2009

Fourth National Report on Human Exposure to Environmental Chemicals

Fourth National Report on Human Exposure to Environmental Chemicals

2009

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

Contents

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

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

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

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

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

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

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

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Introduction

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

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

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and p-Xylene o-Xylene 2 Fourth National Report on Human Exposure to Environmental Chemicals .3-Dichlorobenzene (m-Dichlorobenzene) 1.2'. The process for selection is described at http://www.5.4.3.2'.2'.2’.2'.4'-Tribromodiphenyl ether (BDE 28) 2.5'-Hexabromobiphenyl (BB 153) Volatile Organic Compounds (VOCs) Benzene Chlorobenzene (Monochlorobenzene) 1.2-Dichloropropane 2.2'.1.5-Pentabromodiphenyl ether (BDE 99) 2. 2009 Acrylamide Adducts Acrylamide Glycidamide Total and Speciated Arsenic Arsenic.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 2.3-Tetramethylbutyl] phenol) Triclosan (2.3.4'.4’-Trichloro-2’-hydroxyphenyl ether) Non-dioxin-like Polychlorinated Biphenyls 2.5.2'.2'.4'.2'.4.2-Tetrachloroethane Tetrachloroethene Tetrachloromethane (Carbon tetrachloride) Toluene 1.3'.1.4.4'-Tetrabromodiphenyl ether (BDE 66) 2.cdc.4.5'-Tetrachlorobiphenyl (PCB 49) 2.5'-Hexabromodiphenyl ether (BDE 153) 2.2-Dichlorobenzene (o-Dichlorobenzene) 1.3.2-Trichloroethane Trichloroethene (Trichloroethylene) m.2-bis[4-Hydroxyphenyl] propane) 4-tert-Octyl phenol (4-[1.4.2'4.4’.5'-Tetrachlorobiphenyl (PCB 44) 2.4.4-Tribromodiphenyl ether (BDE 17) 2.5'.1.4.5-Dimethylfuran Ethylbenzene Hexachloroethane Methyl-tert-butyl ether (MTBE) Nitrobenzene Styrene 1.6-Pentabromodiphenyl ether (BDE 100) 2.4.5’.4'-Pentabromodiphenyl ether (BDE 85) 2.4’. Paradichlorobenzene) 1.html.4'.4.1-Dichloroethene (Vinylidene chloride) cis-1.3.5.4'-Tetrabromodiphenyl ether (BDE 47) 2.4-Dichlorobenzene (p-Dichlorobenzene.2-Dichloroethane (Ethylene dichloride) 1. Chemicals reported for the first time in the Fourth National Report on Human Exposure to Environmental Chemicals.4.6-Heptabromodiphenyl ether (BDE 183) 2. Table 1. Total Arsenic (V) acid Arsenobetaine Arsenocholine Arsenous (III) acid Dimethylarsinic acid Monomethylarsonic acid Trimethylarsine oxide Disinfection By-Products (Trihalomethanes) Bromodichloromethane Dibromochloromethane (Chlorodibromomethane) Bromoform (Tribromomethane) Chloroform (Trichloromethane) Environmental Phenols Benzophenone-3 (2-Hydroxy-4-methoxybenzophenone) Bisphenol A (2.4.2-Dichloroethene Dichloromethane (Methylene chloride) 1.6.What’s New in this Report What’s New in this Report In this Fourth Report.4'.2'3.4'.5.4.1.2'.gov/exposurereport/chemical_selection.6'-Hexabromodiphenyl ether (BDE 154) 2.2.1-Dichloroethane 1.3’. 75 new chemicals are added for the 2003-2004 survey period and are listed in Table 1.2-Dichloroethene trans-1.2-Dibromo-3-chloropropane (DBCP) Dibromomethane 1.1-Trichloroethane (Methyl chloroform) 1.

4-dichlorophenol and 2. Details of this procedure are provided in Appendix A.5-dichlorophenol for the 1999-2002 survey periods.What’s Different in this Report What’s Different in this Report The Fourth Report uses a new procedure to estimate percentiles when the percentile estimate falls on a value that is repeated multiple times (e.. 2003-2004) have been re-computed by use of this improved procedure. 2003-2004 data for these other pesticides will be provided on this website as soon as they are available. Some results reported previously have been changed or removed due to improvements in analytical measurement or recognition of an analytical issue (e. Only slight differences should be noted when one compares the recomputations to previous releases of the Report. Explanations for each change are provided in Appendix B. 2001-2002. urinary 2. Percentiles for all three NHANES survey periods (1999-2000. Affected analytes were serum beta-hexachlorocyclohexane for the 2001-2002 survey period.. and polycyclic aromatic hydrocarbons (PAHs) for one or more of the 1999-2002 survey periods. the presence of an interference) that produced results of inadequate quality. Data for other pesticides are included only for 1999-2000 and 2001-2002.g. and these data will be included in the next release of the Report. Fourth National Report on Human Exposure to Environmental Chemicals 3 .g. five results that all have the value 90.1). 2003-2004 data for the organochlorine pesticides and the dialkyl phosphate organophosphorus insecticides are included in the Report.

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

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

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

Therefore. This improved procedure makes each repeated value unique by adding a unique negligibly small number to each repeated value. Taylor JK. Boca Raton (FL). Lewis Publishers. 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. Fourth National Report on Human Exposure to Environmental Chemicals 7 . we have improved the procedure for estimating percentiles to better handle this situation. Appendix A gives the details of the new procedure for estimating percentiles. occasional percentile estimates may differ slightly in the current Fourth Report than in the Third Report. 1987.Data Sources and Data Analysis Report.

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

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

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

interval) 61.9 (54. see Data Analysis section) for Survey year 03-04 is 3. 2006).3) 70. Commercially.0 (53.6 (51.6) 71. 2004).7) 58.1-61. EPA.4-89. Since acrylamide has limited volatility and high water solubility.4-60.2-59.8 (52.2-91..1) 55.2) 57.9-105) 86.4) 57. Smaller scale applications of polyacrylamides include additives to paperboard used for food packaging. 2005). FDA.5 (44.0 (67. Natural substances in the food are converted to acrylamide.1-57. 2002).7) 75th 79.5 (79. gels. These estimated intakes are hundreds of times lower than occupational exposures.0 (57. and peripheral neuropathy following chronic Acrylamide Geometric mean and selected percentiles of hemoglobin adduct concentrations (in pmol/g hemoglobin) for the U.1 (83. but can covalently bind to form adducts with proteins. environmental releases of acrylamide can enter aquatic systems and soils where it degrades within days and does not bioaccumulate (U.7) 54.2-118) 98.1-64.2-70. 2006. acrylamide is synthesized and used in the production of polyacrylamide polymer. although additional exposures from cosmetic products could add a similar amount (NTP-CERHR.1) 101 (95.2 (62.0) 85.4-60.4-83.4) 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. and in some cosmetics.0 (69.7 (65. and in the synthesis or compounding of dye materials. 79-06-1 General Information Acrylamide is a small organic molecule existing as a white crystalline powder in its pure state.9-61.2-77.6-108) 61.8 (91. 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. Animal studies indicate that acrylamide is well absorbed.8 (57..0-115) 156 (120-203) 146 (129-163) 149 (125-179) 218 (172-271) 197 (172-223) 1792 1874 2994 Limit of detection (LOD. as an absorbent in disposable diapers.0 μg/kg for adults (FAO/ WHO.1 (88. EPA.S. FAO/WHO.5-80.9) 63. and well below doses known to cause nerve damage or carcinogenicity in animals. drinking water. it was discovered that acrylamide is formed when starch-rich foods.9 (69. Recently. In the general population.7) 73.4 (54.7-60.3 (53. and from dermal contact with products that contain residual acrylamide.9) 75.4 (51. in permanent press fabrics..S. 2005).6-66.6) 90. In 1997.2) 57. widely distributed in tissues. 2005.2 μg/kg/day (U.0-58. such as potatoes and some grains. Acrylamide is not thought to accumulate in the body at environmental doses.0-66.2 (75. EPA reference dose of 0.3-2.4 (54.0) 57.0-108) 152 (139-175) 126 (111-142) 108 (86.7 (58. the main source of exposure is from the diet.S.S. are heated at temperatures used for frying and baking. Fourth National Report on Human Exposure to Environmental Chemicals 11 .1) 62.1 (52.1 (73.6) 50.6) 73. 1990.4 (53.7) 96.6-61.0. and cosmetics (NTP-CERHR. 2005).6 (81.6-65.3-71. Survey Geometric mean (95% conf. ocular and dermal irritation from direct contact with acrylamide containing materials.1 (47.3) 86.6) 90th 141 (124-155) 03-04 03-04 03-04 03-04 03-04 03-04 03-04 59. Elimination occurs mainly in the urine as mercapturic acid conjugates. 2005).0-49.S.6 (56.6-75.9) 57.4) 57. but are generally above the U.5-85. Fennell et al.8-57.1) 53. People may be exposed to acrylamide from foods. 217 million pounds of acrylamide were produced commercially in the U.1-64.2-67.5) 58.6-104) 82.3 (55.8 (81.9 (60. smoking.7 (55.9) 58.2-114) 163 (147-191) 96. acrylamide has produced upper airway irritation following inhalation of high levels.1) 46.Acrylamide Acrylamide CAS No. and binding agents.8-55. mineral processing.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. and is either metabolized to the reactive epoxide.3) 63.4 (59. 2004.2 (58. 2005).5 (74.7-64. Tareke et al.7 (63. 1994). (NTP-CERHR.5) 66.5 (52. soil conditioners.4-76.9-52. and an average daily intake is estimated as 0.2-93. in some sealing grouts. glycidamide. Polyacrylamides are useful water-compatible polymers used in water treatment. pulp and paper production. population from the National Health and Nutrition Examination Survey. or to glutathione conjugates (Calleman et al. In humans.4) 100 (89.

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 64.9-77.2) 55.8 (44. Puppel et al.4) 46. 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. uterine. reproductive effects (reduced litter size. 2005) have been demonstrated in animals..9) 75.9) 87. scrotal.1-62..4) 53.1-56.7-62.6-62. Glycidamide Geometric mean and selected percentiles of hemoglobin adduct concentrations (in pmol/g hemoglobin) for the U.7 (57. 2005.. fetal death.7) 74.9 (81.4) 83. 2006). EPA at: http://www.4-59.8) 45.2) 87. 2008).9-64.6-90.3) 59. 2005). Puppel et al.3-101) 95.1) 56. Mucci et al.4-98. and to increase DNA reactivity when glutathione availability is reduced (Klaunig et al.3) 59. 2005) and sperm DNA adducts (Xie et al. and neuronal DNA reactivity (Doerge et al. 2009).1 (66. altered gene expression in testicular tissues (Yang et al. 2005.1 (82.0 (80. 2005.0) 94.5 (83.1) 62. 2002.0-62. 2002. Vesper et al.. Adducts are formed when either acrylamide or glycidamide react to form a permanent covalent bond with hemoglobin in the blood. Rice. In addition. gov/iris/ and from the Food and Agriculture Organization of the United Nations and WHO at: http://www. see Data Analysis section) for Survey year 03-04 is 4.2 (56. Hagmar et al. U..8) 60.0. 1997.who.. Several of these studies have shown that smokers have adduct levels that are three to fourfold higher than non-smokers. although different analytic methods can affect results.4-103) 79. 2005. 2005.4 (57. 2008).epa.7) 90. Maniere et al.7 (87.9) 65. respectively) are markers of integrated acrylamide exposure over the preceding few months.4 (81.pdf. population from the National Health and Nutrition Examination Survey.4 (61. 2005. 2005). 2006) have been demonstrated after acrylamide dosing.8 (51. to increase the unscheduled synthesis of DNA in tumor susceptible tissues (Klaunig et al.7 (61.3 (56.4 (56.1) 60. 2006).7 (84. U.5) 71.3) 59. 2005.7-64.7) 60.8-48.S. 2005).2) 65.0 (52. Acrylamide is clastogenic and can produce dominant lethal mutations.S.9-62..8-49. Animal studies have shown that acrylamide can cause nerve damage (neuropathy).0) 118 (103-126) 121 (112-134) 113 (94..9 (58.5) 87.0 (75.1-70.9 (57. thyroid. adrenal.Acrylamide occupational exposures.4-65. levels of AHA adducts decline but may remain detectable for several months (Hagmar et al.9-76. After exposure ceases. probably through its epoxide metabolite.2-91....0-93.9-78.5-94.S. interval) 59.S. male germinal cell injury. 2005. Axonal degeneration. 2003.1 (56. 2006. 2004)..2-90.5-64. Klaunig et al... 2005).5 (42.9) 59. Biomonitoring Information Acrylamide and glycidamide hemoglobin adducts (AHA and GHA...9-138) 143 (130-159) 96. most non-smokers had levels less than about 100 pmol/gram hemoglobin. IARC classifies acrylamide as probably carcinogenic to humans. 2004. EPA.1-60.int/ ipcs/food/jecfa/summaries/summary_report_64_final.4 (90.2 (72.5-92.5) 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.3-78.8-61.1 (57.4 (51.7) 61. 2001). Schettgen et al. 1997..3) 85. Survey Geometric mean (95% conf. The degree of formation of the more toxic glycidamide and levels of GHA can be influenced by polymorphisms in several of the enzymes that metabolize acrylamide (Duale et al..1) 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 59.6-64.5 (56..6 (90.2-68. presynaptic nerve terminal binding (LoPachin.6 (66.5 (59.5) 75th 85. and cancer (mammary. EPA. NTP-CERHR.1 (70. Younger children may have slightly higher levels possibly due to increased intake of acrylamide-containing foods relative to body size (Dybing et al. glycidamide (NTP-CERHR. Glycidamide has been shown to react with DNA (Doerge et al. 2005.5-66.0 (70. Vesper 2005) and smoking (Bergmark.. Additional information is available from U. 12 Fourth National Report on Human Exposure to Environmental Chemicals . 2005. Schettgen et al. and other sites) (FAO/WHO.2 (63. 2005. dominant lethality).5) 90th 130 (120-141) 03-04 03-04 03-04 03-04 03-04 03-04 03-04 71. AHA levels have been shown to increase with dietary intake (Hagmar et al.7-86.

Bruze M.. Yang JS. Tornqvist M. Zhang S. Adv Exp Med Biol 2005. Simultaneous analysis of hemoglobin adducts of acrylamide and Fourth National Report on Human Exposure to Environmental Chemicals 13 . Food and Drug Administration (FDA). 2/3/09 Hagmar L. Chicago.who. February. 2001). et al. Granath F. Churchwell MI. Calleman CJ. Bergmark E. McDaniel LP. LoPachin RM. Toxicol Sci. Determination of hemoglobin adducts in humans occupationally exposed to acrylamide. J Agric Food Chem 2008.561:21-37. 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. Relationships between biomarkers of exposure and neurological effects in a group of workers exposed to acrylamide.27(4):219-226. AHA levels were several fold to several hundredfold higher than levels in non-exposed non-smokers (Bergmark et al. Scand J Work Environ Health 2001.int/ipcs/ food/jecfa/summaries/summary_report_64_final.Acrylamide In occupational settings. Andersen M. 2009 Jan 8.10(1):78-84. Mutat Res 2005. gov/~dms/acrydata. Mutat Res 2005.pdf. 1993.580(1-2):119-129. Health effects of occupational exposure to acrylamide using hemoglobin adducts as biomarkers of internal dose. Monograph on the Potential Human Reproductive and Developmental Effects of Acrylamide. Adv Exp Med Biol 2005. Human exposure and internal dose assessments of acrylamide in food. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. et al. Paulsson B. [Epub ahead of print] Dybing E. Nordander C. Mucci LA. Aprea P. Differences in hemoglobin adduct levels of acrylamide in the general population with respect to dietary intake. Rosen I. Osterman-Golkar S. Beland FA. Wirfalt E. Bridson WE. and 39% of workers with levels above 1000 pmol/gram hemoglobin had these symptoms (Hagmar et al. DNA damage and DNA adduct formation in rat tissues following oral administration of acrylamide. Toxicol Sci 2005. Toxicol 2005. Snyder RW. NIH Publication No.3:406-412. Acrylamide neurotoxicity: neurological. et al. Hagmar L. morphological and molecular endpoints in animal models.43:365–410. Available at URL: http://cerhr. Chem Res Toxicol 1997 Jan. Costa LG.. et al.120(1):45-54. 2/3/09 Klaunig JE.. Calleman CJ. smoking habits and gender. Fennell TR. Acrylamide intake through diet and human cancer risk.. Illinois. Available at URL: http://www. Wu Y. Available at URL: http://www. 2001. Spicer R.561:49-62. In another study. Bergmark E.Toxicol Appl Pharmacol 1994. Toxicol Appl Pharmacol 1993. and Research Strategies. Doerge DR. Kamendulis LM. National Toxicology Program. Godard T. Food Chem. Laurentie M.niehs. Fennell TR. Guffroy M. Perez et al. He F.580(1-2):157-165. Metabolism and hemoglobin adduct formation of acrylamide in humans. Acrylamide is metabolized to glycidamide in the rat: evidence from hemoglobin adduct formation. Bergmark E. Mutat Res 2005. Mechanisms of acrylamide induced rodent carcinogenesis.pdf. 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. Tian G. 6013-6019. Uncertainties. Kautiainen A.. Center for the Evaluation of Risks to Human Reproduction (NTP-CERHR). 054472.85:447-459. 2/3/09 Perez HL. 64th Meeting: Summary and Conclusions (FAO/WHO). 8-17 February 2005. Cheong HK. DNA adducts derived from administration of acrylamide and glycidamide to mice and rats. Survey data on acrylamide in food: individual food products. Churchwell MI. Italy.cfsan. symptoms of numbness or tingling in the extremities did not occur in exposed workers whose AHA levels were below 510 pmol/gram hemoglobin.56. July. Malmberg B. 2006. Bjellaas T.126(2):361-371. Haugen M. smokers and nonsmokers.html#u1004. Twaddle NC. Axmon A. Doerge DR. Biomarkers of human exposure to acrylamide and relation to polymorphisms in metabolizing genes. Summer SCJ. da Costa GG. Burgess J. The Updated Exposure Assessment for Acrylamide. 1994). 2004 Acrylamide in Food Workshop: Update Scientific Issues. et al. 2005. Rome.fda. April 13-15. Hemoglobin adducts of acrylamide and acrylonitrile in laboratory workers. Alexander J. Tornqvist M. Duale N.nih.580(1-2):131-141. Magnusson AL. Chem Res Toxicol 1990. Hagmar et al. Joint FAO/WHO Expert Committee on Food Additives. 2004. Farmer PB. Calleman CJ. Finding a measurable amount of acrylamide or glycidamide hemoglobin adducts in blood does not mean that these levels of acrylamide or glycidamide hemoglobin adducts cause adverse health effects. References Bergmark E. 1999). CFSAN/Office of Plant and Dairy Foods. Wilson KM. Maniere I. Paulsen JE.gov/chemicals/ acrylamide/Acrylamide_Monograph. DiNovi M and Howard D. He F. Costa LG. Becher G.

epa. Yang HJ. Drexler H. Weiss T. Angerer J.S. Han DU. EPA). Agudo A. Ospina M. 2/3/09. U.561:89-96. Letzel S. Broding HC. Vesper HW. Gray JG. Slimani N. 2/3/09 Vesper HW. Angerer J. Karlsson P. Mutat Res 2005. Liu K. Chemical Summary for Acrylamide. propylene oxide. A first approach to estimate the internal exposure to acrylamide in smoking and non-smoking adults from Germany. Lee SH. Marko D. EPA). Adduction of biomacromolecules with acrylamide (AA) in mice at environmental dose levels studied by accelerator mass spectrometry. Adv Exp Med Biol 2005. Schettgen T. Tjønneland A. Determination of haemoglobin adducts of acrylamide and glycidamide in smoking and non-smoking persons of the general population.epa. acrylonitrile and acrylamide-biomarkers in occupational and environmental medicine. Angerer J. Rydberg P. Choi JH. Acrylamide. Toxicological effects of acrylamide on rat testicular gene expression profile. Ospina M. Analysis of acrylamide. Automated method for measuring globin adducts of acrylamide and glycidamide at optimized Edman reaction conditions. Int J Hyg Environ Health 2003. J Agric Food Chem 2002. Environmental Protection Agency (U. Meyers T. Anal Biochem 1999. Benetou V. September. Rice JM. Rapid Commun Mass Spectrom 2006. Lee MH.274(1):59-68. Mutat Res 2005 Feb 7. Cross-sectional study on acrylamide hemoglobin adducts in subpopulations from the European Prospective Investigation into Cancer and Nutrition (EPIC) Study.207(6):531-9.gov/iris/subst/0286. Tareke E.gov/chemfact/s_acryla. Schettgen T. Available at URL: http://www.htm.20(6):959-64. 1994.Acrylamide glycidamide by gas chromatography-mass spectrometry. Available at URL: http://www. The carcinogenicity of acrylamide.S. Han CH.50(17):4998-5006. Tjaden Z. Schettgen T. Chae C. a carcinogen formed in heated foodstuffs.580(1-2):3-20. J Agric Food Chem 2008. Sun H.S.580(1-2):71-80.S. Integrated Risk Information System (IRIS). Environmental Protection Agency (U. Kutting B. revised 1/3/06.134(1-3):65-70.56(15):6046-53. Washington (DC). Hallmans G. Rossbach B.19(4):527-34. Fueller F. Vesper HW. Hemoglobin adducts of ethylene oxide. Toxicol Lett 2006. Licea-Perez H. Xie Q. Fu D. Office of Pollution Prevention and Toxics. Tornqvist M. et al. Ingham L. et al. Puppel N. DNA strand breaking capacity of acrylamide and glycidamide in mammalian cells.163(2):101-8. Drexler H. Int J Hyg Environ Health 2004.txt. 14 Fourth National Report on Human Exposure to Environmental Chemicals . U. Eriksson S. Toxicol Lett 2002. Myers GL. Reprod Toxicol 2005. Smith A. Liu Y. Meyers T. Pilot study on the impact of potato chips consumption on biomarkers of acrylamide exposure. Ding X. Drexler H. Jin Y.206(1):9-14.

090-.120 (.66 (1.48-2.12 (2.070-.104-.066 (.160 (.14) .180 (.050 (.126) . Cigarettes contain about 1.50-1.39) 3.150) .99) 2.360) .04 (1.220-.220) .120 (.23 (2.57) 2.260) 1.17 (1.054 (.77 (1.68) .060 (.S.201) .96-4.060-.060 (<LOD-.050 (<LOD-.190-.052 (<LOD-.090-.690 (.53 (1.030-. The smoke produced by burning tobacco contains at least 250 chemicals that are toxic or carcinogenic.20) 1.015.66) 1.160 (. DHHS.820) .88 (.600-1.77 (1.043-. DHHS.063) .200) 1.05 ng/mL.63-2.20 (.310) 90th 1.02 (.87-3.22) 2.137-.142-.071) .302) . 83% of measurements had an LOD of 0.99) 2.05.080) < LOD .43 (1.990 (.180) .089) Age group 3-11 years 99-00 01-02** 03-04 .85 (1.910-1.047-.154-.23 (1.060-.076-. and more than 50 compounds present in ETS are known or reasonably anticipated to be human carcinogens (NTP.505 (.070 (<LOD-.960-1.62) 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.110) .55 (1.510 (.015 ng/mL.44) 2.96 (1.00) .44) 2.110 (.100-.44 (1. respectively.068) .S.280 (.080-.65 (1.120-. stroke.40) .050-.68 (1.60-2.997-3.163) .21 (.02) 1.230) . Persons exposed to secondhand tobacco smoke (environmental tobacco smoke [ETS]) may have adverse health effects that include lung cancer and coronary heart disease.17 (.95) 1.621-1.312) .050) .710 (.088-.110 (.061) < LOD .084) .840) 3.70-2. and 17% had an LOD of 0.057-.540-.790) .63 (2.01) 3.15 (2.70) 2. cardiovascular disease.54 (1.580-1.68) 2.630 (.78) 2.140 (.090-.131 (.726) .32) 1.39 (1. ear problems. population from the National Health and Nutrition Examination Survey.44 (2.14-1.730 (.20) .120-.300) .350 (.050-. Fourth National Report on Human Exposure to Environmental Chemicals 15 .059-.26-1.470-.175 (. and various other disorders (U.234) .086 (.070) .33-2.30) 2.130 (.Cotinine Cotinine CAS No.50 (1.48-3.060 (<LOD-.144 (.54) 1.506 (.190-.00) 1.164 (.5% nicotine by weight (Kozlowski et al.030-.050 (<LOD-.09-3.110-.164 (.197) . producing roughly 1–2 mg of bioavailable nicotine per cigarette (Benowitz and Jacob.50-4.110 (.148-.14) .93) .040 (.30) 2.220) .620 (.19-2.770-1.060) . which may vary for some chemicals by year and by individual sample.053 (<LOD-.310-1. and 0.066-.193) .140-.950-1.110 (.900-1.21-1.12-4.058 (. 1998).068) .28) .110-.180) .16) .47-3.160) .210 (.670) .580) .09-2.260-1.190-.047-.120) .040 (.480-1.145) .160-.020-.79) 3.19) .50) 3.20-2.040 (.187) .350-.120 (.950 (.49) 1.066) .740-1.160) .620-1.070) .059-.860 (.49) 1.630 (.75) 1.520 (.080 (.12) 1.050 (<LOD-.30) * . 2004).137 (.580 (.080-.76 (1.96) 2.42 (1.030-.080) < LOD < LOD .110 (.428-.167 (.94) 1.23 (.45) 1.087-.11) .106-.180) .84-3.080-.140 (.308 (.400-.087 (.180) .850 (.500 (.625) .22) 2789 3152 2937 3210 3667 3383 Females Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 * .120 (.110-.071 (.130) .32-2. 486-56-6 Metabolite of nicotine (a component of tobacco smoke) General Information Tobacco use is the most important preventable cause of premature morbidity and mortality in the United States.S.077) .533-.28-1.770) .075 (.198) * .060-.240 (..38-2. acute respiratory illness.12 (1.42-4.080-.213) .230 (.110) . acute respiratory infections.34 (1. < LOD means less than the limit of detection.410) .153-.20 (1.930 (.077) .094) .62 (2.073) < LOD .080 (.163 (. 2006).120 (.15) 2.920 (.35 (2.21-1.310) . Survey Geometric mean (95% conf.050) .660) . maternal exposure during pregnancy can result in lower birth weight.216 (.060 (.310-1.108) * .54) size 5999 6819 6320 Total years 99-00 01-02** 03-04 50th .18-3. and 03-04 are 0.77 (2.19) 1.139) * .05) 1. and exacerbated asthma (U.23-2.54 (1.49) 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.89) 1.800 (.81-2.01 (1.160 (.070) 75th .53-4.450-. The consequences of smoking and of using smokeless tobacco products are well known and include an increased risk for several types of cancer.02) 1.17) .180) .630 (.062 (.124 (.030 (.770) .320) .115-.480-.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 .050 (<LOD-.740-1.990) .66-3.040-.040-. 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.087) < LOD < LOD .540 (. Children exposed to ETS are at increased risk for sudden infant death syndrome. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.350-.83-2. 2004). see Data Analysis section) for Survey years 99-00.430-1.370-.32-2.55-2.150) .92 (1.140-.188) .570-1.180 (.052 (<LOD-.88 (1. emphysema.570 (. ** In the 2001-2002 survey period.09-3.111-.

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

Cotinine as a biomarker of environmental tobacco smoke exposure. 1999-2002. Pirkle JL. Turner DM.gov/eid/rmca/critdocs/ criteriadoc/33. J Pharmacol Exp Ther 1999.114(6):853-858.S. Pollack HA. George CF. et al. Giovino GA.gov/ntp/roc/eleventh/profiles/ s176toba. available at URL: http://mtn. [online]. Filter ventilation and nicotine content of tobacco in cigarettes from Canada. 1988-1991.S. Current Intelligence Bulletin 54: Environmental tobacco smoke in the workplace. Herrera B.291(3):1196-1203. International Agency for Research on Cancer. Brody DJ.280:135-140. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Modin G.S. Aiba M.275:1233-1240. Benowitz NL. Jacob P. Houseman TH. Strauss WJ. Kira S.fr/ENG/Monographs/ allmonos90. Herrera B. Jacob P III. Mowery PD. Int Arch Occup Environ Health 1991. Tob Control 1998. Atlanta (GA): 2005. Vol 38.Cotinine and public health officials determine whether people have been exposed to higher levels of ETS than are found in the general population. Bernert JT. Dollery CT. U. Warner K. Clin Pharmacol Ther 1994. JAMA 1998.94(2):314-320. National Center for Fourth National Report on Human Exposure to Environmental Chemicals 17 .4:313-316. DHHS). National Institute for Occupational Safety and Hygiene (NIOSH). Department of Heath and Human Services. Racial/ethnic differences in serum cotinine levels among adult U. Benowitz NL. 4/13/09 International Agency for Research on Cancer. Health Effects of Exposure to Environmental Tobacco Smoke: The Report of the California Environmental Protection Agency.18:188-204. Giovino G. Benowitz NL.php. Vol 83. IARC Monogr Eval Carcinog Risks Hum. Coordinating Center for Health Promotion. Sosnoff CS.pdf. Available at URL: http://www. Trends in the exposure of nonsmokers in the U.iarc. Nicotine metabolism and intake in black and white smokers. Ethnic differences in N-glucuronidation of nicotine and cotinine. 4/13/09 Perez-Stable EJ. Perez-Stable EJ. Environ Health Perspect 2006. Third National Report on Human Exposure to Environmental Chemicals.gov/library/ secondhandsmoke/.S Department of Health and Human Services (U. Brody DJ. Schwartz SS. Office on Smoking and Health [online] 2006. population to environmental tobacco smoke: the Third National Health and Nutrition Examination Survey.php. Tobacco Smoke and Involuntary Smoking. and the United States. Pechacek TF. Mehta NY.fr/ENG/Monographs/allmonos90.gov/tcrb/monographs/10/. Centers for Disease Control.pdf. Metabolism and disposition kinetics of nicotine. Pechacek TF. Centers for Disease Control and Prevention.cancer.280:152-156. U. Absorption and metabolism of nicotine from cigarettes. Summary of Data Reported and Evaluation [online] 1986. Available at URL: http://ntp. 2004. 4/13/09 Iwase A. Respiratory nicotine absorption in non-smoking females during passive smoking. Bernert JT. Biomonitoring data can also help scientists plan and conduct research about exposure to ETS and about its health effects. Exposure of the U. Metabolism of nicotine to cotinine studied by a dual stable isotope method. Am J Public Health 2004. Lewis PJ. Smoke-free laws and secondhand smoke exposure in US nonsmoking adults. Available at URL: http://monographs. IARC Monogr Eval Carcinog Risks Hum. Tob Control 2006. 1999. Pickett MA. National Toxicology Program (NTP). Richter PA. Caraballo R.S Department of Health and Human Services (U.cdc. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Vogler GP. 4/13/09 U. The Health Consequences of Involuntary Exposure to Tobacco Smoke: A Report of the Surgeon General — Executive Summary. June. The Health Consequences of Smoking: The Surgeon General’s Report—Executive Summary. Summary of Data Reported and Evaluation [online] 2004. 1988-1991.S. Pharmacol Rev 2005.7:369-375. Available at URL: http://monographs. iarc. JAMA 1996. the United Kingdom. Fong I. 4/13/09 Centers for Disease Control and Prevention (CDC). 4/13/09 National Cancer Institute (NCI). Sweeney CT.niosh. et al.S. Kozlowski LT. Flegal KM.surgeongeneral. U. Jacob P III. Decrease in the prevalence of environmental tobacco smoke exposure in the home during the 1990s in families with children. Tobacco related exposures.56:483-493. Caudill SP. National Center for Chronic Disease Prevention and Health Promotion. Pirkle JL. DHHS). BMJ 1975. Benowitz NL. Smoking and Tobacco Control Monograph 10 [online].nih.63:139-43. Coordinating Center for Health Promotion. Soliman S. Benowitz NL.niehs. 1991. Epidemiol Rev 1996. Maurer KR.S. References Armitage AK.15:302-307.S. Department of Heath and Human Services.57(1):79115. Available at URL: http:// cancercontrol. Etzel RA. cigarette smokers: the Third National Health and Nutrition Examination Survey. population to secondhand smoke: 1988-2002. Hukkanen J. 11th ed. In Report on Carcinogens. Jarvis MJ. JAMA 1998. Schober SE. Jacob III P. Centers for Disease Control and Prevention. Curtin LR. Tobacco Smoke.

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

N.140) < LOD .130-. General population exposure to DEET occurs from skin application and from inhalation of aerosol formulations. DEET is metabolized via hydroxylation and dealkylation pathways and eliminated in the urine within approximately 24 hours (Selim et al. 2002).110 (<LOD-. DEET can be applied to clothing and the skin to repel biting insects. including seizures and encephalopathy. Its use is recommended for prevention of several vector-borne diseases. 2005).epa. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 2003).250) < LOD .170 (.100-.130-.120-.S. Exposure can also occur from consuming food contaminated by DEET on hands or that was sprayed nearby. About 3-8% of dermally applied DEET is absorbed.130 (.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 . 134-62-3 General Information N. DEET has low acute toxicity.100-.EPA at: http://www.110-.110 (.190) < LOD .180 (.N-Diethyl-meta-toluamide (DEET) CAS No. DEET is not registered for use on agricultural commodities.100 (<LOD-.140) < LOD . Fourth National Report on Human Exposure to Environmental Chemicals 19 .gov/pesticides/.. (Kolpin et al.140) < LOD . DEET is also used in combination with dermal sun screens (U..100-. DEET is not genotoxic.110 (.160) < LOD .N-diethyl-meta-toluamide (DEET) is an insect repellent that was first marketed in 1957. Most reports of adverse effects from overexposure to DEET involve skin reactions (Bell et al.130 (. Human health effects from DEET at low environmental doses or at biomonitored levels from low environmental exposures are unknown.130-.140 (. and it has not been rated by IARC or NTP with respect to human carcinogenicity. There are over 225 insect repellents brands containing DEET.S.130-.130 (. (U.S.240) < LOD . 1998). 1998). population from the National Health and Nutrition Examination Survey.449 and 0.1.EPA. have been reported as result of self-poisoning by ingestion or excessive dermal application.110 (. DEET is not a developmental or reproductive toxicant in animals (U.180) < LOD .270) 688 678 518 700 598 956 Limit of detection (LOD. Sudakin and Trevathan.220 (. Urinary N.N-Diethyl-meta-toluamide (DEET) N.560) < LOD . People in outdoor occupations may apply DEET more frequently or use higher concentration formulations resulting in higher levels of exposure. 1995.220) 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 .100-. which may vary for some chemicals by year and by individual sample. Additional information is available from U.130) < LOD . One survey detected DEET in 74% of sampled streams in the U.210) 480 580 672 829 825 1126 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .170 (.180 (.100-.130) < LOD . and they range in concentration from 4% to 100%.180 (. 2002). see Data Analysis section) for Survey years 99-00 and 01-02 are 0. 2003). Survey Geometric mean (95% conf.120-.210 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD .110 (.S.EPA.N-Diethyl-meta-toluamide (DEET) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.S.. Neurological effects in humans.140-. EPA. < LOD means less than the limit of detection.110 (<LOD-.110-.100-.150) < LOD . but higher DEET concentrations and different formulations may result in greater absorption (Sudakin and Trevathan.520) < LOD .S. After absorption.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 .

population from the National Health and Nutrition Examination Survey.230-.410 (.690 µg/L were measured in eight park employees who applied 71% DEET once a day (Smallwood et al.500) 480 580 672 828 825 1126 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .S.490) < LOD . Urinary levels of DEET were characterized only at the 90th and 95th percentiles of the U. representative subsamples from NHANES 2001-2002.190 (.N-Diethyl-meta-toluamide (DEET) Biomonitoring Information Urinary levels of DEET reflect recent exposure.190-.200 (.. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD .N-Diethyl-meta-toluamide (DEET) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.270 (.240) < LOD .280-1.N.350-. Urinary DEET levels as high as 5.630) < LOD .280 (. In this survey period.130 (<LOD-. Urinary N.230) < LOD . Survey Geometric mean (95% conf.250) < LOD .480 (.330 (. 20 Fourth National Report on Human Exposure to Environmental Chemicals .330 (.290-.S.580) 964 1191 1013 1343 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .410-. 2007).170-.410 (.640 (.270) < LOD .250-.440) < LOD . DEET was detected in 10% of 60 Latino children in eastern North Carolina farm worker households (Arcury et al. 1992).320) < LOD .300 (.550) 688 678 518 699 598 956 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.270-.500 (.390-. 2005).270 (<LOD-. Biomonitoring studies on levels of DEET provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of DEET than are found in the general population.190 (.140-. the limit of detection was lower than for the NHANES 1999-2000 survey period (CDC.370) < LOD .350) < LOD .500) size 1977 2534 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD 90th .150-.150) < LOD . Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.300) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .93) < LOD ..240-.190 (<LOD-.370-. Finding a measurable amount of DEET in urine does not mean that the level of DEET causes an adverse health effect. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.350) < LOD .250 (.230-.320 (.

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

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

Lynch BS. Shin HC. Reidy JA. DirectorateGeneral Health and Consumer Protection.59(9):625-628. Reidy JA. Ema M.nih.69(22):2611-2625. 2003. Pyo MY. Chem Res Toxicol 2001. Calafat AM..jrc. Matthews JB. Environ Sci Technol 2002. Cunha G. Kawamura N. Life Sci 2001. Munro IC. Caudill SP.nih. Environ Health Perspect 2008. Nippon Eiseigaku Zasshi 2004. Koulova AI. Gender differences in the levels of bisphenol A metabolites in urine. 2/4/09 European Commission.pdf. Measurement of bisphenol A in human urine using liquid chromatography with multi-channel coulometric electrochemical detection. Rhomberg et al. Exposure of the U. Hanaoka T. and other organic wastewater contaminants in U. Leranth. NTP-CERHR Panel Report on Reproductive and Developmental Toxicity of Bisphenol A. 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. Bisphenol A.780(2):365-370. Watanabe C. MacLusky. Hlywka JJ. Yoshinaga J. Kim CS. Urinary concentrations of bisphenol A and 4-nonylphenol in a human reference population. Evaluation of developmental toxicity in rats exposed to the environmental estrogen bisphenol A during pregnancy. Han SY. Estimation of intake level of bisphenol A in Japanese pregnant women based on measurement of urinary excretion level of the metabolite. Hughes C.113(4):391-395. Ecotoxicity and the Environment (CSTEE). U. Available at URL: http://ec. Yang M.pdf . 2/4/09 Fujimaki K. Kim JC. Kim YH. vom Saal FS. Weight of the evidence evaluation of low-dose reproductive and developmental effects of bisphenol A.149:988-994. streams.68(1):121-146.4’-Isopropylidenediphenol (Bisphenol-A) Summary Assessment Report. National Toxicology Program Center for the Evaluation of Risks to Human Production (NTP-CERHR). Environ Health Perspect 2005.10:875-921. Barber LB. NC. Serizawa S. Ikka T.niehs. Available at URL: http://ecb. Kiguchi M. bisphenol A glucuronide. Needham LL. Barr DB. Imai H. Urinary bisphenol A and plasma hormone concentrations in male workers exposed to bisphenol A diglycidyl ether and mixed organic solvents. Howdeshell KL.S. Timms BG. Three-generation reproductive toxicity study of dietary bisphenol A in CD Sprague-Dawley rats. Needham LL. et al.137(3):353-362. and Hardy MP. Bradley S.J. Available at URL: http://cerhr. Barr JR. Brussels. Pharmaceuticals. Arakawa C. National Institutes of Health.35(2 Pt 1):238-254.116(1):39-44. 4. Thomas BF. Proc Natl Acad Sci USA 2005. Hara K.Environmental Phenols References Akingbemi BT. Furlong ET. Ye X. 1999-2000: a national reconnaissance.gov/ntp/htdocs/liason/ LowDosePeerFinalRpt. Italy. Thurman EM. Fujii S. Doull J. Kolpin DW. Available at URL: http://cerhr. 5: 505-523.S. 2008. Ispra.it/DOCUMENTS/ Existing-Chemicals/RISK_ASSESSMENT/SUMMARY/ bisphenolasum325. Han SS. Tsugane S. Reprod Toxicol 2001. Calafat AM. K. 2/4/09 National Toxicology Program’s Report of the Endocrine Disruptors Low-Dose Peer Review (NTP). 2007. Needham LL. C. Rat two-generation reproductive toxicity study of bisphenol A. Haighton LA. May 22. Occup Environ Med 2002.S. National Toxicology Program. Joint Research Centre Institute of Health and Consumer Protection.gov/chemicals/bisphenol/bisphenol. Watanabe S. Cohen JT. Zacharewski TR. November 26. Kroes R. J Chromatogr B Analyt Technol Biomed Life Sci 2002..59(4):403-408. Sottas CM.36(6):1202-1211. Richter CA. In vitro and in vivo interactions of bisphenol A and its metabolite. Regul Toxicol Pharmacol 2002. Keimowitz AR. Wong LY. Ekong J. Myers CB. Department of Health and Human Services. hormones. niehs. Zaugg SD. September.eu/ health/ph_risk/committees/sct/documents/out156_en. Toxicol Sci 2002. et al. Tyl RW. Twomey K. European Commission. 2/4/09 National Toxicology Program Center for the Evaluation of Risks to Human Production (NTP-CERHR). Bisphenol A prevents the synaptogenic response to testosterone in the brain of adult male rats. population to bisphenol A and 4-tertiary-octylphenol: 2003-2004. niehs. Meyer MT.312(2):441-448. Barton L. J Am Dent Assoc 2006.pdf . Belgium.145:592-603. NTP-CERHR Panel Report on Reproductive and Developmental Toxicity of Bisphenol A. Brine DR. National Institute of Environmental Health Sciences. N. Rubin C.102(19):7014-7019. Joskow R. Available at URL: http://ntp. McConnell EE. August 2001. 2/4/09 Ouchi K. et al.gov/chemicals/bisphenol/BPAFinalEPVF112607. Hum Ecol Risk Assess 2004..pdf. Chung MK. An evaluation of the possible carcinogenicity of bisphenol A to humans. Exposure to bisphenol A from bis-glycidyl dimethacrylatebased dental sealants. Koh WS. 2002.nih. Estrogenic chemicals in plastic and oral contraceptives disrupt development of the fetal mouse prostate and urethra. Endocrinology 2004.pdf.Scientific Committee on Toxicity. and Hajszan. 32 Fourth National Report on Human Exposure to Environmental Chemicals . Klinefelter GR. T. Harazono A. Marr MC. Calafat AM. Szigeti-Buck. Endocrinology 2008. with estrogen receptors alpha and beta. Biochem Biophys Res Commun 2003. Cha SW. Furukawa M. Park S.14(2):149-157. Kuklenyik Z. Research Triangle Park.europa. Gray GM. Human Health.

Kim SY.44(4):546-51. Filser JG. Fourth National Report on Human Exposure to Environmental Chemicals 33 . bisphenol-A.147(6 Suppl):S56-69. Food Chem Toxicol 2002. Environ Health Perspect 2005. Jang JY. Vom Saal FS. Chem Res Toxicol 2002. Lordo RA. Csanady GA. Wilson NK. et al. Witorsch RJ.40(7):905-12. An observational study of the potential exposures of preschool children to pentachlorophenol. Chang SS. Biological monitoring of bisphenol a in a Korean population. An extensive new literature concerning low-dose effects of bisphenol A shows the need for a new risk assessment. Arch Environ Contam Toxicol 2003. Environ Res 2007. III. Colnot T. Lee SM. Nagel SC. vom Saal FS. Dekant W. Endocrine mechanisms mediating effects of bisphenol A at levels of human exposure. Welshons WV. Metabolism and kinetics of bisphenol A in humans at low doses following oral administration. and nonylphenol at home and daycare. Morgan MK.Environmental Phenols Volkel W.103(1):9-20.15:12811287. Hughes C. Yang M. Endocrinology 2006. Chuang JC. Sheldon LS.113(8):926-33. Kawamoto T. Low-dose in utero effects of xenoestrogens in mice and their relevance to humans: an analytical review of the literature. Large effects from small exposures.

.357 (. Urinary 4-tert-Octylphenol (4-[1.40) * 03-04 03-04 03-04 .600) 1.50) .600) .70 (1.600-1. The alkylphenol ethoxylates enter the environment through human use of products containing them. Alkylphenols also have been used as plasticizers and antioxidants in plastics and resins. testicular atrophy.40) 1. During the 1980s and 1990s.Environmental Phenols 4-tert-Octylphenol CAS No.70 (1.400 (.00 (1. 2003.200-. which may vary for some chemicals by year and by individual sample.80) 2.40) 1.40 (1. and was quickly eliminated from the blood (Certa et al.20-2.80 (1. Bian et al.500-1.50-2. through sewage. < LOD means less than the limit of detection. In 1999-2000. Saito et al. 2004).60-3.10) 1. Nonylphenol ethoxylates are more commonly used than octylphenol ethoxylates.3.900 (.20) 1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.500) .300 (<LOD-.. have demonstrated estrogenic effects particularly when injected at high doses in animals. and through manufacturing waste streams (Warhurst. 2002).40) 2.300-.000 tons of alkylphenol ethoxylates were produced annually worldwide. Indoor and to a lesser extent.400 (.500) .600-1.20-2.900 (.300 (<LOD-. Octylphenols and nonylphenols can also enter the environment directly from manufacturing waste streams. and some of their degradation products are toxic to aquatic life. 4-octylphenol monoethoxylate was detected in 43.30 (.500) 75th . They are biodegraded to the corresponding alkylphenol (octylphenol or nonylphenol).389 (.600-1. 1995.10 (1. In rats.30) 1.50) 1. textiles.369 (.3-Tetramethylbutyl] phenol) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. is used to manufacture alkylphenol ethoxylates.20 (1. pesticides. and to alkylphenoxycarboxylates.10-2.30 (1.500-1. Commercial formulations of alkylphenol ethoxylates usually contain a mixture of oligomers and isomers.700-1. and emulsifiers.300 (<LOD-. 2000.50) 1.g.2.. population from the National Health and Nutrition Examination Survey.30 (1.60-3.60-3. 2000.40) 2. the various alkylphenols have also been used as emulsifiers and modifiers in paints..70 (1.20-2. Blake and Boockfor. and impaired spermatogenesis (e. an alkylphenol. 2006.10 (.10 (. 1997.80 (1.600) .268-.300 (<LOD-..400) 1. streams in 30 states (Kolpin et al. Human exposure to alkylphenols and alkylphenol ethoxylates may occur through ingestion of contaminated foods (e. 34 Fourth National Report on Human Exposure to Environmental Chemicals . altered neonatal sexual development. These high dose parenteral effects of 4-tert-octylphenol have included altered sex hormone levels and hypothalamicpituitary suppression. see Data Analysis section) for Survey year 03-04 is 0.20-2. including 4-tert-octylphenol.90) 2.299-.20) 2.20-2.20) 314 715 1488 03-04 03-04 * * . 1996).30) 90th 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Ying et al.600) ..800-1.10) 2.30-2..50-3.. over 500.60) 613 652 1092 Limit of detection (LOD.507) * < LOD .900 (.60-3. leading to inhalation as another potential exposure route (Rudel et al. which are anionic surfactants used in detergents. 2002).200-.50) .00 (.497) * .g. Laws et al.30) 2.50) 1. Several alkylphenols.20-2.20) size 2517 Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th .500) . Katsuda et al.90) 2.50 (1. Human health effects from 4-tert-octylphenol or the corresponding octylphenol ethoxylates at low environmental doses or at biomonitored levels from low environmental exposures are unknown.400 (.600-1.477) ..300-.00) 1229 1288 03-04 03-04 03-04 * . and some personal care products.900 (.600-1.S.300 (<LOD-.60-3.600-1.00 (. In the 1990s. industrial cleaners.30 (1.5% of 139 U.500 (.. altered estrus cycles and reproductive outcomes. fish) and drinking water. orally administered 4-tert-octylphenol was well absorbed. and the polyethoxy chain may consist of up to 50 ethoxy units. Less frequently. and from contact with some personal care products and detergents. 140-66-9 General Information 4-tert-Octyphenol. outdoor air may have detectable levels of 4-tert-octylphenol and 4-tert-octylphenol monoethoxylates.1.900 (. to shorter chain alkylphenol ethoxylates. The alkylphenols can bioaccumulate in some fish.60) .S.30 (1.70 (1. several European nations banned the use of alkylphenol ethoxylates in domestic detergents and other uses.60) 1.60-3. did not bioaccumulate.274-.80 (1. Disposition in humans has not been studied sufficiently. impaired steroidogenesis. Survey Geometric mean (95% conf.

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.890-2. Yoshida et al. 2004).78 (1. Sweeney et al.03 (1.02-4.470-1.64 (. the urinary concentrations of 4-tert-octyphenol were near or below the detection limit (Inoue et al.00) 2.06 (2.410 (.31 (1.S.349) * < LOD .40-4.50 (2.15) 1. or their corresponding ethoxylates with respect to human carcinogenicity.25) 90th 1.269 (.500-1. IARC and NTP have not rated octylphenol.78) 3.470) 75th .270-. Fourth National Report on Human Exposure to Environmental Chemicals 35 .384) * .850 (.630-1.25) 2.96-4. 4-tert-Octylphenol is not considered directly genotoxic.260 (<LOD-.610) .33 (2.Environmental Phenols Myllymaki et al.60 (1.276 (..3.05-2. (2008) showed that urinary levels of 4-tertoctyphenol were detectable in slightly greater than half of the participants of the U.43) 1.320 (<LOD-.65-3.31-2..470-1.68-2.620) . 2004.620-1.00) 1. 2001.00) 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 .33) 3.170-.71) 2. Kawaguchi et al.530) .280-.370 (<LOD-.910 (. Calafat et al.570) .43) 1. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.560) .85 (1.53-3.400) .00 (.. population from the National Health and Nutrition Examination Survey. Survey Geometric mean (95% conf.300 (<LOD-.11) 2. 2001).450) .270 (.62 (1.68) 2. 2005. at lower or environmentally relevant doses (Blake et al. Biomonitoring Information Urinary levels of 4-tert-octyphenol reflect recent exposure.62 (1.730-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. representative subsample of NHANES 2003-2004.11) 1.29) 2.540-1. 1999).18-4.. 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.03 (1.40 (1.00) 2.270 (.11-2.207-.740 (. Tyl et al.59) 1.460 (. nonylphenol.41) .67-2.43-3.54) * 03-04 03-04 03-04 .S.59 (1.00 (. 2003.160-.17 (... Urinary 4-tert-Octylphenol (4-[1.81 (1. In a small number of adult Japanese volunteers.740 (. 2000.1.860 (.73) 2.22) .76 (2.450) 1.24) 612 651 1091 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.10-2.08) 1.25-2.337-.78) 1228 1286 03-04 03-04 03-04 * .550-1.770 (.3-Tetramethylbutyl] phenol) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. Nagao et al.199-.62) .420) .380 (<LOD-.03-6.435 (.14) 314 713 1487 03-04 03-04 * * .36-3. It is unclear if estrogenic or other effects occur in animals through oral dosing.20 (1.640-1.

57(2):255-266. population to bisphenol A and 4-tertiary-octylphenol: 2003-2004.37(20):4543-53. Bolt HM. Watanabe G.15(6):683-692. Song L. Blake CA. J Chromatogr B Analyt Technol Biomed Life Sci 2004.116(1):39-44. Boockfor FR. McCoy GL. Yoshimura Y. Thurman EM. Arch Toxicol 1996. Tyl RW. Rudel RA. Taya K. Environ Sci Technol 2003. Infantile 4-tert-octylphenol exposure transiently inhibits rat ovarian steroidogenesis and steroidogenic acute regulatory protein (StAR) expression. Inoue K. Meyer MT. Xu L. and sertoli cell number. Seto H. Millette CF. Ito R. Myers CB. Food Chem Toxicol 2006. Qian J. Toxicol Lett 2001. Reproductive effects in male and female rats from neonatal exposure to p-octylphenol. Roche JF. Maekawa A. An environmental assessment of alkylphenol ethoxylates and alkylphenols. Makino T. Nakagomi M. Exposure of the U.54(1):154-167. Furlong ET. Spengler JD. Chronic administration of the environmental pollutant 4-tert-octylphenol to adult male rats interferes with the secretion of luteinizing hormone.S. Maekawa A. Muller AM. Nair-Menon JU. 2/4/09 Ying GG. Needham LL. Effects of 4-tert-octylphenol given in drinking water for 4 months on the male reproductive system of Fischer 344 rats. Seely JC. polybrominated diphenyl ethers. Williams B. et al. Camann DE. Cooper RL. Barber LB.18(1):43-51. 2003. prolactin. Fail PA. Haavisto TE. Paranko J. Wiegand HJ. Ono H. testis size. Environmental fate of alkylphenols and alkylphenol ethoxylates--a review. Nagao T. Taya K. Available at URL: http:// www. Sweeney T.799(1):119-125. Brine DR. Myllymaki SA. Laws SC. Zaugg SD.207(1):59-68. Ye X. Bodman GJ. 1999-2000: a national reconnaissance. et al.36(6):1202-1211. et al. Katsuda S. Measurement of 4-nonylphenol and 4-tert-octylphenol in human urine by column-switching liquid chromatography-mass spectrometry. Effects of neonatal exposure to a high-dose p-tertoctylphenol on the male reproductive tract in rats. Kawaguchi M. Stir bar sorptive extraction and thermal desorption-gas chromatography-mass spectrometry for the measurement of 4-nonylphenol and 4-tert-octylphenol in human biological samples. Saito I. Wong LY. Irreversible effects of neonatal exposure to p-tert-octylphenol on the reproductive tract in female rats. Brooks AN. Toxicol Sci 2000.30(2 Pt 1):81-95.pdf. Yoshida M. Inoue K. Okada F. Raychoudhury SS. Kolpin DW. Fedtke N. streams.uk/resource/reports/ethoxylates_alkylphenols. Regul Toxicol Pharmacol 1999.co. Indoor air pollution by alkylphenols in Tokyo. Two-generation reproduction study with para-tert-octylphenol in rats.S. Nicol L.165(3):217-226. Blake CA. Reprod Toxicol 2004. hormones. Kawaguchi M. Toppari J. Korn LR. Katsuda S.folliclestimulating hormone. Endocrinology 2000.121(1):21-33. Reprod Toxicol 2001. Brody JG. Wang X.Environmental Phenols References Bian Q.14(5):325-332. Onuki A. Biol Reprod 1997. The toxic effects of 4-tert-octylphenol on the reproductive system of male rats.44(8):1355-1361. Pharmaceuticals. 1995. Anal Chim Acta 486:41-50. Yoshimura S. Chen J. Usumi K. Watanabe G. nonylphenol. Maternal exposure to octylphenol suppresses ovine fetal follicle-stimulating hormone secretion. Estrogenic activity of octylphenol.foe. Environ Int 2002. Reidy JA. and other endocrine-disrupting compounds in indoor air and dust. Toxicokinetics of p-tert-octylphenol in male Wistar rats. and other organic wastewater contaminants in U. Kookana R. 36 Fourth National Report on Human Exposure to Environmental Chemicals . Certa H. Horie M. Boockfor FR.71(1-2):112-122. bisphenol A and methoxychlor in rats. Izumi S. Saito Y. alkylphenols. Toxicol Appl Pharmacol 2000. Marr MC. Carey SA. Yoshida M. Takai N. and testosterone. Toxicol Appl Pharmacol 2005. et al. pesticides. Warhurst AM. Environ Health Perspect 2008. Calafat AM. Indoor Air 2004. Environ Sci Technol 2002. Ferrell JM. Sakui N.28(3):215-226. Karjalainen M. Phthalates. Takenaka A.141(7):2667-2673.

Veldhoen et al. toothpastes. Triclosan has been added to soaps. Lyman and Furia. 2007. but not by race/ethnicity and sex. Triclosan can remain present in the oral saliva for several hours after the use of toothpaste containing triclosan (Gilbert et al. 2008)... Triclosan can be absorbed across skin into the blood stream. 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. Fourth National Report on Human Exposure to Environmental Chemicals 37 .. 2007). IARC and NTP do not have ratings with respect to human carcinogenicity. and has also been impregnated into some kitchen utensils. and wound disinfection solutions.2 µg/L was comparable to the median level (8..S. In 1999-2000. Finding measurable amounts of triclosan in the urine does not mean that the levels of triclosan cause an adverse health effect.. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Calafat et al.. 2007). triclosan was found in 57.. In animal studies.. young girls.. Triclosan has a low bioaccumulation potential in fish. 2000. 1976. General population exposure results from dermal and oral use of products containing triclosan.6% of 139 U.S. deodorants. and medical devices.. 2008 has shown higher levels during the third decade of life and among people with the highest household income. Matsumura et al.. mouthwashes. In a U... There is some concern that widespread use of triclosan and other biocides can alter antibiotic resistance in bacteria (Aiello et al. 2004). representative subsample of NHANES 2003-2004. acne medications. and has not been considered mutagenic or carcinogenic (Bhargava and Leonard. 3380-34-5 General Information Triclosan is a phenolic diphenyl ether used for over 30 years as a preservative and antiseptic agent. In animal and human studies. 2002). the median urinary triclosan level of 7. It acts by inhibiting bacterial fatty acid synthesis. Biomonitoring Information Urinary triclosan levels reflect recent exposure. Calafat et al. Triclosan enters the aquatic environment mainly through residential wastewaters. 1988.. Mezcua et al. In the body it is conjugated to glucuronides and sulfates (Bodey et al. a process that can result in the formation of small amounts of 2. 2007.2 µg/L) of children 6-11 years of age who participated in NHANES 2003-2004 (Wolff et al. it has low acute toxicity. streams sampled in 30 states (Kolpin et al. toys.. In a study of 90 U. 2006). Moss et al. Some reports show endocrine effects are observed in amphibians and fish (Foran et al. 1969). 2005. it is excreted over several days in the feces and urine as primarily as unchanged triclosan (Kanetoshi et al. 1987). Triclosan is not considered teratogenic at maternally toxic doses.S.8-dichlorodibenzo-p-dioxin (Aranami et al. 1996. Human health effects from triclosan at low environmental doses or at biomonitored levels from low environmental exposures are unknown. Triclosan formulations may rarely cause skin irritation.Environmental Phenols Triclosan CAS No. 2000). (Sandborgh-Englund et al. It can be photochemically and biologically degraded.

29-12.32-14.6 (30.2) 13.90-10.43-13.4 (12.1 (45.5) 13.45-10.40-17.3-35.1) 9.3 (9.7 (39.9-61.3 (11.1) 9.0 (36.1 (15.8-60.6-15.6) 12.5) 11.1) 13.45-13.9 (50.9-236) 193 (90.93 (7.70-16.1) 11.6 (10.2 (27.2 (25.55 (4.1) 14.60 (8.5-14.4) 90th 249 (188-304) 03-04 03-04 03-04 8. population from the National Health and Nutrition Examination Survey.0) 9.6-14.9) 32.86-12. Survey Geometric mean (95% conf.4.6) 10.48-10.6-37.20 (7.3-31.4’-Trichloro-2’-hydroxyphenyl ether) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.0 (26.7-318) 224 (186-272) 236 (115-336) 356 (169-580) 385 (308-506) 314 713 1487 03-04 03-04 13.2 (10.6 (12.S.3 (8.0-73.2 (13.2-14.6-111) 33.00-8. population from the National Health and Nutrition Examination Survey.8) 9.0 (8.9) 75th 47.Environmental Phenols Urinary Triclosan (2.2-58.89-11.0-15.4) 357 (225-456) 203 (87.6 (9.0-213) 213 (160-272) 453 (263-1150) 260 (127-513) 358 (276-480) 612 651 1091 38 Fourth National Report on Human Exposure to Environmental Chemicals .4) 73.8-85.50-10.5 (11.8-63.20-13.16 (6.4’-Trichloro-2’-hydroxyphenyl ether) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.4-19.3-67.5) 20.1) 7.20-10.2-46.5-341) 245 (163-334) 597 (372-992) 450 (254-750) 461 (383-527) 613 652 1092 Limit of detection (LOD.3 (26.3) 10.20 (7.7 (14.7) 292 (151-432) 132 (78.4-163) 304 (134-566) 261 (198-317) 157 (113-380) 655 (310-890) 472 (406-522) 314 715 1488 03-04 03-04 16.0) 49.6-65.7 (9.0-19.4-18.6) 237 (175-294) 182 (138-217) 384 (294-506) 336 (225-480) 1228 1286 03-04 03-04 03-04 13.0 (11.2 (37.0 (34.38-18.6) 31.8) 7.1) 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 9.7 (28.0) 65.50) 10.1) 50.6) 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 9.80 (5.8 (21.8-127) 37.40-11.4 (11.9) 8.2) 9.6-14.1-39.5-250) 574 (461-716) 380 (258-430) 1229 1288 03-04 03-04 03-04 14.5) 66.10) 84.1) 9.72-13.S.5-86.3) 6.9 (8.4.2-58.4) 75th 43.8) 14.20-11.60 (6.6-20.6) 39. Survey Geometric mean (95% conf.4 (38.9 (33.3-15.4) 7.4 (32.7 (11.1 (8.4) 25.45 (5. interval) 12.8-112) 30.9) 7.48 (8.54 (8.74 (5.3) 47.30-14.21 (6.82 (8.7) 123 (36. interval) 13.92-12. Urinary Triclosan (2.3.18 (5.2) 12.10-9.00 (4.9 (11.11-11.0-15.1) 9.8) 116 (39.2 (11.4) 51. see Data Analysis section) for Survey year 03-04 is 2.94 (7.7) 10.22-10.6) 90th 212 (172-241) 03-04 03-04 03-04 9.4) 317 (231-433) 144 (96.

Calafat AM.8-dibenzodichloro-pdioxin as a photodegradation product of triclosan in water and wastewater samples.45 Suppl 2:S137-S147.17(5):637-644. Teitelbaum SL. Fourth National Report on Human Exposure to Environmental Chemicals 39 . Aquat Toxicol 2006. Chemosphere 2007. Howes D. et al. streams. Pharmaceuticals. Disposition and excretion of Irgasan DP300 and its chlorinated derivatives in mice.80(3):217-227. Windham G. Ogawa H. Fernandez-Alba AR. Meyer MT. hormones.Environmental Phenols References Aiello AE. Clapson DJ. phthalates. Urinary concentrations of triclosan in the U.23(5):579-583.S. 4. Williams PE. et al. Bennett ER. Wigmore H. Gunderson MP. The oral retention and antiplaque efficacy of triclosan in human volunteers.. Pilot study of urinary biomarkers of phytoestrogens. Zaugg SD. Okui T. Kanetoshi A.4. Erratum in: Aquat Toxicol 2007. Williams FM. Moss T. Katsura E. Ferrer I.24(3):209-218. Odham G. Shiratsuchi H. Nagao Y.116(3):303-307. Food Chem Toxicol 2000. Chelimo C. Lyman FL. Aguera A. Kolpin DW. J Invest Dermatol 1976. Thurman EM. Biol Pharm Bull 2005. et al. Gilbert RJ. Britton JA.7/2. Ebersole R. Needham LL.28(9):1748-1751. Bhargava HN. Sandborgh-Englund G. Br J Clin Pharmacol 1987. Osachoff H. Aranami K.69(20):1861-1873.38(4):361370. Evidence of 2. 1999-2000: a national reconnaissance. Randomized trial of a hexachlorophene preparation and P-300 bacteriostatic soaps.83(1):84. Veldhoen N. Mar Environ Res 2000.67(4):532-537.524:241-247. J Toxicol Environ Health A 2006. Larson EL. Furia T. Benson WH. Hirano M.4’-trichloro-2’hydroxydiphenyl ether). Furlong ET. and phenols in girls. Ye X.115:116-121. Bodey GP.38(2):64-71. Environ Health Perspect 2008. Environ Health Perspect 2007. Toxicology of 2. The bactericidal agent triclosan modulates thyroid hormone-associated gene expression and disrupts postembryonic anuran development. Pinney SM.S. Percutaneous penetration and dermal metabolism of triclosan (2. IMS Ind Med Surg 1969. Environ Sci Technol 2002. Barber LB. Triclosan: applications and safety. Anal Chim Acta 1004. 4’-trichloro-2’-hydroxydiphenyl ether. et al. Ekstrand J. Effects of nonylphenol and triclosan on production of plasma vitellogenin and testosterone in male South African clawed frogs (Xenopus laevis). Wolff MS.66:1052-1056. Hong HC. and other organic wastewater contaminants in U. Readman JW. Am J Infect Control 1996. Matsumura N. Ishibashi H. Wong LY. Consumer antibacterial soaps: effective or just risky? Clin Infect Dis 2007. Skirrow RC. Leonard PA. Reidy JA. Hernando MD. Foran CM. Arch Environ Contam Toxicol 1988. Photolytic degradation of triclosan in freshwater and seawater. Adolfsson-Erici M. Levy SB. Mezcua M. Gomez MJ. population: 2003-2004. Watanabe N.50(1-5):153-156. Pharmacokinetics of triclosan following oral ingestion in humans. Kaneshima H.36(6):1202-1211. Developmental evaluation of a potential non-steroidal estrogen: triclosan.

General population exposure to PCP may occur by inhalation of contaminated air.350) < LOD .78) 1. PCP has been detected in soils.350 (.350 (.S.76) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .90) 1. PCP is absorbed rapidly and well by all exposure routes.350 (. ingestion of contaminated food or water.10 (<LOD-1.350) < LOD .94 (1.58-2.. Human exposure to PCP has become less common. and it is used primarily as a preservative for wood to be used outdoors (e.350-.860-2.62 (.770 (.70) .67) 1.09) .350) < LOD .350) < LOD . PCP cannot be used on wood in residential or agricultural buildings.660 (.00) 2.48 (.350-.590-1.350 (. other polychlorinated benzenes.350 (. PCP also may be eliminated in urine as a metabolite of hexachlorobenzene. are eliminated in the urine.25 and 0.350-. 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.04) 1.08-3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.00) 1.33) .350-.65 (.98 (1.890-1.350-.350-.50) 1.90 (1.350-. 40 Fourth National Report on Human Exposure to Environmental Chemicals .350-. mollusicide. Human health effects from PCP at low environmental doses or at biomonitored levels from low environmental exposures are unknown.37 (.48-2.350 (.Fungicides Pentachlorophenol inhale it or absorb it through exposed skin. In the environment.980 (. algaecide and insecticide.350-2. with repeated or chronic exposure.65 (.350-.350-.630 (.51) 1.. has been restricted. PCP is eliminated over a few days (Braun et al.350 (. 1986).350-1. Workers who manufacture or apply PCP may Urinary Pentachlorophenol Also a Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.350 (.83 (2. high dose exposure to PCP can induce a hypermetabolic state and excessive heat production as a result of uncoupling mitochondrial oxidative phosphorylation.45-2. PCP is distributed to most tissues and is not extensively metabolized.94 (1. After a single dose.350-1. hypertension.80) .30 (.40 (.350-2.10 (1.350) < LOD .70) 2.350) < LOD .76) 1.350) . Since 1984.42) 973 1190 1021 1338 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .23 (.g.30) .960) 1. water and sediments because of the large amounts that were produced and used historically.37) .350 (.10) 1.990 (<LOD-2.350 (. To-Figueras et al. utility poles and fence posts).350-.350-. plants.350) < LOD .680-1.42) 696 680 521 696 603 951 Limit of detection (LOD.75) 2.650 (.350 (.32 (. and possibly of lindane (IPCS..500-2. the elimination half-life may be a week or more (Uhl et al.73 (1.33-2.350) < LOD . Acute.350 (. 1976.76) .510-5.5.350 (.350-1.350 (.350) 90th .350) < LOD . 1979). PCP use in the U.350) < LOD .10 (.350) < LOD .350-.60) 1.510-3.30) 1. and dermal contact with PCP-treated products. After absorption. The parent compound and conjugates.350 (.480-2.390 (.350 (.30 (1. < LOD means less than the limit of detection.54-2.10) 1. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.350-.350-.350-. Survey Geometric mean (95% conf.350-2.650) 1.S. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.530) 1.350-.90) 2.350) < LOD . air.350 (. herbicide.350) < LOD .47-3. and metabolic acidosis were observed in CAS No.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 . so it is relatively non-persistent.350 (.350) < LOD .350) < LOD .850-2.350-1. 1997). which may vary for some chemicals by year and by individual sample. population from the National Health and Nutrition Examination Survey.58-2.53) 482 577 681 826 831 1125 99-00 01-02 99-00 01-02 * * * * . Kohli et al.30) 1.350 (.390 (.47-5.00) 1.30 (.990-2..350-..350-.350-.60) 1. and animals.18 (<LOD-1.890 (. along with small amounts of tetrachlorohydroquinone and conjugates. Effects including hyperthermia. PCP is degraded by sunlight and metabolized rapidly by microorganisms.91 (1.350) < LOD .350-2. bactericide.00 (.64) 1.350 (.350) < LOD < LOD 75th .350-.350-2.350-.01 (<LOD-1. 2002.

19) 2.430) < LOD .67 (1. chronically administered high doses of PCP were hepatotoxic. and adversely affected thyroid function (U.360-. Fourth National Report on Human Exposure to Environmental Chemicals 41 .84) 1.560-.78) 1.990 (.650 (.470 (.850 (.360 (.67-3.09 (<LOD-2.290) < LOD .910-1.40) 1.21-2. and the FDA has established a standard for bottled water.780-1.950-1.. interval) Selected percentiles ( 95% confidence interval) Sample 95th 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 ..270-.08) 696 680 521 695 603 951 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.800) < LOD 1.25 (1.490) < LOD .300 (.560) < LOD .cdc.25-2.34 (.epa.S. 1989). 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.35-2.26 (1.94 (1. inhalation.510-.400 (..52) 1. 1989)..19) 2.340-.55) 973 1190 1021 1337 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * . Among adults in the NHANES 1999-2000 subsample.290-.25) 1.e.560) < LOD . 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.75 (<LOD-2.270-.90) 1.950-1.500-.94-3.95) 3. 1995). carcinogenic.6 and 14.9 mg/L.700-2. 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 (4.330-.590-1.52 (1.26 (1. In a small sample of U..310) < LOD . respectively) (Seifert et al.650) 90th 1. 2004.300 (. The U. respectively) (Becker et al.EPA.13 (.gov/ toxpro2.78) 1.30) 1. children in the 1980’s.00-1.18 (1.40) 1.35) 1. Survey Geometric mean (95% conf.240-.510-. Death can result from seizures and cardiovascular collapse.29-3.780) < LOD .82 (1.51) 1. population from the National Health and Nutrition Examination Survey.710-1..260 (.35-2.500-1.67 (1.S. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.82) 1.10 (1. 2003).220-. 1991).630 (.40) 1.35) 1.320) < LOD .67 (1.atsdr.290-.21 (.320) < LOD .950-1.69 (1.30 (.250 (.320) < LOD < LOD 75th .370 (.430-.10-2.830) < LOD .250 (.300 (.48-2.800-1. Pentachlorophenol is not mutagenic or teratogenic.350) < LOD .590) < LOD .25-1. IARC has determined that pentachlorophenol is possibly carcinogenic to humans. environmental levels) and health effects is available from the U.25 (1.650 (. 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.19) 2.84 (1. van Raaij et al.40) 1.310-. EPA at: http://www..79) 1.08 and 5.320 (.900-1. OSHA has established an occupational standard.67 (1.56) 1.52 (<LOD-1.06) 1. EPA has developed standards for PCP in drinking water and the environment.83 (1. or skin absorption.500 (.99) 482 577 681 825 831 1125 99-00 01-02 99-00 01-02 * * * * ..11) 2.16-1.S. In animals.580-.00) 1.610 (. More information about external exposure (i.S.420) < LOD .84-4.380-.75) 1.09-1.html. 2000). the 95th percentile of urinary PCP levels was about fiftyfold higher than that for 6-11 year olds in NHANES 2001-2002 (Hill et al.25-2.220-.19 (1.gov/ pesticides/ and from ATSDR at: http://www. 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.730) < LOD .440 (.52 (<LOD-1.760 (.06 (.570 (.00-1.280) < LOD . In NHANES 2001-2002 subsamples. 2003).16 (.36) .57 (.55) 1.94 (1.06-3.57 (1.67-2.920 (.67-3.73 (1.0 mg/L. the median and 95th percentile urinary PCP levels were approximately three times lower than comparable values in German adults (2.30-2.Fungicides adults and children severely exposed to PCP through ingestion.30) 1.75) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .40-2.40) 1.67 (1.92) 1.18) .S.

Available at URL: h t t p : / / w w w. Needham LL. Braun WH. To T. Environmental Protection Agency (U.105(1):78-83. Environ Health Perspect 1997. Arch Environ Contam Toxicol 1989. 206:15-24. Becker K. Shealy DB.org/documents/jmpr/jmpmono/2002pr08. 2002. The metabolism/ pharmacokinetics of pentachlorophenol in man and a comparison with the rat and monkey. Santiago-Silva M. To-Figueras J. Arch Environ Contam Toxicol 1989. Blau GE. Phillips DL. Metabolism of hexachlorobenzene in humans: association between serum levels and urinary metabolites in a highly exposed population.71:99108. Effects of hexachlorobenzene and its metabolites pentachlorophenol and tetrachlorohydroquinone on serum thyroid hormone levels in rats. Pesticide residues in urine of adults living in the United States: reference range concentrations. Pentachlorophenol measurements in body fluids of people in log homes and workplaces. EPA). Seiwert M. Rodamilans M. Seifert B. Cline RE. Helm D. Krause C. U.S. Schmid P. htm. Can J Biochem 1976. Seiwert M. Hill RH Jr. Barrot C. available at URL: http://www. Schulz C. 4/21/09 van Raaij JA.4:289296. hair. drinking water and indoor air. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children. 42 Fourth National Report on Human Exposure to Environmental Chemicals . Holler JS.18:475-481. urine. International Programme on Chemical Safety (IPCS). Lindane. Seifert B. 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. Dev Toxicol Environ Sci 1979. The metabolism of higher chlorinated benzene isomers. Notten WR. Gregg M. Engel R. Needham LL. et al. et al. et al. Otero R. Schulz C.inchem. Kaus S. 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. References Becker K.Fungicides Finding a measurable amount of PCP in urine does not mean that the level of PCP causes an adverse health effect.54(3):203-208. 11/30/2004. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. r e g u l a t i o n s . Fast DM. Uhl S. Schlatter C. house dust. Baker S. PCP: Human Risk Characterization [online]. Int J Hyg Environ Health 2003.58:182-186. Pharmacokinetics of pentachlorophenol in man. Pesticide residues in food-2002-Joint FAO/WHO meeting on pesticide residues. Environ Res 1995. Bailey SL.10:552-65. Toxicology 1991: 67(1):107-16. Jones D. van den Berg KJ. Bragt PC. Chenoweth MB.S. Head SL. 4/21/09 Kohli J. J Expo Anal Environ Epidemiol 2000. Hill RH. Sala M. The German Environmental Survey 1990/1992 (GerES II): reference concentrations of selected environmental pollutants in blood. Biomonitoring data can also help scientists plan and conduct research about PCP exposure and health effects. Arch Toxicol 1986. Smith SJ.18(4):469-474. Safe A. Hill RH Jr.

19 (.570-1.552 (.600) < LOD .EPA.03) 1.498 (. 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.389-.. and sanitizers.570-. 90-43-7 General Information Ortho-phenylphenol (OPP.30-2.60 (1.632) Selected percentiles ( 95% confidence interval) Sample 95th 2.630) < LOD .480-1. OPP is efficiently absorbed from the gastrointestinal tract and through the skin.636) * .836) * .20 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.624) * .509 (. whereas SOPP is not volatile and is more water soluble.3.50 (1.638) * .00 (1.85) 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 .91) 973 1190 1018 1339 99-00 01-02 99-00 01-02 99-00 01-02 .00) . Cnubben et al.30-7. small amounts of OPP have been measured in human adipose tissue (Onstot and Stanley. Workers who manufacture.493 (. such as fruits and vegetables.34) 1.497 (.92 (. 1998).07 (.600) < LOD .02) 1.10) 1.710-2.490 (<LOD-.88) 1. formulate.EPA.645) * .50 (1. < LOD means less than the limit of detection.50) .30) < LOD 1.50) < LOD .80-3.50-3.40-7.420 (<LOD-.780) < LOD .490 (<LOD-.560-8.610-1. however.550-1. on ornamental plants and turfs. Most agricultural food applications have been revoked. which may vary for some chemicals by year and by individual sample.14 (<LOD-3.40-5. 2002.17 (. are antimicrobial agents used as bacteriostats.20-2.386-.76) 1.20) < LOD 1. fungicides.600-1.770 (. or 2-phenylphenol) and its water-soluble salt.349-. leaving the chemical residue OPP. OPP is considered to be moderately toxic after acute oral doses in animal studies.760-2.61) 2. 2006).800-3.370-.496 (.40-2.S.10) .50-4. and as a wood preservative.840-1. OPP is volatile.580-1. interval) .640) < LOD . EPA. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.466 (.610 (.00 (1.00 (1.3 and 0.540-2. Both have been used in agriculture to control fungal and bacterial growth on stored crops.00-2.00) .20) 2.10) .10) 1. OPP was detected in 40 of 60 different canned beers at concentrations in the low parts per billion (Coelhan et al.Fungicides ortho-Phenylphenol CAS No.570-2.930 (.890 (.50 (1.60-2. SOPP is applied topically to the crop and then rinsed off.80) 1.09) 2.30) 1.10 (1.450 (<LOD-.00 (1.10) 2. 1989).S.880-2.890 (.860 (.490 (<LOD-. OPP is still used as a disinfectant fungicide for industrial applications.27 (.402-.450 (<LOD-..567 (.621) * .85) 2.90) 1. and it has limited water solubility.590-2.364-.20) < LOD 2.22) 2.50) 1.830 (. In the past. it was used in home sanitizers for surfaces. but OPP and SOPP are still used on pears and citrus (U.470 (<LOD-.00) < LOD . 2006).508 (.970 (.500-2.90 (1.22 (.28 (.850 (.696) * .820 (.410-.90) ..670) 2. inhalational.450 (<LOD-.740 (.30) < LOD 90th 1.389-.790) 2. General population exposure can occur via dermal. in paints.50) < LOD .490 (<LOD-.770 (.90) 2.20 (. 2006). Fourth National Report on Human Exposure to Environmental Chemicals 43 .23) 480 577 681 827 830 1125 99-00 01-02 99-00 01-02 .10) .60 (1.390-.30) < LOD .50) < LOD .690-1. or oral routes from residential use and by ingesting treated food or food that was in contact with treated surfaces or equipment.742) * .600) < LOD 75th .90 (1.860) * 99-00 01-02 99-00 01-02 99-00 01-02 .370-.33 (. Available evidence suggests that OPP does not accumulate in the body.60 (1.90) .28-3.490 (<LOD-.23) 695 680 520 695 603 953 Limit of detection (LOD.80 (2.950) < LOD .600-1.10 (1.40-5. or apply these chemicals may be more highly exposed than the general population. Human health effects from OPP at low environmental doses or at biomonitored levels from low environmental exposures are unknown. Estimated human intakes have been below recommended intake limits (U. 2006). population from the National Health and Nutrition Examination Survey.570 (.750-2.570 (.710) 3. Timchalk et al.890) 1.433-.690) < LOD .40 (. 1998.20-3. Both chemicals degrade within hours to weeks in the environment (U.S.10-2.520 (.10-1.80) 1. and it is eliminated rapidly from the body as OPP glucuronide and sulfate conjugates (Bartels et al.50-2.20 (1.600-1.370-.60-3. Survey Geometric mean (95% conf.350-1.600) < LOD 1. sodium ortho-phenylphenate (SOPP).30 (1.S.

38) 973 1190 1018 1338 99-00 01-02 99-00 01-02 99-00 01-02 .568) * . Zhao et al.43) 3.89 (1.670 (.780-14.558) Selected percentiles ( 95% confidence interval) Sample 95th 2.382 (.09 (1.88-4.gov/pesticides/.900) < LOD . Urinary ortho-Phenylphenol (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.02 (.980 (.420 (<LOD-.18) 2.26) 1.96-4.93) .453 (. 1997.. CDC.900-1.880-1.270-.670) < LOD .20) < LOD 3.11 (.46) < LOD 1.0) 1. 1999.61 (.28 (<LOD-4.33) 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 .31) < LOD . 44 Fourth National Report on Human Exposure to Environmental Chemicals .620-1.93 (1. Nakagawa et al.460-.43 (1.43-2.580) < LOD .910-1.91) 695 680 520 694 603 953 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. Smith et al.473) * .940-2. reproductive. or..950) < LOD .780 (.09-3.01) 1.440 (.24-2.00 (1.17 (.91 (1.17 (.360 (<LOD-.09-6.06-4. 1992.600-1.311-.24-2.29) 1.690 (.860 (.75 (1.910 (.75 (1.28 (2. 2000. These metabolites may induce carcinogenicity via nongenotoxic regenerative hyperplasia of the bladder (Appel.62) .21 (.514 (. 2005). IARC has classified SOPP as a possible human carcinogen.4) 3.08-1. 1984.EPA 2006).21-2.470 (<LOD-.410 (<LOD-.550 (.59) .11) < LOD 90th 1.04-4.656) * . OPP or SOPP produced carcinomas of the bladder only after phase II detoxification pathways were saturated. 2002).361-.30) 480 577 681 826 830 1125 99-00 01-02 99-00 01-02 ..610) < LOD 1.470) < LOD .EPA at: http:// www.12) < LOD 1. Brusick.38-3. interval) .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.S.74 (1.84 (1. 2002.. Pathak and Roy. population from the National Health and Nutrition Examination Survey.620-1.550-.06 (1.750 (.S. 2005. but no neurologic.11 (.580-1.47) . Survey Geometric mean (95% conf.590) * .650-1. 2005).980 (<LOD-1.17) 2.750-2.810-1. 1999.78 (2.25-6.17) * 99-00 01-02 99-00 01-02 99-00 01-02 .86 (1. Dermally applied OPP was not carcinogenic in a 2-year experimental study in animals (NTP. and it has classified OPP as not classifiable with respect to human carcinogenicity.81) 1.53) 1.. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.640-1.08) 1. Detectable levels were seen in over half the U.52 (.96 (1.990) < LOD .21) 1..11-1. OPP was not found to be mutagenic.61 (2.S.380 (.670 (.353-.43-2.13) 1.840 (.510 (<LOD-. leading to production of two metabolites.EPA 2006). 1986). Murata et al.44 (1.00 (..40-13. Biomonitoring Information Urinary OPP levels reflect recent exposure.69 (1. Bomhard et al.51-3.27) < LOD ..455-.444 (.810) < LOD . Finding a measurable amount of OPP in urine does not mean that the level of OPP causes an adverse health effect. 1998.510-. 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.05-2. population in the subsamples from NHANES 1999-2000 and 2001-2002 (CDC.33-2. Additional information is available from U.560) < LOD 75th .420 (<LOD-.385 (.93) .97 (2.750 (.860 (.64 (2.343 (.38) 1.770-2.11) 4.320 (<LOD-.S.791) * .248-. Volunteers exposed to 0.93) 1.07) 2..403-.epa.S.58) 2. 1984. U. 2002.29) 1.484) * .570) < LOD 1. or developmental toxicity was observed (Bomhard et al. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.480-. In high dose animal studies.96 (1.38) 2.500) < LOD . Ito et al.33) . Kwok et al. by possible genotoxic mechanisms (Hagiwara et al.496 (.666) * .970) 1.06-5.800-1.301-..32) 1.550) < LOD .910 (<LOD-1.08-2.Fungicides anemia.329-. less likely.32) 3. 1993.508) * .560-2. ortho-phenylhydroquinone and ortho-phenylbenzoquinone.96) 1.410 (<LOD-.61 (1.59) 1. U.291-.12-2.

March 1986. Toxicol Appl Pharmacol 1998. 2005. Kwok ES. Glas K. Moore GA. Third National Report on Human Exposure to Environmental Chemicals. St John MK. Atlanta (GA). Determination and levels of the biocide ortho-phenylphenol in canned beers from different countries. Ito N. 2006.nih. Narang A.S. Tayama S. Environmental Protection Agency (U. Bomhard EM. Gierthy J. Office of Toxic Substances. J Agric Food Chem 2006. Elliott GR. Comparative in vitro-in vivo percutaneous penetration of the fungicide ortho-phenylphenol. Moriya K. Kawanishi S. Freyberger A. Christenson WR. Inoue S. Timchalk C. Analysis of genotoxicity and the carcinogenic mode of action for ortho-phenylphenol. Fourth National Report on Human Exposure to Environmental Chemicals 45 . Mutat Res 1993. O-phenylphenol and its sodium and potassium salts: a toxicological assessment. Ito N. Detection and characterization of DNA adducts formed from metabolites of the fungicide ortho-phenylphenol. Bromig KH. Meuling WJ. EPA-560/5-89-003. Reregistration Eligibility Decision (RED) for 2-phenylphenol and salts (Orthophenylphenol or OPP). Smith RA. Arch Toxicol 2000. Shirai T.gov/ntp/htdocs/LT_ rpts/tr301. Herbold BA. Bormett GA. Imaida K. Coelhan M. Buchholz BA. Selim S. Regul Toxicol Pharmacol 2002. Sangha G. Environmental Protection Agency (U. Bartels MJ. Long-term toxicity and carcinogenicity study of sodium o-phenylphenate in B6C3F1 mice. Richter M. Oxidative damage to cellular and isolated DNA by metabolites of a fungicide orthophenylphenol.32(6):551-625. Leser KH. EPA). Fukushima S.28(6):579594. Timchalk C. Urinary physiologic and chemical metabolic effects on the urothelial cytotoxicity and potential DNA adducts of o-phenylphenol in male rats. Brzak KA. 4/13/09 Onstot JD. McNett DA. Murata M.150(2):402-413. J Agric Food Chem 2002. 1989. 90-43-7) in Swiss CD-1 mice (dermal studies).22(10):809-814.54(16):5731-5735. Moldeus P. Bartels MJ. Turteltaub KW. Drugs. Eastmond DA.(56):399-407. Dose-dependent binding of ortho-phenylphenol to protein but not DNA in the urinary bladder of male F344 rats. Mendrala AL. Vogel JS. food additives and natural products as promoters in rat urinary bladder carcinogenesis.45(5):460-481. In vivo genotoxicity of sodium orthophenylphenol: phenylbenzoquinone is one of the DNA-binding metabolite(s) of sodium ortho-phenylphenol. The pharmacokinetics and metabolism of 14C/13C-labeled ortho-phenylphenol formation following dermal application to human volunteers.20(5):851-857. Cano M.43(7):14311437. van de Sandt JJ. Stanley JS. U. July 28. Roberts AL.Fungicides References Appel KE. Bartels MJ.74(2):61-71.. Hakkert BC. Cnubben NH. Hirose M. J Chromatogr B Biomed Sci Appl 1997. Pathak DN. Hagiwara A. Identification of SARA compounds in adipose tissue.S. Available at URL: http://www. 4/9/09. Zhao S. Available at URL: http://ntp.50(11):3351-3358. Bartels MJ.pdf. Arnold LL. Nakagawa Y. IARC Sci Publ 1984.286(2):309-319. NTP Technical report on the toxicology and carcinogenesis studies of ortho-phenylphenol (CAS No. Brusick D.S.EPA). Carcinogenesis 1999.S.703(12):97-104. U. et al. National Toxicology Program (NTP). Crit Rev Toxicol 2002. Christenson WR. Centers for Disease Control and Prevention (CDC). rat and man. Brendler-Schwaab SY. Shibata M. Fukushima S.gov/oppsrrd1/REDs/ phenylphenol_red.17(8):411-417. Xenobiotica 1998. Determination of orthophenylphenol in human urine by gas chromatography-mass spectrometry.niehs. Eadon G. Roy D. The carcinogenicity of the biocide ortho-phenylphenol. Hagiwara A. Relationship between metabolism and cytotoxicity of ortho-phenylphenol in isolated rat hepatocytes. Hum Exp Toxicol 1998. Toxicol Appl Pharmacol 1999. Biochem Pharmacol 1992.epa. Food Chem Toxicol 1984.35(2 Pt 1):198-208. Comparative metabolism of orthophenylphenol in mouse. EPA 739 R-06004.159(1):18-24. Sangha GK. et al. Environ Mol Mutagen 2005.pdf.

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

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

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

sulfonamide. Striley CA. Identification of human urinary metabolites of acetochlor in exposed herbicide applicators by high performance liquid chromatography-tandem mass spectrometry.248(2-3):115-122. Number 15.EPA): http://pmep. Hodgson E.S. Hsiao JJ. Third National Report on Human Exposure to Environmental Chemicals. March 2006. Lefevre PA.17(6):559-566. Comparative metabolism of chloroacetamide herbicides and selected metabolites in human and rat liver microsomes. Larsen GL. Quistad GB. Casida JE.24(10):1003-1012. Fourth National Report on Human Exposure to Environmental Chemicals 49 .S. Hum Exp Toxicol 1996. Volume 65. pages 3682-3690. Sanderson WT. Sci Total Environ 2000.108(12):1151-1157. J Agri Food Chem 1989. Coleman S. Barr DB. and metolachlor herbicides in rats. Peter CJ. Thurman EM. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. Roberts AL. J Expo Sci Environ Epidemiol 2007. Furlong ET. Wratten SJ. Andrews HF. et al. acetochlor. Tinwell H. Centers for Disease Control and Prevention (CDC).pdf. Report of the Food Quality Protection Act (FQPA) Tolerance Reassessment Progress and Risk Management Decision (TRED) for Acetochlor. Rose RL. EPA). U. Chem Res Toxicol 1998. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. Kinney PL. Hein MJ. 2000. Atlanta (GA).S. J Expo Anal Environ Epidemiol 2005. Sci Total Environ 2000. Camann DE. Finding minimal herbicide concentrations in ground water? Try looking for their degradates. et al.S.html. Heederik D. 5/30/06 U. reservoirs and ground water in the Midwestern United States. Federal Register: January 24. Wilson AG. Burkhardt MR. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. Environ Health Perspect 2003.Herbicides References Ashby J. Olsson AO.cce. Alavanja MC. and other herbicides in rivers. Kier L. Linderman R. Feng PCC. Barr DB.37(4):10881093. EPA 738-R-00-009. 1998. Dialkylquinonimines validated as in vivo metabolites of alachlor.S. Deddens JA. 2005. Occurrence of sulfonylurea. Barr DB. Reynolds SJ. Linhart SM.cornell. Available at URL(non U. Jefferies PR. et al. Available at URL: http://www. imidazolinone. Kolpin DW. Hladik ML.248(2-3):123-133. Environmental Protection Agency (U. Environmental Protection Agency (U. Green T. Acetochlor (Harness) Pesticide Petition Filing 1/00.15(6):500-508. Evaluation of the potential carcinogenicity and genetic toxicity to humans of the herbicide acetochlor. Whyatt RM.111(5):749-756.edu/profiles/herbgrowthreg/24-d-butylate/acetochlor/acetochlor_pet_100. Davison KL. Bravo R. Comparative metabolism and elimination of acetanilide compounds by rat.15(9):702-735.gov/oppsrrd1/reregistration/REDs/acetochlor_tred. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. Battaglin WA.39(17):6561-6574. Environ Health Perspect 2000. Environ Sci Technol 2005. 5/30/06. Curwin BD.11(4):353359. Barr JR. EPA). Feil VJ. epa. Ward EM. Xenobiotica 1994. Hines CJ.

Urinary levels of alachlor mercapturate were generally not detectable in the NHANES 2001-2002 subsample (CDC. 2003). 1998. Alachlor is highly toxic to freshwater fish and slightly toxic to birds and some invertebrates. U. 1997. hemosiderosis. Feng and Wratten. 2000. WHO.EPA.EPA. 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. WHO.. IPCS.. 2003). 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. 1998. In 1993-1995. 1996.EPA. 1999.gov/pesticides/.. EPA at: http://www. Alachlor has a soil half-life of a few weeks. but this metabolite is not a marker of exposure to most plant metabolites or environmental degradates which are often more prevalent in the environment. 1996. 1996). It is absorbed by plants and inhibits plant protein synthesis. Human health effects from alachlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 1999 and 2007. 1995..S. ranged from 0.. 1998). alachlor is quickly absorbed after oral doses and mostly excreted as metabolites within a week (IPCS. (2003) showed that 2. U.epa. the latter may account for some observed effects (Davison et al. including corn. 1998). and uveal degeneration.2% of a reference population had detectable alachlor equivalents by immunoassay in their urine. Finding measurable amounts of alachlor mercapturate in the urine does not mean that the levels of alachlor mercapturate cause an adverse health effect..EPA considers alachlor to be a probable human carcinogen at high doses.S. General population exposure to alachlor may occur through consumption of contaminated food or drinking water. Alachlor itself is not considered mutagenic. USGS. 1989. WHO. Hill et al. but not likely at low doses. 1998. U. NTP and IARC do not have ratings regarding human carcinogenicity. as measured through conversion to deethylamine. Hines et al. but another metabolic pathway can produce 2..S. Since the late 1980s alachlor use has been declining. It is both metabolized in plants and degraded microbiologically in agricultural soils into as many as 19 metabolites and degradates. Tessier and Clark. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 2003).EPA.Herbicides Alachlor CAS No. 1988. and on non-crop land for general weed control. stomach. Hladik et al. 15972-60-8 General Information Alachlor is a chloroacetanilide type herbicide with restricted usage for preemergent control of grasses and broadleaf weeds on agricultural cropland. WHO. alachlor has demonstrated hepatotoxicity. and field workers. but shows little bioaccumulation. Because it can be absorbed through skin. whereas 60% of applicators had detectable amounts. corn cropland was treated with alachlor. and thyroid only at either maximum tolerated doses or related to species-specific pathways (Heydens et al. Kolpin et al. 1995).. soybeans. formulators.. In animals. 2005).6-diethylaniline and its reactive metabolite.S. Additional information about is available from U. mean values of urinary concentrations of alachlor metabolites. U. In chronic animal testing.S. Biomonitoring Information Urinary levels of alachlor mercapturate reflect recent exposure. Animal carcinogenicity studies have demonstrated tumors of the nasal turbinates. Alachlor has low potential for acute toxicity. 2000. 50 Fourth National Report on Human Exposure to Environmental Chemicals . peanuts and other crops.S. 2003). 1998).S. but has not shown developmental or reproductive toxicity in mammalian systems (U. about 20-25% of the U. mercapturate conjugates were predominant metabolites. though positive genotoxic results are reported for several metabolites of alachlor (Brown et al. People exposed to alachlor will excrete alachlor mercapturate in their urine (Driskell et al. 2005.S. the dermal exposure route is potentially significant for applicators.1 to 1. 1994.1 mg/L at various collection times (Sanderson et al. In a study of applicators and workers exposed to alachlor.. Estimated human intakes have been below recommended limits (U.EPA. Jefferies et al. In animal studies.

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

S. J Ag Food Chem 1995.43(9):2504-2512. Roberts AL.S. March 2006. Thelin GP. Third National Report on Human Exposure to Environmental Chemicals. Bull Environ Contam Toxicol 1996. Life Sci 1988.248(2-3):115-122. Barr DB. Kolpin DW. Biagini RE. Hsiao JJ. Biagini R. Thurman EM. Available at URL: http:// www. Available at URL: http://www. J Agri Food Chem 1989.pdf. Whyatt RM. Geological Survey (USGS). 1999.php. and metolachlor herbicides in rats. Jefferies PR. Quistad GB. Feng PCC. Supplemental Technical Information (available on-line only). Quistad GB. Wratten SJ. Hull RD. Shoemaker DA. reservoirs and ground water in the Midwestern United States.int/water_sanitation_health/dwq/chemicals/en/alachlor. Hum Exp Toxicol.43(25):2087-94. Geneva. Heydens WF. Circular 1291. Sci Total Environ 2000. Andrews HF. revised February 15. Kimmel EC. Atlanta (GA). Wilson AG. Geological Survey (USGS). Environ Health Perspect 2003. Hill RH Jr.24(10):1003-1012. Sanderson WT. World Health Organization. Dialkylquinonimines validated as in vivo metabolites of alachlor. Casida JE. Sci Total Environ 2000. Reregistration Eligibility Decision (RED) Alachlor. Hill AB. who. imidazolinone.org/documents/pds/pds/pest86_e.gov/nawqa/pnsp/pubs/circ1291/ supporting_info.44(18):1325. Comparative metabolism and elimination of acetanilide compounds by rat.gov/oppsrrd1/ REDs/0063. Finding minimal herbicide concentrations in ground water? Try looking for their degradates. Environ Sci Technol 2005.htm.inchem.18(6):363-391. Am Ind Hyg Assoc J 1995. MacKenzie B.pdf.111(5):749-756. 2/27/09 Jefferies PR.S. Background document for development of WHO Guidelines for Drinking-water Quality. 2005. Feil VJ. 98-4245 (by Barbash JE. Available at URL: http://www. Linhart SM.248(2-3):123-133.395(2-3):159-171. 2007. Alachlor in Drinking-water. Ann Occup Hyg 2003. Burkhardt MR. Shealy DB. Kinney PL. Tessier DM. Clark JM. DNA adduct formation by alachlor metabolites.47(6):503-517. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. Quantitative assessment of the mutagenic potential of environmental degradative products of alachlor. 86.Herbicides References Battaglin WA. Occurrence of sulfonylurea.37(4):10881093. acetochlor. Centers for Disease Control and Prevention (CDC). Environmental Protection Agency (U. EPA). Larsen GL. 1996. Available at URL: http://water. U. EPA 738R-98-020. Casida JE. Sacramento. Kolpin DW. 2/27/09 U. Thake DC. Striley CA. sulfonamide. An evaluation of the carcinogenic potential of the herbicide alachlor to man. Xenobiotica 1994. 2/27/00 52 Fourth National Report on Human Exposure to Environmental Chemicals .56(9):883-889. Barr JR. Lau H. Identification of a major human urinary metabolite of alachlor by LC-MS/MS. Davison KL.39(17):6561-6574. Casida JE. Henningsen G. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. 1997. 1998. Erratum in: Life Sci 1989. 2003. Gilliom RJ). Brown KK. Water-Resources Investigations Report: Distribution of Major Herbicides in Ground Water of the United States Water Resource Investigations Report No. 1992-2001. Tolos W. International Programme on Chemical Safety (IPCS). Dialkylquinoneimine metabolites of chloroacetanilide herbicides induce sister chromatid exchanges in cultured human lymphocytes.56(6):853-859.usgs. Hines CJ. Hladik ML. The Quality of Our Nation’s Waters Pesticides in the Nation’s Streams and Ground Water. California. 1999. Hines CJ. Mutat Res.epa. et al. et al. World Health Organization (WHO). ALACHLOR. Camann DE. 4/2/09 U. Chem Res Toxicol 1998. Peter CJ. Furlong ET. and other herbicides in rivers. Driskell WJ. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. Kier LD. Biological monitoring of commercial pesticide applicators for urine metabolites of the herbicide alachlor. Martens MA.S. WHO/ FAO Data Sheets on Pesticides. No.11(4):353359. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. Deddens JA. Brown MA. December 1998.

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

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

3/11/09 Arcury TA.61(4):331-355. Sanborn JR. Gillis JH. The effects of atrazine on female wistar rats: an evaluation of the protocol for assessing pubertal development and thyroid function. 2005). 3/11/09 Laws SC. Simpkins JW.inchem. Eldridge JC. World Health Organization.htm.gov/toxprofiles/tp153. Barr DB. Stoker TE. J Expo Anal Environ Epidemiol 2005.. 2001). Heederik D.76(1):190-200. Fleenor-Heyser DG. Biagini RE. Goldman JM. Eldridge JC. Saiz SG. Maroni M.atsdr. Cooper RL. Lioy PJ. Wetzel LT. Third National Report on Human Exposure to Environmental Chemicals. Atlanta (GA). References Adgate JL. Hayes TB.58(2):366-376. Ferioli A. Stoker TE.Herbicides Biomonitoring Information Urinary levels of atrazine mercapturate reflect recent exposure. Curwin BD. Barr DB. McElroy WK. et al.. Determination of urinary residue levels of the N-dealkyl metabolites of triazine herbicides. Moseman RF. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample. Chen H.html. Tyrey L. J Toxicol Environ Health 1994. Shoemaker DA. Freeman NC. et al.. Geneva. 1996. Ferrell JM. Toxicol Sci 2003. Brown KK. Stevens JT. Pesticide urinary metabolite levels of children in eastern North Carolina farmworker households. Biological monitoring of human exposure to atrazine. Steroids 1999. diamino-S-chlorotriazine and hydroxyatrazine.2 μg/L in 15 farmers studied several days after spraying the pesticide (Curwin et al. WHO/ FAO Data Sheets on Pesticides. et al. Toxicol Sci 2000. The geometric mean of urinary atrazine mercapturate was 1. Breckenridge CB. atrazine was detected in only four children (Arcury et al. Striley CA. Cooper RL. Aldous CN.. Pest Manag Sci 2005. 2000).cdc. Short-term effects of chlorotriazines on estrus in female Sprague-Dawley and Fischer 344 rats. 82. Goodrow MH.115(8):1254-1260. In a small number of field workers. Stuart AA. Collins A. et al. 2007). Lucas AD. Gillis JH.43(2):155-167. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Jones AD. Hines CJ. 2001 [online]. Grzywacz JG. No. Perry et al. Stoker TE. A risk assessment of atrazine use in California: human health and ecological aspects. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. Bersani M. Biomonitoring studies on levels of atrazine mercapturate provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of atrazine than are found in the general population. Cottica D. Available at URL: http://www. Centers for Disease Control and Prevention (CDC).109(6):583-590. Clayton CA. Hein MJ. Determination of atrazine metabolites in human urine: Fourth National Report on Human Exposure to Environmental Chemicals 55 . Through immunoassay atrazine equivalents (detected mostly as atrazine mercapturate). Blewett C. Environ Health Perspect 2007. ATRAZINE. Catenacci G.99(8):5476-5480. Ferrell JM. Hermaphroditic. J Toxicol Environ Health 1994. levels of atrazine mercapturate were generally not detectable (CDC. Carr WC Jr. Agency for Toxic Substances and Disease Registry (ATSDR). International Programme on Chemical Safety (IPCS). Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. Sanderson WT. Proc Natl Acad Sci USA 2002. Laws SC. Wetzel LT. et al.org/documents/pds/pds/pest82_e. 2005). In small studies of Maryland residents in 19951996 (MacIntosh et al. Pubertal development in female Wistar rats following exposure to propazine and atrazine biotransformation by-products. Reynolds SJ. The mammary tumor response in triazine-treated female rats: a thresholdmediated interaction with strain and species-specific reproductive senescence. Noriega N. Vonk A. Ann Occup Hyg 2003.. atrazine mercapturate was infrequently detected at the detection limit of < 1 μg/L. Mendoza M. Toxicol Lett 1993. 2003. Bradway DE. Cooper RL.43(2):155-167. Quandt SA. Eberly LE.64(9):672-678. Short-term effects of chlorotriazines on estrus in female Sprague-Dawley and Fischer 344 rats. Finding measurable amounts of atrazine mercapturate in urine does not mean that the levels of atrazine mercapturate cause an adverse health effect.30(2):244-247.. et al. Seiber JN. Deddens JA. Toxicol Sci 2000. urinary concentrations ranged from 5-1756 μg/L (Lucas et al. Tapia J. demasculinized frogs after exposure to the herbicide atrazine at low ecologically relevant doses. In a study of 60 farm worker children.53(2):297-307. In the NHANES 2001-2002 subsample. 2005. Available at URL: http:// www. Environ Health Perspect 2001. Schmid J.. Pfeifer KF. 1999) and 83 Minnesota children with multiple urine collections during 1997 (Adgate et al. Extrom PC.69(2):217-222. 1993). Toxicological profile for atrazine. Lee M. Barr DB. Atrazine disrupts the hypothalamic control of pituitary-ovarian function.47(6):503-517. Barbieri F. the urinary geometric mean levels for herbicide applicators in Ohio and Wisconsin were about 6 μg/L (Hines et al. J Agric Food Chem 1982.15(6):500-508. Gammon DW.

The Quality of Our Nation’s Waters. Dagenhart D. 1992-2001. Geological Survey (USGS). MacIntosh DL. Induction and inhibition of aromatase (CYP19) activity by various classes of pesticides in H295R human adrenocortical carcinoma cells.gov/scipoly/sap/meetings/2003/june/ finaljune2002telconfreport.gov/nawqa/pnsp/pubs/ circ1291/supporting_info. J Toxicol Environ Health A 1999. Chem Res Toxicol 1993. Toxicol Appl Pharmacol 2002. March 2006. 2003b. U. Pesticides and Toxic Substances. Hammerstrom KA. revised February 15.67(2):198-206. 0062. Dryzga MD. Toxicol Sci 2000.182(1):44-54. Boerma J. Stoker TE.S. EPA Office of Pesticide Programs. Toxicol Sci 2002. EPA).pdf. J Expo Anal Environ Epidemiol 1999. Cooper RL. Supplemental Technical Information (available on-line only). Kastl PE.php. A review of epidemiologic studies of triazine herbicides and cancer. Exposure parameters necessary for delayed puberty and mammary gland development in LongEvans rats exposed in utero to atrazine. A longitudinal investigation of selected pesticide metabolites in urine. Interim Reregistration Eligibility Decision For Atrazine. Environmental Protection Agency (U. Needham LL. White paper on potential developmental effects of atrazine on amphibians. Singzoni B. EPA).gov/oppsrrd1/REDs/ atrazine_ired.epa. Ryan PB. Available at URL: http://www. Available at URL: http://water. Cooper RL. Rayner JL. Sanderson JT. A risk characterization for atrazine: oncogenicity profile. Wetzel L. Lansbergen GW.9(5):494-501. Determination of the effect of tridiphane on the pharmacokinetics of [14C]-atrazine following oral administration to male Fischer 344 rats.S. Timchalk C.Herbicides development of a biomarker of exposure. Christiani D.58(1):50-59. The effect of atrazine on puberty in male Wistar rats: an evaluation in the protocol for the assessment of pubertal development and thyroid function. Delzell E. Fenton SE. Guidici DL.6(1):107-116.10(7):479. Ann Epidemiol 2000. Case No. Stevens JT. Laws SC. Osborne DW. Circular 1291.S. Guidici DL. 3/11/09 U.usgs.S. Available at URL: http://www. The effects of atrazine metabolites on puberty and thyroid function in the male Wistar rat. Office of Prevention. 6/1/09 U. Langvardt PW. Breckenridge CB. Stoker TE. Toxicology 1990.S. Tortorelli J. Environmental Protection Agency (U.61(1):27-40. Pesticides in the Nation’s Streams and Ground Water.epa. Wood C. Laws SC.27(6):599612. Crit Rev Toxicol 1997. Toxicol Appl Pharmacol 2004. 4/2/09 56 Fourth National Report on Human Exposure to Environmental Chemicals . Urinary biomarkers of atrazine exposure among farm pesticide applicators.56(2):69-109. May 2003a. Environmental Fate and Effects Division. 2007.pdf. Washington (DC). Sathiakumar N. van den Berg M. Perry M.195(1):23-34.

670-1. but at higher levels they are herbicidal.210-.07 (. which may vary for some chemicals by year and by individual sample.310 (. Fourth National Report on Human Exposure to Environmental Chemicals 57 .55 (1.490 (.4-D may occur during residential applications.13) < LOD . and delayed Urinary 2.27-2. It was first registered with U.690 (.49) 477 546 677 797 823 1070 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD . and aquatic environments. with a half-life of several days to several weeks. dizziness. agricultural. by direct contact with agricultural and residential areas after applications. 4-D.420-.22) < LOD .410) < LOD .00-2. population from the National Health and Nutrition Examination Survey. It is not well absorbed through the skin.40) 1.690 (.952 and 0. and it is often mixed with other chlorophenoxy acid herbicides (such as dicamba. At low levels. It is rarely detected in ground waters (USGS.10 (<LOD-1. MCPA. although dermal exposure may be significant for herbicide manufacturing plant workers exposed to high concentrations of 2. and by consuming food or drinking water contaminated with 2. Acid and salt forms are much less toxic to fish and aquatic invertebrates than the ester forms.4-Dichlorophenoxyacetic Acid CAS No. Sauerhoff et al.310) < LOD . Intentional overdoses and unintentional high dose exposures to chlorophenoxy acid herbicides have resulted in weakness.400) < LOD .4-D has low acute toxicity.Herbicides 2.20 (<LOD-1. 2007).10) < LOD 1.930 (.02-1. renal and hepatic injury. the chlorophenoxy herbicide 2.540-.690 (. hypotension. Human health effects from 2.43) 1.4-D were used in the U. 2005).230 (<LOD-.4-dichlorophenoxyacetic acid (2. Recent estimates of chronic intakes of 2.20 (.70) 1.350) < LOD < LOD < LOD .27 (.960-1.4-D is eliminated mostly unchanged in the urine with an elimination half-life ranging from 10 to 33 hours (Arnold et al.680-1.320) 90th .S.4-D have been below recommended intake limits (U..910) < LOD . 2. it acts as a plant growth hormone.27 (1.250 (<LOD-.690-1. 2.24 (.2.560-.22) 962 1135 1015 1278 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD . It is poorly bound in soils.05-2.4-D or exposed for prolonged periods. 2.16) < LOD .810-1. abdominal pain.4-Dichlorophenoxyacetic acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.EPA.560-1.610-.260 (<LOD-. 1977).21) 1.210 (<LOD-. these herbicides can enhance plant growth.4-D can be applied either as an aqueous salt or as oil-soluble esters. myotonia.550-1. nausea.EPA. in 2001 (U.730 (.330 (.S.930-1..S.32 (1.51 (1.760 (.4-D at low environmental doses or at biomonitored levels from low environmental exposures are unknown.440-1.. 1989. General population exposure to 2.370-.250 (<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 . headache.03) 695 659 520 668 589 892 Limit of detection (LOD. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.490) < LOD < LOD < LOD .4-D is rapidly absorbed via oral and inhalation routes. < LOD means less than the limit of detection. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 1.66) < LOD 1.48) < LOD 1.910) 1.4-D) controls broadleaf weeds in residential.30 (<LOD-2. and mecoprop). Once absorbed.EPA in 1948.S. 2. 94-75-7 General Information Widely used throughout the United States. 1974.80) 1.230-. Similar to other chlorophenoxy herbicides.10 (<LOD-1.660) 1. Survey Geometric mean (95% conf. As much as 62 million pounds of 2.610 (.740 (. 2004).S. Kohli et al.420) < LOD .910) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .08) < LOD .890 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.60) 1.890) < LOD .

EPA 2005).S.790) 1. or to contaminants in the herbicide formulations (specifically 2.490 (.410) < LOD < LOD < LOD . IPCS.480 (.S. 2005). U. 2. Hill et al.4-D levels were detectable in less than a quarter of the individuals studied.4-Dichlorophenoxyacetic acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.56) .810-1.19) .410) < LOD 1.35) < LOD .4-D does not have significant reproductive. Frank et al.4-D had urinary levels several hundred to several thousand times higher than the 95th percentiles of the NHANES subsamples (CDC. Post-application levels in farmers and home gardeners were dependent on Urinary 2.4-D are eye irritants.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 . 2004).340 (. eyes.700 (.790) < LOD .670 (.4-D production plant workers and a few forestry workers spraying 2. 1995).17 (.890) < LOD 1.720 (.05) .4-D reflect recent exposure.39) < LOD 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 2001.590 (<LOD-1. The acid and salt forms of 2. 1989).. IPCS.29) 477 546 677 796 823 1070 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD . 1996. In previous samples of the U.820-1. 2005. such as soft tissue sarcoma and non-Hodgkin’s lymphoma. 2005. U.330-.. in small samples of children (Hill et al.550-. liver.73) . Knopp et al.14 (. 1996. 1985.40) 695 659 520 667 589 892 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. 2006.780) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .670 (<LOD-1.27-1.410) 90th . 2005).270 (<LOD-.990-1.350 (<LOD-.470) < LOD .640 (. myotonia.32 (<LOD-2. 2. Survey Geometric mean (95% conf.740 (.780-1.560-.08 (.610-. 2005. thyroid. 2005.580-. CDC. and of adults and children (Baker et al.EPA. Average post-application urinary levels of 2.S. It is unclear whether these associations are related to the chlorophenoxy herbicides.660 (.380 (<LOD-. urinary 2.410 (<LOD-.Herbicides neuropathy (Bradberry et al.7.380-. U.EPA at: http://www. Biomonitoring Information Urinary levels of 2. U.41 (1.08 (. Epidemiological studies have reported associations of several types of cancer. developmental...590 (<LOD-1.920) < LOD 1.08 (.570) < LOD .440 (.. 2005).270-..S.340-. 2003.S. Kutz et al.gov/pesticides/. Kolmodin-Hedman and Erne.S. 1996.EPA. IARC considers the chlorophenoxyacetic acids group of chemicals as possibly carcinogenic to humans. 2000).epa. adrenals and gonads (NTP..610-.560-.670 (.. IPCS. 1980.4-D was not found to be genotoxic or carcinogenic in animal studies (Garabrant and Philbert. 1992)..780 (. 2002.8-tetrachlorodibenzo-pdioxin) (Garabrant and Philbert.620-. with the exposure to chlorophenoxy herbicides as defoliants or contaminated herbicides. 58 Fourth National Report on Human Exposure to Environmental Chemicals ..13 (.13 (. 2005).850) < LOD .780) . 1995.3.380 (<LOD-.380) < LOD . 1994).660) < LOD .S.890-1.520-. 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.24) 1.980) < LOD 1.390) < LOD < LOD < LOD . 2. other exposures. Pearce and McLean.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.810-1.930-1. IOM.EPA. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 1. population (Hill et al. or teratogenic effects in chronic rodent studies (Charles et al. Acute high doses administered to laboratory animals produced ataxia. Additional information is available from U. population from the National Health and Nutrition Examination Survey.680) < LOD . and evidence of histological injury to the kidneys.16) 1. 2002.26) 962 1135 1015 1277 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .

J Toxicol Environ Health 1992.4-D) epidemiology and toxicology. Wilson RD.71(2):99-108. 1992). Driskell WJ. Finding a measurable amount of 2. and the use of protective clothing or equipment (Arbuckle et al. Survival and Growth Curves from NTP Toxicity Studies. Occup Environ Med 1994.4-D in urine does not mean that the level of the 2. Arnold EK. Exposure of homeowners and bystanders to 2.37(2):277-291.. Kutz FW.4-Dichlorophenoxyacetic Acid). Developmental toxicity studies in rats and rabbits on 2.4-D and 2. TOX-63 Peroxisone Project (2.4-D): exposure and urinary excretion. Bailey SL. Harris SA.5-T). Toxicol Sci 2001. Bus JS. Updated March 7. Garabrant DH.32(4):233-257. et al. Board on Health Promotion and Disease Prevention. Head SL.4-D than levels found in the general population. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children. Shealy DB. Review of 2. 2.. Arch Toxicol Suppl 1980. Biomonitoring studies of 2. Alexander BH. 2005). 3/17/09 Knopp D. Barr DB.nih.edu/catalog. Kolmodin-Hedman B.51(3):152-159. et al.nap.10(6 Pt 2):789-798. J Expo Anal Environ Epidemiol 2000. geometric mean urinary levels of 2. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. Beeson MD.php?record_id=10603. Gupta BN. Ritter L. Barr DB. Ripley BD.4-D in urine provide physicians and public health officials with reference values so that they can determine whether other people have been exposed to higher levels of 2..4-D). Mandel JS. Dhar MM. Selected pesticide residues and metabolites in urine from a survey of the U. Brody D. Reynolds SJ. Washington (DC): National Academies Press. 2005 Charles JM. Estimation of occupational exposure to phenoxy acids (2. 3/17/09 Fourth National Report on Human Exposure to Environmental Chemicals 59 . Heederik D. et al.4. the number of acres to which it was applied (Curwin et al. Third National Report on Human Exposure to Environmental Chemicals. Carter-Pokras OD. 2005). Available at URL: http:// www.4-D will result in an adverse health effect. Dichlorophenoxyacetic acid. Tandon JS.4-dichlorophenoxyacetic acid (2. Campbell RA. 914. 2003. Kohli JD. Baker SE. Environ Res 1995. The pharmacokinetics of chlorinated phenoxy acid herbicides: a literature. Beasley VR.Herbicides the time since application. Crit Rev Toxicol 2002. Arch Environ Contam Toxicol 1989. International Programme on Chemical Safety-INCHEM (IPCS). Quantification of selected pesticide metabolites in human urine using isotope dilution high-performance liquid chromatography/ tandem mass spectrometry. Hill RH Jr. Frank R. Curwin BD.15(6):500-508. Chapman P.18(4):469-474. Erne K. References Arbuckle TE. J Expo Anal Environ Epidemiol 2005 Nov. Biomonitoring for farm families in the farm family exposure study.4-dichlorophenoxyacetic acid in man. Needham LL.gov/index. Mandel et al.27(1):23-38.4-D were highest in the farmers who applied the 2. Needham LL. cfm?objectid=06FF8DA6-E5A1-90CD-3F26562CEC5CDDE5. Available at URL: http:// www. Committee to Review the Health Effects in Vietnam Veterans of Exposure to Herbicides (Fourth Biennial Update. Arch Environ Contam Toxicol 1985.4-dichlorophenoxyacetic acid and its forms.. 2006. Fast DM. To T.31(2):121-125.4:427-435. Harris et al. Philbert MA.4:97-100.4 dichlorophenoxyacetic acid (2. the amount of pesticide applied. Hein MJ.60(1):121-131. Atlanta (GA). Solomon KR. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.4-dichlorophenoxyacetic acid (2.31 Suppl 1:90-97. Xenobiotica 1974. National Toxicology Program (NTP).4-dichlorophenoxyacetic acid in the chemical industry: results of a five year biological monitoring study.htm. Baker S.4-. In farm families. 2005. Murphy RS. Sanderson WT.org/documents/jmpr/jmpmono/v96pr04.S. Pesticide residues in urine of adults living in the United States: reference range concentrations. Forestry workers involved in aerial application of 2. Absorption and excretion of 2.4-D. Biomonitoring of herbicides in Ontario farm applicators. Smith SJ. Cole DC. Honeycutt R. Khanna RN. Tables. Cook BT. Baker BA. Gregg M. Sirons G J.inchem. Hanley TR Jr. Hill RH Jr. Available at URL: http://ntp. J Environ Sci Health B 1992. Acquavella JF. general population. Holler JS. Centers for Disease Control and Prevention (CDC). Scand J Work Environ Health 2005. Vet Hum Toxicol 1989. van Ravenzwaay B.31 Suppl 1:98-104. 3/17/09 Institute of Medicine (IOM).niehs. Sircar KP. Stephenson GR. 2005. TOX-63: TOXICITY REPORT CURVES. Pesticides residues in food: 1996 evaluations Part II Toxicology. Assessment of exposure to 2. Scand J Work Environ Health 2005. Veterans and Agent Orange: update 2002.4:318-321. other family members had levels ranging only slightly higher than the 95th percentile levels in NHANES 1999-2000 and 2001-2002 subsamples (CDC.

usgs.php.4-dichlorophenoxyacetic acid (2. June 2005.EPA). EPA 738 F-05-002.4-D RED Facts.htm. Toxicology 1977. Office of Prevention Pesticides and Toxic Substances.gov/oppsrrd1/ REDs/factsheets/24d_fs.S. S. May. March 2006. Pesticides in the Nation’s Streams and Ground Water. 3/17/09.S. 2007. Gehring PJ. Braun WH. Blau GE.epa.8:3-1U. Available at URL: http://water.S. gov/oppbead1/pestsales/01pestsales/market_estimates2001. Environmental Protection Agency (U. Available at URL: http://www. 4/2/09 U. Available at URL: http://www. Pesticide industry sales and usage . Washington (DC): U. 2. 1992-2001. The Quality of Our Nation’s Waters.2000 and 2001 market estimates.gov/nawqa/pnsp/pubs/ circ1291/supporting_info. Geological Survey (USGS). Circular 1291.Herbicides Sauerhoff MW.epa.EPA). 3/17/09 U.pdf. 2004.S. 60 Fourth National Report on Human Exposure to Environmental Chemicals .EPA. The fate of 2.S. Supplemental Technical Information (available on-line only).4-D) following oral administration to man. Environmental Protection Agency (U. revised February 15.

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

220) < LOD 1192 1346 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .200 (<LOD-.440 (<LOD-. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2538 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 580 831 1127 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD .2. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2537 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 580 830 1127 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD . population from the National Health and Nutrition Examination Survey.500) < LOD 1192 1345 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . see Data Analysis section) for Survey year 01-02 is 0. Survey Geometric mean (95% conf.200 (<LOD-. 62 Fourth National Report on Human Exposure to Environmental Chemicals .Herbicides Urinary Metolachlor mercapturate Metabolite of Metolachlor 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. < LOD means less than the limit of detection. population from the National Health and Nutrition Examination Survey.240) 679 701 957 Limit of detection (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.740) 679 700 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.S. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. which may vary for some chemicals by year and by individual sample. Survey Geometric mean (95% conf.S.670 (<LOD-.

Feil VJ. Jefferies PR. Sci Total Environ 2000. sulfonamide.epa. Comparative metabolism and elimination of acetanilide compounds by rat. U. Centers for Disease Control and Prevention (CDC). 3/26/09 U. Alavanja MC. Heederik D. Environ Health Perspect 2000. Striley CA. Brown KK.37(4):10881093.248(2-3):115-122.html. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. Ward EM. April 1995. 2005. streams and groundwater. Background document for development of WHO Guidelines for Drinking-water Quality. Metolachlor in Drinkingwater. Sanderson WT. California. Linhart SM. Atlanta (GA). Comparative metabolism of chloroacetamide herbicides and selected metabolites in human and rat liver microsomes. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models.Herbicides References Battaglin WA. Pesticides in U. Shoemaker DA. revised February 15.int/water_sanitation_health/dwq/chemicals/ metolachlor. Peter CJ. Wratten SJ. Hsiao JJ. Water-Resources Investigations Report: Distribution of Major Herbicides in Ground Water of the United States Water Resource Investigations Report No. Hodgson E. and metolachlor herbicides in rats. Hladik ML. 6/1/09 Whyatt RM. Geological Survey (USGS). Burkhardt MR.S. Sci Total Environ 2000.gov/nawqa/ pnsp/pubs/wrir984245/text.gov/oppsrrd1/ REDs/0001. imidazolinone. Furlong ET.111(5):749-756. Environ Health Perspect 2003.php. Available at URL: http://www. Circular 1291.gov/nawqa/pnsp/pubs/files/051507. Thelin GP. EPA). EPA 738R-95-006. Xenobiotica 1994. Kolpin DW. Gillion. Available at URL: http://www.39(17):6561-6574. 2003.47(6):503-517. Casida JE. Finding minimal herbicide concentrations in ground water? Try looking for their degradates.who. Reynolds SJ. and other herbicides in rivers. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. et al. Reregistration Eligibility Decision (RED) Metolachlor. The Quality of Our Nation’s Waters Pesticides in the Nation’s Streams and Ground Water.248(2-3):123-133.usgs. Larsen GL. reservoirs and ground water in the Midwestern United States. Andrews HF. et al. Hein MJ.S.S.pdf 3/30/09 Hines CJ.S. Gilliom RJ). March 2006. Thurman EM.ESTfeature_gilliom. Coleman S. J Agri Food Chem 1989. 1999. Kolpin DW.108(12):1151-1157. 98-4245 (by Barbash JE.41:3409-3414.11(4):353359.24(10):1003-1012. 3/27/09 Fourth National Report on Human Exposure to Environmental Chemicals 63 . 1992-2001. Barr DB. Dialkylquinonimines validated as in vivo metabolites of alachlor. Feng PCC.pdf.pdf. Available at URL: http://water. 4/2/09 U. Barr JR. Supplemental Technical Information (available on-line only).15(6):500-508. usgs. Roberts AL.S. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. Linderman R.gov/nawqa/pnsp/pubs/circ1291/ supporting_info. R. Davison KL. Third National Report on Human Exposure to Environmental Chemicals. Sacramento. Chem Res Toxicol 1998.usgs. Environ Sci Technol 2007. Available at URL: http://water. Geological Survey (USGS). Environmental Protection Agency (U. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. Environ Sci Technol 2005. 2007. 1998. Deddens JA. Available at URL: http://water. J Expo Anal Environ Epidemiol 2005. Quistad GB. Biagini RE. Curwin BD. Ann Occup Hyg 2003. acetochlor. World Health Organization (WHO). Barr DB. Occurrence of sulfonylurea. Kinney PL. Rose RL. Camann DE.

4.7. population from the National Health and Nutrition Examination Survey.3.5-T at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 2.4. 93-76-5 General Information 2. with the exposure to chlorophenoxy herbicides as defoliants Urinary 2.4. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1814 2538 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 430 580 618 831 766 1127 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 891 1192 923 1346 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 652 679 483 701 531 957 Limit of detection (LOD.8-tetrachlorodibenzo-p-dioxin (TCDD) led to the discontinuation of 2. 2007). Human health effects from 2.4.4.4. renal and hepatic injury.4-D were used as defoliants in the Vietnam War (e. myotonia.Herbicides 2.5-T degrades to 2. Teratogenic and developmental effects have been reported in studies of multiple rodent strains treated with high doses of technical grade 2. < LOD means less than the limit of detection. Kohli et al. abdominal pain. but higher levels are herbicidal.. Nelson et al.5-T. which may vary for some chemicals by year and by individual sample. 1992).4.5-Trichlorophenoxyacetic Acid CAS No. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. hypotension. Given the commercial unavailability of 2. Agent Orange).4. Mohammad and St. it is not well absorbed through the skin.5-T was once applied as either an aqueous salt or as an oil-soluble ester. Once absorbed into the body. the general population is unlikely to be exposed to it..4. 2. 2004).. nausea.5-T is eliminated mostly unchanged in the urine.. 64 Fourth National Report on Human Exposure to Environmental Chemicals .1. 1974).5-T) is a chlorophenoxy acid herbicide that is no longer registered for use in the United States.4. 2. 2. 1992. such as soft tissue sarcoma and non-Hodgkin’s lymphoma.5-T has been rarely detected in ground waters (USGS.4. see Data Analysis section) for Survey years 99-00 and 01-02 are 1.2 and 0. Although 2.4.5-trichlorophenol and other degradates. Omer. these herbicides can enhance plant growth. The half-life of 2.5-T and 2. Intentional overdoses and unintentional high dose occupational exposures to chlorophenoxy acid herbicides have resulted in weakness.4.5-T (Holson et al. At low levels.5T is rapidly absorbed via oral and inhalation routes.. with an elimination half-life of approximately 19 hours (Arnold et al. 1989.5-T in soil varies with conditions. Ester forms of 2. Epidemiological studies have reported associations of several types of cancer..4.5-T use as a herbicide in 1985.5-Trichlorophenoxyacetic acid (2.4. 1986.4.5-Trichlorophenoxyacetic acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. Chlorophenoxy herbicides act as plant growth hormones. headache.S. ranging from several weeks to many months. and delayed neuropathy (Bradberry et al. and concern about contamination with 2. Survey Geometric mean (95% conf. dizziness.g.

Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Biomonitoring studies on 2.5-T in urine also provide physicians and public health officials with reference values so that they can determine whether other people have been exposed to higher levels of 2.5-T does not mean that the level will result in an adverse health effect. 1996.5-T than levels found in the general population.3. 2004). In the NHANES 1999-2000 and 2001-2002 subsamples (CDC.5-T were generally below the limit of detection. U. IARC considers the chlorophenoxyacetic acids group of chemicals as possibly carcinogenic to humans. It is unclear whether these associations are related to the chlorophenoxy herbicides. 2..4. Survey Geometric mean (95% conf.4.7.Herbicides or contaminated herbicides. Mean urinary levels of 2.S.EPA. or to contaminants in the herbicide formulations (specifically 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.5-T itself is not mutagenic. urinary levels of 2. Urinary 2. 2002.5-Trichlorophenoxyacetic acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. Pearce and McLean.4.gov/pesticides/. other exposures. similar to results of NHANES II (19761980).4.000 times higher than the detection limit for the NHANES 2001-2002 data (Kolmodin-Hedman and Erne.epa. Biomonitoring Information Urinary levels of 2. 2005).4. Fourth National Report on Human Exposure to Environmental Chemicals 65 .4.4. 2003. IOM. 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. Finding a measurable amount of 2.4.5-T reflect recent exposure. Additional information is available from U.S.S.4. 1980).5-T also were below the limit of detection (Kutz et al. 1992). population from the National Health and Nutrition Examination Survey. 2005.5-T measured after a day of exposure in a few asymptomatic herbicide applicators were 35. in which urinary levels of 2. IPCS.EPA at: http://www.8-tetrachlorodibenzop-dioxin) (Garabrant and Philbert.

Kolmodin-Hedman B. J Toxicol Environ Health 1992. Bradberry SM.S.32(4):233-257.5-trichlorophenoxyacetic acid (2.4.23(2):65-73.4-.EPA).4.31 Suppl 1:1825.4. Centers for Disease Control and Prevention (CDC). Fundam Appl Toxicol 1992.epa.5-t mixture.5-T in four-way outcross mice. St Omer VE. Fundam Appl Toxicol 1992. Dhar MM. Tandon JS. Holson JF. Gaylor DW. Proudfoot AT. Brody D. McLean D. Developmental toxicity of 2.4-dichlorophenoxyacetic acid (2.S. Available at URL: http:// www.4. Vet Hum Toxicol 1989. Neurobehav Toxicol Teratol 1986. Environmental Protection Agency (U. Washington (DC): National Academies Press. Developmental toxicity of 2. gov/oppbead1/pestsales/01pestsales/market_estimates2001.2000 and 2001 market estimates.htm.5-trichlorophenoxyacetic acid (2.inchem. II. Pesticide industry sales and usage . Atlanta (GA).S. 3/17/09 Institute of Medicine (IOM). et al. Absorption and excretion of 2. Dichlorophenoxyacetic acid.19(2):298-306. McCallum WF. Review of 2. Erne K. 2005.37(2):277-91. general population.4:318-21. 210:250-255. Beasley VR. Multireplicated dose-response studies with technical and analytical grades of 2. Veterans and Agent Orange: update 2002. The pharmacokinetics of chlorinated phenoxy acid herbicides: a literature. LaBorde JB. discussion 5-7.4. 3/17/09 Kohli JD. Poisoning due to chlorophenoxy herbicides.19(2):286-297. Holson JF. Committee to Review the Health Effects in Vietnam Veterans of Exposure to Herbicides (Fourth Biennial Update. Crit Rev Toxicol 2002. U. et al. Mohammad FK. 914.5-T).EPA. 2004.4.nap. Gupta BN.4-D/2. Available at URL: http:// www. Third National Report on Human Exposure to Environmental Chemicals.4. 2003.8(5):551-60. Nelson CJ. Board on Health Promotion and Disease Prevention. Toxicol Rev 2004.edu/catalog. S. Khanna RN.pdf. Estimation of occupational exposure to phenoxy acids (2. Behavioral and developmental effects in rats following in utero exposure to 2. Murphy RS.Herbicides References Arnold EK. 3/17/09 66 Fourth National Report on Human Exposure to Environmental Chemicals . Sircar KP.org/documents/jmpr/jmpmono/v96pr04. Vale JA. Pesticides residues in food: 1996 evaluations Part II Toxicology.5-T). Arch Int Pharmacodyn Ther 1974. Gaines TB. Kutz FW. May.4. Sheehan DM. Wolff GL. LaBorde JB. Selected pesticide residues and metabolites in urine from a survey of the U. Office of Prevention Pesticides and Toxic Substances. Multireplicated dose-response studies in four inbred strains and one outbred stock of mice. Philbert MA. Carter-Pokras OD. I. International Programme on Chemical Safety-INCHEM (IPCS). Agricultural exposures and non-Hodgkin’s lymphoma.5-T). Scand J Work Environ Health 2005.4-D and 2. Gaines TB. Arch Toxicol Suppl 1980. Cook BT. Available at URL: http://www. 2.31(2):121-125. Garabrant DH. Washington (DC): U.5-trichlorophenoxy acetic acid in man. Nelson CJ. Pearce N.php?record_id=10603.4-D) epidemiology and toxicology.

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

Carbamate Insecticides

Carbofuran

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

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

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

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

Selected percentiles
( 95% confidence interval)

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

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

years 99-00 01-02

50th < LOD < LOD < LOD < LOD

75th < LOD < LOD

90th

* *

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

* * * * * *

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

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

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

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

482 578 681 827 831 1125

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

* * * *

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

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

973 1190 1021 1340

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

* * * * * *

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

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

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

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

696 680 521 696 603 953

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

68

Fourth National Report on Human Exposure to Environmental Chemicals

Carbamate Insecticides

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

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

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

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

Selected percentiles
( 95% confidence interval)

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

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

years 99-00 01-02

50th < LOD < LOD < LOD < LOD

75th < LOD < LOD

90th

* *

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

* * * * * *

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

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

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

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

482 578 681 826 831 1125

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

* * * *

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

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

973 1190 1021 1339

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

* * * * * *

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

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

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

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

696 680 521 695 603 953

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

Fourth National Report on Human Exposure to Environmental Chemicals

69

Carbamate Insecticides

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

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Carbamate Insecticides

Propoxur

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

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

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Carbamate Insecticides

Urinary 2-Isopropoxyphenol
Metabolite of Propoxur

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

Selected percentiles
( 95% confidence interval)

Sample 95th < LOD < LOD size 1917 2503

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

years 99-00 01-02

50th < LOD < LOD < LOD < LOD

75th < LOD < LOD

90th

* *

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

* * * * * *

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

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

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

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

456 574 655 820 806 1109

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

* * * *

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

936 1178 981 1325

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

* * * * * *

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

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

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

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

664 677 500 696 585 931

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

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Fourth National Report on Human Exposure to Environmental Chemicals

Carbamate Insecticides

Urinary 2-Isopropoxyphenol (creatinine corrected)
Metabolite of Propoxur

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

Selected percentiles
( 95% confidence interval)

Sample 95th < LOD < LOD size 1917 2502

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

years 99-00 01-02

50th < LOD < LOD < LOD < LOD

75th < LOD < LOD

90th

* *

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

* * * * * *

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

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

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

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

456 574 655 819 806 1109

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

* * * *

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

936 1178 981 1324

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

* * * * * *

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

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

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

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

664 677 500 695 585 931

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

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Carbamate Insecticides

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

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Fourth National Report on Human Exposure to Environmental Chemicals

Organochlorine Pesticides

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

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

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

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

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

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

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

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

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

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Organochlorine Pesticides

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

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Fourth National Report on Human Exposure to Environmental Chemicals

Organochlorine Pesticides

Aldrin

CAS No. 309-00-02

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

Dieldrin

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

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

Selected percentiles
( 95% confidence interval)

Sample 95th < LOD < LOD size 2275 1946

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

years 01-02 03-04

50th < LOD < LOD < LOD < LOD

75th < LOD < LOD

90th

* *

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

* * * *

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

756 588 1519 1358

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

* * * *

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

1057 946 1218 1000

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

* * * * * *

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

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

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

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

559 456 512 485 1045 881

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

Fourth National Report on Human Exposure to Environmental Chemicals

77

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

064) 90th .30 (8.10 (<LOD-16. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.1) 13.124) .083-.100-.180) .3 (18.8-17.110 (.70 (7. population from the National Health and Nutrition Examination Survey.4) < LOD < LOD 16.112-.110 (.103 (.147 (.2-15.048 (<LOD-.049-.098 (.0) 21.9 (13.8 (11.7) 15. population from the National Health and Nutrition Examination Survey.4) 95th 20.3-21.8) 14.064 (.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 .069) < LOD < LOD . Survey years 01-02 03-04 Geometric mean (95% conf.9-23.2) Sample size 2159 1952 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD 10.9 (13.3 (14.5 and 7.062-.055 (.109 (.090-.0) 19.093) .138) .177) Sample size 2159 1952 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD .170) .150 (.070 (<LOD-.102 (.058) < LOD .130) .1-18.0 (10.50 (8.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.6 (15.059 (.1-19.9 (14.7-22.6 (14.8 (18.080) .6-33.00 (8.090-.8-17.158) .190) .6) 9.80-9.0 (11.180) .149) . Serum Dieldrin (whole weight) Also a Metabolite of Aldrin Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U.130 (.100-.50) 15.4 (12.9 (12.070-.2) 12.080-. Survey years 01-02 03-04 Geometric mean (95% conf.4 (12.062 (. see Data Analysis section) for survey years 01-02 and 03-04 are 10.1) 15.60-10.9 (12.088-.6) 16.8 (9.140-.103 (.3 (13.110) .109-.40-10.S.1-24.4-18.100 (. 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 .056-.130) .6) 19.080 (.4-17.120 (. < LOD means less than the limit of detection.202) 539 456 484 487 980 885 < LOD means less than the limit of detection for the lipid adjusted serum level.80-10.8-25.8.090-.054-.130-.5-15.7 (15.077-.120 (.00-14.8) < LOD 8.8) 15. which may vary for some chemicals by year and by individual sample.6-24.100-.4) 539 456 484 487 980 885 Limits of detection (LOD. Fourth National Report on Human Exposure to Environmental Chemicals 79 .0) < LOD 9.5-17.116) .130-.0-25.6-24.109-.160 (. which may vary for some chemicals by year and by individual sample.140) .4) 19.060) .160 (.054-.075) < LOD .7) 716 587 1443 1365 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD 9.100) .1-16.077 (.5) 21.8-24.120) .150 (.5-17.7 (<LOD-15.2) 15.9-22.112) 95th .1) < LOD 9.0-21.108-.113 (.7 (14.063-.100) .070) .8-19.138 (.1) 14.40-9.130-.139 (.242) .110-. 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 9.3 (18.7-19.1 (18.090 (<LOD-.073-.089 (.90) 90th 15.096-.139 (.5 (16.S.117) < LOD .110 (.1 (13.190) .160) .4) 14.062 (.80 (<LOD-10.140 (.086-.130) .6 (15.3 (19.1) 20.0 (10. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.053 (<LOD-.2) 11.084-.4) 20.182) 716 587 1443 1365 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD .090 (.054-.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 8.120-.30 (8.110) .2) 14.5 (<LOD-11.1) 10.0 (15.101) .5) 15.5) 19.1) 15.4) 21.120 (.9-38.

Edwards JW. Stehr-Green. Li AA. Patterson DG Jr. Revised Feb. J Toxicol Environ Health. Daniel SE. Available at URL: http://www. pp. Chung KL. 4/21/09 Hoyer AP. Roy ML. Evaluation of epidemiologic and animal data associating pesticides with Parkinson’s disease. Buckland SJ. Handbook of Pesticide Toxicology. plasma dieldrin. Reprod Toxicol 2000.html. Available at URL: http://www. David VL. Soto AM. 15.usgs. Facca A. Frey JM. Jorgensen T. Tully DB.fda. McIntosh LJ. Patterson DG Jr.150:263-271. International Programme on Chemical Safety (IPCS). Sanchez-Ramos J. Jr and Laws ER. 2 Classes of Pesticides. J Toxicol Environ Health 1989. 1989. Jr. Turner W.cfsan. Toxicol Lett 1992. Ellis H.htm. Available at URL: http://pubs. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Six high-priority organochlorine pesticides.14:95-102.gov/toxprofiles/ tp1. Mann D. Demographic and seasonal influences on human serum pesticide residue levels. 80 Fourth National Report on Human Exposure to Environmental Chemicals . PA. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. References Agency for Toxic Substances and Disease Registry (ATSDR). Organochlorine exposure and risk of breast cancer. Olea N. 731-915. 2007 [online]. Mink PJ. Environ Health Perspect 1995. Exp Neurol 1998. 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. Pesticides in the Nation’s Stream and Ground Water. Environmental Health Criteria 91. Corrigan FM. Mumtaz MM. Eds.Organochlorine Pesticides in the NHANES 2001-2002 and 2003-2004 subsamples (Edwards and Priestly 1994). Needham LL. Sonnenschein C. Effect of occupational exposure to aldrin on urinary D-glucaric acid. Shore RF. 4/21/09 Bates MN. toxicology.cdc. Brock JW. et al. United States Geological Survey (USGS). Teta MJ. Serum organochlorine levels and breast cancer: a nested case-control study of Norwegian women. 4/21/09 Jorgenson JL.91(1):122-126.27:405-421. Chemosphere 2004. Cancer Epidemiol Biomarkers Prev 2000. Fernandez MG. Kanthasamy A. bioaccumulation. Academic Press. Narahashi T. Lancet 1998. Neurotoxicol 2005.inchem. Kitzazwa M. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.66(4):229-234.atsdr. J Occup Environ Med 2005.103(Suppl 7):113-122.html. Hartvig HB. either singly or in combination. Toxicological profile for aldrin/dieldrin [online]. 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.54:1431-1443. Organochlorine insecticides in substantia nigra in Parkinson’s disease.26:701-719. Kanthasamy AG. Wienburg CL. Finley B. Grandjean P. Vol. Cox. The E-SCREEN assay as a tool to identify estrogens: an update on estrogenic environmental pollutants. Grajewski B. Inc. Priestly BG. and lymphocyte sister chromatid exchange. Environ Health Perspect 2001. Rosellini RA. Chlorinated Hydrocarbon Insecticides.gov/~dms/ pesrpts.64-65 Spec. Smith AG.109(Supp1):113-139. Aldrin and dieldrin: A review of research on their production environmental deposition and fate. Psychopharmacology (Berl) 1987. Food and Drug Administration (FDA). Int Arch Occup Environ Health 1994.gov/ circ/2005/1291/. VT. Andersen A. No:429-436. Carlson JN. Chapin RE.47:1059-1087. 1992-2001. 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.352:1816-1820. Aldrin and Dieldrin [online]. Ginsburg KS. Available at URL: http://www. Schulte P.59:229-234. Song S.9:1357-1367. and epidemiology in the United States. are nonestrogenic in transfected HeLa cells. In Hayes WJ. August 2008. Garrett N. Exposure to low doses of the environmental chemical dieldrin causes behavioral deficits in animals prevented from coping with stress. Dieldrin-induced neurotoxicity: relevance to Parkinson’s disease pathogenesis. 6/1/09 Ward EM. Anantharam V. Serrano FO. et al. Toxicity of dieldrin for dopaminergic neurons in mesencephalic cultures. Part A 2000. Basit A. New York.org/documents/ehc/ ehc/ehc91. September 2002.

63 (8.82-11.5.9) 37.0 (<LOD-12.3 (25. and 03-04 are 14.0-67.2 (21.0-61.8) 663 752 595 998 1497 1383 20 years and older Gender Males 99-00 01-02 03-04 * 11. buildings.3 (<LOD-19.9 (31.5) 37. fish.4 (22.1 (17.8-43. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.5. interval) Selected percentiles ( 95% confidence interval) Sample 95th 44.8 (10.37 (8. Since 1992.4 (10. Survey Geometric mean (95% conf.6) 48. Until 1988. the technical grade product of each chemical contains 10%-20% of the other chemical.7-14.4) 37.8 (10.20 (<LOD-11.6 (9.7 (34.0-33. 1994.5 (41.9) 31.8-32.3 (21.Organochlorine Pesticides Chlordane CAS No.3-45.S.0) 20.5) 21.5-42.36-11.5) < LOD < LOD < LOD < LOD 13.4 (<LOD-12.5) 793 1049 963 868 1200 1015 Females 99-00 01-02 03-04 Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * 11.9 (26.3-24.7) 28.9 (26. respectively.7-25.2-26.6 (16.0) 75th 20. foods high in fat such as meat.5-13.0) 37.8-20.2) 36.3) 10.9) 23. and dairy products are the usual sources of exposure to these chemicals in the general population.7 (42.8) size 1661 2249 1978 Total years 99-00 01-02 03-04 50th < LOD 11.10 (8.1) 30. population from the National Health and Nutrition Examination Survey.8-61. from the early 1950’s until the mid-1980’s.3-49.2-49.8 (17. lawns.0-18.0-13.7 (10.6) 11. As a result of the manufacturing process.2) * 12.0) 27.30-11.1) 30.5) 628 557 462 350 501 493 559 1031 898 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.90 (8.8 (18.6) 39.2 (9.8-33.7) 35.0 (20.2) 22.0 (16.1-51.5-40.5-47.8.7-56.7) 19.5 (34.3 (9.4) 18.1-25.2) < LOD 11.2) < LOD 11.1 (20..2) 37.S.7 (17. Fourth National Report on Human Exposure to Environmental Chemicals 81 . which may vary for some chemicals by year and by individual sample.5) 44.5-38.9 (21.8) 27.7 (43.0-25.9) 13.0 (32.9) 17.6 (9. 2007).9 (11.2 (41.2 (10.9 (15.8-23.6 (43.8-73.2 (37.0) 21. 76-44-8 General Information Chlordane and heptachlor are structurally related organochlorine pesticides and were used in the U.9) 47.5 (8.1) 16.2) 46.3) 37.6) < LOD 11. 1994).0) 41.4) 29.0 (37. Technical grade chlordane had contained 7% trans-nonachlor.1) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * 12.4-14.8) 52.6-45.1 (<LOD-12.5-65. 10.1 (25.3-32.9) 36.10-11.6-12.1-25.70 (<LOD-10.1) * 11.9) 39.9-21.5 (<LOD-12.1) 22.6) 36.8-33.8-31.6) 8. chlordane was used to kill termites and other insects on agricultural crops.9-42.9) 11.20-11.6) 48.9 (17.3 (11.5-43.8 (40.6-24.7-70.4) < LOD 11.6-18.1-65.7) 9.3) 10. Consequently.4 (35.6) 49.9 (11.2) 34.8-42.8 (17.S. Heptachlor and chlordane and their metabolites bioaccumulate in fatty animal tissues. Both of these chemicals and their metabolites can cross the placenta and are excreted into breast milk.7-12.7 (34.3) 41.1 (15.3) 18.0-12. 57-74-9 Heptachlor CAS No.9) 10.5-44.1-15.1) * 11.5) 38.6) 20.5) 10.10-18.3 (20.2-28.5) 56.4-21.1) 90th 34. Heptachlor was used as a soil and seed treatment and for termite control in and around buildings until 1988. see Data Analysis section) for Survey years 99-00.9 (29.9-38.1-19. and 7.1) < LOD < LOD < LOD < LOD < LOD 8.6) 9.4) 22.2-56.5 (31.9) 11.4) < LOD < LOD < LOD 23.7 (32.8) 52.4) 12.2 (36.6) 9.4 (30.2-49.3 (27.7-39.20-10.0 (26.5) < LOD < LOD 9.7 (<LOD-32.4 (30.2) 33.9) 23.1 (27. and in soil.5 (33.9-21.4-45. 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. in addition to trace amounts of numerous other related compounds (ATSDR.4 (31. 2007).2-21.4-51. 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.7) 19.3-45. Chlordane is not currently produced or used in the U.5) 9.8 (42.74 (<LOD-10.7 (<LOD-13.1 (11.6-53.2 (28.89-10.8) 53.8) 44.7) 42.6) 23.9-40.3-43.6-24.7 (19.1 (16.9 (18.1 (<LOD-12.1 (44.6 (25.9 (36.9 (15.5-41.4-40. 01-02. Both pesticides are persistent in soils and sediments and have been detected in water from agricultural run-off and near production and disposal facilities (ATSDR.7) 31.3) 18.1 (<LOD-12.3 (28.2 (39. < LOD means less than the limit of detection.8) 18.4) 39.1-50.5-32.69-10.0) 31.1 (40. heptachlor use has been limited to treatment of fire ants near power transformers.3 (26.

063 (.070) < LOD < LOD < LOD < LOD < LOD .058 (.286 (.060 (<LOD-.076) < LOD .068) 75th .230-.058-.146) < LOD < LOD .208 (.100 (<LOD-.210 (.115-.130-.140 (. chronic doses of heptachlor have produced liver enlargement and injury.320 (.100 (.400) .130 (.300 (.140 (.150-.320) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.075 (.210-. 2001.440) .290-.180-. Chronic feeding studies with either chlordane or heptachlor have demonstrated reduced fertility.108-.225 (.063-.189 (.165-.070 (<LOD-. and breast milk is a major excretion route in lactating women.291) size 1661 2249 1978 Total years 99-00 01-02 03-04 50th < LOD .242-.370 (.057-. Elimination of all these chemicals from the body occurs over months to years.110 (<LOD-.110-. population from the National Health and Nutrition Examination Survey.230-.061-.160) .080 (.104) .S.150 (.220 (.048-.130 (.330 (.230 (.170-.260-. Smith.220-.130-.092) .190-. 2007).250 (.207 (. Rogan.053-.380) .053-.370 (.146) .340) . high doses of either chlordane or heptachlor block inhibitory neurotransmitters and result in central nervous system toxicity.350) . 2002.120-.269 (.S.069 (<LOD-.340) . Epidemiologic studies have not demonstrated teratogenic or developmental effects (Baker et al. 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.063 (. FDA established allowable residues of chlordane.170) .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.062) < LOD .300) .150) .160) .320 (. 1977a.074-.070-.070-.290-.320) 663 752 595 998 1497 1383 20 years and older Gender Males 99-00 01-02 03-04 * .070 (<LOD-.077) .106-.047 (<LOD-. and heptachlor epoxide in foods and bottled water.150 (.300) .258 (.Organochlorine Pesticides (Dallaire et al. Chlordane is metabolized primarily to oxychlordane and to a lesser extent. Takahashi et al.370 (.070 (<LOD-.430) .245-.050 (<LOD-.231) .091) .062) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * .140 (. neonatal mortality.230) .240-.083 (.258-.223) . and the U.280 (.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 * * * * .057 (.180) .128 (.204 (.126 (.270 (.560) . Human health effects from either chlordane or heptachlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 2007.260 (.080 (.250 (.130 (.310 (.077) . 1996. characterized by seizures and paralysis.S. 1981). 2006).220-.090-.150 (. which may vary for some chemicals by year and by individual sample.080) .080) .302) . both chlordane and heptachlor induced hepatic cytochrome P450 enzymes and increased the incidence of liver tumors (NTP.160) . and NIOSH and ACGIH have recommended workplace exposure levels for each pesticide.180) .260 (.300) .280) .168-. and inhalation exposure.200-. and alterations in immune function of offspring.057) * .270 (.148) .240 (.071 (.130) .200-.290 (.216-.250-. interval) Selected percentiles ( 95% confidence interval) Sample 95th . No clear evidence of excessive cancer rates was demonstrated in human epidemiologic studies (ATSDR.079) .227) < LOD .190-.055-.104-.063) ..300) . to heptachlor.200 (.120-.070) .140) .410) .360) .280-.189-. In laboratory animal studies.120-. Survey Geometric mean (95% conf.049 (<LOD-.140-.063 (.087-. 1986).058-.246-.280-.207) ..100-.190-. dermal.080) .240-.140 (.115 (.066-.315 (.070 (.073 (.170) .064) < LOD .348) .510) .350 (.271 (. 1986). 1991). EPA has established environmental criteria for chlordane and heptachlor. Le Marchand et al.203-.280-.130-.073) < LOD < LOD < LOD < LOD .320 (.136) .240) . heptachlor.126) . which is also persistent in the body (ATSDR. Chlordane and heptachlor are absorbed after oral.170) .130) . Acute.290) .082 (. 1977b.310) .230-.100-.130-.063 (.066 (. The major metabolite of heptachlor is heptachlor epoxide.056 (.070-.300-..170) .140-.199-.320) .077) .050-.213) * .400) .063) * . 82 Fourth National Report on Human Exposure to Environmental Chemicals .253-.450) .148-.160 (. IARC. Shindell and Ulrich.450) .320 (.090) .260 (. Subtle neurodevelopmental effects have been observed rodents after prenatal exposure to heptachlor (IPCS.270 (.170) .310) .290-.310-.130-.077) .133) 90th .112 (.280 (.350 (.079) < LOD < LOD < LOD . IARC considers chlordane and heptachlor as possibly carcinogenic to humans.068-.287) .066-. The U.373) .430) .286 (.065-..067 (.119 (.090) . OSHA has established occupational exposure criteria.070 (<LOD-.120 (.180-.290) .210 (.066 (<LOD-.149 (.083) .310) .230 (.068) . 1991.200-.

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

3) 10.8 (18.9 (12.3 (<LOD-25.S.8) 21.5) < LOD 14.2) 26.0-17.0-19. interval) Selected percentiles ( 95% confidence interval) Sample 95th 24.9-25.40) 15.2) 15.3) 27.7 (16.0) 13.6 (16.0-54.8) 13.1-38.10-13.1) 13.1-15.90 (<LOD-9.3) 18.7-25. population from the National Health and Nutrition Examination Survey.6) 22. 84 Fourth National Report on Human Exposure to Environmental Chemicals .8 (13.6 (8. and 03-04 are 14. 01-02.3) 23.8. Survey Geometric mean (95% conf.8 (<LOD-23.2-16.3) 16.9) 15.8) 20.7-18.8) 19.8 (18.6 (16.2) 13.3 (13.7 (10.2-27.4 (11.8) 15.4) 21. respectively. and 7.4 (<LOD-54.9-29.5 (11.7 (13.1) 23.Organochlorine Pesticides Serum Heptachlor epoxide (lipid adjusted) Metabolite of Heptachlor Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U.6) < LOD < LOD < LOD 27.2 (<LOD-62.0) 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 13.2 (<LOD-25.1-16.9 (15.8) 19.5 (<LOD-21.5 (<LOD-32.5) 760 1047 956 829 1212 1007 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 7.8-24.0-17.1-29.1 (16.3) 22.5) 598 553 460 336 503 490 539 1041 888 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.8) 14.3-18. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.0) size 1589 2259 1963 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th 90th 15. 10.4) 18.8) 14.8 (15.8-23.20 (<LOD-9.6-17.0 (15.8-46.1 (19.9-23. < LOD means less than the limit of detection.6 (13. which may vary for some chemicals by year and by individual sample.6) 13.5 (11.1) 20.4 (<LOD-19.8-24.0-16.6.5 (18.8) 16.4 (15.2 (18.8-24.8 (13.7-19.8) 13.5 (10.2-17.3) 18.6 (11.6) 14.0 (11.2-27.6-21.50) < LOD < LOD < LOD 17.2) 20.9-29.6 (<LOD-27.5.9) * * * Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 8.6 (14.5) 19.2 (<LOD-16.6 (12.4 (11.3) 18.9-16. see Data Analysis section) for Survey years 99-00.

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

8 (71.9 (19.7-29.6 (15.5-95.9) < LOD < LOD < LOD 20.8 (28.9 (<LOD-14.4-35.5-87.9-40.1) 62.5) 77.5) 36.7 (13.1-28.6) 13.9 (28.0-143) 112 (68.5) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * 20.1) 31.3) 15.3 (45.9 (51.4-52.9) 14.7) 78.7 (35.9-20.2 (64.5-69.3-30.6) 25.0) Selected percentiles ( 95% confidence interval) Sample 95th 79.0 (14.5-19.6 (16.2 (26.5) 19.6) 10.9-36.3 (56.4-36.7) 35.8 (28.3-50.0 (16.5-17.1-16.4) 107 (84.0-23.9 (66.8 (13.2) 19.2-18.2 (14.1) 78.3 (49.3-86.5.4) 20.4) 48.3) 32. interval) 18.4 (30.0 (62.0) < LOD < LOD 8.5.6) 54.7) 15.8 (45.1 (41.1 (22. < LOD means less than the limit of detection. see Data Analysis section) for Survey years 99-00.2) 30.7) 56. 86 Fourth National Report on Human Exposure to Environmental Chemicals .1 (17.3-21.1 (10.9) 51.1-126) 67. and 03-04 are 14.5 (15.2 (7.1) 17.1 (48.8-19.4-22.4-18.2-18.6 (57.1) 17.0) 13.7 (30.0 (29.9-89.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.0-93.6-66.0-123) 74.2) 39. which may vary for some chemicals by year and by individual sample.5) 90th 55.8 (19.8-41.9-58.6-20.7) 59.9) 51.8 (11.3 (14.0-20.2 (60.3-58.5-111) 68.4 (11.6-22.3) 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.2 (36.86-13.8 (16.2 (15.8-77.1) 18.6 (56.7-21.9) 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 (12.9 (47.8-16.7) 28.0) 19.0-22.7-17.7-18.5-20.8) 19.6 (56.9-64.9 (15.6 (52.0-59.3) 30.8-19.6) 34.1) 17.1) 17. respectively.8 (12.6-19.3) 25.4 (45.8 (42.8 (28.9 (15.4-23.2 (14.7-23.0-37.6 (32.0 (15.4) 16.6) 56.5-36.0 (13.3) 16.5 (25.5) 48.9-65.5) 78.8 (49.6 (<LOD-14.9-69.7-22.3) size 1933 2286 1955 Total years 99-00 01-02 03-04 50th 17.8) 80.7 (11.8-90.8-90.6-88.5) 35.3-57.5) 26.3) 18.1) 14.1-18.7-32.3 (16.2-23.7-77.1-16.4) 59.0 (42.7 (59.1) 78.0-68.0 (42.1-55. and 7.7-160) 86.0 (48.3) 19.4 (28.2-37.8.2-21.1-51.2-16.7) 17.7 (28.3 (17.9 (36.8-21.6 (50.3-39.1) 30.5) 14.4-62.5) 9.7-20.8) 47.8 (26.6) 56.8-67.0 (60.5) 20.1-22.5 (13.0-93.1-34.2 (19.6) 84.3-74.2 (27.7-113) 68.2) < LOD 10.1) 17.7) 73.5 (44.70 (<LOD-12.0) 75th 31.1) 16.8 (26.4-67. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.1) 32.6) 60.0-38.8 (30.1) 17.5) 14.6) 82.2 (59.0 (15.7 (74.1) 18.0) 664 758 589 1269 1528 1366 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 17.2) 34.2-17.2) 20.1) 17.2-88.4 (12.2) 17.9-22.7) 52.7 (16.8 (<LOD-20.9-35.8 (17.8) 51.3 (14.3-32.6-54. 10.8-129) 74.8-110) 59.9) 14.3) 32.8-16.0 (16.5 (45.1 (47.9 (29.0-113) 68.7) 14.5) 30.0) 40.7 (59.0-23. 01-02.7-38.8-79.9-45.8 (26.1 (65.4 (16.0) 49.9 (51.0) 33.2) 59.1-34.5) 22.8 (15.7) 78.0-24.3 (58.4 (67.0 (13. population from the National Health and Nutrition Examination Survey.4) 55.7 (18.7-35.8 (13.5 (15.9-65.10 (<LOD-11.3) 30.9 (16.1-20.7-34.0) 18.4) 19.6-82.3) 18. Survey Geometric mean (95% conf.2 (25.0 (19.3) 36.S.

405) .104 (.630) .087 (.290-.113) .510-.090-.390 (.202 (.500) .760 (.125 (.141) .100-.550 (.099-.119) Selected percentiles ( 95% confidence interval) Sample 95th .108 (.161-.510 (.160-.340-.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.684) .100-.096) .330 (.400 (.131) .190-.390 (.300-.085-.122) .081-.127) < LOD < LOD .220 (.085-.096-.110 (.210-.250) .286-.116-.090-.830) .110) .220 (.240) .690) .210) .161) . Survey Geometric mean (95% conf.092 (.580 (.093-.081 (.124) .590 (.395) .120) .410-1.117) .112 (.400-.240) .112 (.062 (.145-.230 (.100 (.113) < LOD .450) .141) .220 (.134) .565) 922 1062 955 1011 1224 1000 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 * .400) .310 (.180-.371) .440-.390 (.190-.390) .390 (.310-.580 (.180-.190-. which may vary for some chemicals by year and by individual sample.093-.470-.430-.460) .420 (.390) .310-.220 (.260) .310-.120) .060) .410-.250) .232) .082) .490 (.173-.310) .090-.210-.242) .120-.186 (.122) .109 (.690) .430-.380 (.490 (.130) .340) .090 (.220) .460-.128 (.080 (.130) .085-.470 (.191 (.103 (.350-.590) .130) .070 (.220 (.327 (.367) .079-.090 (<LOD-.080-.565) .370 (.190-.171-.497-.170 (.098 (.237) .324 (.680 (.130) .091-.135 (.109 (.190-.099-.280) .960) . population from the National Health and Nutrition Examination Survey.470 (.130) .409-.111 (. Fourth National Report on Human Exposure to Environmental Chemicals 87 .420) .640 (.150) .110 (.250) .108) 75th .310-.183 (.580 (.630) .430-.210) .100) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.116 (.272-.220 (.094 (.490) .237) .520) .119) < LOD < LOD < LOD .840) .205 (.041 (<LOD-.480) .540) .320-.400-.091) .110 (.111-.080-.158-.105 (.330-.343 (.060 (<LOD-.520 (.285-.320-.130) .600 (.288 (.680) .120-.150) .350 (. interval) .110 (.047-.089 (.390-.180-.100-.093) .097) .240 (.104-.279-.270-.068-.211) 90th .651) .330-.186-.400 (.559) .114) .395-.234) .080-.140) .080) .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 .055 (<LOD-.098 (.160 (.800) .600) .240-.106 (.220 (.360-.417 (.060-.110 (.360-.100 (.Organochlorine Pesticides Serum trans-Nonachlor (whole weight) Metabolite of Chlordane Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U.370 (.210 (.078-.458 (.260) .240) .069) .103 (.092 (.084-.20) .470 (.126) .210) .110-.090-.130) .220 (.490-.397-.461 (.093-.098) .930) .460) .190-.630) .340-.090-.558) size 1933 2286 1955 Total years 99-00 01-02 03-04 50th .177-.120-.106 (.078 (.S.079-.090) .120) .054-.120 (.210 (.594) .470-.116) .120 (.440) .090-.288-.130 (.573 (.830) .110 (.100-.520 (.120) .125) .120 (.129) .071 (<LOD-.108) .210 (.061-.355 (.106 (.301-.069-.590 (.130 (.414 (.096-.098-.317 (.095-.300) .080-.

org/documents/iarc/ vol79/79-12. et al. Bioassay of heptachlor for possible carcinogenicity. Ayotte P. Poland.8:1-123. Jaraczewska K.150:981-990. Sci Tot Environ 2006. Environ Health Perspect 2002. Willman E. Covaci A. Berkowitz GS. Aune M. Bioassay of chlordane for possible carcinogenicity. Odland JO. Determinants of serum polychlorinated biphenyls and organochlorine pesticides measured in women from the child health and development study cohort. 1994-1997 organochlorine compounds.nih. Darnerud PO.nih. Granath F. 1979-1980. Hertz-Picciotto I.pdf.org/ documents/cicads/cicads/cicad70. Loo S. Chlorinated Hydrocarbon Insecticides. International Agency for Research on Cancer (IARC) . Academic Press. Bjerselius R. Bleiweiss IJ. 2001. Brower S. Wohlleb JC. Evaluation of human exposure to the heptachlor epoxide contamination of milk in Hawaii. 4/21/09 Baker DB. organochlorine pesticides and polybrominated diphenyl ethers in human umbilical cord serum. Environ Health Perspect 2002.atsdr. maternal serum and milk from Wielkopolska region. Jr and Laws ER. 2 Classes of Pesticides.110:617-624. et al. Kolonel LN.html. Circumpolar maternal blood contaminant survey. Mortality of workers employed in the manufacture of chlordane: an update.cdc. Trends in birth defects for a Hawaiian population exposed to heptachlor and for the United States. Senie R.259(3):374-377. Dewailly E. Jr. 4/21/09 Agency for Toxic Substances and Disease Registry (ATSDR). In Hayes WJ. Stehr-Green P.330:55-70. Lawrence River (Quebec. Voorspoels S. KalubaSkotarczak A. Barker J. Lulek J.28:497501. Takei G. Dewailly E.htm. Handbook of Pesticide Toxicology. May 1994.inchem. Atuma S. 4/21/09 Dallaire F. Available at URL: http://www. Hawaii Med J 1991. Organochlorine exposures and breast cancer risk in New York City women.9:1-109. Natl Cancer Inst Carcinog Tech Rep Ser 1977b. LeMarchand L. Head SL. Vol.html. Drews K. Arch Environ Health. Chashchin V. 1963-1967.gov/ntp/ htdocs/LT_rpts/tr009. Hansen JC.84:151-161. Chlordane and heptachlor [online]. 1993. Muckle G. Bull Environ Contam Toxicol 1981:27:506-511. Baker DB. 9/25/07 International Programme in Chemical Safety (IPCS). International Agency for Research on Cancer (IARC). 4/21/09 James RA. Van Oostdam JC. Vol. Temporal trends of organochlorine concentrations in umbilical cord blood of newborns from the lower north shore of the St.inchem. 2006. Available at URL: http://www. Environ Health Perspect 2003. Wong L. Inc.111:349355. Glynn AW.niehs. Organochloride pesticide residues in human milk in Hawaii. et al. Available at URL: http://ntp. An evaluation of serum pesticide residue levels and liver function in persons exposed to dairy products contaminated with heptachlor. 1986. Tartter P. Pollutants in breast milk.htm.cdc. Laliberte C. et al. Keller JA.gov/ntp/ htdocs/LT_rpts/tr008. National Toxicology Program (NTP). Smith AG.atsdr.50(3):108-118.110(8):835-838. Wolff MS. Dendle WH. Eds. Estimation of Human Exposure to Heptachlor Epoxide and Related Pesticides in Hawaii. 1991 pp. Sci Total Environ 2004.pdf. Shindell S and Ulrich S. New York. Concise International Chemical Assessment Document 70 Heptachlor [online].Summaries & Evaluations. gov/toxprofiles/tp12. Saidein D. JAMA 1988. Toxicological profile for heptachlor and heptachlor epoxide [online].gov/toxprofiles/tp31. 731-915. J Occup Med 1986.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR).org/site/foundation/ research/projects2. Toxicological profile for chlordane [online]. Available at URL: http://www.niehs. Gilman A. Royce W. Distribution of polychlorinated biphenyls. Available at URL: http://www. A Report to the Hawaii Heptachlor Research and Education Foundation. 79.41:145–148.372:20-31. Arch Pediatr Adolesc Med 1996. 88 Fourth National Report on Human Exposure to Environmental Chemicals . 6/1/09 Rogan WJ.html. Natl Cancer Inst Carcinog Tech Rep Ser 1977a. Available at URL: http://www. August 2007. Siegel BZ. 6/1/09 National Toxicology Program (NTP).heptachlor. Charles MJ. Environ Res 2000. Organochlorines in Swedish women: determinants of serum concentrations. Available at URL: http://ntp. Takahashi W. Canada).

0-35.2) 30. DDT can be absorbed after ingestion.2) 155 (59. population from the National Health and Nutrition Examination Survey. Fourth National Report on Human Exposure to Environmental Chemicals 89 .5-54.S.6 (25. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.p'-Dichlorodiphenyltrichloroethane (DDT) (lipid adjusted) Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U.0) 20.0) 40.1’-dichloro-(2.2-95. It is still used in some countries.p’-DDD (4% or less). when virtually all use of it was banned.8-17. and water.S. respectively. < LOD means less than the limit of detection.4) < LOD < LOD < LOD 61.3 (<LOD-31.9-34. and trace amounts of several related compounds.p’-DDT (65%-80%).5) size 1679 2305 1965 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * * 11.8) 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. 1991).7 (19.0 (10.3 (27.8.5) 23. and dairy products. continues to be the primary source of DDT exposure. It was produced and used in the U. which is a mixture containing p. after World War II until 1972.4 (23.2-65. see Data Analysis section) for Survey years 99-00. Food imported from countries that still use DDT may contain the chemical or its residues. DDT and DDE can cross the placenta.8-23. Smith. o.0) 19.3-590) 293 (104-541) 48. 17.9-28. inhalation.8) 15. air.90 (<LOD-12. which may vary for some chemicals by year and by individual sample. population. sediments. 2002. DDT and DDE are distributed to all body tissues with the highest concentrations found in adipose tissues (ATSDR.3) 22.S. p.8-39. DDT was used at one time as a treatment for head and body lice.p’-DDT (15%-21%).10 (<LOD-12.6 (31. In the general U.2 (<LOD-40.8-26.7. interval) Selected percentiles ( 95% confidence interval) Sample 95th 28.6) 635 566 461 356 514 490 564 1061 890 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. Only a small proportion of DDT is metabolized and excreted (Smith. Gunderson. Both Serum p.5 (23. as well as in plant and animal tissues.0 (21.1-27.6 (22.3 (<LOD-21.2) < LOD < LOD 9.3) 21.9) 17.5-36.5 (23.1) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 12. and 03-04 are 20.2-dichloroethenylidene)-bis[4-chlorobenzene] (DDE) and 1. including 1.50-11. DDT is converted to DDE and several other metabolites.5 (14.3) 28. depending on conditions.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 10.3-236) 24.9 (10.1) 31. 2008.10-13.3) 21.1’-(2.3-16.1 (33.00 (<LOD-10. 1991).70 (8.0 (18.Organochlorine Pesticides Dichlorodiphenyltrichloroethane (DDT) CAS No.0 (18.7 (15.5) < LOD < LOD 9.6 (9. In the body. resulting in fetal exposure. 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.2-bis(p-chlorophenyl) ethane (DDD). DDT is converted in the environment to other more stable chemical forms.1 (<LOD-39.9 (10.9) 29.2 (11. food.9 (10.7) 12.9 (<LOD-20.9) < LOD < LOD 9.8) 36. fish.5) 25. particularly meat. particularly for endemic vector and malaria control.0-15. Survey Geometric mean (95% conf.6-33. and 7.4. These chemicals are highly persistent in soil.7) < LOD 18. The biodegradation half-life of DDT in soil varies from 2 to 15 years. 1988). DDT usually refers to the technical product.0-37.0-53.4) < LOD 17.0) 26. or dermal exposure. 01-02.6 (<LOD-25.7-16.5 (15. although DDT and DDE intakes have decreased over time (FDA.0-27.1 (23.1-71.9) 14.8) 30.0-155) 83.9 (21.

1997).087 (. 2002.. tremor. and seizures.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 .230) .170-.140-.. reproductive organ abnormalities.150 (<LOD-. other organochlorines.105-. Studies of DDT exposure and pancreatic cancer.084 (.150 (<LOD-.128 (.098-.180) .150-. and duration of lactation.240) .086 (.150) ..167) size 1679 2305 1965 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * * .074-.00) .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 altered behavior after neonatal exposure (Eriksson and Talts. population from the National Health and Nutrition Examination Survey. Several reviews of cancer epidemiologic studies have concluded that a link between DDT and breast cancer is inconclusive (Beard. 2006). both DDT and DDE may induce specific cytochrome P450 isozymes (Nims et al. 1956).114-. 2000...530 (.220) .203) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result. have not been consistently demonstrated (Beard.343) < LOD .063 (<LOD-.. which may vary for some chemicals by year and by individual sample. Snedeker. In laboratory animals. Beard. premature delivery. Hayes et al. 2006.p’-DDE can produce anti-androgenic effects (Gray et al. Longnecker et al.400 (.220) .190-1.054-.108 (. resulting in exposure to nursing infants (Rogan.071-. Jusko et al.142 (. Calle et al.106-. 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. 2001)... Animal studies reported reduced fertility. Jusko et al. Epidemiologic studies of children with environmental exposure to DDT and DDE have not demonstrated neurologic or developmental abnormalities (Gladen et al. Reproductive effects in humans affecting birth weight.Organochlorine Pesticides chemicals are excreted in breast milk.290) .080-.048 (<LOD-. DDT may bind to estrogen receptors (Chen et al.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..068-.150-.160-.051 (<LOD-.g.180 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th . 2002.530) .180) .106) .130 (<LOD-.240 (. 2006). 2006. 1998).146 (.146 (.. 2006.130 (<LOD-.130-.201 (.250-1. although the risk for preterm delivery may be related to maternal DDE levels (Longnecker et al.190 (. Mariussen and Fonnum.120-.064 (.078 (. overt signs of acute human toxicity include vomiting. 2004.143) < LOD < LOD . Gladen and Rogan.S. 1995.097) 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 .330-4. 90 Fourth National Report on Human Exposure to Environmental Chemicals .075) 1.130 (<LOD-.065-.p’-DDD and p.095) < LOD .. In high dose. fertility.62 (.059-.34) .170) . 1996). 2002. 2001).140) . Human health effects from DDT at low environmental doses or at biomonitored levels from low environmental exposures are unknown.200 (.170 (.627) . 2002.069) .570-4. and leukemia have also been inconclusive (ADSDR. 2006). and o.132-.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. Survey Geometric mean (95% conf.230) . accidental exposures.400) .180-..079) < LOD < LOD .078-.120 (<LOD-. 2001). lung cancer.071 (. Gray et al.260) .061) < LOD < LOD < LOD .190 (.00 (.189-.26) 1. polychlorinated biphenyls.180 (.01) .112 (.250 (.420) . A workplace standard for DDT has been established by Serum p.106) < LOD < LOD . 2001). dioxins and furans). It is difficult to attribute outcomes in human studies solely to DDT because of potential co-exposure to other persistent organohalogen chemicals (e.313 (.

Declining DDE levels over time have also been observed in the German population. and 7.Organochlorine Pesticides OSHA and a guidance established by ACGIH.gov/ toxpro2. 2004). In general. see Data Analysis section) for Survey years 99-00. population declined by about fivefold to tenfold. NTP considers DDT as being reasonably anticipated to be a human carcinogen.8.0-114) 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. 1991).. mean serum levels of DDT and DDE in the U. Stehr-Green. Heudorf et al. Link et al. 1989). Compared to females in the NHANES 1999-2000 subsample. the lipid-adjusted geometric mean levels of DDT and DDE were each fivefold to tenfold higher than the 95th percentile and geometric mean levels. and the most recent median levels for German adults and children are similar to levels in this Report (Becker et al. compared to levels observed in this Report (Anderson et al.S.gov/ pestcides/ and from ATSDR at: http://www.. population from the National Health and Nutrition Examination Survey.S.html.6 (81.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. IARC classifies DDT (p.atsdr. 8. Biomonitoring Information DDE persists in the body longer than DDT. In a population-based sample of men and women from eastern Slovakia. Fourth National Report on Human Exposure to Environmental Chemicals 91 . respectively. 1998. 2004). 2003... Since the 1970’s.. for males and females in the NHANES 19992000 subsample (Pavuk et al. EPA at: http://www. 2002. 2005). Survey Geometric mean (95% conf.e.7-129) 297 (256-344) 338 (303-376) 268 (217-332) 108 (97.6.cdc.S. environmental levels) and health effects is available from the U.epa. 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. respectively... 2003). and 03-04 are 18. 01-02. 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 (84.7-119) 113 (100-140) 93. Smith. 2002. so serum DDE levels may be an indicator of historic exposure and may be higher than DDT levels in the same person. 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. mean DDE levels were about fivefold higher among women of southern Spain exposed by virtue of Serum p. More information about external exposure (i. levels of DDT and DDE increase as a person ages as a result of cumulative exposure (ATSDR.p’-DDT) as a possible human carcinogen.

56-3.22-1.92 (3.07) 1.66) 1.80) 1.51-8.71) 32. interval) 1.8) 15.39 (3.4) 9.41-12.820-1.59 (4.p’-DDT.01-1.58) 75th 3.03-4.75) 1.52 (1.70-3.62-6.6) 9.78 (4.06) 3.43-4.0 (9.02 (2.4 (8.635) 1.80 (2.30 (1.63-15.69 (.23 (7.726) .18-1.51 (1. High mean levels of whole blood DDT (about 3.385-.14-9.99) 1.24 (1.9-17.9 (15.32-1.88 (2.60-13.54) 8.64-2.1 (8.45 (1..32-9.56-2.56) 2.66) 3.68 (2.994-2.14 (1.91) 3.68-4.p’-DDT were below the limits of detection.01-5.77 (1.01-15.58) 1.561 (.10) 2.14) 2.63 (1.1) 12. 2001-2002 and 2003-2004 subsamples.25 (.2) 26.48 (6.87-16.6 (17.8 (13.47) 3.82 (1.51) 3. 2004).490 ng/L) were found many years ago in a study of pesticide workers in Argentina (Radomski et al.59) 6.8 (9.730) .97-4.27) 3.4-19.488-.37-16.96) .6) 9.43-4.81) 11.90-8.93 (7.9 (26.31-12.S.25) 1.3) 937 1069 955 1027 1229 1001 Females 99-00 01-02 03-04 Race/ethnicity Mexican Americans 99-00 01-02 03-04 3.29 (1.75) 2.16-1. or p.7-20.16 (2.34 (7.13 (1.57-3.76) 1.13-2.9) 7.39-1.32 (1.54-7.10-1.34) 6.18-4.96) 1.796 (.3) 16.49 (1. 2005).25-16.88-35. 2004).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.38 (1.2 (9.01-11.p’-DDT (Stehr-Green.19) 4. Finding a measurable amount of p.26 (1.40 (3.28) 1.1) 40.75 (8.860 ng/L) and DDE (about 14.1 (9.01) 1.85-4.26) 3.56-6.58) 1.32-1.31 (1.87 (5.3) 13.32 (1.11 (2.34-3.55-9.p’-DDT.53) 7.54 (1.19-14.534-.516 (..2 (9. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.46 (1.5) 7.76-3.51-49.17-3.5) 10.25 (1.6) 13.57-2.80) 1.00 (.43-8.8-90.963-1.7-19.2) 19.35) 1.0) 657 566 457 416 515 487 732 1053 888 Non-Hispanic blacks 99-00 01-02 03-04 99-00 01-02 03-04 Non-Hispanic whites 92 Fourth National Report on Human Exposure to Environmental Chemicals .53) 1. o.82) 1.22 (7. population from the National Health and Nutrition Examination Survey.623 (.1) 7.50-17.34-11. 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.51-15.71) 12.91 (6.25-14.91-3.70) 1.79) 4.49 (6.5) 5.50 (2.68) 2.30-1. Workers involved in production or application of DDT developed neurologic abnormalities associated with blood levels around 100-300 mg/L.79) Selected percentiles ( 95% confidence interval) Sample 95th 11.40-4.24) 1.39) 1. 1989).36-2.4) 14.611-1.69 (2.37 (1.24-17.14-1.59 (1.46 (1.12 (.18 (6.61-2.81 (1.63 (6.91-2.77 (1.3) 10.6) 12.8 (14.0) 2.870 (.01-1.12 (6.419-.76 (2.11-1.57) 2.00-1.21) 90th 7.57 (3.430-.69) 8.83 (1.59) 3.07) 1.75) 6.75 (4.33-1.55 (2.p’-DDE in serum does not mean that the level of the chemical causes an adverse health effect.69) 4.05 (3.66) 1.64) 3.90) 22.57 (1.92) 1.47 (1.13) 4.18-3..25) 8.14) 2.20 (.01) 1.36-1.6) 8.03-1.7) 9.36 (3.27-1.51) 1.53-15.6 (9.00) 7.02) 1.30-1.3 (8.40-4.81 (7.965-1.52 (3.71 (5.52-6.7 (8.40-8.9-38.31-2.15-4.18-1. serum levels of o.10) .646) .8) 686 758 588 1278 1540 1368 20 years and older Gender Males 99-00 01-02 03-04 1.71 (6.22) . less than one percent had detectable serum levels of o. 1971).500-.57-13.17 (3.81-18.8 (13.26-10.4 (12. which is similar to the overall geometric mean of 260 ng/g lipid in the NHANES 1999-2000 subsample (Bloom et al.36) 3.01-11.5) 16.30 (1.92 (3.38 (1.04-1.520 (. In a subsample of NHANES II (19761980) participants.456 (.06) 1.3-43.66) 4.9) 5. In the NHANES 1999-2000.57 (1. Serum p.39-2.07 (5.85-10.12-1.2 (19.48-4.6) 9.34) 2.41 (1.63 (1.72) 1.00 (6.37-10. Survey Geometric mean (95% conf.37-1.557) 1.Organochlorine Pesticides nearby agriculture (Botella et al.66-4.6) 11.2-32. 309 versus 268 ng/g lipid.80) 3.32) 1.0) size 1964 2298 1956 Total years 99-00 01-02 03-04 50th 1.18) 1.05) 1.02-8..79) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 . 1991).84 (3.66-2.7-48.53 (2.10-5.21) 3.6) 9.4) 13.3 (9.26-2.65 (1.43 (5.65) 1.49 (1. considerably higher than levels in this Report (Smith.46-2.7) 13.04 (6. Consumers of Great Lakes sport fish had mean serum DDE levels that were only slightly higher than nonconsumers.2 (6.36-11.680-1.72) 1.69 (1.890-1.37-4.84-3.45 (1.81-5.66-17.6 (8.09-1.59 (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.97 (3.85 (1.44) 1.76) 1.61 (1.6 (7.49) 8.590 (.0 (12.7) 16.600) .5) 22.

respectively. * 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 93 . and 7. 01-02. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD < LOD size 1669 2279 1946 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD < LOD 90th * * * Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 667 756 588 1002 1523 1358 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 796 1059 949 873 1220 997 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 632 565 458 354 507 486 560 1045 880 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. and 03-04 are 20.8. < LOD means less than the limit of detection. which may vary for some chemicals by year and by individual sample. population from the National Health and Nutrition Examination Survey. 17.S.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. see Data Analysis section) for Survey years 99-00.4. Survey Geometric mean (95% conf.Organochlorine Pesticides Serum o.7.

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

html. Cueto C. Thun MJ.111:349355. Becker K. Organochlorines in Swedish women: determinants of serum concentrations.1-dichloro2.cfsan. Eriksson P.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Int J Hyg Environ Health 2003. Swanson MK. Wolf CJ.355:7889. Food and Drug Administration (FDA). Am J Epidemiol 2002. Hayes WJ. Ostby J. Maternal serum level of 1. et al. Fourth National Report on Human Exposure to Environmental Chemicals 95 .cdc. Environ Health Perspect 2003. lindane (g-HCH). PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. Falk C. Olea-Serrano MF. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population.106(5):279-289. Botella B. and polythelia among male offspring. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. a biostable metabolite of dichloro(diphenyl)trichloroethane (DDT). Longnecker MP. Klebanoff MA.155(4):313-322. selected elements. Needham LL. Environ Res 2004. Angerer J. Jusko TA. Zoellner I. Cerrillo I. Durham WF.. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Am J Public Health 1995.54:1431-1443. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. Neurotoxicol 2000. Hurd C. Available at URL: http://www. Brock JW. Zhou H.162:890-897. Kashyap R. Savitz DA. Seiwert M. Charles MJ.gov/ toxprofiles/tp35. Klebanoff MA. Available at URL: http://www. Biochem Pharmacol 1997. Sci Tot Environ 2006. Prenatal DDT exposure in relation to anthropometric and pubertal measures in adolescent males. Gabrio T. Levels of DDT. Lancet 2001. and dichloro(diphenyl)ethylene (DDE). DDE. Willman EJ. CA Cancer J Clin 2002. Bhatnagar VK. Herrman T. Gunderson EL. Moysich KB. Granath F. Baker RJ. Krause C. Jr. Beard J. hypospadias. Piechotowski I. et al. Lambright C. Link B. Atuma S.gov/~dms/ pesrpts. Gladen BC. Brock JW. Organochlorines and breast cancer risk. Glynn AW. Transcriptional activation of the human estrogen receptor by DDT isomers and metabolites in yeast and MCF-7 cells. Heudorf U. 4/21/09 Anderson HA. Hediger ML. Saiyed HN. Maternal DDT exposures in relation to fetal and 5-year growth.58:1185-1201. Jr. et al. Vorojeikina DP. Patterson DG Jr. Chemosphere 2004. Olson JR. Talts U. Longnecker MP. et al. Bull Environ Contam Toxicol 2004. India. Garrett N. Hum Reprod Updat 2001. Schulz C.52:301-309.atsdr. Hanrahan L. Bates MN. Furr J. et al.71(6):1200-1209. and HCB residues in human blood in Ahmedabad. August 2008. Effects of environmental antiandrogens on reproductive development in experimental animals. Biomonitoring of persistent organochlorine pesticides. Ellis H. et al.205:297-308. Exposure of women to organochlorine pesticides in Southern Spain. Paepke O. et al.html. Arnold SF. The Great Lakes Consortium. Olson J.21(1-2)37-48. Barr DB.fda.96:34-40. dietary intakes of pesticides.112(17):1761-1767. Drexler H. and Mirex among male Lake Ontario sportfish consumers: the New York State Angler cohort study. Current internal exposure to pesticides in children and adolescents in Germany: blood plasma levels of pentachlorophenol (PCP). DDE and shortened duration of lactation in a northern Mexican town. Chen CW. September 2002. The effect of known repeated oral doses of chlorophenothane (DDT) in man. dichlorodiphenyldichloroethylene. HCH. Crespo J. Needham LL. Environ Res 2005. Davis MD. Parks L. Olea N. Rogan WJ. hexachlorobenzene. Chemosphere 2005. Darnerud PO. Notides AC. Henley SJ. Zhou H. Burse VW. JAMA 1956.7(3):248-264. Int J Hyg Environ Health 2002. Gray LE Jr. 4/21/09 Gladen BC. Lepom P. and DDD [online]. Toxicological profile for DDT. Kulkarni PK. Bloom MS. Environ Health Perspect 2004. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population.97(2):178192. Gray KA.2-bi(p-chlorophenyl)ethylene and risk of cryptorchidism. Association between maternal serum concentration of the DDT metabolite DDE and preterm and small-for-gestational-age babies at birth. Epidemiology 2006.17(6):692-700. Klebanoff MA. Needham LL. DDT and human health. FDA total diet study. Environ Health Perspect 1998. Katz SH. et al. Rivas A. Zaidi SS. Buckland SJ. J Assoc Off Anal Chem 1988. Kaus S.72:261265. and other chemicals. Koepsell TD. April 1982 to 1984.206:485-491.358:110-114.53(8):1161-1172. Aune M. Vena JE. Neonatal exposure to neurotoxic pesticides increases adult susceptibility: a review of current findings. Calle EE. Frumkin H. Profiles of ortho-polychlorinated biphenyl congeners. Bjerselius R. Greenfield TA. et al.85:504508.

Jr and Laws ER. Smith AG. Rey AA. Inc. Chemosphere 2004. J Toxicol Environ Health Part A 1998. Stehr-Green. Lubet R. et al. Academic Press. Reddy AB. In Hayes WJ. Environmental exposure to PCBs and cancer incidence in eastern Slovakia. Jones CR. Petrik J. Blood levels of organochlorine pesticides in Argentina: occupationally and nonoccupationally exposed adults. Rogan WJ. Demographic and seasonal influences on human serum pesticide residue levels.27:405-421. DDE. and DDD in male rat liver and cultured rat hepatocytes.150:981-990. Nims R. Radomski JL. Neurochemical targets and behavioral effects of organohalogen compounds: an update. Pesticides and breast cancer risk: a review of DDT.53:455-477.20(2):186-193. Comparative pharmacodynamics of CYP2B induction by DDT. Snedeker SM. Thomas PE. New York. Fonnum F. children and newborn infants. Cerhan JR.36:253-589. Jr. Eds. Astolfi E.54:1509-520. J Toxicol Environ Health 1989. Schecter A. Fox S. Toxicol Appl Pharmacol 1971. DDE. 731-915. 96 Fourth National Report on Human Exposure to Environmental Chemicals . 2 Classes of Pesticides. PA.Organochlorine Pesticides Mariussen E. Chlorinated Hydrocarbon Insecticides. Lynch CF. Deichmann WB. and dieldrin. Handbook of Pesticide Toxicology.109:35-47. Arch Pediatr Adolesc Med 1996. Crit Rev Toxicol 2006. Vol. Pavuk M. et al. 1991 pp. Pollutants in breast milk. Chovancova J. Environ Health Perspect 2001.

Endrin has been detected in soils. endrin usually is not detected in serum of exposed individuals. endrin has been detected with declining frequency in U. Because it is metabolized so rapidly.S. 1992). Endrin was not widely used as a termiticide. All uses of the pesticide in the U. which may vary for some chemicals by year and by individual sample.40 (<LOD-6..50) < LOD < LOD < LOD 5. fatty infiltration. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 1992. 1992). Skeletal abnormalities and cleft palate in the offspring were associated with endrin when it was fed to pregnant laboratory rodents (Chernoff et al.30) < LOD 5.40) < LOD 547 433 487 446 1000 831 Limit of detection (LOD. Endrin was used as an insecticide.20 (<LOD-5. is no longer manufactured in the U. unlike aldrin and dieldrin. population from the National Health and Nutrition Examination Survey.30 (<LOD-6. or discarded. unless the dose is high and the exposure is very recent. IPCS.. inhalation or dermal exposure routes. 1992).60 (5. High doses produced renal tubular necrosis and diffuse kidney degeneration in animals.10 (<LOD-5.40) < 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. see Data Analysis section) for Survey years 01-02 and 03-04 are 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.S.8. < LOD means less than the limit of detection. General population exposure can occur after ingestion of endrin residues on food items imported from countries where endrin is still used.S. Survey Geometric mean (95% conf. 1987). Over time. Smith.50) < LOD 5. and occasionally at low levels in sediment and surface waters. 1979.S. 72-20-8 General Information Endrin. a stereoisomer of dieldrin. Ketoendrin is a major photodegradation product (IPCS. endrin can persist for years. 2008).Organochlorine Pesticides Endrin CAS No. 1981).. manufactured. Further conversion occurs to 12-ketoendrin and various conjugated metabolites which are excreted in urine and feces. Fourth National Report on Human Exposure to Environmental Chemicals 97 . An epidemic of acute endrin poisoning. At high doses.10 (<LOD-5. rodenticide and avicide. and inflammation (Smith.40-5.70) < LOD < LOD < LOD 730 539 1457 1286 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 5.09 and 7. endrin blocks inhibitory neurotransmitters in the central nervous system resulting in excitation and seizures (Narahashi et al. Endrin is absorbed rapidly after ingestion.. characterized by generalized seizures in previously healthy persons occurred in Pakistan when sugar contaminated with endrin was ingested (Rowley et al. largely the result of historical agricultural application or run off from contaminated soils (ATSDR. In the body. 1991). Human health effects from endrin at low environmental doses or at biomonitored levels from low environmental exposures are unknown. anti-12hydroxyendrin. Depending on soil conditions. or from contact with contaminated soils and sediments in areas where endrin was applied. total diet surveys (FDA. EPA. 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. Kavlock et al.S. Hepatic effects of endrin exposure have included necrosis.20 (<LOD-5. 1996. Endrin does not accumulate in body tissues (IPCS. have been cancelled by the U. interval) Selected percentiles ( 95% confidence interval) Sample 95th 5. endrin is converted rapidly to its major metabolite.

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

et al. Gray LE. Olea N. Ellis H.96:34-40. Rowley DL. Available at URL: http://www. Olea-Serrano MF. Food and Drug Administration (FDA). 4/21/09 Bates MN. Garrett N. Turner W. Narahashi T. Kavlock RJ. Vol. Available at URL: http://www. Toxicology 1979. Frey JM. Liddle J. Endrin [online]. I. Roy ML.gov/toxprofiles/tp89. Grajewski B. Hanisch RC. Fetotoxic effects of prenatal exposure in rats and mice. Chernoff N. No:429-436. Gray J. Convulsions caused by endrin poisoning in Pakistan.fda. Schulte P. Academic Press.64-65 Spec. Whitehouse DA. Ginsburg KS. Sokal D. Smith AG. pp. Fourth National Report on Human Exposure to Environmental Chemicals 99 . 2 Classes of Pesticides. Saleem M.gov/~dms/ pesrpts. Chlorinated Hydrocarbon Insecticides. Rab MA. Patterson DG Jr. Jr. Buckland SJ. Perinatal toxicity of endrin in rodents. Sodium and GABA-activated channels as the targets of pyrethroids and cyclodienes. Rogers E. Toxicology 1981. Toxicological profile for endrin [online]. Cerrillo I. August 1996.79(6):928-934. Exposure of women to organochlorine pesticides in Southern Spain. Handbook of Pesticide Toxicology. 4/21/09 Kavlock RJ. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR).9:1357-136. Pediatrics 1987.htm. Cancer Epidemiol Biomarkers Prev 2000.13:155-165.inchem. New York. II.21:141-150. 1991.54:1431-1443. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Hardjotanojo W. Crespo J. Andersen A. Ward EM. Hanisch RC.cfsan. Rivas A.org/documents/ehc/ehc/ ehc130.html. 731-915. Gray LE. et al. Toxicol Lett 1992. Eds. et al. Patterson DG Jr. Burse VW. Inc.atsdr. August 2008. Available at URL: http://www. Fetotoxic effects of prenatal exposure in hamsters. 4/21/09 International Programme on Chemical Safety (IPCS). Needham LL.html. Botella B. Jr and Laws ER. et al. Chernoff H. Environ Res 2004. Chemosphere 2004. In Hayes WJ.cdc. Perinatal toxicity of endrin in rodents. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Gray JA. Environmental Health Criteria 130. 1992. Serum organochlorine levels and breast cancer: a nested case-control study of Norwegian women.

2-31. Gunderson. Therefore.4 (18.2-15.Organochlorine Pesticides Hexachlorobenzene CAS No.4) < LOD < LOD 22.7 (15.3) 24.4-16. 31.3 (22.0 (18.7) < LOD < LOD 24.S.9) < LOD < LOD 20.6-33. 2005).5-15.2 (14.3 (22.6 (21. HCB is slowly metabolized.0 (18. 1997).8 (15.7-21.4) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * 13.3 (12.0) < LOD < LOD 15. Hexachlorobenzene has entered the environment as a result of industrial activities and pesticide applications.5 (14.6-TCP) (To-Figueras et al.0-19.7-30.5-TCP) and 2.7 (19. Workers in chemical manufacturing industries may be exposed to HCB via inhalation or dermal pathways.3 (16.1) * * 15. It is a persistent chemical and bioaccumulates in both aquatic and terrestrial food chains (ATSDR. Urinary metabolites include pentachlorophenol (PCP).5-14. 1988). see Data Analysis section) for Survey years 99-00.0 (14.3-20.8) size 1702 2277 1961 Total years 99-00 01-02 03-04 50th < LOD < LOD 14. 2.6) < LOD < LOD 14.4. particularly by consuming fish.5-trichlorophenol (2.6) < LOD < LOD 25.7) < LOD < LOD 75th < LOD < LOD 90th * * 15.3) < LOD < LOD 29. < LOD means less than the limit of detection.7-16.8 (26.1) < LOD < LOD 15.0 (25.4 (22. air.4) < LOD < LOD 23.9-20.5-18. 01-02.7 (27.6 (24. which may vary for some chemicals by year and by individual sample.6) < LOD < LOD 24. and foods with a high fat content.0) * * 15.5 (13..4) < LOD < LOD 14.7-16.7-22. distributes widely throughout the body.4.9) < LOD < LOD 19. HCB has been detected in fewer foods since the 1980s (FDA.7-15. primarily as a fungicide and seed treatment until the U.9-24.0-16.5-15.5 (13.8-15.2 (14.S.6-19. breast milk is an additional route of elimination in nursing women.9) < LOD < LOD 28.9-32.3-26.4) < LOD < LOD 18.9 (14.2 (24.9) 19.5-14.4) < LOD < LOD 19.9 (23. HCB is well absorbed after oral administration. and elimination occurs by renal and fecal routes.7 (15. 1976).8 (22. The FDA dietary surveys have shown that over time. and sediment (Barber et al.5-33.3 (14.1-20. 100 Fourth National Report on Human Exposure to Environmental Chemicals .6 (23. 2002).3 (20.1-16.0) < LOD < LOD 24.6-26. population from the National Health and Nutrition Examination Survey. these metabolites can also be produced after exposure to other chlorinated compounds (Kohli et al.6-44.4) < LOD < LOD 33. and 03-04 are 118..8) < LOD < LOD 27.9) < LOD < LOD 16.4 (18.2) < LOD < LOD 13.7) * * 14.9) < LOD < LOD 15.6-trichlorophenol (2. wildfowl.8) 583 554 460 350 511 488 636 1052 888 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.2) < LOD < LOD 29.3) < LOD < LOD 20.2 (13. Survey Geometric mean (95% conf.2-15. 2008.7-29.9 (25.9-30. HCB may be created as either a byproduct or an impurity in the manufacturing process for certain chemicals and pesticides. and 7. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.0-28.4. or game taken from areas with HCB contamination.6-32.9 (25.7) 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..8. EPA cancelled its use in 1984.0-25.4 (11.4. Although it is not manufactured as an end-product in the U. 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.1 (14.6) 591 747 588 1111 1530 1373 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * 14.. and accumulates in fatty tissues where it persists for years.9-15.3-22.S.4-15.1 (14. water.0. The general population may be exposed to HCB through diet. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD 28.1 (17.4.9) < LOD < LOD 20.9-17.0) < LOD < LOD 15.3) * * 15.7-26.1 (13.5) < LOD < LOD 18.6) < LOD < LOD 26. 118-74-1 General Information Hexachlorobenzene (HCB) was used from the 1930’s to the 1970’s in the U. and has been detected in soil.2 (17.S.6) < LOD < LOD 26. respectively.

With chronic exposure.086-.092 (. HCB interferes with normal heme synthesis. 1960). which is manifested by increased deltaaminolevulinic acid synthase activity and decreased uroporphyrinogen decarboxylase activity.095) < LOD < LOD 75th < LOD < LOD 90th * * .099) < LOD < LOD .123 (.111) < LOD < LOD .182 (.085-.092-.145-.095-.225 (. 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.097 (. The U.104 (. and liver and thyroid cancers (ATSDR.094 (.111-. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD .171 (. immunologic abnormalities. anorexia.atsdr. and many died before 2 years of age (Peters et al.159-. very high.163-.086) < LOD < LOD .226) 807 1058 957 895 1219 1004 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * . environmental levels) and health effects is available from the U.html.121 (.102) < LOD < LOD .173) < LOD < LOD .epa.S.174-.062-.140 (.092 (.087 (.078 (. and weakness.S.203) < LOD < LOD .079 (.186 (.090 (.088-.064 (.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 * * . arthritis.147-.143-.097) < LOD < LOD .069) * * .148-. Biomonitoring Information Serum concentrations reflect the body burden of HCB.090-.083) < LOD < LOD .156 (.175) < LOD < LOD .S. population from the National Health and Nutrition Examination Survey.157 (.123 (.089-. a consequence of these heme abnormalities is a condition known as acquired porphyria cutanea tarda.065 (.gov/toxpro2.258) < LOD < LOD .129) < LOD < LOD .073-.176) < LOD < LOD .125 (.098 (. 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.086-.145-.094) < LOD < LOD .100) < LOD < LOD .176-.135-.120 (.088-. as well as hypertrichosis.091-.090 (.132) < LOD < LOD .cdc.179 (.167) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * . 2002).081-.gov/pesticides/ and from ATSDR at: http://www.163) < LOD < LOD . thyromegaly.163 (..157-.212) size 1702 2277 1961 Total years 99-00 01-02 03-04 50th < LOD < LOD .089-.126) .191 (.152) < LOD < LOD .095 (.095) * * .114-.130) < LOD < LOD . In humans.090 (.203) < LOD < LOD . and the FDA has established a bottled water standard for HCB.107) < LOD < LOD . EPA at: http://www.081 (.155) < LOD < LOD . Fourth National Report on Human Exposure to Environmental Chemicals 101 . Infants were exposed transplacentally and through breast milk.107-.099) < LOD < LOD .123 (.141) < LOD < LOD .114-. IARC classifies hexachlorobenzene as possibly carcinogenic to humans.097) .127-.099) < LOD < LOD . EPA has established a drinking water standard.072-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.122) < LOD < LOD . Schmid. Chronic feeding studies in animals have demonstrated kidney injury.167 (. More information about external exposure (i. acute doses produce central nervous system depression and seizures.178-. This condition.118) < LOD < LOD . reproductive and developmental toxicities.082-.118-. and NTP classifies hexachlorobenzene as reasonably anticipated to be a human carcinogen.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. which may vary for some chemicals by year and by individual sample. 1982.109) * * .092 (. Survey Geometric mean (95% conf.115 (.060-..069) < LOD < LOD .160 (.102 (.077-. Human health effects from HCB at low environmental doses or at biomonitored levels from low environmental exposures are unknown.Organochlorine Pesticides chemical.095 (.169-.196) < LOD < LOD .088-.113-.085) * * .118-.147 (.e.190 (. ACGIH has developed workplace exposure limits for HCB.

. Reference values updated. however. Hexachlorobenzene in the global environment: emissions. Bjerselius R. Lackman. only 4. FDA total diet study. Gabrio T. 2003).110(8):835-838. Zoellner I. In a representative sample of the 1998 German adult population. 4/21/09 Glynn AW.71(6):1200-1209. selected elements. In the 1976-1980 NHANES subsample. Over the past two decades. Organochlorines in Swedish women: determinants of serum concentrations. Bradman A. and the geometric mean concentration of HCB in whole blood was 0. Bertram et al. et al. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Jones D.44 mg/L. Gocmen A. Hexachlorobenzene content in human whole blood and adipose tissue: experiences in environmental specimen banking. Jones KC.39(12):744-749. As a result of the lower limit of detection in NHANES 2003-2004. 2002. Otero R..81(2):82-85. 1986. IARC Sci Publ 1986.111:349355. Sala M. Eskenazi B.77:173182. J Assoc Off Anal Chem 1988. Link et al. but overall. Residency near industrial or agricultural areas has been associated with higher serum HCB levels (Barber et al.html. distribution. lower than the limit of detection (on a lipid adjusted basis) in NHANES 1999-2000 and 20012002. Available at URL: http://www. Int J Hyg Environ Health 2002. Becker K. Lackmann GM. Food and Drug Administration (FDA).. Chemosphere 2005..Organochlorine Pesticides in the NHANES 1999-2000 and 2001-2002 subsamples. but approximately five times higher than the overall geometric mean level in 2003-2004 (Becker et al. Biomonitoring of persistent organochlorine pesticides. Barr DB. 2002. more HCB levels were quantified. Kemper FH. Gunderson EL.58:1185-1201.. 102 Fourth National Report on Human Exposure to Environmental Chemicals .9% of participants had quantifiable levels (Stehr-Green. 2002. et al.. Temporal trends of organochlorine concentrations in umbilical cord blood of newborns from the lower north shore of the St. Lackmann. Available at URL: http://www. Toxicological profile for hexachlorobenzene update [online]. April 1982 to 1984. Ozalla D. Environ Health Perspect 2003. Finding a measurable amount of hexachlorobenzene in serum does not mean that the level of the hexachlorobenzene causes an adverse health effect.fda.. 2005. 2002.135(4):400404. Seiwert M. Peters HA. declines in background HCB levels ranging from around 50%90% have been documented in studies using cord blood (Dallaire et al.gov/ toxprofiles/tp90. Lepom P. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. 2002). dietary intakes of pesticides. Paepke O. Polychlorinated biphenyls and hexachlorobenzene in full-term neonates.. Fenster L. Factors predicting organochlorine pesticide levels in pregnant Latina women living in a United States agricultural area. 2002) and among children (Link et al. Dogramaci I. September 2002. References Agency for Toxic Substances and Disease Registry (ATSDR). Laliberte C. Sweetman AJ.17:388–399. J Exp Sci Environ Epidemiol 2007. Bryan GT.html. Muller C. Safe A. Granath F. HCB levels were directly related to age. 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. Link B. 4/21/09 Barber JL. van Wijk D. Bertram HP. Kaus S.gov/~dms/ pesrpts. 2005). Muckle G. et al. Atuma S. trends and processes. Sci Tot Environ 2005. Urinary porphyrin excretion in a human population highly exposed to hexachlorobenzene. Krause C. 1999). Cripps DJ. respectively. Epidemiology of hexachlorobenzene-induced porphyria in Turkey: clinical and laboratory follow-up after 25 years. Kohli J. 2006). The metabolism of higher chlorinated benzene isomers. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003.349:144. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. than the limits of detection (on a whole weight basis) in NHANES 19992000 and 2001-2002 (Herrero et al. Can J Biochem 1976. levels. Holland NT. Schulz C. Biol Neonate 2002. Canada).. August 2008. Darnerud PO. Herrman T. Glynn et al. factory workers chronically exposed to HCB and residents near the factory had serum HCB levels that were 150 to 50 times higher. Herrero C. and other chemicals. Arch Neurol 1982. Aune M. et al.cdc. FDA Pesticide Program Residue Monitoring 1993-2006 [online].54(3):203-208. 1989).cfsan. Ayotte P. Schwartz JM.. Agerelated increases of HCB in body fat and serum have been consistently noted in general population studies (Becker et al. 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. Environ Health Perspect 2002.atsdr. Bradman et al. Arch Dermatol 1999. Dewailly E. Lecha M.205:297-308. Santiago-Silva M. HCB detection in serum also was proportional to age. Dallaire F. Piechotowski I. 2005).. In Spain. Lawrence River (Quebec.

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

3 (42.8) 52.0) 7.6-37.6-18.4 (11. each result has been multiplied by 1.0-23. environmental levels declined. and delta.2-20.6) 35.8.0 (33.5) 632 563 460 403 513 487 702 1051 887 Non-Hispanic blacks Non-Hispanic whites Limits of detection (LOD.Organochlorine Pesticides Hexachlorocyclohexane CAS No.6-135) 69. HCH does not bioaccumulate to an appreciable extent in plants (ATSDR. which may vary for some chemicals by year and by individual sample. population from the National Health and Nutrition Examination Survey.4 (16.7-26.6) 47.90) 7.50) 8.1 (9.2-22.7-69.1 (21.2) 62.87 (9.8-54.7) 73. As pesticide applications of HCH were increasingly restricted or eliminated.2) 13.70-19.9) Selected percentiles ( 95% confidence interval) Total * * 50th < LOD < LOD < LOD 75th 19.5) 11.61-12.6 (17.1-37.2-46. exists in several isomeric forms.3) 14.5-123) 49.9-51.3 (13.4 (12. beta. and sediment as a result of historic production and use. < LOD means less than the limit of detection. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.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 21.1 (18.6 (40. The other isomers can be formed during the synthesis of lindane.1-15.2-42.9-14. water.0) 71.8 (17.5 (16.3) 51.5 (24.4-111) 84.9 (9.4) 44.6) 36.1-32. 2005).9-24. **In survey period 2001-2002.1 (12.3) 25.4 (8.6) 16. interval) 9.0-21.5 (43. HCH isomers are lipophilic. Lindane has a half-life of about two weeks in soils and water. respectively.3-38.3 (42.90-8. Lindane (1%) lotion and shampoo are available by prescription for singleuse application to treat human scabies and head lice.S.6-20.7) 23.89 (<LOD-9.2-98.7 (53. 6.4) 11.6-89. EPA cancelled agricultural uses of lindane (ATSDR.8 (33.0-20.90-8.4) 21. commonly known as lindane.76.5) 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.8-16.7) 18.5 (8.7 (29.2-87.1-16.5) 29.7) 97.1 (9.4-50.8-19.7) 32.7) 10.2 (50.3) 37.9-21.7 (25.9) 81. 104 Fourth National Report on Human Exposure to Environmental Chemicals . see Data Analysis section) for survey years 99-00.3-56.2 (34. so they can accumulate in fatty tissues of animals. 01-02.9 (30.68 (<LOD-10.1) 12.7 (62.1-49.46-11.2 (29.8) 7. 58-89-9 General Information Hexachlorocyclohexane (HCH).7 (30.1 (27.2) 142 (99.3 (62.43 (<LOD-9.2 (48.8 (64.4-45.7 (13. containing about 64% alpha and 10%-15% gamma isomers.9 (32.3) 34.5528.4) 901 1067 952 992 1224 1007 Females 11.9-56.0) 17.7) < LOD < LOD < LOD < LOD < LOD < LOD 37. It is no longer produced or sold in the U.4) < LOD 9.6 (22.45) < LOD Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 99-00 01-02** 03-04 16.7-20.8) * * * * * * 15.0 (19.3-85. 608-73-1 beta-Hexachlorocyclohexane CAS No.2-55. can be used as an insecticide and has been used to kill soil-dwelling and plant-eating insects. and 7.70 (8.7 (35.7-96.6-47. Survey years 99-00 01-02** 03-04 Geometric mean (95% conf. However.9) 45.1) 13.6-14. Technical grade HCH is a mixture of all four isomers.5) 22.S.20-16.1-36.2) 9.56-12.9-178) 48.60-13.70-12.36. and have been used either as fungicides or to synthesize other chemicals.80 (<LOD-14.6-62.8 (9.1) 71.5) 14. In 2006.0 (8.0 (37.0) 35.4) < LOD < LOD < LOD 46.0-70.8) 12.8 (10. and 03-04 are 9.0 (<LOD-12.8 (23.4) 27.2) 36.4) 51. particularly alpha and gamma have been detected widely in air.8) 95th 68.7-69.9 (40.4 (52.6-42.09) < LOD Gender Males 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD 14.6) 50.0-34. formerly referred to as benzene hexachloride.1) 31.1-32.0) 41.6) 18.7-96.8) 27. 2005). HCH isomers.9 (26.30-11.7-166) 70. 319-85-7 gamma-Hexachlorocyclohexane CAS No.9 (50.8 (21. the U.5 (14.70 (6. gamma.7) 10.2 (18.9 (62.0 (14.8-199) 134 (85.8-68.0) 8.3 (26.7) 27.1 (30.9 (11.9) 15.0 (35.7 (<LOD-16.5 (11.S.8-87.8) < LOD 10.4-73.0-111) 70.2-17.04-10. The gamma isomer.1) 12.6 (33.5) 40.8 (32.5-29.2-52.6 (10.5) 90th 42.1 (11.9) 17.5 (37.6) 653 758 589 1240 1533 1370 20 years and older 10.6 (16.1-27.1 (16. including alpha. See the section “What’s New” at the beginning of this Report for details.4 (50.2-67.5) 16. soil.2 (9.66-12.4) 10.8) 39.2 (31.80 (6.7) 56.0-70.9-81.

410-.250 (.040-.234 (.118 (.210) .240 (.090 (. and memory loss (Nigam et al..139 (.174) . probably by blocking inhibitory neurotransmitters in the central nervous system. Pesticide applicators or agricultural workers could be exposed to HCH by inhalation and dermal pathways. U.340) .173-.160) .050-.410) . resulting in a half-life of about seven years.331 (.Organochlorine Pesticides exposure to HCH is through the diet.350) .310 (.089-.125) < LOD < LOD < LOD .110) .110-.080-.058) < LOD Gender Males 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD .350 (. from 6% of samples in 1982-1984 to 2% in 1994 (FDA.059-. paresthesias. which may vary for some chemicals by year and by individual sample.521 (.175 (.32) .086) < LOD < LOD < LOD < LOD < LOD < LOD .062 (.092 (.210-.065 (.120 (.051 (<LOD-.S..064 (.620-1.056-.120 (.066) Selected percentiles ( 95% confidence interval) Total * * 50th < LOD < LOD < LOD 75th .230-.120-.100-.150) .124-.305) .250 (.254) 95th .070-.216 (. See the section “What’s New” at the beginning of this Report for details.442 (.110) .221-.222 (.091) .100-.460) .057-.05) .620) . HCH isomers are absorbed after inhalation.480 (.250) .150-.140) .220 (. EPA has established a drinking water standard. The beta isomer accumulates in fatty tissues and is metabolized more slowly.047-.160-.480) .410 (.100-.400) .210 (.420-. 1971.100 (.320 (. 1983).083 (.290 (.412 (.070-.131-.130 (.560) .S.081-.191-.120-. Rogan..144 (.460 (.220) . 1981).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.220-.250 (.280-.190) .100) . hepatic enzyme induction.090 (. Survey years 99-00 01-02** 03-04 Geometric mean (95% conf.450-.210 (.290) .710) .S.382-.240-.390 (.130-.580-1.067 (.080-.057) < LOD Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 99-00 01-02** 03-04 .470 (.290 (. 2002).190) . ingestion. HCH crosses the placenta and is also excreted in breast milk (Radomski et al.260) .250-. Distribution is mainly to fatty tissues.290) .200-.096) .297-.140 (.360 (.. HCH isomers are metabolized to chlorophenol metabolites that are excreted in the urine (Angerer et al.077) < LOD .01 (.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 .308-.410) .051-.050 (<LOD-. **In survey period 2001-2002.180-.404) .214) .110) .080 (.119) .510) .450) .078 (. respectively.360) .190-1.048 (<LOD-. When animals were chronically fed lindane at high doses.330 (.100 (.200 (.140) .167 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.100) . Fourth National Report on Human Exposure to Environmental Chemicals 105 .057-.814) .170-.310) .560 (.065 (.470) .080-.910 (. Acute high doses of lindane after ingestion or excessive skin application of the 1% lotion have produced seizures in humans.056-.146-.700) .400) .300-.103 (.060) .170-.072 (.120-. The U.080 (.450 (.372 (.150 (.050 (.073-.069) .270 (.661) 901 1067 952 992 1224 1007 Females . After dermal application of lindane 1% lotion.098 (.319) .083) . Workers who directly handled HCH have complained of headache.070 (.120) .290 (. 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.090-.050 (.050-.310) .070-. population from the National Health and Nutrition Examination Survey.130) .390-. 1996.118-.200-. Human health effects from HCH isomers at low environmental doses or at biomonitored levels from low environmental exposures are unknown.077) < LOD .058 (<LOD-.080) * * * * * * .103) 90th .050 (<LOD-.570 (. Saxena et al. FDA pesticide monitoring program has shown a temporal decline in the detection of lindane.064) .287 (.340-.281 (.260) .103-. and seizures.294-. tremors.050-.080) .380 (.501) .587) 653 758 589 1240 1533 1370 20 years and older .480 (.068-. 1986). enlarged livers. ataxia. the serum half-life was about 20 hours among children (Ginsburg et al.120) .250-.680) .840) .191-. and FDA has established a bottled water standard and food residue tolerances for lindane.370-.600) .140) .070) .. or dermal exposure.089) .220-.5528.360-. Acute high dose toxicity in rodents affects the central nervous system producing decreased activity.280-.190-.067) . each result has been multiplied by 1.090 (.150) .244-.070 (. and nephropathy developed (IPCS. OSHA and ACGIH have established workplace standards and guidelines. 1977).050-. Gunderson 1988). 2008.260-.37) 1.062 (.690) .050) .580 (.330-.057 (<LOD-. for lindane. interval) .120 (.160 (.

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

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

Needham LL. Arch Toxicol 1981. Kashyap R.inchem. Zoellner I.9(4):417-424.html. Sturgeon SR. et al. Seiwert M. Krause C. et al. Wood PH. Paepke O.71(6):1200-1209. and other chemicals. Arch Pediatr Adolesc Med 1996. Granath F. Becker K.96:34-4Food and Drug Administration (FDA). Piechotowski I. and HCB residues in human blood in Ahmedabad. Cancer Causes and Control 1998. Kutty D. Lowry W. available at URL: http://www. Rothman N. 4/21/09 Ginsburg CM. Lindane.cdc. org/documents/jmpr/jmpmono/2002pr08. et al.72:261265. Falk C. et al. Buckland SJ.20(2):186-193. Gunderson EL.gov/~dms/pesrpts. Herrman T.cfsan. Kulkarni PK. Blood levels of organochlorine pesticides in Argentina: occupationally and nonoccupationally exposed adults. Pesticide residues in food-2002-Joint FAO/WHO meeting on pesticide residues. Brock JW. Environ Health Perspect 1998. Available at URL: http://www. Saxena MC. children and newborn infants. Toxicol Appl Pharmacol 1971. Raju GS. Schulz C.120:1-82. Bates MN. Rey AA. Garrett N. Absorption of lindane (g benzene hexachloride) in infants and children. gov/toxprofiles/tp43.106(5):279-289. Cerrillo I. Link B. April 1982 to 1984.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). 4/21/09 Anderson HA. Ellis H. Serum hexachlorocyclohexane residues in workers engaged at a HCH manufacturing plant. Deichmann WB. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. Needham LL. Available at URL: http://www. Glynn AW.27:405-421. Potischman N.91:998-1000. Olea-Serrano MF.150:981-990.58:1185-1201. PA. The Great Lakes Consortium. 4/21/09 Kutz FW. Maass R. August 2008. Darnerud PO. Organochlorine pesticides and polychlorinated biphenyls in human adipose tissue. Occupational exposure to hexachlorocyclohexane. Bottimore DP. Bjerselius R. Nigam SK. Zaidi SS. India.html.57(4):315-320. Karnik AB. J Assoc Off Anal Chem 1988. Bhargava AK. Levels of DDT. Rev Environ Contam Toxicol 1991. Aune M. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. et al. Demographic and seasonal influences on human serum pesticide residue levels. August 2005. Olson J. International Programme on Chemical Safety (IPCS). et al. Lepom P. Angerer J. Heinrich R. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. VI. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Gabrio T.111:349355. Botella B. Rogan WJ. Chemosphere 2005. Majumder SK.205:297-308. Toxicological profile for hexachlorocyclohexanes update [online]. 108 Fourth National Report on Human Exposure to Environmental Chemicals . Kaus S. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Exposure of women to organochlorine pesticides in Southern Spain. Astolfi E. Hanrahan L. Burse VW.atsdr. J Pediatr 1977. Atuma S. Pollutants in breast milk. Needham LL. Rivas A. FDA total diet study.fda. Int J Hyg Environ Health 2002. Biomonitoring of persistent organochlorine pesticides. Krishna Murti CR. HCH. selected elements. Stehr-Green. Reisch JS. J Toxicol Environ Health 1989. Organochlorines in Swedish women: determinants of serum concentrations.48:127-134. Brinton LA. Chemosphere 2004. Bai KM.54:1431-1443.htm. Siddiqui MKJ. Visweswariah K. dietary intakes of pesticides. Int Arch Occup Environ Health 1986.52(1):59-67. Metabolism of gammahexachlorocyclohexane in man. Int Arch Occup Environ Health 1983. 2002. Saiyed HN. Placental transfer of pesticides in humans. et al. Patterson DG Jr. Environ Res 2004. Environ Health Perspect 2003. Bhatnagar VK. Radomski JL. Bull Environ Contam Toxicol 2004. Serum concentrations of organochlorine compounds and endometrial cancer risk (United States). Olea N. Crespo J.

and 7. which may vary for some chemicals by year and by individual sample.6.0 (14. 1991). aquatic organisms.7) < LOD 66. Ingested mirex that is not absorbed is eliminated in the feces within about 48 hours.4) 617 548 459 398 500 484 688 1049 884 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.4-230) 18.1 (<LOD-65.1 (<LOD-104) < LOD < LOD < LOD < LOD 39.5 (<LOD-42. < LOD means less than the limit of detection. where it has a half-life of 12 years.70 (<LOD-15.S.5.10-37.4) < LOD 63. sediments.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. respectively. especially those from persons living in the southeastern U.8 (<LOD-73.0) * * * 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. (Kutz et al.3 (15. Mirex can cross the placenta and be excreted in breast milk. animals. In studies conducted in the 1970’s and 1980’s.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 16.8) < LOD 15.6 (<LOD-108) 9. and foods. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.6 (<LOD-23. The most likely sources of human exposure to mirex are eating fish from contaminated water or living in areas with soil contaminated by historic mirex manufacturing.70-40.4 (8. it is a highly persistent chemical in the environment. Mirex contamination of Lake Ontario and adjacent waterways has been well documented (ATSDR. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 57.2-230) 13.0 (12.6-305) 15. Survey Geometric mean (95% conf.. population from the National Health and Nutrition Examination Survey.2) 51. 01-02.6) < LOD < LOD < LOD < LOD 71. soil.4) < LOD 15. Mirex is absorbed through the skin and from the gastrointestinal tract.6 (<LOD-31. Mirex is not metabolized in the body.8 (12.S.70-24. Occupational exposure is limited to workers at sites where mirex contamination is present.7 (<LOD-47.5-82. disposal. mirex was detected in human adipose samples. 1995).5-425) 40. 2385-85-5 General Information Mirex has not been produced or used in the U. Formerly.3 (15. EPA have issued public health advisories or warnings that fish from contaminated lakes and rivers may contain mirex. since 1977. resulting in exposure to newborns and nursing infants.6) size 1853 2257 1951 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th 15.S.S.8. see Data Analysis section) for Survey years 99-00.5 (9. 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. 10.6) 9.3) < LOD < LOD < LOD < LOD < LOD < LOD < LOD 15.1 (13. after which it is widely distributed in the body and stored in fat. water. Mirex binds strongly to soil. its major uses were as a flame retardant additive and as a pesticide to kill fire ants and yellow jackets in the southeastern U.1 (8. or pesticide application.90-29. 1985. and 03-04 are 14.Organochlorine Pesticides Mirex CAS No..5-291) 11.0 (<LOD-108) < LOD < LOD 50.3-225) 15. Some states and the U.10 (<LOD-15.40 (<LOD-13. Mirex has been detected in air. where it was applied directly to soil and by aerial spraying.S.7 (12. Fourth National Report on Human Exposure to Environmental Chemicals 109 .0-374) 11.5 (<LOD-115) 153 (30.7) 8.2 (7.

gov/toxpro2.084) * * * Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .220) . and 4.093 (.170) size 1853 2257 1951 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .. Smith.268) < LOD . as well as in a subsample of NHANES II (1976-1980) participants.100 (<LOD-.089-.450 (.8. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.430 (.410 (.atsdr. 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.html. 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. serum mirex levels were generally below the limits of detection (Stehr-Green. In addition.240) < LOD < LOD < LOD < LOD < LOD < LOD < LOD . and the FDA monitors foods for pesticide residue and has established an action level for mirex in fish tissue.090-1.37) .106 (. environmental levels) and health effects is available from the ATSDR at: http://www.108 (.052-. 1989).054 (<LOD-. 2001-2002.090-1.077 (<LOD-.450) 1. population from the National Health and Nutrition Examination Survey.170-3. Biomonitoring Information In the NHANES 1999-2000.470) .e.062-.256 (. which may vary for some chemicals by year and by individual sample.080-1. 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.080-1.310 (.140 (<LOD-. Survey Geometric mean (95% conf.055-.635) < LOD .08 (..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 .S.73) .079 (<LOD-. 1995.92) . Laboratory animals fed high doses developed liver enlargement and liver tumors.102) < LOD < LOD < LOD < LOD .370 (.02) . developmental abnormalities including cataracts and edema in the offspring have been reported (ATSDR. In samples obtained between 1994 and 1997. IARC classifies mirex as possibly carcinogenic to humans. and NTP classifies mirex as reasonably anticipated to be a human carcinogen.090 (<LOD-. The geometric mean mirex levels of the Inuit mothers were 8.090-1.470 (. More information about external exposure (i. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD .470) .100 (<LOD-.690) . EPA has established environmental standards for mirex.41) . 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.7 ng/g of lipid. reproductive toxicity included decreased fertility and testicular damage.064 (<LOD-.S.610) < LOD < LOD < LOD < LOD .174) 617 548 459 398 500 484 688 1049 884 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the lipid adjusted serum level.79) .170) 887 1052 949 966 1205 1002 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .070-1.cdc.220 (<LOD-.510) < LOD < LOD ..106) < LOD .Organochlorine Pesticides exposures are unknown.112 (. 1991). 2004).110 (<LOD-.79) .170) < LOD .053-. and 2003-2004 subsamples. 2005).059 (<LOD-. 110 Fourth National Report on Human Exposure to Environmental Chemicals . 7.090 (<LOD-.090 (<LOD-. The U.

Chashchin V. Watts DL. August 1995. Available at URL: http://www. Toxicological profile for mirex and chlordecone [online]. 4/21/09 Bloom MS. 1991 pp. 1994-1997 organochlorine compounds. Gilman A. Hansen JC. Jr. Inc. Swanson MK. Rev Environ Contam Toxicol 1991. Bottimore DP. Kutz FW. Leininger CC. Profiles of ortho-polychlorinated biphenyl congeners.330:55-70. Chlorinated Hydrocarbon Insecticides. Vena JE. Organochlorine pesticides and polychlorinated biphenyls in human adipose tissue. Stroup CR.97(2):178192.27:405-421. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 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. Academic Press. Van Oostdam JC.cdc. The human body burden of mirex in the southeastern United States. Moysich KB. 2 Classes of Pesticides. Environ Res 2005. Eds. hexachlorobenzene. Strassman SC. PA. Vol.120:1-82. et al. Sci Total Environ 2004. Stehr-Green. J Toxicol Environ Health 1989. New York. Jr and Laws ER. and Mirex among male Lake Ontario sportfish consumers: the New York State Angler cohort study. Wood PH. Carra JS. dichlorodiphenyldichloroethylene. In Hayes WJ. Circumpolar maternal blood contaminant survey. Demographic and seasonal influences on human serum pesticide residue levels. Kutz FW. Smith AG. Dewailly E.gov/toxprofiles/ tp66.Organochlorine Pesticides effect. Odland JO.15:385-394. J Toxicol Environ Health 1985. 731-915.html.atsdr. Fourth National Report on Human Exposure to Environmental Chemicals 111 . Handbook of Pesticide Toxicology. et al. References Agency for Toxic Substances and Disease Registry (ATSDR). Olson JR.

0) 2.40 (2.S.60 (4.950 (<LOD-1. Formation of 2.5-TCP) and 2.20-36.30) < LOD 4. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. other organochlorines.63) 18.0 (4.0) < LOD 973 1178 1021 1319 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .4.4.57 (<LOD-15.80) < LOD 1.40 (2.940-3.60-8.19 (<LOD-6.0) < LOD 5.0 (4. Occupational exposures.40) < LOD 4.50-25.50 (1.6-trichlorophenol (2.30-40.42 (<LOD-12.27) 696 661 521 696 603 939 Limit of detection (LOD.30-44. 2.40) < LOD 6.00-3.0) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 1.71 (<LOD-8.80 (1.90-33. Historically.6-TCP were used as intermediates in the production of certain pesticides.50 (2. Such workers would probably Urinary 2.80 (2.0) < LOD 11.5-Trichlorophenol CAS No.72) < LOD 1.60 (.0) 2. however.40 (.4.80-41.8) 21.20) < LOD 1.Organochlorine Pesticides 2.50-16.30-27.7) 24.50-63.0) 14.0 (3.30 (.0) 5.4. may occur by inhalation or dermal routes. EPA.980-3. 88-06-2 Metabolites of Organochlorine Pesticides and Other Environmental Chemicals General Information The chlorophenols.00-8.50 (.31 (<LOD-9. 2006).40 (1.9 (<LOD-121) 9.40 (2.30-27. interval) Selected percentiles ( 95% confidence interval) Sample 95th 16.6-Trichlorophenol CAS No. 1999).6-TCP was also used as a wood preservative and may still be used in production of some fungicides (ATSDR.0 (3.30) < LOD < LOD < LOD < LOD < LOD 1.5TCP and 2.3.4. General population exposure may occur by ingesting contaminated food or water and by inhaling contaminated air. surface water.20) < LOD 90th 5.5-trichlorophenol (2. public drinking water systems did not detect 2. are metabolites of several organochlorine chemicals.S. Environmental sources of these compounds include industrial discharges or run off from pesticide facilities or disposal sites.. 1999). 2.4. but they may be produced as by-products during manufacturing of other chlorinated aromatic compounds.03) 9.71 (<LOD-8.4.0 (5.40-11. which may vary for some chemicals by year and by individual sample.980-3.4.0) < LOD 11.6-TCP).27) 482 570 681 815 831 1112 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD 1.60) < LOD 8. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.40-18.40) < LOD 1.10-3.6-TCP in any of the samples (U.4.9.30-27.0) 2.920-3.0) 2. Survey Geometric mean (95% conf.42 (<LOD-8. and sediments.900-2.40 (1.27) size 1994 2497 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD 75th 1.30-11.5-trichlorophenol. hexachlorobenzene.00 (3.40 (. 95-95-4 2.60-18. population from the National Health and Nutrition Examination Survey.20) < LOD 5. including hexachlorobenzene and hexachlorocyclohexanes.50) < LOD 1.0) < LOD 21. Trichlorophenols have been detected in fish taken from waters near waste water treatment and industrial discharges (ATSDR.00 (2.S. recent sampling of U. < LOD means less than the limit of detection.0 (8. 112 Fourth National Report on Human Exposure to Environmental Chemicals . Exposure to trichlorophenols also may result from metabolism of lindane.00-3. usually at herbicide production or waste incineration facilities. and polychlorinated benzenes (Kohil et al.0) 2.20 (4.40 (2.8-tetrachlorodibenzo-p-dioxin occurs during the synthesis of 2. 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.4.4.0) 2.30-3.5-Trichlorophenol Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.0 (4.60 (2.4. Trichlorophenols are no longer manufactured commercially.0) < LOD 5. 1976).0) < LOD 5. soils.20-71.9 and 0. Both chemicals have been detected in air. 2.7.

4) 5.3 mg/L reported in German adults aged 18-69 years (Becker et al.S. 2004).02-3.82 (<LOD-32.16) < LOD 90th 5.4 (6. Neither 2.4. More information about external exposure (i..2 (2. interval) Selected percentiles ( 95% confidence interval) Sample 95th 11.0 mg/L.31) < LOD 2.05-17. the 95th percentile urinary 2.69 (2.46 (1.4) < LOD 3.e. recent small studies have not demonstrated increased exposure to trichlorophenols in workers who dredged contaminated soils or incinerated waste materials (Agramunt et al.55 (4.75 (<LOD-6.0) 7.86 (3.4.6) 4. Among 6-11 year old children in NHANES 1999-2000. 1995) were similar.1) 2.43 (2.24) < LOD 5.4) < LOD 3.5-Trichlorophenol (creatinine corrected) Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.17) 9.78-19.1 (<LOD-58.33) < LOD < LOD < LOD < LOD < LOD 2.49 (1.6-TCP. Radon et al. environmental levels) and health effects is available from ATSDR at: http://www.05-8. was similar to the corresponding percentile for 6-11 year olds in NHANES 1999-2000 (Hill et al.90 (4.6-TCP had increased rates of hepatic tumors..11) 482 570 681 814 831 1112 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD 1.24) < LOD 1.16 (.57 (<LOD-7.6) 4. 1989).atsdr.79-4.4.8 (5.5) < LOD 12.20-6. However.5-TCP or 2.64 (4..6-TCP as reasonably anticipated to be a human carcinogen. NTP classifies 2.11) size 1994 2496 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD 75th 2.53-3. 2003). IARC classifies combined exposures to polychlorophenols. In the same 2-6 year old children. and lymphomas.75 (3.4. 1995) and up to 19 times higher than the 95th percentile value of 1.2) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 2.93-11.4.36 (1.gov/toxpro2..2) < LOD 5.00-19.32) < LOD 4.920-2.37) 16.13-13.. 7.4.68 (<LOD-8.6-TCP were developmental or reproductive toxicants in animals (ATSDR 1999). in addition to dioxins.8) < LOD 9.78 (3.4. the 95th percentile urinary 2.50) < LOD 2. which includes trichlorophenols.4.67 (1..820-2.4..4.44 (.73 (<LOD-8.24 (3. Laboratory animals chronically fed high doses of 2.37-11.19-4.80 (1.43) < LOD 12.44 (1.47-8.4..6-TCP at low environmental doses or at biomonitored levels from low environmental exposures are unknown.00-29.5-TCP nor 2.67 (1.9) 12.5) 11.69-18.88-16.60-3.57 (3.57 (<LOD-7. Biomonitoring Information In the NHANES 1999-2000 and 2001-2002 subsamples. furans.3) < LOD 973 1178 1021 1318 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * . IARC considers the experimental evidence for animal carcinogenicity inadequate for 2. At lower doses.6) 4.6-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.78) < LOD 1.24-11.980 (<LOD-1. 2003).5-TCP. animals showed hepatocellular abnormalities.02) < LOD 7.3 (5.29 (1.5-TCP among adults in this Report and in a nonrandom subsample from NHANES III (Hill et al.4.81 (<LOD-9.74) 11. urinary 2. but almost twenty times higher than 95th percentile values reported in German adults aged 18-69 years (Becker et al.html. and other chlorinated compounds.9 (5.5-TCP and limited for 2.19-12.95 (3..62-20.3 mg/L in a nonrandom subsample from NHANES III (Hill et al. Human health effects from 2.83-12.2) 2.28-25. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. leukemias.7 (4. 2003.Organochlorine Pesticides be exposed to mixtures of chlorophenols.cdc.6-TCP levels at the 95th percentile were up to eight times higher than 3.4. 1989). The 95th percentiles for 2. Survey Geometric mean (95% conf.27-17.53-3.00) < LOD 4.24) < LOD 6.68-4. Urinary 2. population from the National Health and Nutrition Examination Survey.8) 4. Fourth National Report on Human Exposure to Environmental Chemicals 113 . as being possibly carcinogenic to humans.15) < LOD 2.37) 696 661 521 695 603 939 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.

89-6..10) 6.67) 4.74 (2.00 (4.80-6.99) 6. 2004).84) 2.60 (2.6-TCP exposure and health effects.4. 2003).20-23.14 (2. see Data Analysis section) for Survey years 99-00 and 01-02 are 1.54) 6.80-20.70-3.4 (8.18) Selected percentiles ( 95% confidence interval) Sample 95th 25.5-46.4-17.8-13.0-54.00-21.60-3. which may vary for some chemicals by year and by individual sample.60) 6.90 (3.0-50.3) 23.0) 6.45-9.20-3.20-6.0-38. Biomonitoring data will also help scientists plan and conduct research about 2..30-33.4 (9.9) 694 677 519 696 602 931 Limit of detection (LOD.36 mg/g creatinine. In harbor workers exposed to chlorophenol-contaminated river silt.9 (11.92 (2. interval) 2.57 (<LOD-2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.2) 481 574 678 820 830 1109 99-00 01-02 99-00 01-02 2.98-11.18-3.5-TCP and 2.32) * 3.60 (3.90-8.00 (2.0 (11.08 (2.85) * 3..30-2.8) 18.12) 2. similar to the limit of detection for this Report (Anderson et al.70-6.90 (4.80-7.6-19.80-25.65) 15.0 (8. 114 Fourth National Report on Human Exposure to Environmental Chemicals .4.40-4.58-3.01-6.6 (12.0 (14.28) 24.30-11.74-3. Urinary 2.0) 12.32) 3.70) 5.6-TCP level.4.95-6.60) < LOD 5.3-26.4.40-2.31 (3.4 (10.89 (3. Urinary 2.0 (7.0) 13.00-4.73-9.4.30-2.4.70) 3.80 (3.4.90) 2.0-37.5-TCP or 2.09-7.0 (13.8) 32. Sawmill workers exposed to chlorophenol wood preservatives had urinary 2.45 (2.47 (3.33-4.4.40) 2.40) 2.6-TCP than are found in the general population.59) 4.06) * 2.52 (2.0) 10.0 (15.0-18.56 (3.80 (2.4.0) 19.6-17.4.48-26.0 (12.9) 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 2.91-4.60 (3.0 (14.7 (13.3 (11.0) 7.4.4.3.5-TCP (0.55-3.5-TCP and to the median 2.0 and 1.3) 20. for males in NHANES 19992002 (Agramunt et al.40) 3.7) 21.40-14.53) 2.6-22..0 (4.0) 9.50-5.0) 7.70) 1.8 (9.4 (17. respectively.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.75 (8.58 (1.80 (2.60-37.02) 2.10-3.6-Trichlorophenol Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.0) 13.3 (11. Survey Geometric mean (95% conf. Finding a measurable amount of 2.6) 26.44) 75th 4.4.2) 12.9) 13.0 (9.1 (8.04) 2.52-3.78 (2.46-3.0) 14.20 (3.70) 5. the median urinary 2.7-3.6 (11.2) 25.0 (20.6 mg/g creatinine) and 2.65 (5.28) * 2.6-TCP (0.5 mg/g creatinine) were similar to the limit of detection for 2.4.70-6.1 (10.0 (6.6-TCP were monitored in a group of hazardous waste incinerator workers from 19992002.6TCP values.30) 4.4.72-10.8-24.85 (2.5-TCP or 2.0-43.40 (2.7) 33.10 (5.40) 4.31) * 2.25-11.0 (6.0-68.80) 1.95) 3.00 (1.S.0) 14. was about six times lower than the median urinary levels for males in this Report (Radon et al.4.0 (8.4.3-17.09) 15.2-0.0) 17.76) 3.20) 4.0) 13.59-6.23) 2.4.69 (3.26 (2.45 (5. Biomonitoring studies on levels of 2. 0.20 (3.51-12.0) 19.10) 2.10-3.10-2.5-TCP or 2.60-21.Organochlorine Pesticides A small study of adults who ate Great Lakes sport fish reported a mean urine 2.4.40-7.0 (16.07 (<LOD-3.0-38.1-25.68 (<LOD-2.0) 11.0-41.0 (14.5-TCP or 2.40-32.9 (13.67-12.23) 3.2 (14.0) 10.78 (2.66 (8.7 mg/L.36-5.6) 970 1178 1019 1325 99-00 01-02 99-00 01-02 99-00 01-02 2.63) 90th 15.32-4.40-2.3) 37.7-16.6) 21.24 (2.95 (4.40 (2.87-14.6-TCP in urine does not mean that the level of 2.6TCP causes an adverse health effect.0) 11.98-7. population from the National Health and Nutrition Examination Survey.7) * 99-00 01-02 99-00 01-02 99-00 01-02 4.53) 4. 1991).70 (2.0) 13.50 (2.70 (2.49 (6.0 (6.6-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. 1998).79 (5. Mean values of 2.7 (9.0 (15.0-44.5-TCP level of 0.36 (1.8-15.35-3.1) 16.0) 15.5-TCP and 2.45) < LOD 11. < LOD means less than the limit of detection.23-2.4.0) 9.0 (20.0) 17.

5) 11.76) 4.55-2.38 (2.4) 9.19-5.1 (8.72) 32.63) * 4.11) 10.30-2.9-32.66-4.83-6.10) 4.8) 12.54 (2.87) 2.0 (9.79-17.50 (2.42) 2.9-34.00) 4.10-9.53) * 2.52) 2.18-2.10 (6.24 (1.26-13. Fourth National Report on Human Exposure to Environmental Chemicals 115 .5 (10.00) 4.4.71 (3.9-64.59 (2.8) 21.78) 2. interval) 2.76) 1.87) * 2.0) 8.88) 4.Organochlorine Pesticides Urinary 2.91 (7.6) 8.2 (7.1-21.09-3.65-2.44 (3.0 (11.08-2.3-23.23) 4.88) 5.78 (2.72-16.16-10.56 (7.3-37. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.25 (3.99-2.5) 12.40 (7.33) * 2.83 (3.8 (7.63) 4.67-17.90 (1.40 (2.06) 11.60 (4.5) 8.9) 19.04-16.06-2.88) 4.6 (12.23 (1.8) 19.4) 4.8) 11.02 (1.22-9.88) * 2.73) 5.14-2.91 (3.9) 7.56) < LOD 11.25 (3.77) 2.98) 10.6 (5.87-6.2) 19.65) 18.47-5.00 (2.8 (8.7) 6.87 (3.9) 481 574 678 819 830 1109 99-00 01-02 99-00 01-02 2.1-32.0 (6.63-15.63-13.33 (1.62-15.05 (3.68) 2.81) Selected percentiles ( 95% confidence interval) Sample 95th 21.6 (10.41-6.75) 75th 4.83-5.26 (6.58 (4.5 (8.6-Trichlorophenol (creatinine corrected) Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.96) < LOD 4.22 (<LOD-2.53 (3.35 (3.6) 13.63 (<LOD-2. Survey Geometric mean (95% conf.89-2.32 (2.6 (9.02) 3.82 (8.27-9.38-5.9 (9.1) 694 677 519 695 602 931 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.52 (5.25-17.1) 14.5) 11.20-2.77-4.29-4.38 (4.1) 11.50-8.49) 4.82 (3.6) 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 2.41 (3.9) 8.43 (<LOD-2.26) * 99-00 01-02 99-00 01-02 99-00 01-02 4.6 (9.00 (3.56-5.92) 4.25-2.6) 12.2 (12.4) 8.5) 9.52) 2.0) 10.14-13.13-6.51-21.42 (2.63 (2.78) 90th 12.33 (7.7) 25.7-36.94-13.98 (1.3) 8.5 (7.6 (22.21-11.51) 18.9-29.6) 970 1178 1019 1324 99-00 01-02 99-00 01-02 99-00 01-02 2.65-21.13 (1.49-3.15 (6. population from the National Health and Nutrition Examination Survey.91-2.17) 13.04-2.70-9.4 (11.87-7.43 (2.01 (3.29-4.65) 2.3 (9.28-4.1 (13.81) 2.29 (6.22 (1.06) 4.82-2.S.6-31.17) 2.76-8.2 (8.73-22.17-4.46-14.43-7.18-4.15 (1.5-28.60-2.88) 1.48-2.4 (12.05 (6.6 (6.90) 2.53-11.2 (13.88-7.53) 4.95-2.88 (2.76) 2.22-2.81-9.22 (3.7 (14.51 (2.9) 8.33-2.32-19.89) 10.52 (3.82) 2.25-15.38) 22.83-6.68) 2.9 (9.

Wegner R. Needham LL. Seifert B. December 2006 Draft. Int Arch Occup Environ Health 1991. Anderson HA. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population.EPA). Jones D. Urinary excretion of chlorinated phenols in saw-mill workers. Available at URL: http://www. Smith SJ. Chlorophenol exposure in harbor workers exposed to river silt aerosols. Monitoring internal exposure to metals and organic substances in workers at a hazardous waste incinerator after 3 years of operation.gov/safewater/ccl/pdfs/reg_determine2/report_ ccl2-reg2_ucmr1_occurrencereport.pdf. Toxicological profile for chlorophenols [online].146:83-91. Environ Health Perspect 1998. Corbella J.71:99108. Available at URL: http://www.gov/toxprofiles/tp107. Schulz C.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Environ Res 1995. Shealy DB. Seiwert M. Domingo A. 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]. Am J Ind Med 2004. Toxicol Lett 2003. Szadkowski D. Radon K. Burse VW. The metabolism of higher chlorinated benzene isomers. 5/19/09 116 Fourth National Report on Human Exposure to Environmental Chemicals . Heinrich-Ramm R. Environmental Protection Agency (U. Kohli J. Int J Hyg Environ Health 2003.63:57-62.S.cdc. Head SL. Can J Biochem 1976. Becker K.106(5):279-289.18(4):469-474. U. Luotamo M. Jarvisalo J. Bailey SL. Olson J. The Great Lakes Consortium. Holler JS. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children. Safe A. Hill RH Jr.atsdr. 206:15-24. July 1999. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. et al. Baker S. Arch Environ Contam Toxicol 1989. Needham LL. Kaus S. Aitio A.epa.54(3):203-208. Baur X. et al. html. Gregg M. Lindroos L. Falk C. To T. Pesticide residues in urine of adults living in the United States: reference range concentrations.45:440-445. Fast DM. Poschadel B. Hanrahan L. 4/21/09 Agramunt MC. et al. Hill RH Jr. Pekari K. Domingo JL. S.

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

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

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

758-1.40-1.0) 20.955 (.52) 6.70) < LOD < LOD 1.50-5. interval) 1.290 (<LOD-.11 (.12) 4.7 (14.98-5.67) 3.27-15.44-38.840-1.35-12.0) 10.93 (4.02) 4.38-5.86-15.0) 5.26-6.620-1.0) 11.17-3.02-5.4) 17.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.36-4.1) 13.2 (14.1 (9.91) 4.97) 8.56 (1.70-19.890 (<LOD-2.1 (10.52) * * 1.83 (5.00-7.00-12.56 (4.79-7.00-12.8) 19.07-10.56-13.60 (1.490-2.1-17.70-11.0 (7.50 (2.0 (8.9-18.0) 9.700-1.0) 10.2) 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 1.3) 14.757-2.95) 5.5 (8.7 (12.71-9.55-8.47) * * 1.40-19.810-1.60 (5.21 (.0 (8.56 (6. and 0.0) 12.600 (<LOD-1.33-18.28) 1.50 (.39 (3.90-4.0 (6.89) 9.80) .04) < LOD 1.44 (2.8 (8.90) 2.5 (11.08 (<LOD-2.26 (5.0) 11.599-1.50-36.30 (2.10 (.61 (3.00) 3.74 (8.60) < LOD < LOD 4.35-16.2 (7.0 (5.54 (3.740-2.98-12.4 (7.76 (2.00-27.2) 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.S.00-27.42) .70 (4.08-2.0) 15.80) 2.0) 10.34-3.80) 3.80) 4.80-22.22 (. population from the National Health and Nutrition Examination Survey.00) 3.10 (2.00-19.60-25.90) 3.670-1.1) 10.8) 11.8 (12.72) 5.80-4.6) 18.579-1.5) 15.82-12.0) 7.40-16.97) 90th 7.42-3.63) 1.2.16) 4.0-28.81) 11.30-4.58) Selected percentiles ( 95% confidence interval) Total * * 50th 1.3) 17.7) 11.61) 4. 01-02.5) 20.60-18.58 (3.954 (.10 (2.780) < LOD 3.39 (8.70) < LOD < LOD 75th 3.0) 5.52-11.0 (9.44-3.623-1.0) 10.10 (.970-2.81) 1.57-7.33 (5.32 (. 0.0) 11.48-7.12-19.40-5.0) 11.0-27.0 (8.0 (12.3) 16.2) 14.8) 7.81) 11.860-2.66) * * 1.82) 10.80) 2.29) * * 1.60) .2.4) 18.20 (.50) 2.4) 20.40-11.0) 5.08-15.45 (2.00 (4.13 (2.43-12.05-7.86 (1.73) * * .90 (1.8 (9.93-24.2 (7.13 (2. and 03-04 are 0.4 (9.10-7.6) 7.20 (2.3-15.40 (.10) < LOD < LOD 4.2-20.51) 2.9) 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. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.47) 5.80 (4.94) 3.0) 6.70-23.0 (6.55-6.90-5.717-1.21) 9.2) 16.0 (9.5-16.80) 11.19) 9.96-3.99 (5.53) 4.0) 10.1-23.68-7.2) 16.5-17.58 (2.20 (.20-7.0 (7.8-32.35-11.00 (5.80) 2.0 (7.01) * * 1.74 (8.13-2.71 (2.10) < LOD .0) 6.0 (7.15-12.79 (5.0 (4.2 (14.40-14.46) 10.2 (9.2) 672 678 473 509 696 578 595 948 752 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.80 (2.26-8.20-4.1) 95th 13.50 (4.32) 1.94) * * .750-1.1.37 (3.20 (.530 (<LOD-2.80-24. see Data Analysis section) for Survey years 99-00.30 (2.4 (7.290 (<LOD-1.16 (2.70) .85 (3.14) * * .830 (<LOD-3.03 (. respectively. which may vary for some chemicals by year and by individual sample.80) .70-14.23-5.20-30. < LOD means less than the limit of detection.8 (14.00 (1.0) 6.2 (9.70 (2. 120 Fourth National Report on Human Exposure to Environmental Chemicals .981 (.58 (5.15) 14.9) 14.30 (4.30-6.2 (7.9 (8.4 (9.34-7.60-11.9) 8.2 (11.8) 7.20 (.27-3.

6) 11.00) 8.00-17.60) * * .5) 11.860 (.80) 9.34) < LOD < LOD .93-5.74) 4.40 (3.37 (5.34) * * .1 (9.574-1.41-12.43 (.37-5.2) 5.7) 5.780 (<LOD-1.7) 12.56) 4.94-10.19 (4.28-9.79-9.69) 2.5) 7.750 (<LOD-1. interval) .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.82-26.44 (2.1) 4.9) 12.23) 4.84 (5.2 (8.09-11.66-34.69 (4.924 (.830-1.82-6.67) 4.61-29.52) 4.94-9.09) 2.11-6.790 (.66 (1.83) 8.2) 9.7) 18.26) * * .03-6.76-4.98 (3.6) 9.13) 4.20-8.8) 7. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.37-3.05) .3) 12.35) < LOD < LOD 3.14 (3.S.68-4.98) 9.37 (4.00 (4.83 (7.650-1.3) 16.900 (.53 (6.58) * * 1.40-5.56-13.6) 8.40-14.1 (8.90-8.960 (.02-2.67-19.93-9.773-1.66 (5.00-13.53-11.28 (5.54-4.75 (3.88 (5.5 (4.57 (4.57) 4.4 (4.71) 10.68) < LOD < LOD 3.29) * * .40-3.3) 15.45-11.43 (3.54-2.6) 13.2) 7.855 (.80 (2.5-16.34 (6.890 (<LOD-1.75-7.37) 9.5-13.06-2.47 (3.40-28.98) .32-12.1) 4.566-1.5-32.9 (5.36) * * 1.2) 95th 12.31 (3.5) 8.7 (9.94-23.35 (1.42) 12.3) 5.28) 10.62-5.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.95 (3.71-2.5) 7.94 (4.932 (.7 (8.92-2.920 (.45-5.82-14.31-14.89-3.38) .29 (2.02 (2.53) 9.9) 11.60) 2.549-1.03) 2.0 (8.870-2.94-22.47 (3.570-1.60-9.98-22.50) 7.74) 90th 7.8 (10.6 (9.40-12.608-1.10-13.41) .23 (4.89) * * 1.98) .03) 2.7 (10.57-10.82-14.38 (1.40) < LOD < LOD 75th 2.05 (.75) 2.47) * * .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 1.30 (1.996 (.98-5.61 (1.01-2.500-1.61-13.8) 16. population from the National Health and Nutrition Examination Survey.818 (.90-5.85 (6.40) 4.890 (<LOD-1.80 (6.15-10.88) 2.25) < LOD . Fourth National Report on Human Exposure to Environmental Chemicals 121 .9) 16.1 (11.45-5.75) 14.04 (1.03 (7.54-15.883 (.47) 2.0) 7.73 (1.02 (7.10 (3.1 (6.04-6.77 (6.56) .620-1.5) 12.440 (<LOD-2.54-11.00 (4.8) 8.27) < LOD 2.69) 4.61 (1.9 (9.00-19.55-20.2 (6.8) 12.25) 6.2) 13.54) .633-1.7) 471 576 308 664 821 699 814 1122 921 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .533-1.4) 4.560-1.64-5.2) 5.8) 6.05 (1.28 (2.18 (.2 (10.07 (.76) < LOD .66 (2.24-3.47 (1.820 (.72) 11.09 (.87 (3.1) 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 1.87 (1.9-28.1-15.28 (4.510-1.46) 2.46-5.960 (<LOD-2.1 (10.710 (<LOD-1.66-15.6 (10. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.62) .4) 4.95) 2.81 (1.69-10.88-10.540-1.79-3.80 (7.9 (9.56) 7.51-5.92-5.0) 6.43) 2.93) 9.85) 2.30) 2.78 (2.4 (9.41) Selected percentiles ( 95% confidence interval) Total * * 50th .02-14.34 (6.2) 8.94 (2.42 (3.84) 7.57 (6.75 (7.21-23.1 (7.03 (2.39 (2.81-5.430-1.5-20.67) 1.88-15.4) 13.87-5.

80 (2.95 (2.88) 3.970 (<LOD-2.7 (11.00-18.39-13.90 (6.77-3.0-33.670 (<LOD-1.28 (7.1) 11.22-12.70-5.00) 7.31) 1.33-11.1 (10.80-8.82) 8.70 (8.10 (<LOD-1.2 (7.31-12.7) 15.10-15.24 (2.00-16.5 (9.41) 3.35 (6.0) 13.90 (2. 122 Fourth National Report on Human Exposure to Environmental Chemicals .35-3.00-4.7) 16.5 (8.35) 4.96) 90th 7.20) 3.98-9.70-8.60 (6.01 (2.11-6.67) 4. < LOD means less than the limit of detection.15-2.84-4.670 (<LOD-1.62-17.20-18.67) 3.5) 21. 0.8) 9.00) 3.70-9.30) 3.80) .8) 8.5.0) 12.80) 5.4) 7.99 (3.80) .9) 95th 14.12 (4.16-1.75 (3.80-6.910 (<LOD-2.5.22 (6.66-13.8-20.31-7.90 (1. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th .58.0-24.6-19.1 (10.30) < LOD < LOD .78) 5.4 (10.46-28.0 (10.90) 8.92-17.6) 18.70 (1.3 (9.S.5 (8.0-24.90) 4.40 (2.3 (9.0) 12.88) 10.18 (3.70) 2.20-8.8 (12.27) 9. see Data Analysis section) for Survey years 99-00.63-14. respectively.27) 4.34 (6.60) < LOD < LOD 2.20) 3.6 (10.2 (9.86-10.51) < LOD 1.9) 16.0 (15.90 (2.61-32.18) * * * * * * * * 1.0) 14.80-14.90 (6.0) 18.22 (6.52 (6.29-4.50-4.53 (3.77-14.81-6.1-23.20 (<LOD-2.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Dimethylphosphate (DMP) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.8-17.95-9.37 (3. 01-02. and 03-04 are 0.6-41.34-5.95 (5.7) 14.8 (12.80 (2.30) < LOD < LOD 4.9-14.89 (2.0) 23.58 (1.0) 9.6) 14.0) 19.8-21.60 (5.42 (1.0 (9.97-4.00) 3.4 (14. and 0.3) 10.4) 672 678 498 509 695 579 595 948 757 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.10) 6.9 (7.89) 2.50) .0-19.4-17.60 (2.10 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.49-4.90-31. population from the National Health and Nutrition Examination Survey.45 (3.0 (13.3 (12.3) 8.06 (2.0) 7.00) 8.75 (2.22) 8.6) 14.80 (5.66) 4.50) 5.90 (5.3 (7.80-21.0 (14.80-4.90 (2.2) 14.59-3.580-2.96) 3. which may vary for some chemicals by year and by individual sample.7 (10.00-9.9) 9.00 (.00-4.92) 9.90-15.47-6.9-15.25 (2.740 (<LOD-1.680 (<LOD-1.80-12.90 (6.9 (12.790 (<LOD-1.34-10.40) < LOD < LOD 75th 2.0) 12.3) 20.0 (5.9) 10.27 (7.41-5.29) < LOD < LOD < LOD < LOD 3.80-3.4 (10.20) .04 (3.8-20.50-5.0 (8.34-3.3) 14.17 (7.0) 9.50) 3.0) 13.670 (<LOD-1.9-17.670 (<LOD-1.0) 11.3 (6.15-6.90-15.67-10.00) < LOD .3 (11.0) 11.61 (3.74) * * * * * 1.37) 2.0) 6.650-1.73) 7.0) 14.0-29.10-4.4) 11.64) 10.5) 471 576 310 664 822 717 814 1121 938 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * .0 (7.27 (3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.0 (10.10-10.30) 8.40 (2.8) Sample size 1949 2519 1965 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.27) .7-21.3) 22.90-9.0 (9.7) 10.6 (10.70-9.46-4.14 (6.00-18.5-26.7-19.39 (5.7) 22.6) 952 1187 946 997 1332 1019 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * 1.24-5.30) 3.90 (6.6) 11.72) 2.20-4.

79-6.97) < LOD .27) * * * * * * * * 1.6 (11.9) 16.59-3.7 (10.4) 16.37-5.6) 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 * * * * * * .51-10.82-11.09-11.89-10.5) 13.973 (.620 (<LOD-.28 (1.38 (.38 (2.28) 6.86 (3.78) 4.3) 12.530-1.89-3.7 (8.7) 9.00) 8.11-3.55 (2.9-17.99) 2.6 (11.83 (6.29-2.55) 16.44-6.72) 4.5 (10.72-4.4 (11.9 (9.5 (15.4) 6.8) 16.69-11.99 (4.68) .2) 12.6) 14.30) 7.9 (9.34) < LOD < LOD < LOD < LOD 3.11 (5.93 (2.58 (4.73 (5.38-13.6-19.2 (9.7) 15.6) 952 1187 945 997 1331 1017 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * .4) 7.910 (<LOD-1.27) < LOD .89 (3.4) 15.38 (1.52-3.1 (8.5 (11.3-17.7-23.93-10.12) < LOD < LOD 4.0-21.47-9.54 (7. Fourth National Report on Human Exposure to Environmental Chemicals 123 .4-16.8 (8.07) 2.36 (2.760 (<LOD-1.06 (<LOD-1.2-30.00) 2.6 (12.23-3.30) 2.54-5.42) 7.50-17.12 (7.850 (<LOD-1.75-3.39-17.61 (2.28-12.0) 14.93 (6.5 (8.07) 2.42) 8.93 (<LOD-2.9) 19.82-8.2) 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.30) 8.54) 9.83 (7.810 (<LOD-1.7) 14.0-19.3) 9.2) 16.96-10.5-17.6) 6.43 (2.78-10.70-35.67 (1.86) 9.8) 14.96-11.5 (9.14 (2.74-19.74-4.79-9.63 (2.71 (1.7 (11.4-18.25 (4.3) 8.4) 7.3-15.6 (13.6) 7.29) 3.07 (5.27-13.S.97-4.77) 3.4) 7.75-3.16 (3.0 (11.00 (2.68-4.33) 3.87 (3.4) 9.37) 3.940) < LOD < LOD 1.2) 12.18) 2.50 (6.6 (10.68-19.1) 10.95 (2.3 (7.21-21.34-18.89-13.88-7.6) 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 1.86-3.41 (7.00 (7.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.06) .53-8.88 (1.68-10.92 (5.0 (13.590 (<LOD-.16-14.48 (2.95) 3.950) .7-19.85-8.0 (8.29 (5.2 (9.3) 6.04) 9.32) 2.690 (.00 (<LOD-1.45) 6.03) 3.71) < LOD < LOD 2.3-17.7) 14.30-5.7 (10. population from the National Health and Nutrition Examination Survey.2) 19.890-2.42-19.5) 10.15) < LOD < LOD 75th 2.32-8.94 (5.20-3.05-3.00 (5.3-21.78 (4.78 (6.8) 11.77 (2.5) 8.01-5.67 (7.6) 13.45) 3.95) 90th 8.2) 12.2-15.25-9.2) 15.3-34.55) .51-7.89-3.85-17. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.15 (1.1) 13.80) 3.63 (6.02-4.9 (9.64-11.5) 22.1) 20.780-1.6) 12.27) 1.8 (10.27) 5.9-25.00 (3.91) 3.81 (7.21) * * * * * 1.91-9.1 (13.92) 3.0 (10.7) 12.70-2.6) 95th 16.4-16.03 (2.2) 8.1 (19.00 (<LOD-1. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th .94-14.33-10.920 (<LOD-1.89 (2.2) 10.38) 1.4-15.07-3.77 (2.03 (6. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.09-11.6 (13.29 (2.19) 3.89) 5.

50) 1.05-3.2.98 (2.740-.05-2.60) 2.750-1.65 (2. < LOD means less than the limit of detection.45 (1.54) .49) 2.780 (.730) .990-1.930 (.580-1.970) .30-3.90) 3.46 (1.49) .550 (.41-5.500 (<LOD-.880) < LOD .359-.32 (1.70-7.657) * * .350-.32-1.618) * .680-1.201-.570 (.840 (.690-1. interval) Selected percentiles ( 95% confidence interval) Total * .540 (.960-1.89) 1.560-.20) 3.54-2.42-2.80) 5.570 (.77 (1.57 (1.240 (<LOD-.380) .600 (<LOD-.63 (1.490 (<LOD-.80) 3.670) .00-4.74-5.23-3.460-.08 (2.343 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.75-2.15) 2.73-5.380-.83 (2.13) .750) 1.45 (1.592) * .18 (1.98-3. and 03-04 are 0.749 (.450 (<LOD-.73 (2.86 (1.550 (.55 (3.70 (1.00 (1.90) 2.75 (2.20) 2.580-.29-2.19-1.10-1.45-4. respectively.90 (1.80) 3.600-1.60-4.00) 2.930) < LOD .40 (1.14-1.960) .22 (1.210 (<LOD-. 01-02.04) .30 (.910-1.79) .29) 1.710) .60) 3.425 (.11-3.30) 4.340-.30 (.50-2. see Data Analysis section) for Survey years 99-00. 0.26) .160 (<LOD-.22-3.860) < LOD < LOD .10) 1.21) 3.94 (3.584) .20 (1.20 (1.710 (.79) .22-3.58 (1.570 (<LOD-.510 (<LOD-.03) 1.47 (1.70-2.455 (.449 (.31-3.570 (<LOD-.30) 2.70 (1.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Diethylthiophosphate (DETP) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.89-6.76-6.20-1.08 (2.22-8.20) 2.50 (1.94 (2.390-.34) 2.83 (2.33-2.09. 124 Fourth National Report on Human Exposure to Environmental Chemicals .47) 2.390-.60 (2.59-2.880) < LOD 75th .48 (1.68-5.64 (1.760 (.600-.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 * .720-1.80) 2.36-4.350-.87-3.78) 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 * .20) 1.31-3.09 (.01-1.16) 1.46) 1.80 (1.700) .353-.20-2.950) 90th 1.590-.570) * .459 (.620-1.22-2.45 (2.10) 1.720 (.46 (2.585) * * .1.280-.11-3.710 (.57 (2.20) 1.89) 672 678 478 509 695 553 595 948 745 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.00-2.88) 1.790 (. and 0.27 (3.18 (.01) .20) 3.690 (.980) 1.453 (.69-4.587) * * .31) 2.91) 2.740-1.25-1.74) 3.83) .80 (2.820 (.96-3.592-.98) .690) .95 (2.780 (.90) 2.800 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.720-1.30 (1.16) 2.04) 1.96-5.700) .910) 1.650-.S.54 (2.16-3.949) .960 (.50 (1.30) 1.759) * .820 (.303-.457 (.850) < LOD .780) .38) 1.95) 2. which may vary for some chemicals by year and by individual sample.00) 1.10-1.90-4.32) 3.960) .86) 3.20 (1.830 (.260 (<LOD-.31) 95th 2.910 (.505 (.30 (.398-.37-2.89) .388-.17) 1.95-5.970) 1.740 (.680-1.15) 2.48 (2.17) 1.78) .34) 2.510 (.77-2.336-.50 (1.382-.20 (2.14 (1.30-3.40 (1.50 (1.83) 1.80) 3.76 (1.960) 1.380-.549 (.690-.740 (.930-1.80) 2.50-2.35) 1.880 (.01-3.61 (1.46-3.94) .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 * .73 (1.20-3.27 (2.30) 4.597) * .83) 2.17-4.930) 1.400) .39) 2.97 (2.30-1.20-2.41 (2.70 (1.592) * 50th .13) 2.940) < LOD .570-1.10) 3.810) .26 (2.467 (.59-6.10) 1.440-.50 (1. population from the National Health and Nutrition Examination Survey.

44) 2.42 (.07) 1.43) 2.13 (1.335-.99) 1.88 (1.47 (1.550-1.790) .05-2.580) .00-3.372 (.470 (<LOD-.800-1.700 (.18-2.330-.560-.50) 1.270-.380-.280 (<LOD-.45 (1.97) 1.710 (.910) < LOD .412-.250 (<LOD-.920) .850) 1.318-.06-2. population from the National Health and Nutrition Examination Survey.08-2.630) * .20-2.34 (1.66 (2.710 (.88) .98) 1.485) * * .33) .60) .720 (.04) 95th 2.31-1.77 (3.97 (1.45 (2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.22-3.720-1.14 (2.30) 3.67) .00-1.70 (2.560 (.700 (.08 (2.75 (2.640 (.590 (.32 (.58-6.60 (1.460-1.08 (.377-.57-4.840) .790 (.64 (2.560-.33 (1.67 (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.480-1.11 (.78) 3.24) 4.540-.400) .81) 2.17) 2.739) * .77-3.95) 1.730) .350) .520-.65) 2.62 (2.700 (.310 (<LOD-.00 (3.91 (1.97 (1.42) .08) 1.50 (1.348-.52 (1.680 (.55 (1.28 (1.22 (2.08-3.79) 1.62 (1.07) 1.535 (.285-.43) 2.61-3.38 (1.444-.320-.270-.870 (.690) < LOD < LOD .71) .38-3.380) .710 (.580 (.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 * .32) 5.830 (.07) 1.08-2.530 (.61) 2.07-3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.22) 4.515) * * .97) 2.520 (.82 (2.94) .44-2.57-2.76) 1.460) . interval) Selected percentiles ( 95% confidence interval) Total * .597) * .440-1.990-1.510-.393 (.460 (.80) 2.22) .05) < LOD .20-7.92 (1.740) < LOD 1.645) .07 (.09) .38 (2.234 (.08-3.36) 3.591 (.57 (3.750 (.500-.73 (2.447 (.16-1.23 (.05) 1.92) 3.87 (2.79 (1.22-3.448 (.75) 6.670 (.330 (<LOD-.230 (<LOD-.640 (.590-1.16) 1.580-.480) .400-1.840) 1.23) 2.92-8.04-1.17) 2.510 (.30-2.510 (.380-1.640 (.820) .58 (1.52) 3.300-.368) * .53) .67) 1.61 (3.830) 90th 1.06) 4.89 (1.940-1.870) .760) .05-4.19 (1.390) .75-3.840) 1.72-4.320-.305 (.471-.72 (1.16-2.253-.71 (1.509 (.39 (1.55-3.23) 3.490 (.23) 2.11-2.47 (1. Fourth National Report on Human Exposure to Environmental Chemicals 125 .750 (.90) 2.72 (2.10) 2.42-6.66) .61-3.270 (<LOD-.32) 2.72) 1.11) 1.180 (<LOD-.47-4.02-3.84 (2.49-4.02-3.310 (<LOD-.688) * .760) < LOD 75th .390-1.742) * * .43) 1.250 (<LOD-.05 (1.08-2.69 (3.04-5.136-.64 (2.08-3.22) 1.32) 1.25-3.660-.900) 1.S.49 (1.20) 1.42-8.69 (1.43 (1.880) 1.67-3.60) 1.800) < LOD .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 * .58) 3.740) .370-.403) .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.550-.22-2.08-3.67 (1.310-.29-4.03-2.77-4.453 (.84-6.63 (1.70 (3.02-6.17-2.57 (1.23) 1.552 (.32-1.73-3.470) .550-.60 (2.03-1.72) 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 * .300 (<LOD-.41 (.89-3.82) 2.07) 5.39) 2.930-1.08) 2.99) 2.590) * 50th .820) 1.71) 2.75 (1.07-2.980-1.550) .950-2.

1 (10.5) 30.64-8.70) 5.70 (1.66-5.0-69.0-110) 34.8) 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. which may vary for some chemicals by year and by individual sample.23) 9.79 (1.0) 3.2-33.05) * 2.0) 13.0 (26.9-21.81-3.87-7.10 (1.45) 2.9-51.95 (5.78) 9.18) 6.10) .0) 19.05-3.16) 2.32 (2.2 (19.20-4.0-53.3) 28.6 (9.0-41.00-24.6 (26.7) 47.83-2.70-6.94 (1.10 (1.0-43.0-49.1) 95th 48.1 (25.0 (20.53) 40.81-2.0-50.0) 33.17-2.0) 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 2.50 (2. respectively.44) Selected percentiles ( 95% confidence interval) Total * 2.0-31.54 (3.20 (2.43-7.8) 62.0) 4.77) 38.2) 16.3) 26.0) 28.0 (13.11) 2.9) 17.26) 75th 11.82 (1.80-2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.0 (19.4-22.70 (.90 (1.7 (12.0 (38.0) 31.2) 31.21 (3.2-27.04) 3.1 (26.1) 18.10 (1.77 (1.45) 2.16) * 1.31-6.70 (1.48) 5.8 (12.9 (19.48-2.8) 32.0 (8.91 (4.46 (.70 (7.10-4. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. population from the National Health and Nutrition Examination Survey.53) 1.9 (10.04 (<LOD-2.59 (1.0 (38.21 (1.0 (38.14) 5.60) < LOD 1.71) 5.40) < LOD 1.5.0 (37.9) 18.30-14.78 (1.30) 4.86-3.80) .86 (1.0) 16.59 (1.8) 41.1 (22.19) 2.21 (4.90 (1.0 (24.96) 5.63-6.3 (14.610 (<LOD-1.0-53.79 (2.0) 17.93-3.0 (7.80) < LOD 1.0-92.S.5-20.4-76.0-58.0 (38.470 (<LOD-1.3) 38.0) 45.2 (12.0) 17.0-39.74-2.0-41.6-54.0-47.0) 20.690-3.0) 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 2.3) 33.6 (15.11 (4.3 (12.7-41.23-2.40-16.76 (2.5-45.80-18.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.50-7.54 (1.41-4.0 (17.0 (21.50-5.27-6.71 (4.85 (1.60 (2.4.40) 50th 2.8) 39.8-24.18.2-47.2-26.29-4.10-13.1-19.76 (2.6-27.52 (4.72 (1.13 (1.4 (15.0-110) 42. interval) 1.26 (.7) 20.6-45.0 (38.07-5.41) 1.1) 38.1) 140 (46.50-17.0 (40.65 (4.660-2.90-8.13) 12.30 (.5) 69.0) 8.46-2.0) 28.0-52.04-8.06) * 2.1-46.41) 5.0 (8.30) 11.10) 39.88) 3.0 (38.0 (38.49-2.830-3.0) 16.6) 52.9) 48.9 (19.80) 1.2-27.8 (26.97) 6.83-2.06 (1.0-39.6 (11.64-3.58-2.70) 1.3 (23.0-230) 35.50-2.29-9.10 (7.1 (11.44) 3.09 (4.5-27.53 (1.4 (19.88) 1.42) 1.02 (2.83 (1.1-40.12 (3.1-25.69) 2.6-22.20) 1.29) 2.79-2.0) 32.0) 15.0) 3.3) 31.0 (8.4 (10.0-260) 34.85) * 2.5-40. and 0.0-29.600-2.0-62.53) * 2.25-3.12) 1.8 (22.0-58.5-74.18) 14.1) 38.2-39. see Data Analysis section) for Survey years 99-00.10 (1.4) 38. < LOD means less than the limit of detection.48-2.61 (1. 126 Fourth National Report on Human Exposure to Environmental Chemicals .1-20.9 (23.8) 671 678 498 509 695 579 595 947 757 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.46-6.0) 4. 0. and 03-04 are 0.35-6.50-20.57-2.00 (. 01-02.7 (12.0-62.0 (11.18) 20.3 (12.00 (.80) 90th 38.99 (2.0-41.3 (10.9 (27.44-7.8 (12.67 (1.13 (1.57-2.0) 20.3 (24.36-2.75-14.0) 3.71-2.05) 1.0) 6.530-4.0 (33.23-2.41 (1.98 (1.1 (25.8-21.0 (32.0 (25.41) 1.0) 4.90) 11.0) 3.0) 5.70-17.0) 42.40-4.7-22.5 (24.0) 30.58) 16.40) < LOD 2.2-80.98) * 2.92-5.7 (28.83 (3.92) * 2.44) 2.2-62.0 (20.0) 18.0 (6.19-2.33 (5.830-4.0) 15.1-47.70) 1.4) 19.9) 38.61-2.

2 (15.2-38.83 (.62) 4.16 (1.20-5.67-3.9 (10.4-67.50-5.55 (2.46-5.1) 52.4 (19.75 (1.0 (17.2) 41.95 (2.3 (10.4) 14.2) 36.5 (8.3-19.2 (8.36-13.66) 8.670-1.1) 13.08) 1. population from the National Health and Nutrition Examination Survey.680-4.02) * 1.33) 1.86) * 2.51) < LOD 1.1) 25.9-52.0-71.58-2.870-3.71 (1.48 (4.7-19.2 (9.2) 4.88 (4.79-17.47-17.80-8.1) 27.2-28.5-190) 30.07-2.860 (<LOD-1.96-16.60) 4.39 (1.40-7.9) 12.8) 3.23) < LOD 2.8-43.18) * 2.0 (14.1) 36.7-47.1 (12.3 (8.2) 13.2-34.7) 30.32-3.97 (1.26-2.35) 1.6-49.8-45.75) * 1.1) 17.0) 13.4 (11.86) * 3.33) < LOD 1.00 (4.17) 2.5 (17.5 (41.6) 3.22-2.22-3.46-6.1 (34.68) 47.0 (25.18-1.33) 2.1 (25.7-20.7) 95th 51.4) 3.1-63.9) 3.9) 24.22 (.8 (7.4) 12.9-18.9) 24.07-2.4-34.6 (27.53) 1.19-14.9 (26.1) 15.9) 54.02 (.6-38.95) 90th 32.61-2.3 (10.5-97.38 (3.54-15.44) 9.6) 11.2) 33.6 (24.31) 2.34) * 1.9 (7.8-26.96) 2.4-71.6-51.06) 1.84-13.4 (9.9-37.90 (.7-37.899-2.0) 25.94) 19.76-2.43) * 2.91-2.1 (33.0-118) 29.7) 34.8) 23.72) 2.0-70.5 (6.59-15.2 (22.7) 23.63-5.82) 1. Fourth National Report on Human Exposure to Environmental Chemicals 127 .00) 1.67 (1.25-3.12 (1.7 (10.21 (4.94-20.36 (4.56 (2.8) 11.9-41.16-2.02) 1.2) 471 575 310 664 821 715 813 1121 937 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 1.28) 1.46) 1.15 (.888-1.0 (23.7 (18.890-4.43-12.23-1.0) 10. interval) 1.52 (1.27) 10.6-32.8) 15.99-4.35) .7-43.9 (13.11-2.00) 6.41 (2.1) 25.3 (20.06-1.93) 5.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Dimethylthiophosphate (DMTP) (creatinine corrected) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.7-38.08 (1.4-39.1) 27.23) 37.26-4.83) .16 (1.2-47.59-2.24 (1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.3 (9.2 (16.0 (6.68 (1.5) 70.66 (1.36) 10.9 (39.58-17.29-5.4 (5.9-95.7) 26.3) 28.95-16.46-22. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.69-5.2-70.79 (2.6 (11.2) 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 2.66 (1.0) 48.5 (13.0) 952 1187 945 996 1330 1017 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.19-6.870-3.03) 1.57 (6.38-5.45 (1.7-109) 22.11) < LOD 1.14 (.5) 27.88 (4.17-3.8-37.0-40.7 (24.20) Selected percentiles ( 95% confidence interval) Total * 1.5 (15.7 (11.8-34.S.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.52-4.2) 13.47 (3.95-16.5 (34.4-21.27) 50th 2.6) 112 (40.1-22.48) 1.82 (2.59-2.0 (32.0 (39.3-27.6) 19.2 (21.09 (5.32 (3.6 (7.75 (1.75-6.50 (2.45-1.4 (25.7) 66.19 (1.38-1.9) 3.3) 13.54-2.03-2.14-8.4) 12.94) 1.27 (6.4 (12.1-60.0 (19.27-3.43-2.5 (15.71) 8.8) 32.40 (2.19) 5.930 (<LOD-1.7 (18.870-3.30) 28.9 (19.71-2.67 (1.0 (23.88 (1.37 (1.35 (2.3-42.40 (5.69-18.70 (1.67-16.62 (2.00-16.16 (1.0) 30.40-4.750 (<LOD-1.07) 9.8) 31.91 (6.12) 3.22 (2.6) 3.60 (.80 (1.6) 7.1) 13.01 (.56) 1.28 (1.51) .9-36.37-2.0) 47.70-4.88 (1.6) 23.5-36.5-43.06) 1.18) 3.19) 5.61-22.1 (39.0) 3.61 (1.57) 4.4 (25.33-5.1 (50.64 (1.7) 61.47 (1.38) 5.3-22.06) 75th 9.7) 15.4 (21.

280) < LOD < LOD < LOD < LOD .830 (.640 (.140-.210 (.360-.380-.120-.870 (. population from the National Health and Nutrition Examination Survey.300-1.470-1. 0. and 0.140-.110-.130-.860) .140) .050-.770) < LOD 95th .36) .100 (.770 (.420-.870 (.820 (.300-.380-.610-1.450 (.090 (<LOD-.540 (<LOD-.310-.720 (.870) < LOD .550) .620 (.12 (.160) .320 (.510-1.310 (.700-1.320-.990) .840) .230-. 01-02.170-.330-.650-1.080 (<LOD-.990 (.780) < LOD 1.32) .650) .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 .720-1.290) < LOD < LOD < LOD < LOD .120 (<LOD-.990) .630 (.1.130) .870 (.410) < LOD < LOD < LOD < LOD .190 (. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th 75th .610 (.610 (.870 (.150) .03) .610-.120-.370-.680) .42) .410-.310) < LOD < LOD < LOD < LOD .090 (<LOD-.190 (.090 (<LOD-.730) .530-.30) .850) < LOD .830 (.270 (.162) * * * * * .084-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.090 (<LOD-.350) < LOD < LOD < LOD < LOD .130 (.830) < LOD .090 (<LOD-.700-1.160-.00) .099-.640-1.540) 672 678 498 509 694 579 595 947 757 Non-Hispanic blacks .310) < LOD < LOD < LOD < LOD .860-1.430 (.400-.630 (. < LOD means less than the limit of detection.240 (<LOD-.350) .680-1.260 (.370-.440-1.540) .230) .380-.660 (.290 (<LOD-.900 (.390) < LOD < LOD .090 (<LOD-.130-.700-1.310 (.290) < LOD < LOD < LOD < LOD 90th .940 (.130) .720) .290) < LOD < LOD < LOD < LOD Non-Hispanic whites Limit of detection (LOD.690-1.640) .700-1.560 (.220 (.200) < LOD < LOD .S.680-1.740) < LOD .650 (.470 (.410-1.460 (.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 * * * * * * .20) .490 (.450 (.540) .60) 1.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.760) < LOD .570) .410-.58) .30) .05.130-.730-.171) * * .930 (.180) . 128 Fourth National Report on Human Exposure to Environmental Chemicals .640) . respectively.850 (.820 (.830) .40) .850 (.680 (.190 (.10 (.42) .080 (<LOD-. see Data Analysis section) for Survey years 99-00.10) .15) .117 (.650-1.430-.840) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.140-.390 (.220 (<LOD-. which may vary for some chemicals by year and by individual sample.1.560 (.160) . and 03-04 are 0.460-.10) .210 (.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 * * * * * * * * * .870 (.30) .600 (.650) .13) .450 (.10) .150 (<LOD-.360-.

520-.410-.250-.116 (.210 (.86) .400) .360 (.380-1.09) .700-1.580) .00) < LOD .700 (.440-1.67) .260-.410) < LOD < LOD .570-.700) .86) . Fourth National Report on Human Exposure to Environmental Chemicals 129 . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.360-.120) .220 (.380-.670 (.440 (.161) * * .880 (.410 (.24) .650-1.080 (.140-.100 (<LOD-.60) .070 (<LOD-.01 (.050 (<LOD-.110) .510-.500-1.580 (.62) 1.36 (1.500) .070 (<LOD-.310) < LOD < LOD < LOD < LOD Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.860 (.38) 1.760) .810 (.380-.860-2.190 (.080) .640-1.190-.280) < LOD < LOD < LOD < LOD .330 (.410-.78) .500 (<LOD-.070 (<LOD-.03 (.850 (.220) < LOD < LOD < LOD < LOD .410 (.550 (.340-.03) .990) .720 (.330-.400 (<LOD-.270) < LOD < LOD < LOD < LOD .057-.43) .170) < LOD < LOD .610-1.170 (.780 (.300-.860 (.750) < LOD 95th .390-.650) < LOD .230) < LOD < LOD < LOD < LOD .880-1.090 (.150-.800-1.S.270 (.260) .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 .03 (.19 (.700 (.180-.780) < LOD 1.300-.540 (.320 (<LOD-.720 (.730 (.380-.02-1.140-.710-1.390-.730) .670-1.570 (.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 * * * * * * .940) .100-.520) 672 678 497 509 693 578 595 947 756 Non-Hispanic blacks .140) .084-.330-.080 (<LOD-.110) .090 (<LOD-.570-1.330-.450 (.580) < LOD .070 (<LOD-.410) .360-.300 (.140-.110) .730) .370 (<LOD-.230-.230 (<LOD-.290) < LOD < LOD < LOD < LOD 90th .02) .12) < LOD .600) .470 (<LOD-.580-1.20) 1.111) * * * * * .380 (.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 * * * * * * * * * .740 (.450) .060-.560 (.550 (.200 (.190 (.66) 1.58) 1.670 (. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th 75th .540) .960) .140-.970) .120) .170 (.580 (.740) < LOD 1.360) < LOD < LOD < LOD < LOD .660-1. population from the National Health and Nutrition Examination Survey.24 (.110-.03 (.890 (.990) .200 (.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.600-1.140-.940) .240-.29 (.14) 1.730) .310) < LOD < LOD < LOD < LOD .490-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.540 (.330 (.110) .870) .460 (.

90 (2.63 (3.99) 11.580 (.730 (.960 (<LOD-1.0-40.0-38.70-7.23-6. which may vary for some chemicals by year and by individual sample.07 (1.39 (2.52 (1.0) 2.0 (17.0) 5.750-1.90) .07-3.620-1.82-4.40-7.0-40.30 (1.40 (1.840-3.88-3.07 (3.10-9.83-3.90) . respectively.380-.750-2.38-3.43-4.720) 2.10 (.0) 2.15) 19. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.90-37. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th 2.86) 4. < LOD means less than the limit of detection.600 (.55-4.87) 5.590 (.210-1.59-5.880) 5.40) 2.850) 16.07) 1.0) 2.425-1.30 (2.40 (1.80 (4.07 (3.20-17.830 (.26 (2.0 (17.12-1.0 (5.90-28.170-1.74 (3.53) 20.14) 2.800) 17.30 (.0 (17.67 (2.62-8. population from the National Health and Nutrition Examination Survey.53-7.330 (<LOD-1.0) 2.0) 5.250 (<LOD-.40) 1.63) 32.00 (1.48 (2.87) 12.0) 3.94 (1.68) 2.350-.67) .30-3.0) 2.61 (1.15) 14.900 (.0-38.00) 1.840 (.6) 672 678 498 509 695 552 595 947 752 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.890 (.11 (1.0) 5.0 (16.12) * * * * * * * * .65) 1.910) 2.870) < LOD < LOD .960 (.11) 13.0) 5.640 (.50) 2.640 (.29-10.0) 7.97) 20.49) 17.31-10.60) 1.32-9.30) 95th 19.67 (1.11) .49 (1. see Data Analysis section) for Survey years 99-00.30-7.0-44.48) 13.0 (17.05 (2.85-3.28) .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 * * * * * * * * * .74) 5.770 (<LOD-1.00) .99 (1.07-3.080-1.08.96 (1.70-3.510-.28) 1.800) 90th 13.36-3.1.53 (2.45 (2.83) 2.30) .0 (5.05-3.60) .52) 5.16) 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 . and 0.0) 4.31) .840 (<LOD-1.0) 2.10-3.691 (.40-4.90-9.00-17.10 (3.18) 1.70-17.20) < LOD < LOD < LOD < LOD < LOD 1.260-.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 * * * * * * .110 (<LOD-.14-5.51 (2.350-.14) .46 (1.10-3.0-39.400-1.90) .0) 4.S.94-8. 130 Fourth National Report on Human Exposure to Environmental Chemicals .49 (1.610 (.0-38.90 (1.0 (4.0 (6.39) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.30 (1.42) .1. 01-02.28-9.01) 5.0) 4.21) 3.10 (3.52 (1.770) 2.21-3.40-8.13 (3.66) 4.37) .70) 2.47 (3.97) 20.610) < LOD < LOD < LOD < LOD < LOD 2.83-3.20-4.480-.0) 2.740 (.50) .40-20.20 (1.80) < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 4.03 (.0 (5.42) 2.32 (1.0 (4.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.00-17.00) .36-3.800-4.20-4.76 (1.30-6.35-10. and 03-04 are 0.0 (13.6) 5.90-20.35) 5.05 (3.190-1.55-8.70-30.0 (5.20 (1.370-.24-7.35) 11.33 (4.0) 4.0 (17.51-8.0 (5.0 (7.690 (.94-3.70-50.30 (1.99) 19.00 (.360-1. 0.0 (3.

580 (.53) 27.15) 9.81-17.67 (2.320-1.03) 2.37) 4.04-16.250 (<LOD-.88) 17.540 (.38 (2.580) 1.36 (.890 (.5 (9.390-.96) 2.740-1.370) < LOD < LOD < LOD < LOD < LOD 1.770) .25-9.33-3.27 (2.22) 2.55) 21.8) 7.430) 1.00) . Fourth National Report on Human Exposure to Environmental Chemicals 131 .74 (2.40-12.600 (<LOD-1.5 (8.49-2.02) .01 (1.690-5.57-40.33 (1.12 (4.4) 2.00-19.31-18.35 (.91) 2.56 (1.21-3.57 (.55 (3.56) .7) 5.08) .970-3.4-34.18) 1.470 (.02 (1.47) .850-3.0 (9.14 (1.62-17.370 (.5) 2.04 (1.5) 7.41 (4.83 (4.83-11.57) 8.25-38. population from the National Health and Nutrition Examination Survey.630-1.340-.31-7.2 (8.330-1.340 (.24) 3.1 (5.31) .340-.17 (1.340-.8) 1.748 (.7) 4.71 (.82-11.06 (.580-1.790) 11.9 (11.30 (4.32) 9.14-6.930) .590) 2.64-4.10) 2.500 (.02-4.47) 5.79 (.5) 2.670 (.67) 1.80) 3.88 (2.6) 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 * * * * * * * * * .50) 11.660) < LOD < LOD .820) .33-4.86 (3.51-4.96-8.1) 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.09-3.540-1.47-10.90-6.88 (.710 (<LOD-1.9) 5.67-6.50 (4.240-.89 (2.4 (4.55) 21.44) .780-4.10 (2.830 (.5-40.40-2.650) 90th 10. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th 1.940-4.91-4.57) 1.22-27. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.700) 6.33-5.62 (1.3) 3.960 (.96-25.S.190-1.25 (1.430 (<LOD-.18) 95th 21.48-42.60 (1.840-3.7 (12.98 (4.10-3.48 (4.67) 2.64) 30.85-3.44-11.800-2.69-7.580) 16.820 (.7 (6.84) 9.830-3.620-3.71 (2.65 (2.1) 471 575 306 664 820 697 814 1122 924 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * .41) 18.0 (4.66-47.7) 6.80 (.53) .51-44.40 (.45 (1.8 (20.8) 7.92 (2.450 (.18) * * * * * * * * .86) .8) 2.29-4.270 (<LOD-.48-7.360 (.790 (.8) 4.47-10.9) 6.7) 3.270-.8) 2.0) 4.39) 20.50) .77 (.650 (.12-4.85 (1.370-1.33 (3.31) .1) 2.73 (4.40) 1.17) 5.11) .560 (.07 (2.52 (.02 (.32-6.860-2.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.13 (2.5 (11.07-21.28-6.11-5.43) .97) .260-.700) < LOD < LOD < LOD < LOD < LOD 1.61) Sample size 1949 2517 1927 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .1 (7.310-.03) 16.23-7.474-1.60) < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 4.05) .88-3.150 (<LOD-.2-38.69) 2.56) 2.59 (1.260-.29 (4.75) 5.730-3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.50 (2.3) 2.8-33.

Lunghini L. Castorina R. Garrison RP. accidental. Lu C. Reprod Toxicol 1998a. A clinical neurological. et al. Di-alkyl phosphate biomonitoring data: assessing cumulative exposure to organophosphate pesticides.38(1):91-97. Curl CL. Environ Res 2001.53(1):714. et al. Kedan G. Organophosphorus pesticide exposure of urban and suburban preschool children with organic and conventional diets. Environ Res 1992. Am J Ind Med 2006. Castorina R. Third National Report on Human Exposure to Environmental Chemicals. Hansen S. Fenske RA. The relationship between maternal and fetal effects following maternal organophosphate exposure during gestation in the rat. Chen W. Bradman A. Bozzi N. McKone TE. Barnhart S. J Expo Anal Environ Epidemiol 2005. Anger WK. Fenske RA. 2005. Biologic monitoring of exposure to organophosphorus pesticides in 195 Italian children. 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Temporal association of children’s pesticide exposure and agricultural spraying: report of a longitudinal biological monitoring study. Fenske R.7(5):715-731.37(3):382-395. Environ Health Perspect 2003. Environ Health Perspect 2003.32(5):487-496. Costa LG.49(9):751-760. Astroff AB. Arch Environ Health 1998. Daniell W.14(6):869-889. Environmental and biological monitoring of exposure to organophosphorus pesticides: application to occupationally and non-occupationally exposed adult populations. Sartorelli P. Arcury TA. Centers for Disease Control and Prevention (CDC). Angerer J.60(4):279-286. Abdelrasoul GM. Barr DB. Regul Toxicol Pharmacol 2003. Koch D. Young AD. Kissel JC. Neuropsychological performance among agricultural pesticide applicators. Environ Health Perspect 2005. Boccalon P. et al. Eigenberg DA.111(13):1640-1648. Engel LS. Ann NY Acad Sci 1997. Peterson JC. Orsi D. Lu C. Gillham RA. Pilkington A. Eskenazi B. Seta N. Kissel JC. Curl CL. Jamal GA. Duggan A. Buchanan D. Hawk R. 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The effect of the 14-day agricultural restricted entry interval on azinphosmethyl exposures in a group of apple thinners in Washington State. Richardson RJ. Environ Health Perspect 2000. Shebl MM. Strambi M.108:521-525. Greenhalgh R. Bouvier G. Bravo R. J Toxicol Environ Health 1981. Demers P. Long-term use of organophosphates and neuropsychological performance. Regul Toxicol Pharmacol 2003. Griffith W. Barr DB. Krieger RI.113(12):1802-1807. Grzywacz JG. Harnly ME. Organophosphorus pesticide urinary metabolite levels of children in farmworker households in eastern North Carolina. Sartorelli E. Giordani B. Fenske RA. Barr DB.177:37-41. Berent S.16(5):417-426. Metabolites of organophosphorous insecticides in urine specimens from inhabitants of a residential area. Sciarra G. 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Twenty-four-hour urinary excretion of ten pesticide metabolites in healthy adults in two different areas of Italy (Florence and Ragusa). Chronic neurological sequelae to organophosphate pesticide poisoning. Chrislip D. Salvini S. Steenland K. Narang A.68(3):209-227 Maizlish N. Aprea C. Occup Environ Med 1995. An epidemiological study of the relations between exposure to organophosphate pesticides and indices of chronic peripheral neuropathy and neuropsychological abnormalities in sheep farmers and dippers. Barr DB. Beach J. Bull Environ Contam Toxicol 1994. Fourth National Report on Human Exposure to Environmental Chemicals 133 . Bradman A. Rothlein J. Frasca G. Eskenazi B. Rothlein J. Thompson ML. Association between in utero organophosphate pesticide exposure and abnormal reflexes in neonates. Savage EP. Lasarev M.30(2):98-103. Rodnitzky RL. 4/7/09 Young JG. Office of Prevention Pesticides and Toxic Substances. Buccafusco JJ. Johnson C. Hore P. A behavioral evaluation of pest control workers with short-term. Environ Health Perspect 2006. Heaton RK. Ames RG.52(2):190-195. Saieva C. Lambert WE. Buchanan D.edu/ openbook.113(4):504-508. Neurotoxicol Teratol 1998. O’Malley M. low-level exposure to the organophosphate diazinon. Malathion deposition. Occup Environ Med 2001. Organophosphate pesticide exposure and neurobehavioral performance in agricultural and non-agricultural Hispanic workers. Petchuay C. McCauley L. Muniz J.43(1):38-45. Keefe TJ.pdf. Variation in organophosphate pesticide metabolites in urine of children living in agricultural communities.345(8958):11351139. Scherer J. et al.S. Monitoring of urinary alkyl phosphates in pestcontrol operators exposed to various organophosphorus insecticides.12(2):153-172. Washington (DC): U. Chronic central nervous system effects of acute organophosphate pesticide intoxication. and cholinesterase status of date dusters and harvesters in California. Tumino R. Washington (DC).php?record_id=2126&page=1. Samuels S.12(2):134-141. Berry H.38(4):546-563.26(2):199-209. Smit LA. Masala G. Ruberu DK. gov/oppbead1/pestsales/01pestsales/market_estimates2001. Seiber J. Pedersen L. et al. Sci Total Environ 2004. Int J Occup Environ Health 2006. Arch Environ Health 1975.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Krieger RI. Am J Ind Med 1987. Chronic neurological sequelae of acute organophosphate pesticide poisoning. 2004. Marshall E. Lewis JA. Spurgeon A. Environ Health Perspect 2005.338(8761):223-227. low-level organophosphate exposure on delayed recall. Rohlman D.2000 and 2001 market estimates. Neurotoxicity among pesticide applicators exposed to organophosphates. Irish RM. Neurotoxicology 2005.20(2):115-22. Bravo R. Gladstone EA. Burcar PJ. and spatial learning in monkeys and rats. Weerasekera G. Scand J Work Environ Health 1998. Nell V. Lancet. Lasarev M. metabolite clearance.nap. Arch Environ Contam Toxicol 2000. Wickremasinghe AR.84(5):731-736. Dinoff TM.epa. Occupational exposure to organophosphate pesticides: a neurobehavioral study. Pesticide industry sales and usage . Calvert IA. The presence of dialkylphosphates in fresh fruit juices: implication for organophosphorus pesticide exposure and risk assessments. Santana J. Environmental Protection Agency (U.114(5):691-696. vibration sense and tremor among South African farm workers. National Academy of Sciences. Takamiya K. McConnell R. EPA. 1991. Jamal GA. van der Hoek W. Prendergast MA. Levy LS.44(4):352-357. Effects of occupational exposure to organophosphate pesticides on nerve and neuromuscular function. Muniz J. Neuropsychological effects of long-term exposure to organophosphates in sheep dip. Robson MG. et al. Lancet 1995. et al. Rosenstock L. Pesticides in the Diets of Infants and Children. Daniell WE. U.58(11):702710. The Pesticide Health Effects Study Group. Claypoole K. Jenkins B. Available at URL: http://www. Pilkington A.24(1):18-29. discrimination. J Toxicol Environ Health A 2005. Stokes L. Stephens R. Available at URL: http://books. Effects of chronic. Keifer M. Am J Public Health 1994. et al. Phillips J. Kidd M. Myers JE. 1993 [online]. Visuthismajarn P. Hansen S. J Occup Environ Med 2002. National Research Council (NRC). Terry AV Jr. Stark A.332(1-3):71-80. Vitayavirasak B.S. Arch Environ Health 1988. 1/12/09 Peiris-John RJ. Weisskopf C.52(10):648-653. EPA). London L. Schenker M. Gillham R. Caltabiano LM. Russo J. Mounce LM. Effects of long-term organophosphate exposures on neurological symptoms. S. May. Biological monitoring of organophosphate pesticides in preschool children in an agricultural community in Thailand. Lu C.

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

60-3.0 (9.70-17.20 (2.9 (9.25) 1.22) 2.0) 8.and post-construction structural applications for termite control were to be phased out by 2005 (U. Survey Geometric mean (95% conf. 2005).39) 4.10 (1.3 (11.0) 15.5-24.59-2.60 (5.EPA. Chlorpyrifos is very toxic to fish and aquatic invertebrates and shows modest degrees of bioconcentration.90-8.6-Trichloro-2-pyridinol Metabolite of Chlorpyrifos and Chlorpyrifos-methyl Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.67 (2.59) 2.35) 1.8) 10.80) 1.0 (7.70) 1.50-2.63 (1.89-2. 2921-88-2 Chlorpyrifos-methyl CAS No.62-2.83) 1.60-2.80) 12. 5598-13-0 General Information The chemical 3.70-11. Estimated intakes from diet and water have not exceeded recommended intake limits.43-2.30-9.80-10.44-2.70-5.0) 6.01) 1.51-2.04-10.70-15. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.50 (2.4) 481 573 681 823 832 1113 99-00 01-02 99-00 01-02 1.4.20) 2.28-3.52-2.7-23. Exposure can also result from contact with contaminated surfaces.1-16.51 (1.30-2.29-1.80 (7.30-5.0 (7.02 (7.63 (8.0) 8.37) 5.50 (1. 2007). staying bound to soil particles.61 (1.20-11.0 (13. The general population may be exposed to chlorpyrifos via oral.30-11.3 (10.10) 2.90) 3. and on plants for days to several weeks.44-5.98-15.00) 2.9 (10.84) 1.15 (1.EPA. 1999.80) 2.4-15. Approximately 80.74 (1.40-10.40) 2.20) 2.0) 12. Approximately 21-24 million pounds per year were used domestically from 1987-1998.71 (1.20-16.32-1.60 (2.20-3. USGS. population from the National Health and Nutrition Examination Survey.60-4.3 (8.30-12.76 (1.0) 10.61) 75th 3.14) Selected percentiles ( 95% confidence interval) Sample 95th 10.72) 2.50-2.6) 7.51) 1.20-2. 2002).90 (2.70 (1.90 (3.67 (2.2 (10.90 (1.20 (4.53 (1.13-3.47) 1.50-14.7) 8.80) 4.32) 2.70 (1.10-17.30) 4.71 (6. chlorpyrifos and TCPy were detected in all indoor air and dust samples (Morgan et al.90-7.26) 7.04-10. pre.5.30 (2.50-4.80-8. air.50-8.0 (10.45 (1.05) 1.S.28) 2.47-13. chlorpyrifos was no longer registered for indoor residential uses in the United States.43-2.4 (8. interval) 1. Chlorpyrifos-methyl is an organophosphorus insecticide also used in agriculture and not registered for residential use.0) 14.57 (2.30) 5.20-14.68 (7.20-4.19-3. 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.89 (2.47-11.2) 972 1183 1022 1326 99-00 01-02 99-00 01-02 99-00 01-02 1. After 2001.0) 12.88 (1.66-4.86) 4.80 (1.47 (4.00-24. Inhalational and dermal routes of exposure are important in pesticide formulators and applicators.4 and 0.3) 8.97) 2. Fourth National Report on Human Exposure to Environmental Chemicals 135 .0) 7.60) 5.40-13.22 (1.0) 11.50 (2.30 (2.03) 1.94 (4.81-2..5.79-2. and sprayed to kill mosquitoes.63 (2.24-1.61-7.47-9.16) 2.9) 697 660 521 701 602 947 Limit of detection (LOD.0 (7. Chlorpyrifos is degraded in agricultural soils with a half-life of several months.20) 10. 2002).S. but can be detected in streams receiving runoff from application sites.40) 9.00) 1.30-1.13 (1.00-8.10 (3.9 (7.95 (4.9-18.91) 16.29) 90th 7.67 (1.Organophosphorus Insecticides: Specific Metabolites Chlorpyrifos CAS No.21) 3.36 (4.72-4.95) 7.0 (7.0) 12.0) 9.09 (2.4 (9.91 (1.000 pounds are used per year.19 (1.0 (7.03) 99-00 01-02 99-00 01-02 99-00 01-02 2.37 (1.74-9.97) 2.27 (7.09 (3.99-4.30 (4.10 (5.71 (2.7) 13.20) 4. Chlorpyrifos is a broad spectrum organophosphorus insecticide that has been widely used to control insects on food crops such as corn.0) 12.76 (1. and dust.31-2.02 (1.3) size 1994 2509 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th 1.10) 6.35) 2.40 (5. For instance.40 (5.96) 3.90-4.5) 7.46-2.60-3.24-3.31-2. dermal.87-6. Chlorpyrifos is Urinary 3.60 (4.8) 9.38 (3.25) 3.90 (1.52-12.40-2.97) 7.77 (1. It has low leachability. and inhalation routes.4 (10.66-15.6-trichloro-2-pyridinol (TCPy) is a metabolite of chlorpyrifos and chlorpyrifos-methyl.77-15.1) 5.68-2.8-15.00) 3.37 (4. Chlorpyrifos is not well absorbed through the skin but dermal exposure can be significant when other routes of exposure are low.9) 11.40 (6.97-7.90 (6.40-26. in 142 urban homes and preschools in North Carolina.70-16.64) 3.50-5.78 (7.05-5.0) 10.50 (2.0) 18.0) 10.5 (8.50 (1.10 (4.44 (3.77) 1.92 (1.77-6.55-5. and is infrequently detected in ground water (IPCS.34) 1.0-28.90-2. It also has been applied directly on animals to kill mites.0) 12.30) 4. applied to structures to kill termites.39-2.90) 7.97) 4.50-4.17 (1.02) 1.7) 9.S.

97) 3.2) 6.50 (4.3) 8.32) 1. Human health effects from chlorpyrifos or chlorpyrifosmethyl at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 2006a.56) 5.80-4. Survey Geometric mean (95% conf.72) 2.95 (3.42-2.62-7. TCPy is more persistent in the environment than chlorpyrifos itself (U.6) 10.06-4.45-1.60 (1.43 (4.39-1.00) 1.55) 1.44 (5.03) 1. interval) 1. weakness.98 (6.58 (1.65-11. 2005.83-2.98 (7.82 (3.0) 6.33 (1.73 (1.23-1.27-1.57-2.30-1.78 (1.94-12.57-2.47 (1.82) 8.97 (2.08) 6.75) 6. The metabolite TCPy does not inhibit acetylcholinesterase enzymes.05-1.3) 9.91 (4.06 (5.45 (1.56 (1.34-1..40) 1.5) 5.52 (5.S.39) 6..39 (4.49-2. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”). Slotkin et al.EPA.20 (2.2 (7.01) 99-00 01-02 99-00 01-02 99-00 01-02 3.20-1.19) 3.58-5.14-8.57) 9.8) 9.1 (10.09-3.91 (3. phosphorothioates such as chlorpyrifos are metabolically activated to the “oxon” form which has greater toxicity than the parent insecticide..77) 1.82 (2.91) 10.19-1.42 (6.12-3.72) 1.38) 3.02) 7.58 (1. Roy et al. resulting in excess acetylcholine at nerve terminals.05-8.06 (1.47 (5. Ricceri et al. the detection of TCPy in a person’s urine may reflect exposure to the environmental degradates.79-13.30-4.63 (4..44 (1.36) 1.55 (1.53 (2.92 (1.49-2. In pesticide applicators.74) 1.09 (1.12-1.01) 3.5 (6.69 (1.46 (1.89) 4. and seizures.76 (3.80-11.25-11.86 (1.16 (4. and producing acute symptoms such as nausea.Organophosphorus Insecticides: Specific Metabolites rapidly absorbed following ingestion. 2005.31-1.81) 2.05-3.4) 4.86 (3. Once absorbed.43-10.85) 4.83-11.24-24.64-2.94-14. 2000).62) 1.35) 2.15 (4.85) Selected percentiles ( 95% confidence interval) Sample 95th 8.21-1.85 (2.44 (5.11) 7.88-9.71 (1.22 (4. and other metabolites.1 (7.09-1.24) 5.93 (1.92-2.24-4.54 (2. cholinergic effects. paralysis.0) 16.05-4.05) 3.86 (1.46 (2. Based on animal data and human cholinesterase monitoring during occupational exposure. ubiquitous lowlevel environmental exposures in humans would not be expected to result in inhibition of cholinesterase activity.1-21.92) 3.16) 6.44 (6.59) 3.22 (6.6) 9.1-38.3 (7.47-2.44-6.72-2.80-6.24) 75th 2.31) 1.26-14.33) 2.57) 2.0) 12.7) 7.9 (12.48 (1.68) 1.93) 5.09-2. Chlorpyrifos is eliminated from the body primarily in the urine with a half-life of approximately 27 hours (Nolan et al..5.33 (.88-10.01) 1. 2006b).07) 1.11 (2.91-13.85-4. chronic exposure to chlorpyrifos may be associated with slight alterations in some components of neurophysiologic testing (Steenland et al.66-11. 2006.22-6.87-3.58) 1.49-2.55 (4.23) 14. These organophosphorus insecticides share a mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system.44 (1.0) 481 573 681 822 832 1113 99-00 01-02 99-00 01-02 1..97 (3.88) 6. 2005. In addition to being a metabolite of chlorpyrifos and chlorpyrifos-methyl in the body.24 (1.66 (1. Recent in vitro and in vivo animal studies suggest that effects on neuronal morphogenesis. and behavior may occur at systemically nontoxic doses or at doses of chlorpyrifos that do not result in cholinergic signs (Aldridge et al.31-4..42 (5.93) 2.28) 2.63-2. population from the National Health and Nutrition Examination Survey.60-3.91-4.96) 3.91) 1.91) 2.41 (1.47 (1.39 (2.28) 2.00-8.93 (4.12) 1.S.88-8.70-4.82-4. Overt cholinergic toxicity from chlorpyrifos has been described following suicidal ingestion and unintentional high level occupational exposure. 1984).17-4.97-3.48 (2.22) 1.64 (1. vomiting.80) 3.49 (1.97) 3.62) 90th 5.19-2.33-7.00-13.33 (5.37 (1.58 (4.88 (1.58) 5.940-1.3) size 1994 2508 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th 1.35-1.25-12. Chlorpyrifos and chlorpyrifos-methyl both demonstrate moderate acute toxicity in animal studies. Urinary 3.02 (5.85) 1.14) 1.11 (2. 2002).35) 1.65-15. Thus.59-2. TCPy can also occur in the environment from the breakdown of the parent compounds.07) 5.51 (1.3) 8.19) 6.7) 697 660 521 700 602 947 136 Fourth National Report on Human Exposure to Environmental Chemicals .17-4..24-1.90-9.29 (3.83) 1.56) 2. neurotransmission.81 (3. Metabolic hydrolysis leads to the formation of TCPy. 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. Betancourt et al.0) 10.6-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.99-8.56-2.54) 5.68) 6.91) 1.8) 972 1183 1022 1325 99-00 01-02 99-00 01-02 99-00 01-02 1.85 (3.. Howard et al.93 (2.88 (1.01) 3.64-7.24-5.00 (7.84-6.88-8.99) 1.11-9.95 (1.27-7. 2006.53-5.25-1.76 (2.56 (4.63 (5.66) 1.71) 3.21-6.75 (1.

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

Organophosphorus Insecticides: Specific Metabolites Centers for Disease Control and Prevention (CDC). Sheldon LS.cfm?objectid=6F5E95EB-F1F6-975E7C20F4211536F46F. U. Urinary pesticide concentrations among children. Harley K.114(5):746-751. Fenske RA. Environmental Protection Agency (U.113(2):211-219. Camann D. Pellizzari E. Scand J Work Environ Health 2005. Ryan L. Mandel JS. Bennett DH. Angerer J. Gregg M. Baker S. Environ Health Perspect 2003. A longitudinal investigation of selected pesticide metabolites in urine. et al. Chlorpyrifos. Barr D. Venerosi A. Rauh V. House dust levels of selected insecticides and a herbicide measured by the EL and LWW samplers and comparisons to hand rinses and urine metabolites. Hines CJ. Curwin BD. Int J Hyg Environ Health 2001. Sanderson WT. Hammerstrom KA. Acquavella JF. Biological monitoring of exposure of the general population to the organophosphorus pesticides chlorpyrifos and chlorpyrifos-methyl by determination of their specific metabolite 3.S. Lein PJ. Needham LL. Neurologic function among termiticide applicators exposed to chlorpyrifos. Howell RJ. Bruun D. Hardt J. National Toxicology Program (NTP). Environ Health Perspect 2004. Ann Occup Hyg 2007. Hein MJ. et al. Dick RB.9(5):494-501. Steenland K. Third National Report on Human Exposure to Environmental Chemicals. Bucelli R. February 5. Herrick RF. Bailey SL.73:8-15. Toepel K.10(4):327-340. Head SL. Environ Res 1995.114(2):260-263. Wartenberg D. Toxicol Appl Pharmacol 2005. Kromhout H. 4/7/09 Koch HM. Environ Health Perspect 2005. Eskenazi B. Brain Res Dev Brain Res 2005. et al. 4/7/09 Perera FP. Zhang J. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. Exposures of preschool children to chlorpyrifos and its degradation product 3. J Expo Anal Environ Epidemiol 2005. Gurunathan S. Croghan CW.5. Seidler FJ.15(4):297-309. Toxicol Sci 2006.155(1):71-80.inchem.204(2-3):175-180. Baker BA. J Expo Anal Environ Epidemiol 1999. Morgan MK. Available at URL: http://ntp. Sharma V.5. Environ Health Perspect 2006b. Chlorpyrifos exerts opposing effects on axonal and dendritic growth in primary neuronal cultures. Barr DB.nih. Environ Health Perspect 2006a. Jewell NP. J Expo Anal Environ Epidemiol 2005. 2921-882. Ozkaynak H.108(4):293-300. Available at URL: http://www. Ricceri L. Environ Health Perspect 2000. Developmental neurotoxicity of organophosphorous pesticides: fetal and neonatal exposure to chlorpyrifos alters sex specific behaviors at adulthood in mice. Effects of transplacental exposure to environmental pollution on birth outcomes in a multiethnic population. Striley C. Kinney P. Roy TS. Hore P.31 Suppl 1:98-104. 2005. Bradman A. Levin ED. Temporal variability of urinary levels of nonpersistent insecticides in adult men.6-trichloro-2-pyridinol. Barr DB. Slotkin TA. Jett DA.51(1):53-65. J Expo Anal Environ Epidemiol 2000. Jones PA. Fortuna S. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population. et al. MacIntosh DL. Nolan RJ. Seidler FJ. Reid TM. Freshour NL. Lioy PJ. Executive summary of safety and toxicity information. Robson M. Environmental Health Criteria 198.niehs. International Programme on Chemical Safety-INCHEM (IPCS). Hill RH Jr. Ryde IT.112(10):1116-1124. Seidler FJ. Alexander BH. Lorenzini P. Tsai WY. Pesticide residues in urine of adults living in the United States: reference range concentrations. Bravo R. Barr DB. Chlorpyrifos accumulation patterns for child-accessible surfaces and objects and urinary metabolite excretion by children for 2 weeks after crack-and-crevice application. Freeman N. EPA 738-R- 138 Fourth National Report on Human Exposure to Environmental Chemicals . Cometa MF. Chlorpyrifos: pharmacokinetics in human volunteers. et al.S. Quantitative morphological assessment reveals neuronal and glial deficits in hippocampus after a brief subtoxic exposure to chlorpyrifos in neonatal rats. Heederik D. et al. et al. 1992. Meeker JD. chlorpyrifos. et al.15(3):271-281. mothers and fathers living in farm and non-farm households in Iowa. et al. Shealy DB. Chrislip DW. Weltzien E. Rick DL.111(2):201-205. Atlanta (GA). EPA). Ryan PB. Biomonitoring for farm families in the farm family exposure study. 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. Slotkin TA.org/documents/jmpr/jmpmono/ v99pr03.114(10):1542-1546. Tate CA. Edwards RD.93(1):105-113. Capone F.71:99108.207(2):112-124. Interim registration eligibility decision for chlorpyrifos. Slotkin TA. Lu C.6-trichloro 2-pyridinol in their everyday environments. Environ Health Perspect 2006. Irish R. 1999. et al. gov/ntpweb/index. Comparative developmental neurotoxicity of organophosphate insecticides: effects on brain development are separable from systemic toxicity. Chuang JC.htm. Honeycutt R. Robertson GL. Saunders JH. Levin ED. Howard AS. Adgate JL. Bravo R. Chapman P. Yang D. Toxicol Appl Pharmacol 1984. Freeman N.

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

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

270) < LOD 659 701 920 Limit of detection (LOD.Organophosphorus Insecticides: Specific Metabolites Urinary 3-Chloro-7-hydroxy-4-methyl-2H-chromen-2-one/ol Metabolite of Coumaphos Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.2. Fourth National Report on Human Exposure to Environmental Chemicals 141 . which may vary for some chemicals by year and by individual sample. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2480 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.210) < LOD < LOD 567 815 1099 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1169 1312 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .380 (<LOD-.200 (<LOD-. population from the National Health and Nutrition Examination Survey.200 (<LOD-. < LOD means less than the limit of detection. 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.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 .560) < LOD 659 700 920 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.S. see Data Analysis section) for Survey year 01-02 is 0. 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 . Survey Geometric mean (95% conf.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.670 (<LOD-1.

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

fruits. since 2004. Human exposure to diazinon from dietary sources is expected to be low due to its limited applications to food crops and due to its rapid degradation. Most granular formulations. < LOD means less than the limit of detection.S. vegetable.EPA. diazinon produced wild bird kills before use restrictions were in place. but is rapidly absorbed orally (IPCS.05) < LOD < LOD 644 678 484 700 554 956 Limit of detection (LOD. and forage crops. Diazinon is not well-absorbed through the skin. It is also used for cattle ear tag applications to control flies and ticks and. see Data Analysis section) for Survey years 99-00 and 01-02 are 7. and other metabolites. 333-41-5 General Information The chemical 2-isopropyl-4-methyl-6-hydroxypyrimidine is a metabolite of diazinon. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”).S. in some pest strips. diazinon cannot be sold for residential use. It has been infrequently detected in general groundwater sampling but has been detected in streams receiving runoff from application sites (IPCS. which may vary for some chemicals by year and by individual sample. It is toxic to birds. 1998. 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 1.11) < 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. Metabolic hydrolysis leads to the formation of 2-isopropyl4-methyl-6-hydroxypyrimidine. and particularly when it was ingested in granular form. Inhalational and dermal routes of exposure can be significant for pesticide applicators. 2004).49 (<LOD-2. an organophosphorus insecticide that is used to control insects on nuts. USGS. Diazinon is biologically and chemically degraded in soils with a half-life of about a few weeks. Fourth National Report on Human Exposure to Environmental Chemicals 143 .S. 2004). population from the National Health and Nutrition Examination Survey. Estimated intakes from diet and water do not exceed recommended intake limits (U. about 13 million pounds of diazinon were used annually on agricultural sites in the United States. phosphorothioates such as diazinon are metabolically activated to the “oxon” form which has greater toxicity. Fish and aquatic invertebrates show modest degrees of bioconcentration and are very sensitive to toxic effects.2 and 0. diazinon was widely used in residential and garden application. 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. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.Organophosphorus Insecticides: Specific Metabolites Diazinon CAS No. Prior to 2000. seed and foliar applications are planned to be phased out (U. Once absorbed. 2007). but these uses have been phased out. Survey Geometric mean (95% conf. 1998). Before these restrictions.EPA. Experimental diazinon exposure in people has demonstrated its rapid elimination into urine. aerial. in the past.45 (<LOD-3.7.

the detection of 2-isopropyl4-methyl-6-hydroxypyrimidine in a person’s urine may reflect exposure to the environmental degradate. cholinergic effects.gov/toxpro2. 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. 2-isopropyl-4-methyl-6-hydroxypyrimidine can also occur in the environment from the breakdown of the parent compound. Seifert and Pewnim. agricultural.atsdr. Additional information about external exposure (i. In addition to being a human metabolite of diazinon. Intoxications in humans from intentional overdose. 1998). animal carcinogen. 1992).S. and seizures. Diazinon is not considered to be a mutagen.e. subsamples of NHANES 1999-2000 and 20012002. and producing acute symptoms such as nausea. EPA at: http://www.cdc.S.. environmental levels) and health effects is available from ATSDR at: http://www. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. In animals.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. The U. Olsson et al. In two nonrandom samples of United States adults and children.Organophosphorus Insecticides: Specific Metabolites from dialkyl phosphate metabolite excretion (Garfitt et al.72 (<LOD-4. Thus. 144 Fourth National Report on Human Exposure to Environmental Chemicals ..html and from U. 1986. 1998).EPA considers diazinon unlikely to be carcinogenic in humans. in the 2001-2002 subsample (CDC.76 (<LOD-3.49 μg/L. 2002). Diazinon has moderate acute toxicity in animal studies.. respectively (Baker et al. population from the National Health and Nutrition Examination Survey.epa. Survey Geometric mean (95% conf. resulting in excess acetylcholine at nerve terminals. diazinon does not accumulate in tissues (IPCS.. paralysis. most of the measurements of 2-isopropyl-4-methyl6-hydroxypyrimidine in urine were below the limit of detection. diazinon and other organophosphorus insecticides share a mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system. although the 95th percentiles for children 6-11 years old and for non-Hispanic blacks were 1. In the U. vomiting. and indoor applications have been documented... weakness. Biomonitoring Information Urinary levels of 2-isopropyl-4-methyl-6hydroxypyrimidine reflect recent exposure.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. 2003). 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. 2000. respectively. At high doses.gov/pesticides/.45 and 1. or reproductive toxicant (IPCS.S. 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.S. There has been only limited study of diazinon at systemically non-toxic doses that do not result in cholinergic signs (Anthony et al. 1986 Rajendra et al.

htm.. Diazinon.Organophosphorus Insecticides: Specific Metabolites 2005). Bouchard M. 2007 [online]. International Programme on Chemical Safety-INCHEM (IPCS). References Anthony J. Interim reregistration eligibility decision (IRED. et al. Third National Report on Human Exposure to Environmental Chemicals. Needham LL. Driskell WJ.50(5):505-515. March 2006. Swan SH. Centers for Disease Control and Prevention (CDC). Fenske RA. Effects of chronic intake of diazinon on blood and brain monoamines and amino acids. Dumas P. 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. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine. Oloffs PC.376(6):808-815. Carrier G.gov/ oppsrrd1/REDs/diazinon_ired. 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. Drug Chem Toxicol 1986. 2006). Biochem Pharmacol 1992. Sadowski MA.inchem. 6/1/09 Fourth National Report on Human Exposure to Environmental Chemicals 145 .S. 4/7/09 Lu C.S. Banister EW. Atlanta (GA). urinary 2-isopropyl-4-methyl-6hydroxypyrimidine was detected in less than 14% of multiple samples collected during varied diets (Lu et al. Redmon JB. Biological monitoring of exposure to organophosphorus insecticides in a group of horticultural greenhouse workers. Kruse RL. Barr DB. Swan et al.9(2):117-131.37(4):501-507. urinary 2-isopropyl-4-methyl-6-hydroxypyrimidine levels were below the limit of detection (Bouchard et al. In a small number of men visiting fertility clinics in Missouri and Minnesota. Ann Occup Hyg 2006. 1998. Environmental Health Criteria 198. Drobnis EZ. Brunet RC. Exposure to the organophosphate diazinon: data from a human volunteer study with oral and dermal doses. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.44(11):2243-2250. 2006). Bull Environ Contam Toxicol 1986. Environmental Protection Agency (U. Irish R. Barr DB. Baker SE. Cocker J. Geological Survey (USGS). Seifert J. Banister E. The Quality of Our Nation’s Waters.S. Barr DB.pdf. Rajendra W. Olsson AO. Nguyen JV. 1/14/09 U. Available at URL: http://pubs. Available at URL: http://www. Noisel N. 2005. Liu F. Effect of sublethal levels of diazinon: histopathology of liver. Alteration of mice L-tryptophan metabolism by the organophosphorous acid triester diazinon. Environ Health Perspect 2006. EPA 738-R-04-006. Study for Future Families Research Group.. J Expo Anal Environ Epidemiol 2000.org/documents/ehc/ehc/ehc198. Barr DB. Bravo R. In 54 Canadian greenhouse workers.114(2):260-263. U. Toepel K. Garfitt SJ. May 2004.10(6 Pt 2):789-798. 1992-2001.134(1-3):105-113. revised February 15. Jones K.epa. Semen quality in relation to biomarkers of pesticide exposure. Oloffs PC. Diazinon. Pewnim T. (2003) found that 2-isopropyl4-methyl-6-hydroxypyrimidine was detectable in 96% and 58% of the subjects. Mason HJ. Beeson MD. Quantification of selected pesticide metabolites in human urine using isotope dilution high-performance liquid chromatography/ tandem mass spectrometry.111(12):1478-1484.usgs. Toxicol Lett 2002. Anal Bioanal Chem 2003. EPA).gov/circ/2005/1291/. In 23 children. Environ Health Perspect 2003. Pesticides in the Nation’s Streams and Ground Water. Available at URL: http://www.

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

S. 2001. a malaoxon metabolite and a technical grade impurity tested positive in some chromosomal tests (Blasiak et al.S.Organophosphorus Insecticides: Specific Metabolites direct ingestion of agricultural strength solutions.gov/toxpro2.74 (<LOD-5. 1999. Additional information about external exposure (i. median urinary levels on the conventional diet were similar to the detection limit in the NHANES 1999-2000 subsample (CDC. 2004).S.. Survey Geometric mean (95% conf. 1999). 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. environmental levels) and health effects is available from ATSDR at: http://www. 2005)..e.. some of the postshift urine levels in duster-applicators were thousandsfold higher than the detection limits in the NHANES 1999-2000 subsample. CDC. 2002. Thomas et al. but isomalathion. population from the National Health and Nutrition Examination Survey. Human studies of single oral doses between 0. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 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.. and it is not considered an animal teratogen or a reproductive toxicant. IARC considers malathion not classifiable as a human carcinogen. 2003). 2006).cdc.S. Malathion dicarboxylic acid was infrequently detected in multiple samples from 80 Maryland residents in 1995-96 (MacIntosh et al. but cholinesterase activity was not affected. 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. 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. Malathion does not appear to produce human reproductive or teratogenic effects at environmental levels of exposure (Grether et al. 1993. 1987. Toxicity from unprotected bystander exposure during applications is rare (U. Giri et al. Fourth National Report on Human Exposure to Environmental Chemicals 147 . representative subsample from NHANES 19992000 (Adgate. Of 382 pregnant women living in an agricultural community.EPA.S. Replacing conventional diets with organic diets in 23 children led to a tenfold decrease in urinary levels of malathion dicarboxylic acid. EPA at: http://www. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.. 1996. 2006).5 and 5.gov/pesticides/..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. Malathion itself has not been considered genotoxic (U. Flessel et al. 2005. 30% had detectable levels of malathion dicarboxylic acid at a detection limit about tenfold lower than the detection limit in the NHANES 1999-2000 analyses (Eskenazi et al.EPA. Lu et al.0 mg/kg/day have shown no acetylcholinesterase inhibition or other short term effects (IPCS. 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.. Biomonitoring Information Levels of urinary malathion dicarboxylic acid reflect recent exposure. 2000). 2005)..atsdr.html and from U... 2006).. Biomonitoring studies of malathion dicarboxylic acid provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of malathion than are found in the general population.epa. Finding a measurable amount of malathion dicarboxylic acid in urine does not mean that the level will result in an adverse health effect. 1990).

Malathion (addendum). Giri S. et al. Environ Health Perspect 2006. 2005. Hooper K.132(4):794-795. 4/7/09 Kissel JC. Fenske RA. A toxicokinetic model of malathion and its metabolites as a tool to assess human exposure and risk through measurements of urinary biomarkers. Increased frequency of specific genomic deletions resulting from in vitro malathion exposure. 6/1/09 148 Fourth National Report on Human Exposure to Environmental Chemicals . Lu C. Bouchard M. Barr DB. Environmental Protection Agency (U. Samuel O. Clayton CA. Available at URL: http://pubs.inchem.pdf. Am J Public Health 1987.S.9(5):494-501. Flessel P.56(10):2393-2399. Geological Survey (USGS). revised February 15. Goldhaber M. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides.445(2):275-283. Pesticides residues in food: 2003 FAO/WHO Meeting on Pesticide Residues.usgs. Neutra R. Blasiak J. htm. Barr DB. Genetic toxicity of malathion: a review. Cancer Res 1996. EPA 738-R06-030. Environ Mol Mutagen 1993. EPA). Barr DB.gov/circ/2005/1291/. Dumoulin MJ. Dinoff TM. Arch Environ Contam Toxicol 2000. MacIntosh DL. Available at URL: http://www. Centers for Disease Control and Prevention (CDC). Bravo R. Rappaport E. Toepel K. International Programme on Chemical Safety-INCHEM (IPCS). O’Neill JP. Harris JA. J Expo Anal Environ Epidemiol 1999. Petitti D. metabolite clearance.73(1):182-94.77:1009-1010. Carrier G. Prasad SB.gov/oppsrrd1/REDs/ malathion_red.38(4):546-553. Comparison of organophosphorus pesticide metabolite levels in single and multiple daily urine samples collected from preschool children in Washington State. Albertini RJ. Harley K. July 2006. 1992-2001. Environ Health Perspect 2001. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population.15(2):164-171. Needham LL. Eskenazi B. Giri A. Toxicol Sci 2003 May. Grether JK. Griffith W. Pluth JM. Freeman NC. Pesticides in the Nation’s Streams and Ground Water. The Quality of Our Nation’s Waters. Reregistration eligibility decision (RED) Malathion. Trzeciak A. Atlanta (GA). Eberly LE. Jewell NP. Barr DB. Weltzien E. Krieger RI. Genotoxic effects of malathion: an organophosphorus insecticide using three mammalian bioassays in vivo.112(10):1116-1124. Curl CL. U. Kizer KW: Exposure to aerial malathion application and the occurrence of congenital anomalies and low birthweight. and cholinesterase status of date dusters and harvesters in California. Lu C. Mutat Res 1999.114(2):260-263. 6/1/09 U. March 2006. Bradman A. Sharma GD. Environ Health Perspect 2004. 2007 [online]. Irish R. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample. In vitro studies on the genotoxicity of the organophosphorus insecticide malathion and its two analogues. Hammerstrom KA. Malathion deposition. J Expo Anal Environ Epidemiol 2005. Thomas D.org/documents/jmpr/jmpmono/v2003pr06. Swan SH. Mutat Res 2002. Lioy PJ. Available at URL: http://www.S. Reproductive outcome in women exposed to malathion. A longitudinal investigation of selected pesticide metabolites in urine. Am J Epidemiol 1990. Ryan PB. Jaloszynski P. Brunet RC.74(2):following table of contents. Kedan G. Erratum in: Toxicol Sci 2003 Aug. Nicklas JA. Gosselin NH. et al.Organophosphorus Insecticides: Specific Metabolites References Adgate JL.22(1):7-17. et al. Quintana PJ. Szyfter K.epa.109(6):583-590. Hertz-Picciotto I. Third National Report on Human Exposure to Environmental Chemicals.S.514(1-2):223231.

910) < LOD < LOD .28-4.00 (2.11-4.91-3.70) 2.00) 3.70 (2.0) 3. and oral routes can occur in pesticide and agricultural workers (Muttray et al.00 (2.50 (1.33) 2.0) 3. Methyl parathion is not registered for residential use in the United States.80 (2.50 (1.70 (2. O-ethyl-O-(4-nitrophenyl) phenylphosphonothioate.8 and 0.50) 3. It had been applied to cotton.44) 2.90-9.10) 4.27) 2.10 (3.21 (2. Ethyl and methyl parathion are infrequently detected in groundwater sampling (USGS.60-19.32-3.70-3.90-11.69 (2. Fourth National Report on Human Exposure to Environmental Chemicals 149 . first registered in 1948.48) 90th 2.28 (1. and Nitrobenzene Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.46 (3.50) 1.85 (2.300-.940 (<LOD-2.80 (2.37-2.11) 2.37-4.22-3.1. and eliminated rapidly from the body after absorption (Kramer et al.67) < LOD 1. Once absorbed.01) 695 660 518 679 603 941 Limit of detection (LOD. and aquatic invertebrates. was once a restricted-use insecticide with limited applications on certain agricultural crops.50) 3.19 (.70-6.02) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .910) < LOD < LOD < LOD 1.74) 5. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Urinary para-Nitrophenol Metabolite of Ethyl Parathion. Both are toxic to birds.10-1.40-4.40 (1. Estimated intakes from diet and drinking water have been below recommended limits. Methyl parathion has low water solubility.70 (3.49 (1.36-1. the potential for human exposure to either ethyl or methyl parathion through the diet or drinking water is low. methyl parathion was rapidly absorbed after ingestion.01) 4.. and of the chemical nitrobenzene.70 (<LOD-3.10) 22.24) 479 565 680 813 830 1099 99-00 01-02 99-00 01-02 * * * * < LOD .80) 2. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.21-1. Given its limited use. < LOD means less than the limit of detection.45) 5.30-3.860 (<LOD-1.32-1.770 (.33 (1. population from the National Health and Nutrition Examination Survey. 2002.S.67 (1.60 (4..80 (1.60) 1.EPA.0) 3. Many previous registered agricultural uses of methyl parathion have been cancelled (U.40) 2.40-3. 2003). but by 2003.50-14.09-1.20-5.18-3.57) 1.298-00-0 Ethyl Parathion CAS No.71 (3.61) < LOD 1.92-2.57-4. more slowly absorbed through the skin.0) 3.02-6. 2007)..40-4. with limited applications in agriculture.10 (3. fish. all registered uses were voluntarily cancelled (U.S.32 (1.70) 2.S.60-36.70-6.990-1.79) 4. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.89 (2.Organophosphorus Insecticides: Specific Metabolites Methyl Parathion CAS No.30-16. Morgan et al.05) 4.50 (1. In animal studies.850) < LOD . Metabolism of ethyl or methyl parathion leads to the formation of paranitrophenol.0) 4.00) 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 1.10 (<LOD-6.66 (2.71) 971 1164 1018 1313 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .37-4. 2006).70-3.70) 2.90 (1.30-5. 56-38-2 General Information Para-nitrophenol is a metabolite of the insecticides methyl parathion.50) 2.20) 5.50 (1. Methyl Parathion. 2000).61) < LOD 1.910) < LOD .0) 2.50 (2.15-3.30 (2.72 (3.13-1.41-4.70-6. 1977). which may vary for some chemicals by year and by individual sample. and to a lesser extent. pulmonary. on cereal grains.60-5.50 (2.69) 4. peak domestic use was as high as 5-6 million pounds per year.10-11.790 (<LOD-. binds tightly to soils resulting in low leachability.58) 3.32-1.20 (<LOD-2. Ethyl parathion.28 (1. Methyl parathion use is highly restricted.92) 5.70 (2. Survey Geometric mean (95% conf. Increased risk of exposure via dermal.0 (3.EPA.34 (3. ethyl parathion.62 (1. In the 1990s. interval) Selected percentiles ( 95% confidence interval) Sample 95th 5.47) 2.50-9.26 (1.16) < LOD 1. phosphorothioates such as methyl and ethyl parathion are metabolically activated to the “oxon” forms which have greater toxicity than the parent insecticides.45 (1.12) < LOD < LOD 1.0) 3.60-24. and has a short half-life in soils and on plants.71 (2.40) 4.37) 2.20 (2.40) 1.700 (<LOD-.01-4.30 (1.730 (<LOD-.

01 (2.17) . environmental levels) and health effects is available from ATSDR at: http://www.Organophosphorus Insecticides: Specific Metabolites Metabolites”).72-2.98-7. Human health effects from parathion or ethyl parathion at low environmental doses or at biomonitored levels from low environmental exposures are unknown.07 (1. Thus.20) 3..2) 2. Methyl parathion is not considered genotoxic.33-3.30) 3. Parathion and methyl parathion have high acute toxicity in animal testing.970 (.440 (<LOD-. weakness.95) 1.67 (3.EPA considers methyl parathion unlikely to be carcinogenic to humans.870) < LOD . accidental exposure. gov/toxpro2.96 (1.79) 1.730-1. At high animal doses of methyl parathion.S.44-3.10) 90th 2.38-3.67-2.20) .94-47. Jaga and Dharmani. methyl parathion.html and from U.35-3..26) 17.80 (1.640) < LOD < LOD 1. Additional information about external exposure (i.00 (1. U.15) 3. 150 Fourth National Report on Human Exposure to Environmental Chemicals .10 (1.79 (1. In addition to being a metabolite of methyl and ethyl parathion.cdc.87 (1.39 (1.21-21.15-10.930 (.86 (2. and Nitrobenzene Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.89 (2. cholinergic effects. 2004).3) 2. 2006. 2005.680 (<LOD-1. IARC does not consider ethyl parathion and methyl parathion classifiable as human carcinogens.94-4.33) 479 565 680 812 830 1099 99-00 01-02 99-00 01-02 * * * * < LOD . Survey Geometric mean (95% conf.950) < LOD .830-1.930 (.e.880 (.720-1.S. 1978.60) 2.91 (1.970 (.04 (2.84) 3.76-14.57) 6.57-7.31-3.48-4.89 (2. interval) Selected percentiles ( 95% confidence interval) Sample 95th 4.56-2. or generally to have reproductive toxicity at doses below those causing acetylcholinesterase inhibition in most animal studies (IPCS.23) 1.03) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .96 (1.720 (<LOD-.78 (2.7) 3.90 (1. paralysis.83 (1.16-4.82) < LOD .790-1.20 (3.11-4.370 (<LOD-.08 (1. and unintentional acute or chronic high-level occupational exposure (Hill et al.. Orsorio et al. 1991).33-6.97 (<LOD-4.08) < LOD .790-. vomiting.44-3.25) 1.540) < LOD .530) < LOD < LOD < LOD .60 (1.500) < LOD < LOD .08-3.07) 2.11) 1.78-2.13) 4. and seizures.04) 1.30-1.14-3. population from the National Health and Nutrition Examination Survey.29 (2. 2003.71 (1.93 (2.26 (1.70) 3.21) 1.850-1.43) 4.57-2.310-.00 (1.atsdr.71) 1.01-3.41-2.33-3.29) 1.80 (1. 2006.35-3.690-1..400 (<LOD-.06) 971 1164 1018 1312 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD . Zurich et al.55) 2. Methyl Parathion.97 (2. the detection of para-nitrophenol in a person’s urine may also reflect exposure to the environmental degradate. and other metabolites. retinal atrophy and sciatic nerve degeneration have also been observed (IPCS.60-2.29) 2.82 (2. para-nitrophenol can also occur in the environment from the breakdown of the parent these organophosphorus pesticides and from nitrobenzene.9) 1. Overt cholinergic toxicity and death from methyl and ethyl parathion have been described following suicidal ingestion.. but lists ethyl parathion as a possible human carcinogen. Lores et al.840 (. 2004).45) 695 660 518 678 603 941 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. In large doses.S.940 (<LOD-1.78-2. gov/pesticides/. Recent in vitro and in vivo animal studies suggest that parathion may have additional neuronal and glial cell effects at lower doses (Guizzetti et al.88 (1. Karanth and Pope et al.91) 1.980 (.23) size 1989 2476 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD 75th .1) 2.430 (.800-1.00) 2.05) 4. paranitrophenol. resulting in excess acetylcholine at nerve terminals. 1990.59 (1. 1995. teratogenic.epa. The metabolite.39) 1. does not inhibit acetylcholinesterase enzymes. and other organophosphorus insecticides share a common mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system.92 (2.73 (1. EPA at: http://www.97-10.77-7.01 (.17-4..2) 2.09) 2.78) 2. 1995). ethyl parathion. Urinary para-Nitrophenol (creatinine corrected) Metabolite of Ethyl Parathion.61) 4. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.55 (<LOD-3.13-12. and producing acute symptoms such as nausea...37-1.25 (2. WHO.4 (3.31) < LOD .88) 1. Slotkin et al.

Environ Res 1995. Shealy DB. Rockhold RW. 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.6(2-3):159-173. Jewell NP. Urinary excretion of paranitrophenol and alkyl phosphates following ingestion of methyl or ethyl parathion by human subjects. CDC. Lu C.33(5):270-276.112(10):1116-1124. Pharmacokinetics of methyl parathion: a comparison following single intravenous. Griffith W. Gregg M. J Expo Anal Environ Epidemiol 2005. Organophosphorus pesticide poisonings in humans: determination of residues and metabolites in tissues and urine. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population. Barr DB. Hill RH Jr. ACGIH recommends a BEI of 0. oral or dermal administration. 2005. McCann KG. Curl CL.15(2):164-171. and many residents were symptomatic (Barr et al. 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. DiPietro E. Toxicology 2005. Cline RE.. McClure PC. 2005). Alley CC. 2002. et al.Organophosphorus Insecticides: Specific Metabolites Biomonitoring Information Urinary levels of para-nitrophenol reflect recent exposure. McCann et al.25(5):599-606. Arch Environ Contam Toxicol 1977. Hryhorczuk DO. Environ Health Perspect 2004. Bailey SL. Lewalter J. Role of individual susceptibility in risk assessment of pesticides. 2002). Clark JM. Available at URL: http:// www. Chicago area methyl parathion response.5 mg (500 µg)/g creatinine for workers at the end of shift. Pesticide residues in urine of adults living in the United States: reference range concentrations.110 Suppl 6:1085-1091.S. Needham LL. Baker RC. general population (CDC.. 1995. et al.9:311-320. 1995). Baker SE. Laboratory investigation of a poisoning epidemic in Sierra Leone. Lin LI. Finding a measurable amount of para-nitrophenol in urine does not mean that the level will result in an adverse health effect. Head SL. Centers for Disease Control and Prevention (CDC).56(7):449553. Head SL. Morgan DP. Rev Environ Health 2006. Harley K. Neurotoxicol Teratol 2003. Dharmani C. 2005. Baker S. Pesticide workers may have much higher levels following pesticide applications. Hetzler HL. Barr JR. Effect of organophosphorus insecticides and their metabolites on astroglial cell proliferation. 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. Arch Environ Health 1978. Ashley DL.71:99108. Atlanta (GA). Eskenazi B. Occup Environ Med 1999. Hill RH Jr.110 Suppl 6:1075-1078. Comparison of organophosphorus pesticide metabolite levels in single and multiple daily urine samples collected from preschool children in Washington State.. Hill et al. 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. 2005.. Bradway DE. 2003) and in 482 pregnant females from an agricultural region of California (Eskenazi et al. Barr DB. 2002.215(3):182-190.. Pope C. 4/7/09 Jaga K. Pathak S. Moseman RF.org/documents/jmpr/jmpmono/v95pr14. J Biomed Sci 2002. International Programme on Chemical Safety-INCHEM (IPCS). Leng G. Giordano G.inchem. Methyl parathion: an organophosphate insecticide not quite forgotten. Measurement of p-nitrophenol in the urine of residents whose homes were contaminated with methyl parathion. a range of values several hundred times higher than levels found in the U. References Barr DB.S. Lores EM. Wellman SE. J Anal Toxicol 1990. Moomey CM. Bradman A. Fourth National Report on Human Exposure to Environmental Chemicals 151 . Slach EF. 2005). 2004). et al. Kramer RE.21(1):5767. Turner WE. Third National Report on Human Exposure to Environmental Chemicals. et al.. Costa LG. et al. Environ Health Perspect 2002. Karanth S. Kedan G. Rubin et al. Environ Health Perspect 2002. Runkle KD. population (Olsson et al. 1999). end-of-shift urinary para-nitrophenol levels ranged from 190 to 410 µg/ gram of creatinine (Leng and Lewalter.htm.14(4):213-216. Kissel JC. Guizzetti M. Weltzien E. Age-related effects of chlorpyrifos and parathion on acetylcholine synthesis in rat striatum. Parathion-Methyl (addendum). and levels were similar or slightly lower that those in a small convenience sample of the U.. In a study of workers who handle parathion. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Barr DB.

S. Investigation of a fatality among parathion applicators in California.who.gov/oppsrrd1/REDs/factsheets/0155fct. 6/1/09 World Health Organization (WHO). Case No. Anal Bioanal Chem 2003. Available at URL: http://pubs. Hill RH Jr. EPA-738-FOO-009. Available at URL: http://www. Ames RG. Toxicol Lett 2006. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine. Backer G. Assessment of human exposure and human health effects after indoor application of methyl parathion in Lorain County. 2004. Environ Health Perspect 2002. Environmental Protection Agency (U. 1/14/09 U. Slotkin TA. Dunlop B. Monnet-Tschudi F. Rubin C.04/106. Involvement of glial cells in the neurotoxicity of parathion and chlorpyrifos. Ohio.E. Nguyen JV.S. Interim reregistration eligibility decision (IRED) for Methyl Parathion. Ryde IT. 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. Am J Ind Med 1991. Hill G. 1992-2001. External and internal exposure of wine growers spraying methyl parathion.201(2):97-104. 1/12/07 U. Environmental Protection Agency (U. May 2003.S. March 2006. U. Ethyl parathion. The Quality of Our Nation’s Waters. September 2000.S. 152 Fourth National Report on Human Exposure to Environmental Chemicals . Jung D.epa. Mengle DC. Pesticides in the Nation’s Streams and Ground Water. Environ Health Perspect 2006. Letzel S.114(10):1542-1546. Esteban E.pdf. Methyl parathion in drinking water. Olsson AO.S. revised February 15. Sadowski MA. Seidler FJ. Toxicol Appl Pharmacol 2004. WHO/SDE/WSH/03. Osorio AM. 5/19/09 Zurich MG.Organophosphorus Insecticides: Specific Metabolites Muttray A. EPA). Rosenberg J. Available at URL: http://www.20(4):533-546.110 Suppl 6:1047-1051. Levin ED. Available at URL: http://www. gov/oppsrrd1/REDs/methylparathion_ired. Facts.376(6):808-815. et al. EPA).int/water_sanitation_health/dwq/chemicals/ methylparathion.usgs. 2007 [online].162(2-3):219-224. Yacovac R. Geological Survey (USGS).D.gov/circ/2005/1291/. Honegger P. pdf. Schilter B. Barr DB. R. Kieszak S. Tate CA.epa. 0153.pdf. 1995-1996. Costa LG.

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

840) 669 687 929 Limit of detection (LOD. population from the National Health and Nutrition Examination Survey.780 (.31) . interval) Selected percentiles ( 95% confidence interval) Sample 95th . see Data Analysis section) for Survey year 01-02 is 0.250 (<LOD-. Survey Geometric mean (95% conf.700-1. 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. which may vary for some chemicals by year and by individual sample.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 .700-.850 (.27) .840 (.780 (.470 (.430 (<LOD-. Survey Geometric mean (95% conf.S. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.S.950) < LOD < LOD 1.460) 1165 1316 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .610 (<LOD-1. interval) Selected percentiles ( 95% confidence interval) Sample 95th .21) < LOD .780 (<LOD-1.00) 669 687 929 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.64) .410 (<LOD-1.770) 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 .820) < LOD < LOD .680 (<LOD-.670 (<LOD-1. population from the National Health and Nutrition Examination Survey.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.210-.17 (.210-1.200-.740 (.880) 567 810 1104 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD .760 (<LOD-.740-1.08) 1165 1316 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . < LOD means less than the limit of detection. 154 Fourth National Report on Human Exposure to Environmental Chemicals .780 (<LOD-1.500 (.07) .580-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.94) .2.300-1.670) 567 810 1104 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD .210 (<LOD-.55) .15) < LOD .

Atlanta (GA). Environmental Protection Agency (U.pdf. Pesticides residues in food: 1992 evaluations Part II Toxicology. June 2003.fda. Finalization of interim registration eligibility decision for pirimiphos-methyl. Available at URL: http://www.inchem. Nguyen JV. Case No. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine.epa. Third National Report on Human Exposure to Environmental Chemicals. 4/7/09 Olsson AO. 4/7/09 International Programme on Chemical Safety-INCHEM (IPCS). 2535.376(6):808-815.gov/~acrobat/tds1byps. cfsan. Total Diet Study: Summary of Residues Found Ordered by Pesticide. 2005. July 2006. Sadowski MA. U. org/documents/jmpr/jmpmono/v92pr16. Available at URL: http://www. gov/oppsrrd1/REDs/pirimiphos-methyl_ired. Anal Bioanal Chem 2003.pdf.S. Available at URL: http://www. Food and Drug Administration (FDA). EPA).S.Organophosphorus Insecticides: Specific Metabolites References Centers for Disease Control and Prevention (CDC). 850. 1/14/09 Fourth National Report on Human Exposure to Environmental Chemicals 155 . Market Baskets 91-3-01-4. Barr DB. Pirimiphos-methyl.htm.

1992). Pyrethroids are not well absorbed through the skin (ATSDR. bind to soils. resmethrin. Pyrethroid insecticides are the most common active ingredient in commercially available insect sprays and are also used as structural termiticides. such as piperonyl butoxide. They are also applied on livestock to control insects. 2005. 2006a. 2002).2-dimethylcyclopropane carboxylic acid (55701-05-8 ) trans-3-(2.2-Dichlorovinyl)-2.EPA. 2006b). Human health effects from pyrethroid pesticides at low environmental doses or at biomonitored levels from low environmental exposures are unknown. and synergists. EPA. After absorption from inhalation or ingestion. or carbamate pesticides. agricultural fields.. which are natural chemicals found in chrysanthemum flowers. by either ester hydrolysis or hydroxylation. animal facilities. pyrethroid pesticides have less acute toxicity in animals and people. and sumithrin) are also registered for use in mosquito-control programs in the United States. and greenhouses. Woollen et al.2-Dibromovinyl)-2. About two million pounds of permethrin and one million pounds of cypermethrin have been applied annually (U. They are ranked as having moderate acute oral toxicity. The general population may be exposed to pyrethroid insecticides primarily from the ingestion of food or from residential use. 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. Leng et al. The table shows the urinary pyrethroid metabolites measured in this Report.. and then eliminated over several days in urine and bile (Kuhn et al. 1997.2-dimethylcyclopropane carboxylic acid (55701-03-6) cis-3-(2. 2003. and deltamethrin have been used frequently on cotton. pyrethroids are rapidly metabolized. organophosphorus. where these chemicals prolong sodium channel opening when a nerve cell is depolarized (Shafer et al. WHO. Permethrin is also used in skin lotions and shampoos as medical treatments for lice and scabies. cyfluthrin. Certain pyrethroid insecticides (such as permethrin. Outside the U. Pesticide applicators can be exposed to pyrethroid pesticides via dermal and inhalation routes from powders and liquid formulations. Generally. 2002).. Pyrethroid pesticides have low volatility. Soderlund et al. Unmetabolized pyrethroids have been measured in breast milk.. This class of pesticides has low toxicity in birds and mammals. 2003. Pyrethroid pesticides are used to control a wide range of insects in public and commercial buildings. Compared with other classes of insecticides such as organochlorines. Adverse effects from large doses are related to the action of pyrethroids on the nervous system.Pyrethroid Pesticides Pyrethroid Pesticides General Information Pyrethroid pesticides are synthetic analogues of pyrethrins. followed by conjugation. 1999.2-dimethylcyclopropane carboxylic acid 3-Phenoxybenzoic acid (3739-38-6) 156 Fourth National Report on Human Exposure to Environmental Chemicals .. Dermal exposure with the potential for inadvertent ingestion may occur when lotions or shampoos are applied to treat lice or scabies. 2007).. Soderlund et al. Estimated intakes from diet and drinking water are below recommended limits. they are not persistent in the environment due to their rapid degradation within days to several months. cypermethrin. 2005). deltamethrin has been used for indoor protection against mosquitoes that carry malaria.S. so usage is restricted near water (U.S.2-Dichlorovinyl)-2. and are rarely detected in ground waters (USGS.. There are about 30 different pyrethroid pesticides in use. but pyrethroids are highly toxic to fish and some aquatic invertebrates. 1992). warehouses. in some situations replacing the use of DDT. but may be poorly transferred across the placenta (ATSDR. In agriculture. Pyrethroid pesticides are generally formulated as complex mixtures of different chemical isomers.S.. solvent oils. Woollen et al. 2002.

1991. the pyrethroids are not considered genotoxic in in vitro testing or carcinogenic in animal testing (WHO. tremor. 2001. Richardson JR. choreoathetosis.107(3):173-177. Neurosci Lett 2001. Caudle WM. Toxicol Appl Pharmacol 1991. Abell AD. 2002. Human cases of systemic poisoning are rare and usually result from accidental exposure or intentional ingestion of pyrethroid insecticides. Shin JH. Behavioral and endocrine changes induced by perinatal fenvalerate exposure in female rats. Fredriksson A. Shaw IC.. et al. cdc. 2003.gov/pesticides/ and from ATSDR at: http://www... motor activity. bioallethrin and deltamethrin. Yamada T. Human doseexcretion studies with the pyrethroid insecticide cyfluthrin: urinary metabolite profile following inhalation. dopaminergic. Biochem Biophys Res Commun 1998. cyfluthrin was the most frequent pyrethroid associated with symptomatic effects (irritant respiratory and dermal effects. Signs and symptoms of acute pyrethroid poisoning after massive ingestions include agitation.1/15/09 Aziz MH. Varoli FM. paresthesias) reported in agricultural workers from 1996 to 2002 (Spencer and O’Malley.8(1):197-202. The pyrethroids in general use are not considered teratogenic or to have significant reproductive toxicity (ATSDR. 2000. Thomson BM. on immature and adult mice: changes in behavioral and muscarinic receptor variables.. Spinosa HS. Toxicol Appl Pharmacol 2006. et al. Kim et al. WHO. Transient dermal paresthesias have been reported among pesticide applicators after direct contact with certain types of pyrethroid pesticides. Kunimatsu et al. J Environ Monit 2006. September 2003. IARC considers deltamethrin and permethrin as not classifiable as to their human carcinogenicity. and catecholaminergic pathways and behavioral changes have been demonstrated at subacute and subchronic doses for some pyrethroid pesticides (Aziz et al. Kim TS.8(1):18-21.atsdr. Effects of prenatal exposure to deltamethrin on forced swimming behavior. Leng G. Int J Hyg Environ Health 2002. Kunimatsu T. [Effects of fenvalerate on reproductive and endocrine systems of male rats] Zhonghua Nan Ke Xue 2002. Lewalter J.62:101-108. Eriksson P. Shafer. and striatal dopamine levels in male and female rats. Leng A. Garey and Wolff. Lemonica IP. Elwan MA. Berger-Preiss E. Garey J. Hu et al. Wolff MS. Environ Health Perspect 1999. Bernardi MM. 2002). Moniz AC. Song L. Indoor pyrethroid exposure in homes with woollen textile floor coverings. Sunami O. Estrogenicity of pyrethroid insecticide metabolites. Neurotoxicol Teratol 2005. Wang SL. Go V. Kuhn K. Ray et al. Neurodevelopmental consequences of gestational exposure (GD14-GD20) to low dose deltamethrin in rats. Lazarini et al. Estrogenic and antiprogestagenic activities of pyrethroid insecticides. Kang IH. Hu JY.251(3):855-859. Regul Toxicol Pharmacol 2002. 2001.27(12):1273-1283. Pogo BG. Eriksson and Fredriksson.35(2 Pt 1):227-237. 2002).html. et al. Agrawal AK. Lee SJ. Guillot TS.108(1):78-85. Estrogenic potential of certain pyrethroid compounds in the MCF-7 human breast carcinoma cell line. and seizures (ATSDR. Wieseler B. Zhao RC..205(6):459-472. Go et al.. Garey J. salivation. Idel H. Concomitant exposure to organophosphorus insecticides may increase pyrethroid toxicity by slowing metabolic clearance of the pyrethroid. 2004. 2006. Levsen K. Cruz-Casallas PE. Florio JC.gov/toxpro2. Soderlund et al. Additional information about pesticides is available from U.27(4):609-614. Neurotoxic effects of two different pyrethroids. and permethrin) in the Hershberger and uterotrophic assays..Pyrethroid Pesticides and other ion channels may also explain some pyrethroid effects.html. though a few pyrethroid pesticides and some metabolites have shown weak or inconsistent estrogenic effects on standardized assays (ATSDR.S. Neurotoxicol Teratol 2001. Toxicological profile for pyrethrins and pyrethroids. 2003. 1999. Shukla Y.23(6):665-673.. Generally. 2005). Kuhn KH..gov/toxprofiles/ tp155. 2006.300(3):161-165. Moniz et al. Kamita Y. Seth PK. References Agency for Toxic Substances and Disease Registry (ATSDR). 2005). EPA at: http://www.atsdr. Idel H. Bernardi MM. Fourth National Report on Human Exposure to Environmental Chemicals 157 .cdc. Salzgeber SA.. Pyrethroid pesticide-induced alterations in dopamine transporter function. 2005). In developing rodents. 2006). Ranft U. McCarthy et al. Leng G. Adhami VM. Lazarini CA. Okuno Y. 2003. Wolff MS. Kim IY. Leng G. hypersensitivity. Elwan et al. Sugiri D. Bull Environ Contam Toxicol 1999. 2003. 1998. Xenobiotica 1997. 2005).. Toxicokinetics of pyrethroids in humans: consequences for biological monitoring.211(3):188-197. neurochemical changes in cholinergic. Lack of (anti-) androgenic or estrogenic effects of three pyrethroids (esfenvalerate.50(2):245-255.. Kim HS. Available from URL: http://www. 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.. epa. J Reprod Dev 2004. Miller GW. McCarthy AR. Chen JH. Yang J. In California. Pauluhn J. et al. Assessing estrogenic activity of pyrethroid insecticides using in vitro combination assays. Ose K. fenvalerate.

synergies.who.171:3-59. Soderlund DM.htm.Pyrethroid Pesticides Ray DE. Developmental neurotoxicity of pyrethroid insecticides: critical review and future research needs.gov/oppsrrd1/REDs/ factsheets/permethrin_fs. Available at URL: http://www. Available at URL: http://www. Mechanisms of pyrethroid neurotoxicity: implications for cumulative risk assessment. Pesticides in the Nation’s Streams and Ground Water. 5/26/09 Woollen BH. Mullin LS. Safety of pyrethroids for public health use. Meyer DA. Environmental Protection Agency (U. Available at URL: http://pubs. Pesticide and Evaluation Scheme. June 2006a. Laird WJ. Forshaw PJ.htm.S. Environmental Protection Agency (U. sumithrin synthetic pyrethroids for mosquito control.epa. Marsh JR.epa. Geological Survey (USGS). 19962002. Clark JM.S. Revised February 25.S. Lesser JE. U. Spencer J.gov/ circ/2005/1291/. June 2006b. Crofton KM. resmethrin.gov/pesticides/ health/mosquitoes/pyrethroids4mosquitoes. Environmental Protection Agency (U. Sargent D. Environ Health Perspect 2005.113(2):123-136. April 2002. Pyrethroid insecticides: poisoning syndromes. J Toxicol Clin Toxicol 2000.10. Xenobiotica 1992. 5/26/09 U.186:57-72. 5/26/09 U. EPA). et al.epa. The metabolism of cypermethrin in man: differences in urinary metabolite profiles following oral and dermal administration. Permethrin. and therapy. Permethrin Facts (Reregistration Eligibility Decision Fact Sheet).int/hq/2005/WHO_ CDS_WHOPES_GCDPP_2005. 2005. Sheets LP.pdf. pdf. Toxicology 2002.22(8):983-991.S.38:95-101. Pyrethroid illnesses in California. EPA). 5/26/09 U. Rev Environ Contam Toxicol 2006. Shafer TJ. 2007.S. Reregistration Eligibility Decision for Cypermethrin.usgs. March 2006. 5/26/09 158 Fourth National Report on Human Exposure to Environmental Chemicals . Available at URL: http://www. Available at URL: http://whqlibdoc. 1992–2001. World Health Organization (WHO). O’Malley M.S. EPA).S. Piccirillo VJ.gov/oppsrrd1/REDs/cypermethrin_red.

Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 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. 2006). 2006) and estimated daily intakes based on urinary levels in children were considered to be below acceptable daily intakes (Heudorf et al. In an analysis of 217 urine specimens from a nonrandom sample of United States residents. (2004) reported a geometric mean concentration of 4-fluoro3-phenoxybenzoic acid of 0.. Studies in Germany of 396 children and adolescents (Becker et al..S.. 2005).68359-37-5 General Information The chemical 4-fluoro-3-phenoxybenzoic acid is a specific metabolite of the pyrethroid insecticide cyfluthrin.95 µg/L... Following an indoor application exposure. 2003).2 μg/L) in the U. Cyfluthrin accounted for one-third of pyrethroid-related worker illnesses reported in California from 1996-2002. representative 2001-2002 NHANES subsample (CDC. the mean elimination half-life of cyfluthrin from the plasma was 16 hours (Williams et al. 2006) and 1177 urban adults and children (Heudorf et al. Urinary levels of 4-fluoro-3-phenoxybenzoic acid were generally below the limit of detection (0. 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. 2004).S. 2001. but it can also reflect direct exposure to 4-fluoro-3-phenoxybenzoic acid formed in the environment. the presence of 4-fluoro-3-phenoxybenzoic acid in urine not only reflects the metabolic transformation of cyfluthrin.. Seven individuals participating in floor exercises on cyfluthrin treated carpet demonstrated a rise in the urinary excretion of 4-fluoro-3-phenoxybenzoic acid in the 72 hours following the activity (Williams et al. Biomonitoring Information Urinary levels of 4-fluoro-3-phenoxybenzoic acid reflect recent exposure to cyfluthrin or its environmental degradate. In 57 volunteers entering areas previously spot-sprayed with various pyrethroid pesticides (including cyfluthrin). Leng et al. Biomonitoring studies of 4-fluoro3-phenoxybenzoic acid in urine provide physicians and public health officials with reference values so that they can determine whether other people have been exposed to higher levels of cyfluthrin than levels found in the general population. 2003). 2003).Pyrethroid Pesticides Cyfluthrin CAS No. most of which were dermal and respiratory irritations (Spencer and O’Malley. Cyfluthrin is rapidly metabolized and eliminated from the body. Thus. median urinary levels of 4-fluoro-3-phenoxybenzoic acid were slightly less than the limit of detection in the NHANES 2001-2002 subsample (CDC. Baker et al. 2005. Degradation of cyfluthrin to 4-fluoro-3-phenoxybenzoic acid occurs in the environment. representative subsample in NHANES 2001-2002 (CDC. 2005). Urinary levels for adults and children in these studies were similar (Heudorf et al.. Fourth National Report on Human Exposure to Environmental Chemicals 159 .

population from the National Health and Nutrition Examination Survey. < LOD means less than the limit of detection. 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.2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.Pyrethroid Pesticides Urinary 4-Fluoro-3-phenoxybenzoic acid Metabolite of Cyfluthrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.2 and 0. which may vary for some chemicals by year and by individual sample.S. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. Survey Geometric mean (95% conf. 160 Fourth National Report on Human Exposure to Environmental Chemicals .

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. 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. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.S. Fourth National Report on Human Exposure to Environmental Chemicals 161 . population from the National Health and Nutrition Examination Survey. Survey Geometric mean (95% conf.

Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Ball M. 2005. Arch Environ Contam Toxicol 2004. Kolossa-Gehring M. Berger-Preiss E. Isotope dilution highperformance liquid chromatography-tandem mass spectrometry method for quantifying urinary metabolites of synthetic pyrethroid insecticides. Int Arch Occup Environ Health 2004. 19962002. Angerer J. Rev Environ Contam Toxicol 2006. Angerer J. Heudorf U. Schulz C.Pyrethroid Pesticides References Baker SE. Human exposure to indoor residential cyfluthrin residues during a structured activity program. Ranft U. Angerer J. Seiwert M.77(1):67-72.209(3):221-233. Spencer J. Olsson AO. Williams RL. Hoppe HW. Third National Report on Human Exposure to Environmental Chemicals. Becker K. Krieger RI. O’Malley M. Int J Hyg Environ Health 2003. Int J Hyg Environ Health 2006. Int J Hyg Environ Health 2006. Bernard CE. Angerer J. et al. Hadnagy W. Environ Health Perspect 2001.206(2):85-92. Centers for Disease Control and Prevention (CDC). 162 Fourth National Report on Human Exposure to Environmental Chemicals . Pyrethroid illnesses in California. Sugiri D. Atlanta (GA). Leng G. Heudorf U. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. J Expo Anal Environ Epidemiol 2003.186:57-72.109(3):213-217. Heudorf U.209(3):293-299. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides.46(3):281-288. Drexler H. Barr DB. Idel H.13(2):112-119. Butte W. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine.

870) 1. In the body.28) 671 680 518 701 591 957 Limit of detection (LOD.850 (.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 .160 (. 1999).570 (.710-1.770) .07 (.630-.630) .240) .670 (.32) .340) .740-1.2-dichlorovinyl)-2.790-1.380-.35) 1.110-.202 (.24) 1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.28) 468 580 667 831 816 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .900 (.890 (. more of the trans-metabolite than Urinary cis-3-(2.440 (.11) .120-.280-. and trans-cyfluthrin.2dimethylcyclopropane carboxylic acid in urine not only reflects the metabolic transformation of any of the three pesticides.410) . the presence of trans-3-(2.110 (<LOD-. 1985. 52315-07-8 CAS No.180 (.44 (.200-.600) .690) . which may vary for some chemicals by year and by individual sample.470-1.200) .340) .2-dimethylcyclopropane carboxylic acid is a metabolite formed from trans-permethrin.270 (. population from the National Health and Nutrition Examination Survey.770-1.740 (.Pyrethroid Pesticides Cyfluthrin the cis-metabolite is found in the urine.110-.650-1. trans-cypermethrin.610) .780) .700) .120-.400-.490-1. transcypermethrin and trans-cyfluthrin.330 (.910-5.47 (. The chemical trans-3(2. 1999).2-dichlorovinyl)-2.510 (.2-dichlorovinyl)- CAS No.370 (.220-.150 (.270 (.300 (.2-Dichlorovinyl)-2.140 (<LOD-.550) .250-.580) 1.300-.730 (.460-1.230) .530 (.S.380) .680-3. cis-3-(2.2-dichlorovinyl)-2.600-1.220-.430-.730 (.200) < LOD < LOD < LOD .2-dimethylcyclopropane carboxylic acid formed in the environment from the degradation of these pesticides (George.740-2.270 (.410) .2dichlorovinyl)-2.08) 947 1193 1004 1346 99-00 01-02 99-00 01-02 99-00 01-02 * * .160 (.380 (.12 (. Generally.52645-53-1 General Information Several pyrethroid pesticides are formulated as a mixture of cis.170 (.13 (.21) .670-2.880 (. trans-permethrin.820 (.280 (.740) 1.610) .or trans-3-(2.53) .68) .790) ..500 (. < LOD means less than the limit of detection.77 (.890 (. Kuhn et al. but can also reflect exposure to trans-3(2. Similarly.490-.120-.460-.50) .35) .680 (.110-.640 (.710) .1 and 0.630) .250 (. Cyfluthrin.210) 90th .580-1. cis-permethrin.670-1.960 (.310) .470 (.790-1.670-1.180) . Fourth National Report on Human Exposure to Environmental Chemicals 163 .600 (. 1985.510 (.570-.220-.500 (. and cis-Cypermethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.270-. Survey Geometric mean (95% conf.68 (.68359-37-5 Cypermethrin Permethrin CAS No. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.68) .2-dimethylcyclopropane carboxylic acid in urine not only reflects the metabolic transformation of any of the three pesticides. Kuhn et al.790 (..08) .350) .80) . but it can also reflect exposure to cis-3-(2.15) .490-1.340-.160 (<LOD-. ciscypermethrin and cis-cyfluthrin.380-.2-dichlorovinyl)2.2-dimethylcyclopropane carboxylic acid that is formed in the environment from the degradation of these pesticides (George.370-.420-.330) .920) 1.200 (.43) . The presence of cis-3-(2. Biomonitoring Information Urinary levels of cis.2dichlorovinyl)-2.380-.220-.240) .155-. and ciscyfluthrin.210-.120-.300 (.200-.2-dimethylcyclopropane carboxylic acid is a metabolite formed from cis-permethrin.2-dimethylcyclopropane carboxylic acid Metabolite of cis-Permethrin. The cis-isomer of permethrin has more potent insecticidal activity than transpermethrin.262) * * * < LOD < LOD .510 (.950-2.300-.200) .140 (.630 (.680) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD . see Data Analysis section) for Survey years 99-00 and 01-02 are 0. cis-cypermethrin.1.490-.260 (.730 (.200-.220) .and trans-isomers.460 (.54) .520) .210) .

390 (.33 (.190 (.250) .290) . 2006).440 (.2-dimethylcyclopropane carboxylic acid did not increase at 24-72 hours after exposure to nearby pest control operations (Leng et al.Pyrethroid Pesticides 2.11) 947 1193 1004 1345 99-00 01-02 99-00 01-02 99-00 01-02 * * .14) 671 680 518 700 591 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.12-2. 2003). and cis-Cypermethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.190) . Estimated daily pyrethroid intakes based on urinary levels in the German children were below the acceptable daily tolerances (Heudorf et al.340-.2-dichlorovinyl)-2.170 (.590) .780) 1.450-.080-.67 (.270 (.640) 1.570) .250) 90th .360-1. population from the National Health and Nutrition Examination Survey. urinary trans-3-(2.08) 468 580 667 830 816 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .680 (.900 (.11) .470-1.290 (.440-.200-.130-.160 (<LOD-.370-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Lu et al.590 (.03) 1. In these volunteers. In the same residents. post- Urinary cis-3-(2.260 (.710 (.890) ..2-dichlorovinyl)-2. Survey Geometric mean (95% conf.150-.550-1. 2005).560) 1.230-.140-. In a study of volunteers.300 (.640 (. the median and 95th percentile of urinary levels of cis-3-(2.540 (.580) . These studies indicated that intake is mainly from the diet and that dermal absorption contributes little to intake (Heudorf et al.250-.220 (. though the 95th percentile levels increased several fold after exposure to nearby pest control operations (Leng et al.80) .S.. 2006.104-.550) .250-.300 (.31) .210-..300) .340) .700-2.380) . In a study of urban residents in Germany (Berger-Preiss et al.. the levels at 24-72 hours were slightly less than the 95th percentile in the NHANES 2001-2002 subsample (CDC.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 .260 (.24) . 2001) showed urinary levels of cis.220) ..840 (. Cyfluthrin.340) .390-. Urinary levels of the two chemicals in adults were similar to those in children in these studies (Heudorf et al.680-1.2-dichlorovinyl)-2.67) .750 (.710-3. 2002).220 (.250 (<LOD-.580-1.49) .230 (.560) .450 (.530 (.37) .540) .350 (.320-.550 (. 2006) and 1177 urban adults and children (Heudorf et al.680-1.2-dichlorovinyl)-2.430-. 2004.2dimethylcyclopropane carboxylic acid at the 95th percentile were about half the 95th percentile in the NHANES 20012002 subsample (CDC.410) .780 (.640-.420 (.350) .290) .520) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .2-Dichlorovinyl)-2.440-.700) .840 (.2-dimethylcyclopropane carboxylic acid reflect recent exposure to either their parent pyrethroid pesticides or their environmental degradates.430 (.260) .450-1.290-.370-.700) .920 (.550-1.750-1.880) .182) * * * < LOD < LOD .2dichlorovinyl)-2.270-.280-.2-dimethylcyclopropane carboxylic acids in children were related to residential pesticide use and house dust levels (Becker et al.11 (.. 2005).530 (. 2004). 2001.230-.430-1.250-.. median urinary levels of trans-3-(2.550) .230-..170) < LOD < LOD < LOD .250) .270) .29 (.2-dimethylcyclopropane carboxylic acid levels at the 95th percentile were about one-third of the 95th percentile in the NHANES 20012002 subsample (CDC.640-1.800 (.2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of cis-Permethrin.400-1.2dimethylcyclopropane carboxylic acids at the 95th percentile that were similar or slightly less than the 95th percentiles in the U.300) .and trans-3-(2.190) .830) .380-.260-.890 (. 2005).440 (.180-.. urinary levels of cis-3-(2. 2006. Schettgen et al.380 (.510-1.200-.150-. 2006). 2003).11) 1.200 (.33) .138 (.. 2002). 2005).59) .59) . 2005) In a small group of indoor pest-control operators..150-.690-1.120 (.400 (.600 (.540 (.21) .320) . the levels at 24-72 hours were slightly less than the 95th percentile in the NHANES 2001-2002 subsample (CDC.300-.59 (1.640-1.11) .12 (. 164 Fourth National Report on Human Exposure to Environmental Chemicals .2dichlorovinyl)-2. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.260 (. representative NHANES 2001-2002 subsample (CDC.170 (.and trans-3(2.810 (.500 (.180 (.370-.S.270) .2-dimethylcyclopropane carboxylic acid did not increase. Studies in Germany of 396 children and adolescents (Becker et al.390-.280 (.200) .240 (<LOD-. Other studies have provided evidence that urinary levels of cis.

64-4.910-1.14) 1.23) 2.66) 691 680 518 690 595 954 Limit of detection (LOD.780 (.90) 1.560 (. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.2-dimethylcyclopropane carboxylic acid (Hardt and Angerer.19 (3.410 (<LOD-.42 (2.13) .08-4.490-1.77) 1.440 (<LOD-.5) 2.89 (2.39 (1. population from the National Health and Nutrition Examination Survey.860) .60-4.55-3.560 (.35) 1.55-4.680-1.63) 1.19 (2.11-2.87 (1.63) 1.66) 478 576 675 826 823 1123 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .20 (.17 (.09 (.68-3.700-1.40 (1.25 (1.95) 2.39-5.37 (1.19) 1.56) 2.68) 1.620) < LOD 2.Pyrethroid Pesticides application median urinary levels of summed cis.730) .23 (.470 (. Fourth National Report on Human Exposure to Environmental Chemicals 165 .14-6.77 (1.68) 2.580 (.660) 1.and trans-3-(2.58) 961 1184 1015 1341 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .25-3. The maximum post-application urinary levels.410 (<LOD-.50 (1. which may vary for some chemicals by year and by individual sample.01) 4.28 (2.76-3.55-5.460-.85) 4.670) .49-5.08) 1.56 (1.11-1.700) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.76-4.500-.17-1.14-2. Urinary trans-3-(2.2-dimethylcyclopropane carboxylic acid in urine does not mean that the level causes an adverse health effect.68-2.43) 2. Finding a measurable amount of cis.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 .or trans-3-(2.01 (1.420 (<LOD-. < LOD means less than the limit of detection. 2005).2-dichlorovinyl)-2.910-1.41-14.77) 2. interval) Selected percentiles ( 95% confidence interval) Sample 95th 3.570) 90th 1.12-6.69 (1.94 (1.670) .69) 1.66) .760) .16) 1. trans-Cypermethrin.400-.17 (.7) 2.610) 1.410-.560 (.840-1.940 (.84 (1.520) .54) 4. 2003) were similar to the 95th percentiles for adults in the NHANES 2001-2002 subsample (CDC.91 (1.97-11.550 (.62 (1.2-dichlorovinyl)-2.460-.490 (<LOD-.920-1.500) .49-3.60) .07-3.800-1.81) 2.710 (.480-.48) 4.41 (1. 2005).07 (1. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.59 (1.10) 2.470 (<LOD-.830-1.95) 3.20 (.500 (.970 (.56) 2.S.850-1.2-dimethylcyclopropane carboxylic acid Metabolite of Cyfluthrin.68) 1.28 (1.400 (<LOD-.60) 1.08-6.810-1.2-Dichlorovinyl)-2.54 (1.2dichlorovinyl)-2.27 (1. were up to 27 times higher than the 95th percentile for adults in the NHANES 2001-2002 subsample (CDC.03-1.22 (1. Survey Geometric mean (95% conf.49-3. Biomonitoring studies on urinary levels of cisor trans-3-(2.77) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .03-1.530) .4.820) .56 (1.26 (.750) . however.410-.20 (.520-.4 and 0.2-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. and trans-Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.42) 1.

* Not calculated: proportion of results below limit of detection was too high to provide a valid result.00) 5.86 (2.570 (.15-3.28) 2.12-1.47 (1.57) 3.880-1.45 (1.700-.780) .31 (.37 (1.44) 2.22-2.570 (<LOD-.410-.900 (<LOD-1.39 (1.660) .55 (2.740) .36 (1.87) 1.35 (1.64 (1.07-3.570-.41) 1.91 (1.07-2. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.88) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 1.20 (1.S.11) .850-3.02-1.47-2.13) .31) 1.00 (1.540) .00) 1.61) 1.65 (2.480-.15-3.720-1.880 (.55 (2.31 (2.07) 2.640) .700 (.2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of Cyfluthrin.98 (1.33 (1.580 (.56 (1.60) 2.750) .730) .87-3.07) 2.35) 1.19) .91) 1.56-5.60) 2.12 (.800-1.16 (1.700 (. 166 Fourth National Report on Human Exposure to Environmental Chemicals .26 (1. Survey Geometric mean (95% conf.55 (2.08 (.36) 2.970 (.42 (.580) .22) 1. and trans-Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.30-6.780 (<LOD-.39) 1.3) 2.10) size 1976 2524 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD 75th .780) 90th 1.850) 1.48-2.520 (<LOD-.65) 1.81 (2.30-3.610-.930-1.820-2.880 (<LOD-1.87-8.11) 478 576 675 825 823 1123 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .68) 3.500-.00-5.42) 1.19) 961 1184 1015 1340 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .70 (.27-2.22-1.56-2.87) 1.760 (.60 (1. population from the National Health and Nutrition Examination Survey.2-Dichlorovinyl)-2.07-1.440-.13) 1.720 (<LOD-.91-11.530 (<LOD-.850) .40-2.75 (1.15) 2.33-2.470-.20-2.89) 2.48 (1.560 (.00) 1.74) .470 (.08 (.15-3.67 (2.45-2.27-2.80) 1.720-1.19 (1.Pyrethroid Pesticides Urinary trans-3-(2.11) 691 680 518 689 595 954 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.33-1.15 (1.770) < LOD 2.670) .47-2.800-1.15) 3.34-3.29) 1.34-4.57 (1. trans-Cypermethrin.74) 2.87 (1.530 (.

Angerer J. et al. Schulz C. Hardt J. Int Arch Occup Environ Health 2004. Kolossa-Gehring M.134(1-3):141-145. Idel H. Leng G. George DA. Int J Hyg Environ Health 2006.76(7):492-498. Environ Health Perspect 2006. Third National Report on Human Exposure to Environmental Chemicals. Ranft U. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine. Int Arch Occup Environ Health 2003. Hoppe HW. Ranft U. Pearson M. Indoor pyrethroid exposure in homes with woollen textile floor coverings. Int J Hyg Environ Health 2006. Angerer J. Fourth National Report on Human Exposure to Environmental Chemicals 167 . Berger-Preiss E. Idel H. Berger-Preiss E. Heudorf U. Drexler H. Ball M. Permethrin and its two metabolite residues in seven agricultural crops. Angerer J. Hadnagy W. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Sugiri D.206(2):85-92. Heudorf U. Environ Health Perspect 2001. Biological monitoring of workers after the application of insecticidal pyrethroids. Angerer J.209(3):293-299. Bull Environ Contam Toxicol 1999.68(6):1160-1163. Heudorf U.109(3):213-217. Int J Hyg Environ Health 2002. Butte W.77(1):67-72. Centers for Disease Control and Prevention (CDC). Schettgen T. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides. Angerer J. Drexler H. Toxicokinetics of pyrethroids in humans: consequences for biological monitoring. Seiwert M. Atlanta (GA).62:101-108. Idel H. Pyrethroid exposure of the general population-is this due to diet? Toxicol Lett 2002. Bartell S. Barr DB. Bravo R. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. Lu C. Wieseler B. Leng G. Kuhn K.209(3):221-233. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. J AOAC 1985.114(9):14191423. Levsen K. A longitudinal approach to assessing urban and suburban children’s exposure to pyrethroid pesticides. 2005. Leng G. Int J Hyg Environ Health 2003.Pyrethroid Pesticides References Becker K. Angerer J. Heudorf U. Sugiri D.205(6):459-472.

Biomonitoring studies provide physicians and public health officials with reference values so that they can determine whether other people have been exposed to higher levels of deltamethrin than levels found in the general population..2-dimethylcyclopropane carboxylic acid were below the limit of detection (CDC. 168 Fourth National Report on Human Exposure to Environmental Chemicals .1 μg/L) for the NHANES 2001-2002 subsample (CDC.2-dibromovinyl)-2. 2001) showed that urinary levels of cis-3-(2. 2005). 2001.2-dibromovinyl)-2. The peak mean levels in these children were more than 800-fold higher than the detection limit in the 2001-2002 NHANES subsample.2dimethylcyclopropane carboxylic acid formed in the environment.S. Urinary levels for adults and children in these studies were similar (Heudorf et al.2-dimethylcyclopropane carboxylic acid of 0. deltamethrin has been used against mosquitoes that carry malaria.2-dibromovinyl)-2. in some situations replacing the use of DDT.2-dimethylcyclopropane carboxylic acid in urine does not mean that the level will result in an adverse health effect.2-dibromovinyl)-2. Baker et al. (2004) reported a geometric mean concentration of cis-3(2. in detection of cis-3-(2.2-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)-2.2-dimethylcyclopropane carboxylic acid in the environment (IPCS.2dimethylcyclopropane carboxylic acid reflect recent exposure to deltamethrin or its environmental degradate.2-dibromovinyl)-2.5 μg/L) than the detection limit (0. Studies in Germany of 396 children and adolescents (Becker et al. 2005). Outside the U. 1990). Deltamethrin can degrade to cis-3(2. 2006) and 1177 urban adults and children (Heudorf et al. Following residential spraying with deltamethrin for malaria protection in Mexico. Finding a measurable amount of cis-3-(2. 2006) and estimated daily intakes based on urinary levels in children were considered to be below acceptable daily intakes (Heudorf et al.2-dibromovinyl)2.2-dibromovinyl)-2.2-dimethylcyclopropane carboxylic acid in the urine may reflect exposure to deltamethrin or to cis-3-(2. 2005)..3-0.2-dimethylcyclopropane carboxylic acid is a metabolite of the pyrethroid insecticide deltamethrin.. mean peak urinary levels of cis-3-(2. 2004). Biomonitoring Information Urinary levels of cis-3-(2.39 µg/L..Pyrethroid Pesticides Deltamethrin CAS No. In an analysis of 217 urine specimens from a nonrandom sample of United States residents. In the NHANES 2001-2002 subsample.2-dimethylcyclopropane carboxylic acid at the 95th percentile ranged slightly higher (0. 52918-63-5 General Information Cis-3-(2..2-dibromovinyl)-2.2-dibromovinyl)-2. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. urinary levels of cis-3-(2. Thus..

see Data Analysis section) for Survey years 99-00 and 01-02 are 0. population from the National Health and Nutrition Examination Survey. < LOD means less than the limit of detection. which may vary for some chemicals by year and by individual sample. 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.2-Dibromovinyl)-2. Fourth National Report on Human Exposure to Environmental Chemicals 169 . * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Survey Geometric mean (95% conf.Pyrethroid Pesticides Urinary cis-3-(2.1.S.1 and 0.2-dimethylcyclopropane carboxylic acid Metabolite of Deltamethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.

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

Angerer J. Hoppe HW. Int J Hyg Environ Health 2006.109(3):213-217.htm. Heudorf U. Centers for Disease Control and Prevention (CDC).113(6):782-786. Schulz C. Butte W. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Kolossa-Gehring M. Third National Report on Human Exposure to Environmental Chemicals. Available at URL: http://www. Environ Health Perspect 2005. Grimaldo M. Atlanta (GA).209(3):221-233. 2005. Angerer J. Fourth National Report on Human Exposure to Environmental Chemicals 171 . Angerer J. Torres-Dosal A.209(3):293-299. Deltamethrin. et al.Pyrethroid Pesticides References Becker K. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides. Environmental Health Criteria 97. Environmental health assessment of deltamethrin in a malarious area of Mexico: environmental persistence. Ball M. Environ Health Perspect 2001. et al.77(1):67-72. Seiwert M. Lopez-Guzman OD. Int Arch Occup Environ Health 2004. International Programme On Chemical Safety (IPCS). 5/26/09 Ortiz-Perez MD. Heudorf U. and genotoxicity in exposed children. [online] 1990. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany.inchem. Heudorf U. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine. toxicokinetics. Int J Hyg Environ Health 2006. Batres LE. Angerer J. Carranza C. Drexler H.org/documents/ehc/ehc/ ehc97.

. CDC.. Baker et al. Urinary levels of 3-phenoxybenzoic acid in children were found to be related to residential pesticide 172 Fourth National Report on Human Exposure to Environmental Chemicals . In a small group of indoor pest-control operators. 2005. The mean peak levels in these children were 83-fold higher than the geometric mean for children in the NHANES 2001-2002 subsample (CDC. Finding a measurable amount in urine does not mean that the level will result in an adverse health effect. median urinary levels of 3-phenoxybenzoic acid were slightly less than median levels in the NHANES 2001-2002 subsample (Leng et al. CDC. 52645-53-1 Tralomethrin CAS No. CDC. In 57 volunteers entering areas previously spot-sprayed with various pyrethroid pesticides. a temporal variation in levels was observed and considered to correspond to seasonal spraying of pesticides. 2006). (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. Thus. 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 one study of 145 urban residents in 80 private homes in Germany. Hardt and Angerer..Pyrethroid Pesticides Cyhalothrin CAS No. In an analysis of 217 urine specimens from a nonrandom sample of United States residents. Following residential spraying with deltamethrin for malaria protection in Mexico. 66841-25-6 General Information The chemical 3-phenoxybenzoic acid is a metabolite and an environmental degradate of the six pyrethroid pesticides listed above. 2002.52315-07-8 CAS No. 2004). Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Fenpropathrin Permethrin CAS No. 2005). Biomonitoring Information Urinary levels of 3-phenoxybenzoic acid reflect recent exposure to the parent pyrethroid pesticides. 2005). 2005).. but can reflect direct exposure to 3-phenoxybenzoic acid formed in the environment from the degradation of these pesticides. 2003). 68359-37-5 Cypermethrin Deltamethrin CAS No. 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.. In the New York City study. A study of 396 German children (Becker et al. 2006) showed that urinary levels of 3-phenoxybenzoic acid at the 95th percentile were similar to levels at the 95th percentile for children in the U.. 2003. 2003. Saieva et al. the presence of 3-phenoxybenzoic acid in urine not only reflects the metabolic transformation of any of the six pesticides listed above. 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. Becker et al. urinary 3-phenoxybenzoic acid levels at the 95th percentile were about threefold lower than the levels at the 95th percentile in the 2001-2002 NHANES subsample (Berger-Preiss et al. 2005). 39515-41-8 CAS No..S. 52918-63-5 use and house dust levels (Lu et al. 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.. 2005). Biomonitoring studies of 3-phenoxybenzoic acid provide physicians and public health officials with reference values so that they can determine whether other people have been exposed to higher levels of pyrethroids than levels found in the general population. 2006. 2005. representative NHANES 2001-2002 subsample (CDC. 2005). 2005).

277-.1.260 (.35 (2.28) 1.830) 90th 1.25-1.49 (1.81 (1.62-6.740 (.227-.27-11.226-.05) .300 (.65-2. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.30) 3.280 (.26) 2.75 (1.210-.13 (.350-.26) 2.54) 1.470-.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 .35) 2.427) .32 (2.63-3.340) .34 (2.190-.560-1.160-.364) .430-.190-.362) .90) 1.89-71.760 (.800) 1.530-.73) 1.38 (2.49-2.600 (.780) 4.406) .640 (.01 (1.250 (.12 (.200-.1) 3.840-1.83-11.26-2.320) .246-.250 (.990) .370) .78 (1.200-.71 (1.46) .650 (.276-.454 (.320) .311 (.53) 1.18 (2.369) .02-6.325 (.35) 2.03 (3.55 (1.69 (1.69) 3.1) 3.23 (2.16) 974 1193 1024 1346 99-00 01-02 99-00 01-02 99-00 01-02 .250 (.345) Selected percentiles ( 95% confidence interval) Sample 95th 4.200-.680 (.820) .27-2.820) .42-2.273 (.45-5.940) 1.53-3.700-1.78) 6.710 (. population from the National Health and Nutrition Examination Survey. Fourth National Report on Human Exposure to Environmental Chemicals 173 .30 (1.321 (.340) 75th .530-.428-.92-3.260 (.233-.750) .49 (1.76 (1.46) 2.320) .230 (.850) .63 (3.32-21.35 (1.260-.230-.62-8.960 (.29-1.373) .510-.330) .49-2.520 (.850) .266-.340) 1.16) 483 580 682 831 833 1128 99-00 01-02 99-00 01-02 .33 (2.740 (.374) 99-00 01-02 99-00 01-02 99-00 01-02 .570-1.78) 1.300 (.830-2.417 (.240 (.328 (.27-2.360) .62) 5.190-.271-.288 (.210-.21 (2.288-.33) . Deltamethrin.300 (.12) .45 (2.220-.384) .230-.601) .72 (1.450 (.595) .670 (.730 (.870 (.430-.260 (.247-.700 (.298 (.160-.79) 3.620-1.292 (.292-.510-.265-.300) .290 (.320) .253-.34-6.38 (2.52-4.238-.51-6.64) 697 680 524 701 603 957 Limit of detection (LOD.39) 2.610) .33 (1.550-.295) .240 (.180-.Pyrethroid Pesticides Urinary 3-Phenoxybenzoic acid Metabolite of Cypermethrin.30 (.32 (1.355) .48-2.750-1.18 (1.05) 1.750) .250-.560-.41-2.297 (. and Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.34) 8.60) .190-.41 (1.16-1.490) .420) .S.230 (.314 (.35) 1.25 (2.56-5.440) .44) 5.387) .1 and 0.570-.590 (.434) .390) .336 (.353 (.41) 3.314) .78) 1.41-3.315 (.14-6. interval) .800 (.86 (1.25-7.586) .25 (2.320 (.13) .590-.16) 1.93 (1.25-4.50 (2.36) 1.04-5.43) 3.560-.1) 3.52-5.8) 3.65 (1.51-3.710 (.230-.270 (.630) .330) .270) .267 (.490-.507 (. Survey Geometric mean (95% conf.12) 4.810) 1.48-2.04) .352-.

06-3.43 (2.720 (.224-.700-1.357) .90) 3.67) 1.280 (.37 (1.272 (.150-.240-.309 (.250) .540 (.238-.240 (.35) .930) .63) 1.03-1.270 (.840-1.190-.274 (.240-.220-. Deltamethrin.261-.677) .53 (1.35-3.271-.253) .440-.330) .320) .230-.290-.270) .67 (1.200-.590-1.400) .490 (.07-5.400-.74) 3.321-.09) 3.25) 2.202-.67 (1.640 (.41) 1.44 (1.44) 2.250 (.96 (1.27) 1.09-2.590) .610 (.95) 1.500) .49 (1.21-4.370-.590) .230) .84 (1.510 (.330 (.350) .210-.49) 3.21 (1.55 (1.410-.22 (1.330) 75th .81 (1. Survey Geometric mean (95% conf.09-2.63-3.48 (1.178-.41-4.300-.380-.280 (.490-.274-.234 (.370 (.07) 2.225-.270-.312 (.02 (2.335-.73) 1.52 (1.04 (3. and Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.48) 697 680 524 700 603 957 174 Fourth National Report on Human Exposure to Environmental Chemicals .550 (.960-1.740) .226-.510 (.720) 90th 1.410) .275 (.930) 1.19 (2.437) .17 (.730) .270 (.246 (.280) .760) .278) .04 (.52) 2.300-.94 (1.62) 1.446) .86 (1.49) 1.15-2.210 (.51-7.330) .00) 1.270) .25-5.200-.43-64.39) 1.91 (2.510 (.75-8.19) 2.670) .61-2.17-1.60-4.83) 1.36 (1. population from the National Health and Nutrition Examination Survey.378 (.10 (2.580) .160-.11 (.810) 1.860-1.229-.730) .03 (.550 (.Pyrethroid Pesticides Urinary 3-Phenoxybenzoic acid (creatinine corrected) Metabolite of Cypermethrin.91) .190 (.43 (1.460-.37) 1. interval) .261 (.49-2.216-.365) 99-00 01-02 99-00 01-02 99-00 01-02 .299-.480 (.323 (.0) 3.530-.400-.88-5.40) 2.91-4.630) .310) .401) .00) 1.560 (.329) .490 (.220 (.64-5.372) .362 (.423 (.09 (.650) .72 (1.35 (1.420-.272) .240 (.190-.534) .230-.264 (.00) 5.62) .55) 3.91) 9.32 (2.83 (1.450 (.280 (.329) .750-1.19) 974 1193 1024 1345 99-00 01-02 99-00 01-02 99-00 01-02 .309) .240-.36-6.730-1.92) 483 580 682 830 833 1128 99-00 01-02 99-00 01-02 .330) 1.380 (.11 (.311 (.227 (.43) 1.02-1.530-.304) Selected percentiles ( 95% confidence interval) Sample 95th 3.80) 4.60) 1.40 (1.280) .480-.290) .280-.54 (1.640 (.570) .290) .240 (.25-2.316 (.13-1.240-.16-4.350 (.13 (.35) 1.590) .550 (.328) .210 (.860 (.860-1.13-1.240 (.460-.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 .670) 3.173-.440-.05-3.200-.440-.73-4.250 (.580 (.S.200-.390-.19-6.387) .

205(6):459-472. Bartell S. 2005. et al. Becker K. Hardt J. Centers for Disease Control and Prevention (CDC). Torres-Dosal A. Bravo R. Exposure to indoor pesticides during pregnancy in a multiethnic. Batres LE. Third National Report on Human Exposure to Environmental Chemicals. Biological monitoring of workers after the application of insecticidal pyrethroids. Barr DB. Olsson AO. et al. Leng G. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. Sugiri D. Lu C.46(3):281-288. Int Arch Occup Environ Health 2003. Seiwert M. Indoor pyrethroid exposure in homes with woollen textile floor coverings. Godbold J. Berger-Preiss E. Angerer J. Environ Health Perspect 2005. Int J Hyg Environ Health 2003. Environ Health Perspect 2006. Sugiri D. Lopez-Guzman OD. Berger-Preiss E. Ranft U. Grimaldo M.206(2):85-92. Environ Health Perspect 2003. Angerer J. Lapinski R. Pearson M. Ortiz-Perez MD. Liu Z.209(3):221-233. Int J Hyg Environ Health 2002. Ball M. toxicokinetics. et al.Pyrethroid Pesticides References Baker SE. Fourth National Report on Human Exposure to Environmental Chemicals 175 . Int J Hyg Environ Health 2006.114(9):14191423.76(7):492-498. Idel H. Isotope dilution highperformance liquid chromatography-tandem mass spectrometry method for quantifying urinary metabolites of synthetic pyrethroid insecticides. Obel J. Levsen K. urban cohort. Kolossa-Gehring M. Environmental health assessment of deltamethrin in a malarious area of Mexico: environmental persistence. Barr DB. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. A longitudinal approach to assessing urban and suburban children’s exposure to pyrethroid pesticides. Idel H.113(6):782-786. Atlanta (GA). Berkowitz GS. Leng G. Deych E. Hoppe HW. Hadnagy W. Ranft U. and genotoxicity in exposed children. Carranza C.111(1):79-84. Arch Environ Contam Toxicol 2004.

190-.150 (.158 (.136-.137) .160-.120-.117-.220) .420) .070 (<LOD-.390-.180 (.440 (.150-.190 (.490 (. Antimony can exist in one of four valences in its various chemical and physical forms: -3.270 (.250) .190) .080-. distribution. Two antimony compounds (sodium stibogluconate and antimony potassium tartrate) have been used as antiparasitic medications.130 (.340 (.120 (.250 (.230) .400 (.110-. The absorption.133) * .200 (.300 (.180-.134-.230) .260-. from air and drinking water.500) .430 (.280) .120-.430 (.300-.130 (.095 (.180-.120-.130 (.430 (.350 (.157) .300) .180-.260 (.390 (.460 (.230-.280-.080) .320-.087-.184) .200-.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 .350) .560) .270) .160) .350 (.190 (.S.130 (. 176 Fourth National Report on Human Exposure to Environmental Chemicals .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 .230-.130 (. which may vary for some chemicals by year and by individual sample.220-.136) * .460 (.290-.200-.220-.190-.160) .146 (.210) .100-. 01-02. and pewter.350) .130 (.132 (.200) . +3.390) .098-.160-.350 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.260-.112-.410-.120-.300-.240 (.128 (.148-.340 (.220-.110) .126-.460 (.210) .119-.090) 75th .200-.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 .230) .240 (.310 (.470) .390) .120) . 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.270 (. fireworks.210 (.310) .090-.141-.140) .250-.04. It is used in metal alloys.143 (.280) .150) .093 (.161) .200) .190 (. enamels.130) .300-.320-.132 (.140 (.110 (.280) .200) . metal bearings.145) Selected percentiles ( 95% confidence interval) 50th . and +5.115) .210 (.210) .154-.220-.130) .070 (<LOD-.160 (. storage batteries.320 (.360-.130) .180 (.390-.150) .190 (. and refuse incinerators that process or release antimony.200-.120-.250-.176 (.220) . population from the National Health and Nutrition Examination Survey.130-.330) .144) .170-.270 (.120) .207) . see Data Analysis section) for Survey years 99-00. ammunition.080) .210) . and 0.130-.330 (.197) .160-.710) .470) . Stibine is a metal hydride form of antimony used in the semiconductor industry. and 03-04 are 0.250 (.150-.103) .110-. 0.250 (.190-.070-.170-. often combined with oxygen to form antimony trioxide or with sulfur to form stibnite.210-. Antimony enters the environment from natural sources and from its use in industry.130-.160 (.142 (.160-.250-.180) .260) .130-.230 (.510) .120-.240 (. People are exposed to antimony primarily through food and.460) .110-. 7440-36-0 General Information Antimony is found in ores or other minerals.090 (.310 (.440) .095-.500) .175 (.156-.07.120-.350-.170-.230-. coal-fired plants.140) .120-. or other substances containing antimony is another means of exposure.120 (.120-. interval) .200) .300) .400) .490) .140 (.310) .154) .100 (.130-.400 (.280-.170-.320) Total .108 (.100) . and excretion of antimony vary depending on its oxidation state.180 (.320 (.120 (. sheet and pipe metal.122 (.200 (.130 (.150 (.220-.150-.137) . 0.310-.410) .240-.160) .134 (.120 (.390) .180 (.220-.117-.180) .320-.145 (.170 (.125 (.290-. water.270-.240-.280-.360 (. Workplace exposures can occur at smelters.150 (.280) .160 (.190) . and glass.410) .310 (. Dermal contact with soil.180-.079-. It is also used in paints.140-.400) .100-.140 (.330) .350) .210-.126 (.109-.270 (.120) .260) .090 (<LOD-.270) .350-.160) .210) .170-.350 (.370) . castings.280-.230-.470 (.131-.390) .330 (.220 (.180 (.160) .120 (.330-.350) .360 (. solder.080 (<LOD-.300 (.150-.200 (.260 (.230 (.300) .220) .170 (.110-.250-.154) .178) .400-.330) .340) .360) .190 (.240) .140 (.130-.260) .099 (.130 (.330 (. and as a fire-retardant in textiles and plastics.128 (.150-.320) .390-.230 (.220) 95th .150) .140) .119) .100 (.570) .180 (.400) .200 (.04.190-.169 (.170) .160) .164-.190) .230-.090-. < LOD means less than the limit of detection.130) < LOD . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.180-.135) * .220 (.140) .190) .190-.120) .240 (.350-.400 (.360) .350 (.260 (.280 (.370-.130-.440) .330-.105 (.114) .200 (.108-.150) 90th .140) .Metals Antimony CAS No.240 (.530) .290 (.200 (.310 (. ceramics.088-.280 (.115-. to a lesser extent.320) 787 683 618 554 667 723 768 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.310-.280-.320-.190) . respectively.600) .330) .123 (.140) .

140) .127) .133) .167 (.156-.192-.233-.107-.300) .226 (.148-.164-.265-.108-.069-.185 (.288 (.295 (.265 (.250-.310) .150-. 1973).118 (.200-.156 (.230) 95th .143) .126) .144-.250 (.084) .228-. 1944).128-.076-.195-.176 (.225) .245) .099-.320-. resulting in hemolysis with abdominal and back pain (Dernehl et al.152) .204-.148) * .117-.278) .081 (<LOD-.132) .071-.154-.198) .208 (.321) .196 (.320 (.225 (.121 (.143) 90th .500) .300 (.333-1.121 (.480) .163 (.113-. and route of exposure (Elinder and Friberg.159-.107-.106-.119 (.080 (<LOD-.259 (.193) .333-.217 (.092-.471) .131) .082 (<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. 1958) and occupational exposures (Briegner et al.131-.253 (.310) .317) .320) .108-.129) .471 (.447 (.271-.421) .414) .162-.444) .444) .135) .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.741) .280-.115 (.187) .080 (.255-.147-.238) .250 (. 1995).108-.253-.111-.317) .741 (.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 .129 (.280 (.112 (.173 (.207) .276 (.124 (.135 (. 1986).235-.123 (.209) .138-.122 (.286 (.191 (.438) .138-.170 (.233 (.171) .146-..227-.129 (.417) .333 (.364 (.163 (. population from the National Health and Nutrition Examination Survey.098) .098-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.116-.320 (.109-.248) .193 (.095-.112-.429) .076-.263-. and kidney have been demonstrated in high dose animal studies depending on the dose.203) .125-. 1962).233) .195-.124-.106-. 1953). 1986).188) .120 (.224 (.333 (.317) .250-.087) .318-.338 (.089) .153 (.208-.143) Selected percentiles ( 95% confidence interval) 50th .371 (.114 (.104-.118 (.086 (. 1988..103-.105-.130) .134) . myocardium.269 (.333) .149-.068-.172-.373) .164) .120 (.185 (.229-.167-.103-.159-.268) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.211) .153-..082) . species.140) < LOD .267-..139 (. Histopathologic inflammatory and degenerative changes in the lung.278 (.119-.352 (.135) .272) .400 (.310 (.126-.247) .181) .261) . Dysrhythmias and T-wave changes on electrocardiogram have also been noted after both therapeutic (Berman.173-.239-.069-.115-.148-.135) .108 (. Inorganic antimony salts irritate the mucous membranes.429 (.115 (.203) .130 (.124-. Pulmonary edema may occur in severe cases of inhalation exposure (Cordasco et al.182 (.179-.391) .113) .298 (.338 (.343 (.333-.256 (.124) .173) .425) .082) .109 (.236 (.143) .195 (.277 (.146-.151) .228 (.244-.281-.104-.129) * .417) .176-.238 (.149) .145) . and ulcers (Werrin.097-. Acute antimony poisoning may cause a metallic taste. interval) .250-.185-.255) .250-.068 (.127) .135 (.130) .238) .175 (.727) .111 (.241-.159-.308) .485) .308-.338) .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 . skin. and gastrointestinal symptoms such as vomiting.079 (<LOD-.120 (.181) .123) .132 (.183) .206-. liver.194-.263 (.074 (. Fourth National Report on Human Exposure to Environmental Chemicals 177 .430) .150-.357) .099-.119-.100 (.138 (.181) .122 (.115-.143 (.114 (.313-.267 (.146) .152) .102-.146-.086) 75th .120 (.352) .130) .Metals than for trivalent compounds (Elinder and Friberg.220) .333-.178 (.138) * .117-. abdominal pain.098-.209) .136) .113-.222 (.115 (.266 (.092) .391) .095-.294) Total .085) .205-.167 (.116 (.192) . Acute inhalation of antimony has been associated with irritation of the respiratory tract and impaired pulmonary function (Renes.077) .161) .125 (.30) .380 (.S.199-.357-. An elimination half-life of approximately 95 hours has been estimated after occupational exposures (Kentner et al.109 (.114 (.192 (.061-.147) .117-.186) .213 (.385 (.189 (.096-.315) .131 (.127) .102-. 1954).300) .405) .137 (..115) .230-.173 (.257) .364 (.188-.320-.107-.161) .267) .200-.209 (. diarrhea. The toxicity of stibine after acute inhalational exposure is similar to that of arsine.112 (.075 (.248-.078 (.242-.333 (.160 (.081) .167 (.318-.126 (.200) .241-.214) .178-.209-.139 (.121) .200-. Ming-Hsin et al.228 (.127 (. and eyes.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 .127) .075 (. Human health effects from antimony at low environmental doses or at biomonitored levels from low environmental exposures are unknown.164 (.250) .176 (.

10(3):560-586. Rev Infect Dis 1988.46:931-936. Lenert G. Friberg L. Handbook on the toxicology of metals. Information about external exposure (i. Van der Venne MT. Stead FM. 1998. Yang C-Y. Int Arch Occup Environ Health 1987.51:238-240. VI. Arch Dis Child 1997. Costeloe K.html. Petrucci F. J Trace Elem Med Biol 2002. Cordasco EM. Paschal et al. Chest 1973. stibine. Element reference values in tissues from inhabitants of the European community. 2nd ed. J Occup Environ Med 2004. population. Dezateux et al. Caroli S.e. 1997). Iavicoli et al. O’Regan M. Liao Y-H.. Finding a measurable amount of antimony in urine does not mean that the level of antimony causes an adverse health effect. plasma and urine and a critical evaluation of reference values for the United Kingdom population. Industrial Medicine 1944.521-523. or exposure differences. eds. gallium. Stocks J. Environ Health Perspect 1998.. Antimony... Int Arch Occup Environ Health 1995. EPA. Levels of urinary antimony in infants appeared to be similar to those reported by CDC (2005) for young children (Cullen et al. Matthews T. Antimony trioxide is rated by IARC as a possible human carcinogen. Kentner M. Pozzoli L. arsenic. Carelli G. and future strategies.158:165-190. Nau CA. Centers for Disease Control and Prevention (CDC). Pietra R. clinical efficacy. 2005. Semisch CW. and a drinking water standard has been established by the U.S. A study of 46 elements 178 Fourth National Report on Human Exposure to Environmental Chemicals . Piatnek DA. pp. 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.. Sci Total Environ 1994. Weltle D. Biomonitoring Information Levels of urinary antimony reflect recent exposure. 1991.67:119-123.. Stone FD. Kiberd B. Chemotherapy for leishmaniasis: Biochemical mechanisms. Wu M-T. Apostoli P. 1998) or compiled reference ranges (Hamilton et al.. 1998). Chin Med J 1958. References Berman JD. and 2003-2004. Cheng-Wei L. Third National Report on Human Exposure to Environmental Chemicals. Leinemann M.106:33-39. Nordberg GF. Gallorini M. which may be due to methodologic. Earlier measurements in general populations (Minoia et al. Trace element reference values in tissues from inhabitants of the European community I. Ju-Sun P. Review of elements in blood. Dezateux C. Briegner H. Biological assessment of exposure to antimony and lead in the glass-producing industry.64(2):182-185. Suchenwirth R. Mayne P. Gebel TW. Fuchs A. Delves HT. Buchet JP. 1994) have reported values slightly higher than those in this Report. Arsine..48:93-97. Luedersdorf R. Antimony in blood and urine of infants. Biomonitoring of a worker population exposed to low antimony trioxide levels.)1954.76(2):103-115. Mahieu P. In: Friberg L. Chen J-R.16: 33-39. Human biomonitoring of arsenic and antimony in case of an elevated geogenic exposure. Hamilton EI. Schaller KH. New York: Elsevier. Yu H-S. Bailly R. 1990.atsdr. environmental levels) and health effects is available from ATSDR at: http://www. 2004. even when exposure levels were below workplace air standards (Bailly et al. 20012002. Br J Ind Med 1991. Mayer P. Ming-Hsin H. Atlanta (GA). et al. Kentner et al. Elinder CG.. Pilgrim L. Vouk VB. and antimony in optoelectronic industry workers. Stasney J.13:361-362.59:469-474. Urinary antimony in infancy. Dernehl CU. Dunkelberg. Several investigations of airborne antimony exposures in workers have found urinary levels that are many times higher than those seen in NHANES 1999-2000.cdc. Delves HT. et al. indium. Chia-Yu H. Industrial Medicine and Surgery (Dec.. Iavicoli I.Metals to antimony have been established by OSHA and ACGIH. Alimonti A.76:432436. Roland H. 1986. Ludersdorf et al. Mechanism and treatment of cardiac arrhythmias in tartar emetic intoxication. Experimental and human studies on antimony metabolism: their relevance for the biological monitoring of workers exposed to inorganic antimony. and hydrogen sulfide. Shao-Chi C. Pulmonary edema of environmental origin. 26-42. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Sabbioni E. Kuo-Juie Y. Biological monitoring of exposures to aluminum. Bolten C. Sabbioni E. Industrial antimony poisoning. Konings J. J Clin Pathol 1998. Cullen A.. Wade A. Minoia C. et al. Urinary antimony was not associated with locally elevated soil levels in a study of more than 200 German residents (Gebel et al. 1987). HH. Lauwerys R. Skulsukai G.. 2002. respectively. External and internal antimony exposure in starter battery production. Liao Y-H et al. 1995. Schacke G. gov/toxpro2. Ho C-K.

Paschal DC.Metals in urine. Pirkle JL. Sci Total Environ 1990. Werrin M. Quarterly Bulletin of the Association of Food and Drug Officials 1962. Sampson EJ. Chemical food poisoning. and serum of Italian subjects. Morrow JC.99-108.95:89-105. Renes LE. Industrial Hygiene and Occupational Medicine 1953. Trace metals in urine of United States residents: reference range concentrations. Ting BG. Environ Res 1998. 27:38-45. Jackson RJ. blood. et al. Antimony poisoning in industry.76(1):53-59. Fourth National Report on Human Exposure to Environmental Chemicals 179 .

Arsenic is measurable in most soils.08 (5. and.1) 290 725 1542 03-04 03-04 9.40) 7. chromated copper arsenate (CCA) has been used to treat outdoor timbers and pressure-treated woods to prevent wood rot.1-18. psoriasis. Survey years 03-04 Geometric mean (95% conf.1) 15.7 (11.7-83.74.27) 9. a trivalent compound known as white arsenic) is a common natural and commercial form that can be released into the air during volcanic action. lead.90-14. In nature.2 (13.0 (15.0 (14. were used as treatments for syphilis.8-61.6) 618 722 1074 Limit of detection (LOD.66-8. The United States no longer produces arsenic from mining but imports about 22. and other metals.97) 8. to a lesser extent.9 (8. and monosodium methyl arsenate were used as pesticides but contemporary uses are restricted.0-19.2) 15.Metals Arsenic CAS No.5) 43.3-19. pesticides.0 (11. lead hydrogen arsenate.6-141) 53.8) 30. such as arsenopyrite (FeAsS) and realgar (As4S4). sodium arsenite.2 (51.70-9.84) 8.5-178) 46. arsenocholine.29 (8.4) 60.4 (7.9-34.00 (6.1) 1281 1276 03-04 03-04 03-04 9.2) 46.10-10.4 (26. black.12 (6.4 (48.1-40. +3 and +5). gaseous hydride manufactured in small quantities for use in the semiconductor industry. and in lead-acid storage battery grids.5) 95th 65.5) 66. and as a cosmetic to lighten complexion.57) Selected percentiles ( 95% confidence interval) 50th 7.2 (12.8) 17. Various forms of inorganic arsenic can occur in groundwater from natural sources or as a result of soil application or industrial waste. General population exposure to inorganic arsenic can occur through consumption of drinking water and. and play sets.4 (31.9-62. Although it is still widely used in the United States.5 (36. to a lesser extent. alloys.55 (7.30) 17. and as homicidal poisons.6 (13.3) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites Sample size 2557 03-04 03-04 03-04 7.50 (8.8 (48.4 (24. retaining walls.5 (34. Before the 20th century. copper arsenates.90-11. particularly arsenic trioxide. 7440-38-2 General Information Arsenic is an element that is widely distributed in the earth’s surface in small amounts. In the last century. referred to as inorganic arsenic compounds. 2005).3) 10.5-19.10-7.6-35.80-9.50-14.9) 21.8) 34. trimethylarsine oxide. interval) 8.84) 8.0 (22. from coal burning.5 (40. Arsine (AsH3) is a reactive. CCA-treated wood has been restricted since 2003 and no longer can be used in residential applications such as decks.70 (6. arsenites. and arsenosugars. Since the 1940s.9-46. cancers. mostly for use in wood preservation (ATSDR.8) 7. Arsenic trioxide (As2O3. mental disorders. Roxarsone and other organic arsenicals are anticoccidial agents added to poultry feed.2-61.0 (43.90 (7.90) 16.20 (8.8) 29.6) 11.6-43. population from the National Health and Nutrition Examination Survey.30 (6. Arsenic can combine with such non-carbon chemicals as sulfur and oxygen to form arsenides.34-10.80) 6.5 (23.90 (5.3-15.8) 33.5-52. ocean and fresh waters.7) 65.30 (7.6 (9. semiconductors. Groundwater Urinary Total Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. cacodylic acid. or rarely as elemental metalloids (yellow. it is found in over 200 crystalline or mineral forms.25-9. Arsenic trioxide is approved to treat acute promyelocytic leukemia. grain.6 (32.4-65.7) 24.1) 7. arsenic as elemental metalloids may be used in some ammunition. and arsenates (oxidation states of -3. arsenic compounds. 2001).1 (38.10 (6.S.00-9.70) 8.7-95.2 (41. Various arsenic compounds were used in paint pigments and for tanning animal hides.4) 13.8-77. Gallium.80 (5.9 (17.6 (15.2-20.41 (7. aluminum. and indium arsenides are used in the semiconductor industry.5 (14. 180 Fourth National Report on Human Exposure to Environmental Chemicals . and foods.0-60.34-9.4) 40. the smelting of copper. Also.5) 41.5-41. solders.19-9.8) 7. Arsenic and its compounds have had many uses in the past and present as medicines.3-111) 78. Water sources contain mostly inorganic arsenate.77) 6.90 (7.90-8.90-8.7) 90th 37.12-10.10) 10.90-7. though in some locations arsenite may be prevalent (WHO.2-93. Arsenic can also combine with organic substances in nature to form such organic arsenic compounds as arsenobetaine.2-17.1 (32. and produce.02-8. meats. see Data Analysis section) for Survey year 03-04 is 0.90) 75th 16.9) 68. and gray forms). as alloy in metal bearings.000 metric tons annually.13-8.

8-32.8 (20.2 (12.75 (5. Arsenite is then oxidatively methylated to the monomethylarsonic acid (MMA) and dimethylarsinic acid (DMA) with subsequent excretion primarily in the urine (NRC.0) 12.07-9.47 (6. shellfish.0) 1281 1276 03-04 03-04 03-04 8.8 (11.8 (27.0-38. Inorganic arsenic is well absorbed from the gastrointestinal tract and absorbed to a lesser degree through inhalation.93-9.32 (5.8-75.47 (7.96) 12.3 (27.0-26.6 (10.. WHO.8 (21.47-6.23-7.86-17. Gamble et al.88) 7.06 (4. 2001).6 (17. 2001. are used in enclosed ultraclean operations within the semiconductor industry. Inorganic forms of arsenic demonstrate high acute toxicity.1 (14.61 (7. Ingestion of arsenosugars in kelp and algae can also lead to the excretion of DMA. 2006.9) 618 722 1074 Fourth National Report on Human Exposure to Environmental Chemicals 181 . arsenic does not show biomagnification in the food chain (WHO. Smoking tobacco is also a source of inorganic arsenic. 2007.2) 15. dose level. U. Smelter workers can have significant inhalational exposures to airborne arsenic trioxide for which air standards have been established.4 (40. 2001). Survey years 03-04 Geometric mean (95% conf.1) 58.7 (11.3-41.7) 28.8) 27.0-18.99-9. 2006. and some other seafood can contain organic forms of arsenic including arsenobetaine. Fish.44) 6.1) 7.10-8. as observed in Bangladesh where millions of people have been exposed.7 (9.01) 11. selenium.6-17.0) 26.4) 54. 2007.7) 95th 50. 2001). 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.30-9.4 (11. 2007. 2001). age.7-18.38-10.75) 13. EPA.66-8.9) 13. and arsenosugars.1) 6.10-16.88 (5. though some reduction may occur in the gut prior to absorption.6 (35. inorganic arsenic is widely distributed within the body..33-10.5) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites Sample size 2557 03-04 03-04 03-04 8.S.S.0) 14. 2001). with trivalent inorganic arsenic (arsenite) being more toxic than pentavalent inorganic arsenic (arsenate) (NRC.01) 7.1) 8. cacodylic acid and monosodium methyl arsenate.Metals sources of drinking water often have measurable arsenic and several regions of the United States have naturally higher arsenic levels than the U. The semiconductor dopants. TMAO is also formed in the environment from microbiological action and is a metabolite of arsenic in certain mammals.44-11.31 (6.28-7.20-9. have caused clinical arsenic poisoning. Direct exposure to DMA and MMA may result from use of the two pesticides.3-64. population from the National Health and Nutrition Examination Survey.1) 24. and folate status (Chen et al. In aquatic sediments. gallium arsenide and indium arsenide.0) 33.S.0 (31. dust.8-62.7-35.00 (6.58-10. kelp.2) 90th 30.0-69.25 (6.0) 42. trimethylarsine oxide (TMAO).12-10. EPA’s maximum contaminant level (Hughes. organic arsenic can be converted back to methylated and inorganic arsenic. Chowdhury et al.5 (9.2-46.04) 7.93-8. NRC.7-188) 27. Though modest bioconcentration occurs in some aquatic life. WHO. mine tailings). Children may have additional exposures from ingestion of contaminated soils (e.9 (45.81-9.4-64.5-120) 40.8 (12.45) 5. After absorption.18 (5. arsenocholine.6) 45. 1988).66-8. arsenocholine is converted to arsenobetaine and also to small amounts of TMAO (Christakopoulos et al. interval) 8.9) 53.35) 7. Steinmaus et al.1 (11. but is poorly absorbed dermally (WHO..41) 6.4) 32.11 (5.66 (7.. 2001).7-17.3) 6. 2001. These organic forms of arsenic from seafood are absorbed and quickly excreted in the urine (WHO. Tseng.4 (24.5-17.24 (7. In aquatic organisms.13) 8.0 (17.4 (12. Arsenate is reduced in the body to arsenite (oxidation state +3).7-34.9-56.51) 75th 14.4 (26.25-9. and contact with CCA-preserved wood structures.40) 8.5) 290 725 1542 03-04 03-04 8.59) Selected percentiles ( 95% confidence interval) 50th 7.3-53.3 (24. 2001).33 (6.2-15..2) 40. 2001). 2003.3-62. Inorganic arsenic and its metabolites have elimination half-lives of approximately 2–4 days (Lauwerys and Hoet. Extremely high groundwater arsenic levels.50 (6. so exposure to the general population is extremely limited.04 (5.7 (25.64 (7.4 (42.1-36..76 (6. 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.5) 17.8) 22.3) 9.g.

2006. Acute toxicity resulting from the ingestion of large amounts of trivalent arsenic (e... lung. 2006. leading to a decrease in adenosine triphosphate energy production. which may vary for some chemicals by year and by individual sample.30) 1.50) 2568 95th 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1. Bangladesh. 2004.. 2004). food residue. can cause peripheral sensorimotor neuropathies. 2001). arsenite will inhibit cellular pyruvate dehydrogenase by binding to the sulfhydryl groups of dihydrolipoamide. WHO. hematocytopenias. Cellular glucose uptake.. it may have its own separate toxic action by substituting for phosphate in glycolysis and other pathways. hypertension. Survey years 03-04 Geometric mean (95% conf. 2001). see Data Analysis section) for Survey year 03-04 is 1. 2006) or when exposure occurs in smokers (Chen et al. vomiting. arsenic trioxide) includes hemorrhagic gastritis with nausea. drinking water have not been associated with increased cancer rates (Schoen et al.. 2001). hyperkeratosis.50) 621 725 1078 Limit of detection (LOD. WHO.. < LOD means less than the limit of detection.. and by uncoupling oxidative phosphorylation (NRC. and childhood neurodevelopmental effects in observational human studies.50) 1.0. With chronic exposure. WHO. 2001).10 (<LOD-1.20 (<LOD-1. 2001).S. and bladder cancer (IARC. and DNA repair inhibition (Cohen et al. Chile). increased oxidative stress. Bredfeldt et al. 2006. substitution in phosphate metabolism. renal failure. and hyperpigmentation of the skin (NRC. cytotoxicity. interference in signal transduction pathways.g. OSHA and ACGIH have established workplace standards and guidelines for arsenic exposure and monitoring. 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. NRC. hepatotoxicity.S.10 (<LOD-1.Metals +3) shows greater toxicity than arsenite itself (Aposhian et al. Chronic elevated arsenic intakes have been associated with diabetes. Taiwan.20 (<LOD-1. WHO. * Not calculated: proportion of results below limit of detection was too high to provide a valid result..60) 1.. and altered gene expression. including drinking water sources with elevated arsenic levels (e. and it also will inhibit succinate dehydrogenase. respectively. and peripheral neuropathy may also occur with large doses or after surviving an acute overdose. fatty acid oxidation. 2007. including inhibition of numerous enzymes. and endothelial injury (Kumagai and Sumi. Although arsenate is reduced in the body to arsenite. 2001. some of these effects may take years to develop. apoptosis. Such actions may lead to decreased energy production. but additional or confirmatory research is needed (Kapaj et al. Cohen et al. and production of glutathione may be affected as well.20 (<LOD-1. Arsenic has many actions demonstrated in cellular studies. 2007).30) 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1.10 (<LOD-1. Laboratory studies using inorganic arsenic have shown chromosomal aberrations. and diarrhea. cell transformations. Raml et al. 2006) and newly discovered thioarsenic metabolites may also be as toxic (Naranmandura et al.10 (<LOD-1.80) 1. 1998.20 (<LOD-1. population from the National Health and Nutrition Examination Survey. 2001. noncirrhotic portal hypertension. NRC.g. The risk of lung cancer appears more pronounced when large environmental exposures start in childhood (Smith et al. 182 Fourth National Report on Human Exposure to Environmental Chemicals . U. Studies of arsenic at levels typical of U. Cardiac arrhythmias.S. 2004). which can lead to dehydration and shock. 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. 2007. Acutely.EPA has established drinking water. gluconeogenesis.. 2000. Chronic human intake of arsenic at less than acutely toxic doses. The U. The organic forms of arsenic occurring in seafood have little known toxicity. 2001).50) 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD 1.10 (<LOD-1.60) 1. Chronic arsenic exposure in humans is considered to be a cause of skin. Acute unintentional inhalation of arsine gas can produce hemolysis of red blood cells. peripheral vascular disease..EPA.S..

. 2007. 1998. Daily variation in creatinine-corrected urinary arsenic is relatively small when intake is constant (Calderon et al. Josyula et al.41) 3. Consequently.Metals compounds. 2006). Calderon et al. Though CCA-treated wood contains several thousand times more arsenic than untreated wood... though air levels of arsenic fume and dust are correlated with urinary arsenic levels at higher occupational inhalational exposures (Jakubowski et al. median urinary total arsenic levels in 4052 adults varied with seafood intake. In animal studies.S..S. 2001).70) 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD 2.html. 2006..75 (<LOD-2. IARC and NTP recognize inorganic arsenic and arsenic compounds as human carcinogens. but generally only at maternally toxic doses (WHO.89) 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2..80 (<LOD-4. although urinary arsenic levels were not associated with CCA contact (Shalat et al. urinary arsenic levels have been accepted as a good biomarker of dose (WHO.95) 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. population (Rubin et al. 1999.61 (<LOD-3.33 (<LOD-3.33 (<LOD-3.cdc. 2007. In the German Environmental Survey III of 1998. 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. 2003. 2006.. Fourth National Report on Human Exposure to Environmental Chemicals 183 .atsdr. the median total urinary arsenic in about 200 people was approximately four times higher than that of the U. Levels of total urinary arsenic in the U. higher mean or median total urinary arsenic levels have been reported among people living in specific western areas of North America (Calderon 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. Survey years 03-04 Geometric mean (95% conf. 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. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.. and the FDA has established a bottled drinking water standard. arsenic has been fetotoxic and teratogenic. Pellizzari and Clayton.S. 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. Vahter et al. 2000. gov/toxpro2. 2006). Offergelt et al. Valenzuela et al. Pellizzari and Clayton. 2006).. Additional information about external exposure (i. 2004.50) 1. 2001).19) 3.. population from the National Health and Nutrition Examination Survey.S... 1999). Shalat et al.50) 2568 95th 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2.04 (<LOD-3. population in NHANES 2003–2004 (Schulz et al. and were about two-fold lower than those for the U... 1992. Meza et al. 2008). DMA produced bladder cancer in some chronic rat studies (Cohen et al..18) 3. Pellizzari and Clayton 2006). Caldwell et al... 2008).00) 1.. 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. 2008.. 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. environmental levels) and health effects is available from ATSDR at: http://www. Compared with this Report.. had decreased since the prior 1990– 1992 survey.e. 1999. 2006. 2005) and Urinary Arsenic (V) Acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.. In a Nevada town where groundwater levels were naturally elevated. 2006). 2004.75 (<LOD-2. Shalat et al. 2001).. Caldwell et al. 2000). 1986).69 (<LOD-3.18 (<LOD-3.

a control population of 696 Tacoma residents had median urinary DMA levels similar to those for NHANES 2003–2004 (Kalman et al. and two methylated metabolic products.20 (. DMA has been the predominant metabolite composing the majority of measurable inorganic-related arsenic in the urine (i.30) 10. with DMA.50-6.05) < LOD . 1996.20 (1.3 (9.5) 621 725 1078 Limit of detection (LOD. population (Sun et al. arsenite.80-5.4) 23. 2000. Tseng et al.2-35.7) 13.3) 1284 1284 03-04 03-04 03-04 1.3 (21.6) 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 * * 1.600 (.9) 13. Caldwell et al.20-190) 31. and TMAO. and other factors such as nutrition. arsenite..0-23.83) Selected percentiles ( 95% confidence interval) 50th 1. 4. When seafood intake is avoided. 2005.20) 3.8-40.S.80) 1.. Urinary Arsenobetaine Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.7) 15.00-6.20) 7. population (Ahsan et al.400-. 2001.6 (11.17-1. and TMAO were detected in only 7. Chowdhury et al.6.1-94...g.4 (16.66 (1. Levels of DMA and MMA increase in approximate proportion to the intake of inorganic arsenic.80 (4. geometric mean levels were about 70-fold higher than for the U. 1985.800-1.00 (.55 (1..8) 35. 2008)..00 (1. 2005. Detectable levels of MMA reported in NHANES 2003–2004 were found only at the upper percentiles and. DMA and MMA.3) 95th 35.0 (27.900 (. Some noncancer effects of arsenic (e.40) 5.20) 18. In most human studies. Total arsenic measured in the urine includes all species of inorganic and organic arsenic.S.800-4.7 (13. 1.9 (6. arsenobetaine.1) 18.68) .50) . and duration of exposure are also considered important.00-1. 2008).50) 90th 16.3-39.70 (3.e. 2008). and peripheral neuropathy) have been associated with urinary levels as low as 50–100 μg/L in chronically exposed populations (ACGIH. Blom et al. 2007).900-1.90-29.20 (4. when seafood organic arsenic is subtracted).0) 29. 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.28) 1. MMA.5) 29. in NHEXAS 1995–1996. population in the NHANES 2003–2004 subsample. DMA and MMA compose most (about 75%) of the total arsenic species measured in urine.31-1.8-50.700-1. For residents of Inner Mongolia.6 (25. Aposhian et al.. Arsenate.871-1. Valenzuela et al.7-22.S. Pellizzari and Clayton. < LOD means less than the limit of detection.00-4. In the residents of a Chilean town who consumed water with high levels of arsenic. 2000.800) 1.40-7. Caldwell et al..1) 45.8 (17. 2008.7 (21.30 (2..8 (12. and 0. After recent seafood ingestion. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.4) 31.20-3. 184 Fourth National Report on Human Exposure to Environmental Chemicals .37 (1.93) 1.80 (3.700-1. Great Lakes region residents had median urinary DMA levels that were slightly less than median levels in NHANES 2003-2004 (Caldwell et al.60) 1.6-44.. 2001).90-7.60-3. and urinary DMA represented about 67% of the total urinary arsenic (Hopenhayn-Rich et al.10) 4.50) . Caldwell et al. China.70) 6..19 (. Survey years 03-04 Geometric mean (95% conf.40) 75th 5.0) 4.6 (13.70-21. 2007) with higher levels of arsenic in the drinking water. arsenocholine.4.. median levels of urinary DMA were about 40-fold higher than the adult median reported in NHANES 2003– 2004.9-23.48-2. which may vary for some chemicals by year and by individual sample.0 (26.4-35. dermal keratosis. as evidenced by trace or nondetectable levels of arsenobetaine and arsenocholine in the urine..5 (26.10 (4. The higher percentiles of total urinary arsenic levels in the U..30 (1. 2005..6.00) 3. and arsenobetaine being the main contributors to the total urinary arsenic levels (Caldwell et al... 2008.5) 292 728 1548 03-04 03-04 1.70-21. arsenocholine.1-25. In the late 1980s. WHO..800 (.20-25. interval) 1.00-12.2 (6.5 (14. 2006).40-6.3% of a representative sample of the U.11-1.3) 35. Sun et al.5) 32. These associations are stronger at higher urinary levels. 2000.45 (1.29 (1. respectively.20 (2.62) 2. 2008). Individually measurable species resulting from inorganic arsenic exposure are arsenate. population showed a higher contribution of arsenobetaine (Caldwell et al.1-51. methylation capacity.80 (.Metals other areas of the world (Ahsan et al. Measurable organic arsenic species in this Report are three biologically generated environmental forms. population from the National Health and Nutrition Examination Survey.8.9 (7.74 (1.2-38. arsenobetaine and arsenocholine will greatly increase the level of total urinary arsenic and comprise the highest percentage of the total urinary arsenic level.S. Caceres et al.S.10) 8.500-1. see Data Analysis section) for Survey year 03-04 is 0.. Also.43-1.70 (5.30) 2.800 (. vasospasm. 2003).. 1990.

58 (3.2 (13.44 (1.3 (10.25-7.93 (1.3) 1284 1284 03-04 03-04 03-04 1.62-6.78-5. Survey years 03-04 Geometric mean (95% conf.54 (1. 2006.51-2.55) 1.50-7.2 (4.91) 90th 16.9) 32.638) 1. population from the National Health and Nutrition Examination Survey.50-15.72) 12.15-1.959-1. not to imply a safety level for general population exposure.3 (10.4 (11..82) 4.88) 2.15-1.9 μg/L.938-1.6) 19. Vahter et al.7) 30.11 (.88 (5.877 (.81 (4.37-2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.Metals as with DMA.2 (12. Caldwell et al. The American Conference of Governmental Industrial Hygienists (ACGIH) provides an occupational biologic effect index (BEI) for urinary inorganic arsenic plus metabolites equal to 35 μg/L (ACGIH.3-24.15-4.39-3.29 (4.3) 95th 29. 1992.70) 5.9) 14. In recent years.40 (1. Urinary Arsenobetaine (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.00 (3. WHO.36) 2. 1998.4-21.13-39.5) 26. these levels were much lower than those found in other studies where environmental exposures were highly elevated (Chowdhury et al. 2001).4-28.612-1.67) 4. Finding a measurable amount of arsenic in urine does not mean that the level of arsenic causes an adverse health effect.1) 26.79 (1. Information about the biological exposure indices is provided here for comparison. 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. The 95th percentile of the U.5) 17.5-20.8) 29.5 (18.32-7.05) 1.6-46.9 (13. Sun et al.68 (1.73-6. 2008).80-153) 17.64-29. population for the sum of inorganic related species was 18.7) 17.25 (.45) 1.21) 5.28) 1.29-14.0) 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.00 (1.0 (9.10 (.9-18.4-82. which is below the ACGIH BEI (Caldwell et al.16 (. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. occupational monitoring and research studies have focused on the sum of inorganic-related species (arsenate + arsenite + DMA + MMA) as a measure of inorganic arsenic intake.786-1.S.05 (.40) 1.47 (1.4 (24.531 (..400-..6 (9.78 (3.S.6 (6.909-1.83) 2.1 (26. 2001).43) 14.14 (1..6-29.7) 9.1-36.47 (2. 2007).76-27.18-1.65 (1.83) 8.4) 32.4) 292 728 1548 03-04 03-04 1. Studies of small groups of metal and sulfuric acid smelter workers with varying industrial hygiene conditions have reported urinary inorganic arsenic levels (arsenate + arsenite + DMA + MMA) ranging as high as several hundreds of μg/L during or after work exposure (Jakubowski et al.19-2. Offergelt et al. 2008).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 * * 1.12) < LOD .82) Selected percentiles ( 95% confidence interval) 50th 1..61-6.901-2.30-1.30) 1. 1986.4) 13..1-18.67) 1.2 (12.53 (. 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..91 (4. interval) 1. Fourth National Report on Human Exposure to Environmental Chemicals 185 .9 (25.80) .833-1.51) 5.43) 75th 5.0-36.5 (18.. 2003.6-32.

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

20 (<LOD-1.80) < LOD 621 725 1078 Limit of detection (LOD.S.08 (<LOD-4.44) 2.00 (<LOD-3. which may vary for some chemicals by year and by individual sample. < LOD means less than the limit of detection.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. 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 1.29) < LOD 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. Urinary Arsenous (III) Acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.Metals Urinary Arsenous (III) Acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. Fourth National Report on Human Exposure to Environmental Chemicals 187 . population from the National Health and Nutrition Examination Survey. Survey years 03-04 Geometric mean (95% conf.00) 1.76) < LOD 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 3. see Data Analysis section) for Survey year 03-04 is 1. 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. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.40 (<LOD-1.00 (<LOD-2.S.95 (<LOD-2.

00-15.00-8.59 (6.71-4.18 (6.0) 12.0-16.3 (8.85 (3.16-11.80) 2.11 (3.0) 17.20) 11.78) 4.70-4.77 (3.00 (7.0) 9.50-5.00-11.0) 13.1-18.86-7.97-3.0-12.44 (2.00) 9.67) 8.00 (3.20-12.61-16.14) Selected percentiles ( 95% confidence interval) 50th 3.05) 10.80-6.92) 3.1-22.22) 4.88 (4.95 (4.05) 5.9) 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 3.74) 90th 9.7) 13.6 (9.0-17.0) 95th 16.9) 11.50 (4.3 (7.33) 3.33-4.38 (3.94-3.45) 3.0-19.95-6.00-4.0) 292 728 1548 03-04 03-04 4.06) 5.20-4.0) 10.00) 3.24) 3.00 (5.30) 3.0) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites Sample size 2568 03-04 03-04 03-04 4.5) 12.50-15.7-16.00) 12.0 (8.9 (7.7.32 (8.49) 10.9) 5.19) Selected percentiles ( 95% confidence interval) 50th 3.90) 5.00-13.0) 13.00-22.27-2.00-15.00-5.70-12.00-3.00 (3.69-3.03-6.1 (8.9 (11.29-4.00 (6.25 (4.65-8.82-9.0 (10.3 (8.24-4.89 (3.16 (4.6) 292 728 1548 03-04 03-04 3.45 (8.72 (4.00-15. interval) 3.00) 6.0-18.27 (3.7) 12.0-25.86 (2.7 (10.2) 10.0 (12.31) 4.0 (9.27 (2.86-21.0) 14.00-4.32-10.44) 5.78 (4.73 (3.0 (10.0 (12.00-9.37 (2.71) 3.95-4.55 (2.0) 16.00-4.31-4.60-7.00-4.82) 3.00 (6.00-7.00 (6.00 (3.4 (7.00-4.0) 9. Survey years 03-04 Geometric mean (95% conf.0 (13.16 (2.30 (7.57-5.60-6.71 (4.11) 4.00) 4.34 (3.81 (5.0 (9.17-6. population from the National Health and Nutrition Examination Survey.48 (2.Metals Urinary Dimethylarsinic Acid Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.05) 3.48 (3.0 (10.34 (3.0 (13.00 (5.70) 5.00) 6.17 (2.0) 621 725 1078 Limit of detection (LOD.00-3.12 (3.4) 621 725 1078 188 Fourth National Report on Human Exposure to Environmental Chemicals .0) 17.0 (8.00) 7.12-4.00-11.00 (7.70 (3.00) 4.69 (3.5 (11.00-7.6) 1284 1284 03-04 03-04 03-04 4.00 (3.60-3. Urinary Dimethylarsinic Acid (creatinine corrected) Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.00 (3.65-6.17-4.84-8.70-3.00-11. interval) 3.80-3.0 (11.28) 2.10) 6.71 (3.0 (9. Survey years 03-04 Geometric mean (95% conf.S.90) 2.15) 4.34) 3.00-4.8) 7.0 (14.57 (3.00) 3. population from the National Health and Nutrition Examination Survey.00) 90th 11.14) 3.82-5.32 (4.37 (3.6-18.0-16.90 (3.S.49-4.9) 13.1-15.60-4.00 (5.45) 8.98) 4.00-7.7) 1284 1284 03-04 03-04 03-04 4.61-11.27-5.67) 9.91) 75th 5.46 (4.03 (3.52) 3.13-4.74 (2.0) 11.10) 3.34-4.8) 7.79 (3.80-5.00 (5.00) 6.00 (3.94) 3.09 (7.62) 4.0) 16.69 (3.80) 7.80 (4.34-4.42) 3.00) 5.95-3.84-18.0 (10.5) 95th 13.00-7.00) 75th 6.73) 6.69-6.0) 9.08 (2. see Data Analysis section) for Survey year 03-04 is 1.00-10.00) 6.00-12.00 (5.00-12.0-17.00 (4.0) 11.39-3.92-12.

16 (2. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th 1.22) 3.53) 292 728 1547 03-04 03-04 * * < 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 1.23) 1.40) 1.96-2.05-1.20-1.88 (1.80 (1.20 (1.60-2.S.60) 1283 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.61-3.33 (1.17) 2.43-3.57) 95th 2.18-1.75) 621 725 1077 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.40-3.20 (1.90) 1.30) 1.71-2.28 (1.60) 292 728 1547 03-04 03-04 * * < LOD < LOD 1.52 (2.00 (1.50 (2.20 (1.80) Sample size 2567 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.15-1.60) 2.62) 2. population from the National Health and Nutrition Examination Survey.70-3.46-2.00) 2.985) 1.70-2.50 (<LOD-1. population from the National Health and Nutrition Examination Survey.30) 1.82-2.853-1.61) 2.10-1.28 (1.40) 2. < LOD means less than the limit of detection.30 (1.S.40-2.33 (1.53 (1.88 (1.30 (1.53-2.86) 2.00-2.90) 2.07) 2.30 (1.80 (1.79) 2.53) Sample size 2567 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.00-1.53) 1283 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.70-2.40) 1.30 (2.80-2.20 (1.88-2.20-3.00) 1. see Data Analysis section) for Survey year 03-04 is 0.00-2.31 (1.50) 1.77) 1.58) 2.07-3.80 (1.00 (<LOD-1.90) 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.36) 1.35-3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.82-2.9.90 (1.46 (1.50-2.63 (<LOD-1.85) 2.10 (<LOD-1.80) 1.18-1. Fourth National Report on Human Exposure to Environmental Chemicals 189 .85) 1.70) 2.20 (1.00-1.60 (1.Metals Urinary Monomethylarsonic Acid Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.30-1.10-1.30-1.60 (2.40 (2.30-2.14-1. Survey years 03-04 Geometric mean (95% conf.54) 90th 2.80 (1.11-1.60) 1.86 (2.86 (2.900-1.50 (1.80-2.10) 2.40-3.10 (.90 (2.00) 2.00 (2.93) .00-4.30) 2.10 (1.22 (1.10) 95th 2.20 (1.10 (1.20) 2.45) 3.10-3.40-2.84-3.31-3.73-2.60) 2.816 (<LOD-. Urinary Monomethylarsonic Acid (creatinine corrected) Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.37 (1.34) 2.30) 90th 1. which may vary for some chemicals by year and by individual sample. Survey years 03-04 Geometric mean (95% conf.50) 621 725 1077 Limit of detection (LOD.80 (2.00) 1.00 (<LOD-1.00 (2.10 (.07 (1.36 (1.81) 1.80) 1.86) 3.00) 1.50 (1.70-2.70-2.40 (1.

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

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DMA(V)] in urine of children compared to adults from an arsenic exposed area in Bangladesh.89:145-151. Smith AH. Hughes J.

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91) 2.69 (1.50 (6.56 (1.53) 2. Barium salts have also been available as rodenticides.30) 5.61 (5. In nature.48-4.21 (1.81-3.2) 6.78) 1.40 (1.98) 1.85) 1.70 (1.43) 2.29-5.78-2.91) 6.9) 5.43) 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. soluble forms of barium.93-2.35-1.40) 7.24 (4.47-1.33 (1.44-2.4) 9.70-2.15 (2.73-5.41) 1.49 (1.74-2.80 (5.12) 7.36 (4.00) 4.14 (6.45 (1.87-9.71) 2.42 (1.87-3.25-11.80 (2.19-1. and 0.30-1.91 (2.88 (5.55-7.93-8.15 (6.10 (2.50 (1.90 (1.51 (1.20-1.15-11.40 (1. In single dose animal studies.34 (1. Fourth National Report on Human Exposure to Environmental Chemicals 193 .06-1.70) 3.37 (4.20-8.20 (3.11 (3.14-1.31-2.40) 7.1) 9.24-1.60-6.88) 1.30-2.40-13. and food.99 (4. such as brazil nuts.37) 5.09 (2.54-1. Small amounts of barium can be released into the air during mining and other industrial processes.46) 1.36) 5.40 (5.29-1.70) 4.12 (2.26-1.38 (1.80 (1.Metals Barium CAS No.35 (2.24-1.70) 7.62) 1.90-9.50 (4.44-5. and ceramics.48) 1. 0.30-1.03 (1.86 (4.41-1.00-3.36-1.39) 1.40 (4.37-1.10) 3.00-76.62 (1.27) 2. Urinary Barium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.30) 5. depilatories.50 (1.49-1.64) Sample size 2180 2690 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 2.97 (1.85 (2.95-6. were relatively well absorbed following inhalation (60-80% of a dose) or ingestion (11-32 % of a dose).70) 1.54 (6.28-1.67) 6.43 (1.00 (2.11 (3.45) 7.74-3.20 (1.82-6.19) 2.30-3.76 (3.50 (4.50-1. Barium compounds are used by the oil and gas industries to make drilling muds. Workers employed by industries that make or use barium compounds can be exposed to barium dust. 7440-39-3 Medically.54) 2.70-6.70-3.36 (1.96-2.20) 2.56 (1. it combines with other chemicals such as sulfur or carbon and oxygen. glass.63 (2.81-2.61-8.20-1.86 (4.27 (1.30 (3.15-1.73 (6.82) 1.87-14.70) 5.65-8.g.57-7.11 (2.71 (2.12.50-6.48 (6.49) 11. whereas others are practically insoluble (e.50 (1.26) 2.20-1. and 03-04 are 0.54 (2.15 (1.00) 1.90-2.26-7. The general population can be exposed to low amounts of barium in air.55-3.90) 2.37) 1.71) 95th 6.80-5.50) 1.32) 8.25-1.34 (2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. barium sulfate is used as a contrast medium for taking radiographs of the gastrointestinal tract.90) 4.78) 1.80) 7.10) 5.86-5.22-1.49) 2.73) 1.87-7.05% of the earth’s crust.51) 7.50) 4. Barium compounds are also used commercially in paint.60) 4.76) 1.77-3. barium sulfate and barium carbonate).53-5.70-8.49) 8.60-10.02 (7.60) 1.75-3.12.28) 90th 5.72) 4.50 (5.30 (2.73) 3.8 (6.35 (3.08-8.15-1.66) Selected percentiles ( 95% confidence interval) 50th 1.00) 1.78-3. fireworks.62 (1.57 (5.77) 1.14-6.92) 2.65-5.43 (1.75) 2.61 (3.53) 1.88) 7.30) 8.56 (2.80 (1.70) 1.21 (1.86-4.94-6.20 (4.87) 7.59) 3.29) 5.20-5. see Data Analysis section) for Survey years 99-00. 01-02.80) 6.8) 5.05-2.71-9.80-7.52 (1.22) 6.15) 5.56) 4.50-6.87 (5.00) 6.44 (1.12-1.20-1.51) 2.48-4. are high in barium (Genter.60-3.31 (2.64-3.20-6.74) 3.21-8.90) 2.90-13.08 (6.80 (1.11-1.04-6.47) 4.50 (1.36-1.49) 4.34 (1.38 (1.93 (4.70-5.65 (5.59-11.S.50) 2.68 (1.30) 5. rubber.8) 9.63 (1.38) 8.73 (5.70 (5.01 (4.51) 1.12) 6.35) 5.82) 2.76-7.30-2.60 (1.17-1.35-4.21-2.61 (1.10 (4.56) 1.61 (1.60 (2.37-8.90) 1.50 (4. 2001).54) 1.66 (4.20-8.43 (5.53) 692 683 618 540 667 723 765 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.26) 5.64 (1.30) 2.50-1.60) 1. bricks.39 (1.30) 3.60) 3.65-1.71) 1.87 (6. respectively.4) 7.01-7.70-2.16 (1.63 (8.50) 2.07 (2.65) 1.63) Total 1.16) 5.76-2.41-3.99-5.62) 1.49-9.90 (4.35-1.30 (5.40) 3.30-5.90 (6.54-8.86) 6.32-7.43) 6.60-6.40 (5.80-3.54) 1.57) 3. water.18) 3.30) 4.80-2.46) 1.35 (1.4) 6.72) 1.47-1.63 (5.34) 2.18-1.32-1.40 (1. tiles.30 (5.31.30 (1.77 (3.56 (6.10-4. such as barium chloride.95 (4.65) 1. Ingested soluble barium General Information Elemental barium is a silver-white metal which comprises approximately 0.39 (1.85) 1.18 (6.80 (2.84) 5.09 (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 1.81-2.72) 75th 3.38) 2.88) 4.20-8. population from the National Health and Nutrition Examination Survey.46-1.63) 1.39) 4.22-1. Some barium salts are freely soluble in water.61 (2.76-3.63) 1.48) 1.27 (1.00 (1.12 (2.50 (2.54-1.52 (4. Certain foods.39-1. interval) 1.00-8.40 (5..65) 3.10 (3.04-2.06-2.25 (1.50 (3.50 (1.10-5.60-2.80) 1.

46-22. such as those used in medical radiographic procedures. hypertension.76 (2.47) 10.20 (1.98 (2.47) 1.91 (3.45 (3.58 (2.85-5.777-1.02-5.64) 7.48) 2. Toxicity from soluble barium salts is rare.76) 2. 2001).63) 1.42) 1.04) 1.75) 2.58-6.45) 1.96) 4.38 (1.56-3.38) 1.51) 4.69-9.40 (1.921 (.84-2.32 (2.77-5. The health effects of exposure to barium compounds depend on the dose.50 (4.51 (3.00-1..49 (1.00) 4.78 (2.68) 1.83) 3.50) 2.00-7.11) .29-4. 1990).22-1.54) 2.57-7.24 (5.24-3.58) 4.3) 6.38 (4.91-2.32 (1.51) 6.20) 4. Urinary Barium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.68-3.32) 2.891 (. 1984.36 (1.48-5.70) 4.39 (2. interval) 1.37 (1.59 (1.10 (6.55 (4.97-3.56 (1.29-7.79) 1.28-7.88 (2.36-2.09) 6.96-6.45-8. about 75 % of a dose of soluble barium was eliminated within 3 days (Reeves.01 (5.963 (. a benign condition that may occur among barite ore miners.18 (1.39 (2.10) 6.58) 75th 2.35-3.11-2.29-1.41) 4. Barium is not rated for human carcinogenicity.905 (.2) 6.31 (4.52) 2.33) 6.03-1.8) 4.58 (4.29-4.22-4.24-6.60 (1. paralysis.96) 4.61) 2.24) 3..13-2. Chronic high doses in animals resulted in kidney damage (McCauley et al.68 (3.34-3.42 (4.67-6.16) 11.30 (1. 1994.73-4. water solubility.62 (1.84 (3.12) 2.00 (5.60) 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. chemical form.24 (3.49-1.22-1.55-6.39 (2.33-4.59-7.36 (3.31-1.89 (2.49 (1. and route of exposure.37-2.53 (2.03) 1.23-5.76 (4.87) 1.81-6.36 (5.03) 3.46) 3.51) 4. 1986).57-5.26-1. weakness.25) 4.01 (4.16-1.33 (1.64 (1.55 (1.43) 1.00 (3.00) 1.47) 4.S.76 (3.02 (3.18 (1.31-1.90-2.96 (4.26-1.39-5.08-1.51-3.23-2.54 (1.46 (2.27-3.65 (5.19-1.56) Selected percentiles ( 95% confidence interval) 50th 1. Human health effects from barium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.59) 1.04) 5.28) 5.10) 3.38) 4.86 (2.29 (3.33) 1.16 (1.55 (5.27 (2.24-6.20-8.34 (1.32 (1.62 (4.60 (5. 1989).38-5. NTP.86-7.59) 1.11) .27) 7.82) 1.47-8.56 (1. Insoluble barium salts.41 (2.28-6.36-1.27) 692 682 618 540 667 723 765 1132 1074 Non-Hispanic blacks Non-Hispanic whites 194 Fourth National Report on Human Exposure to Environmental Chemicals .70) 10. vomiting.39-1.75) 2.703-1.44-2.01) 1.08-2.74 (5.41 (1.29) 1.72) 6.57) 2.80-6.06) 2.46) 2.75) 1.45-1.32) 2.22-2.10-1.30) 2.36 (1.39 (3.92) 2.20-2.55 (1.54 (2.44-2.39-10.02) .60 (2.62) 2. Perry et al.45-1.39-1.91) 2.82) 1.53-21.34) 1.68 (3.96 (4.97) 1.36-1..4) 5.35-1.28-1. 1985.27-1.50) 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 1.15-4.47) 1.96) 4.Metals was eliminated primarily in feces and to a lesser extent.31-1.89) 90th 4.71 (5.34-5.88 (6.25 (1. Symptoms following acute high dose include perioral paresthesias. and cardiac dysrhythmias.3 (6.52 (3.54) 1.52) 7.50) 1.03-1.74) 1.47 (2.57-10.26-1.81-6.64) 7.75) 1.37-1.20-1.77) 1. are not absorbed when administered.97-4.02) 4.25-11.76) 1.76-3.41) 5.14-2.24-11.52) 1.48-3.51 (1.19-1.68) 3.915 (.45 (1.56) 4.13-3.832-1.53) .19-2.33 (1.38-7.75-22.80) 4.84-5.21 (1.59 (1.49-1.45-6.29-3.65 (2.83) 2.34-1.81-7.70) 1.06) .80) 3.75-3.97 (4.97 (5. 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.880-1.881 (.28 (1.48-1.48 (1.37 (1.63-4.47 (5.28-11.37) 2.26) 4.2) 5.62 (2.00 (2.23-1.0) 5.99 (2.72 (2.43-6.31) 5. Wones et al. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.61 (4. population from the National Health and Nutrition Examination Survey.99) 1.0) 6.69 (5.04 (2.74) 1.38 (1.76) 2.77) 1.77) Total 1.48 (1.31 (1.52-4.55-5.40-1.96) 7.24-1.38-1.39) 4.41 (1.64 (1. but can occur after intentional or accidental ingestion of barium carbonate in rodenticides (Genter.05-1.38) 1.79-5.19-1.72) 4. diarrhea.40 (1.58) 1.00 (3.84) 2.0) 7.00) 4.44 (1.30 (1.4 (5.68-3.77) 1.35-1.38 (4. Barium blocks cellular efflux of potassium resulting in profound hypokalemia.73-2.36 (3.49-1.2 (3.10-2.42) 1.60 (2.68 (2.40 (1.66 (1.86) 5. Chronic accumulation of inhaled barium dust in the lung tissue may cause baritosis.51 (1.57 (6.99 (4.33-1.52-10.754-1.26-1.91 (3. Following intravenous injection in animals.48 (1.59) 2.64 (1.00) 6. in urine.45) 95th 6.24-1.710-1.60 (1.5) 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 1.92 (4.50) 1.77) 5.73) 2.26-4.03) 2.33 (5.46) 1.29 (1.55) .64 (1.

p.atsdr. 1994. et al. Available at URL: http://ntp. Kopp SJ. Calabrese EJ. Vol 2: Specific Metals. Nordberg GF. Perry EF. PS. Minoia C. 1998). Urinary concentrations in acute poisonings are often hundreds to thousands of times higher than in this Report.gov:8080/cs. Sci Total Environ 1990. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.e. Investigations into the effect of drinking water barium on rats. and radium In: Bingham A. ed. the welders had no obvious adverse clinical effects (Zschiesche et al.64(1):13-23.95:89-105. Studies reporting urinary levels of barium in general populations have found values generally similar to those reported in NHANES 1999-2000.. Epidemiological study of barium in Illinois drinking water supplies. 1985. Information about external exposure (i. and 2003-2004 (CDC. Environ Health Perspect 1990. Morrow JC.pd f&qt=barium+chloride+dehydrate+1994&col=020rpt&n=3&la= en. Finding a measurable amount of barium in urine does not mean that the level of barium causes an adverse health effect. Int Arch Occup Environ Health 1992. Princeton (NJ): Princeton Scientific Publications.. environmental levels) and health effects is available from ATSDR at: http://www. patient population and literature reference intervals for urinary trace elements.nih. 221-252 Komaromy-Hiller G.Metals Workplace standards for external air exposure to various barium salts have been established by OSHA. Ash KO.85:355-359.niehs. McCauley PT. Atlanta (GA). Wones RG. 4/8/09 Paschal DC. 1992).niehs. calcium. 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.. Magnesium. Howerton K. 1986. Biomonitoring Information Levels of urinary barium reflect recent exposure. Welders of barium-containing electrodes had median urinary levels of barium that were 60 times higher than the median levels in this Report..nih. 2001. NTP.28(3):373-388.. Jackson RJ. p.197210. In: Inorganics in drinking water and cardiovascular disease. [online].gov/ntp/htdocs/LT_rpts/tr432. Princeton NJ: Princeton Scientific Publications. 10326-27-9) in F344/N rats and B6C3F1 mice (drinking water studies). Sampson EJ. Environ Res 1998. Reeves AL. Handbook on the Toxicology of Metals. LA. Gallorini M. strontium.html. Centers for Disease Control and Prevention (CDC). In: Calabrese EJ.gov/toxpro2. Ting BG. 1990. Lack of effect of drinking water barium on cardiovascular risk factor.76(1):53-59. ed. A study of 46 elements in urine. eds. Paschal et al. J Toxicol Environ Health.S. blood. Cohressen B. New York: John Wiley & Sons. Perry HM. 231-249. barium. Clin Chim Acta 2000. Advances in modern toxicology. 2000) to levels in NHANES 1999-2000 and 2001-2002. Sabbioni E. Inc. 2001-2002. Fourth National Report on Human Exposure to Environmental Chemicals 195 . Third National Report on Human Exposure to Environmental Chemicals. Apostoli P.. Patty’s toxicology. pp. Pirkle JL. In Friberg L. 2005. Genter MB. Comparison of representative ranges based on U. 1984. Exposure to soluble barium compounds: an interventional study in arc welders. Jr. Schaller KH. EPA.. and a drinking water standard has been established by U. New York: Elsevier.cdc. 84-94. Levy. 1989. Minoia et al. Costa R. Vouk VB. et al. Barium. Powell C. Barium levels determined in clinically submitted specimens were broadly comparable (Komaromy-Hiller et al. and serum of Italian subjects. technical report on the toxicology and carcinogenesis studies of barium chloride dehydrate (CAS no..296(1-2):71-90. 2005.html?charset=iso-88591&url=http%3A//ntp. Stadler BL. eds. et al. Zschiesche W. Trace element reference values in tissues from inhabitants of the European community I. Laurie RD. 5th ed.S.. et al. Pietra R. p. Frohman. National Toxicology Program (NTP). References Brenniman GR. Pozzoli L. Weltle D. Trace metals in urine of United States residents: reference range concentrations. Douglas BH. 2nd Ed. Hypertension and associated cardiovascular abnormalities induced by chronic barium feeding.

130 (<LOD-.S. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. x-ray machines. see Data Analysis section) for Survey years 99-00. are mined for commercial recovery of beryllium.13. 01-02. beryllium is used in instruments. Exposure to beryllium occurs mostly in the workplace. and can be found in mineral rocks. Beryllium is also used in the production of sports equipment such as golf clubs and bike frames. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. near some hazardous waste sites.130 (<LOD-. Low-level beryllium exposure in the general population can occur through breathing air. and refined beryllium is used in mirrors and special metal alloys for the automobile. inhaled insoluble beryllium sulfate was retained in the lungs and nearby lymph nodes. In studies of laboratory animals. Beryllium compounds are commercially mined. nuclear. Burning coal and oil can produce small amounts of beryllium dust that can be released into the air.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 . less than one percent of the inhaled dose was slowly absorbed into the blood and eventually incorporated into the skeleton. or drinking water containing the metal. which may vary for some chemicals by year and by individual sample.13.13. electrical. and machine-parts industries.140 (<LOD-. and volcanic dust. A half-life of 450 Urinary Beryllium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.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 . aircraft. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th < LOD < LOD < LOD 90th < LOD < LOD < LOD 95th < LOD < LOD < LOD Sample size 2465 2690 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . and 0. 7440-41-7 General Information Pure beryllium is a hard gray metal.Metals Beryllium CAS No. < LOD means less than the limit of detection. population from the National Health and Nutrition Examination Survey. and dental bridges. and from breathing tobacco smoke. the lightest of all metals. and 03-04 are 0. soil. Two types of minerals. In medicine. 196 Fourth National Report on Human Exposure to Environmental Chemicals . coal. bertrandite and beryl. computer. respectively. 0.160) < 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. eating food.

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

Apostoli P. Apostoli and Schaller (2001) stated that detection limits in earlier studies were inadequate to estimate nonoccupational exposures. Genetic and exposure risks for chronic beryllium disease. 198 Fourth National Report on Human Exposure to Environmental Chemicals . Urinary beryllium--a suitable tool for assessing occupational and environmental beryllium exposure. Minoia C. Review of elements in blood. Clin Chim Acta 2000. 0. Available at URL: http://www. Paschal et al. 3/27/08 Komaromy-Hiller G.296(1-2):71-90. Ting BG. Ash KO. 2000. Pietra R. Biomonitoring Information Urinary beryllium levels represent recent and accumulated exposure. which approximate this Report’s limit of detection. Environmental Health Criteria.html. Centers for Disease Control and Prevention (CDC). and the 95th percentile for males in NHANES 2001-2002. population were generally undetectable in NHANES 1999-2000. VI. Pozzoli L. Howerton K. and 2003-2004.76(1):53-59. In other studies. less than 0. International Programme on Chemical Safety (IPCS). it is likely that urinary beryllium levels in the U.. Comparison of representative ranges based on U. (1994) noted that analytical methods used in several general population studies appeared to have limits of detection that were insufficiently low (i. Environ Res 1998. They reported urinary beryllium levels ranging from 0. Clin Chest Med 2002. Int Arch Occup Environ Health 2001.atsdr. Hamilton et al. 1990. Sabbioni E.158:165-190. et al. Sci Total Environ 1990. Beryllium [online].e. Element reference values in tissues from inhabitants of the European community.e. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. environmental levels) and health effects is available from ATSDR at: http://www. Sci Total Environ 1994. blood. et al. Gallorini M. Schaller KH.157:388-398.12 to 0.13 μg/L. Given these results. Pirkle JL.gov/toxpro2. Costa R. Trace element reference values in tissues from inhabitants of the European community I. Hamilton EI. and serum of Italian subjects. 1998).org/documents/ehc/ehc/ ehc106. Trace metals in urine of United States residents: reference range concentrations.1 μg/L).. A study of 46 elements in urine. Levels of beryllium in urine for the U. Atlanta (GA) 2005. Finding a measurable amount of beryllium in urine does not mean that the level of beryllium causes an adverse health effect. Maier L. Minoia et al.htm. patient population and literature reference intervals for urinary trace elements.23:827-839.15 μg/L in workers exposed at the recommended threshold limit value (Apostoli and Schaller.74:162-166.Metals (i. References Apostoli P. HLA-DPB1 and chronic beryllium disease: a HuGE review. McCanlies EC. Paschal DC. Kriess K.. 106. 1990. Andrew M. Jackson RJ.S.95:89-105. 20012002. Van der Venne MT.S.S. Weston A. Am J Epidemiol 2003. and the fact that most NHANES participant levels were undetectable. Sabbioni E. plasma and urine and a critical evaluation of reference values for the United Kingdom population.. Third National Report on Human Exposure to Environmental Chemicals.cdc. 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.inchem. Sampson EJ. 2001). population are lower than levels in workers. urinary levels for general populations have been either undetectable or had different detection limits than in this Report (KomaromyHiller et al.. Morrow JC.

300-.00-1. and incineration of municipal waste materials.393 (.30) .300-.500 (.216-.400 (.600 (.600 (.500-.60 (1.10) 1.500-.600-.500-.80) 1. < LOD means less than the limit of detection.20) .10 (1.304-.200-.500) .20-1.500-.421 (.300-.700-1.500 (.300-.300 (.300) .368-. plastic stabilizers.50-1.900 (.90) 1.333 (.900-1.30) 1.900-1.800-1. cadmium use has declined in response to environmental concerns (http:// minerals.400-.200 (.300-.30-1.300 (.20) 1.398) < LOD < LOD < LOD < LOD < LOD < LOD .400) < LOD .400-.40 (1.500 (.600) 1.600) 90th 1.S.800-1.400 (.00 (.600) .395 (.400-.400) < LOD .900-1.00 (.300-.800) 1. interval) .60 (1.400 (.500) .400-.304 (.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 * * * * * * . respectively.10 (1.00-1.400 (.20 (1.20 (.14.400 (.50 (1.S.60 (1.900-1.300 (<LOD-. coatings and plating.289-.400-.500 (.900-1.400-.300) .300 (. or copper smelters (U.10) 1.283 (.500-.900-1.400) .300 (.300-.426-.449) Selected percentiles ( 95% confidence interval) 50th . and nonferrous alloys.00 (.80) 1.800) .500) .600 (.10 (.900-1.300) 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 .600) . lead.50 (1.304 (.400) .313 (.441) * .500-.60) Total * .700) .500) .344) . during refining of lead and copper from sulfide ore.309-.10 (1.600 (.412 (.300) . U.700 (.300 (.10) 1.90) 723 898 910 905 1044 856 2135 2231 2081 4207 4772 4525 6-11 years 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .700-1.700) .700-1.500) .800 (.600) .300 (.359-.20) 1.500-.300-.200-.366) * * .300 (.300 (.10) 1.10 (1.50) 1.200 (<LOD-.40 (1.00 (1.500-.900-1.600 (. as zinc sulfide) and to a lesser extent.600 (.00 (1.600-.300-.900-1.600 (.403) .20) .300 (.300 (.60 (1.800 (.427) * .20) 1.usgs.300 (.500-.700) .50-1.3.600 (.500 (.00-1.367-.275-. Cadmium also may be emitted into the air from zinc.500-.300-.00 (.452) .10 (1. Other uses include pigment production.00-1.50 (1.10 (1.200-.500-.40 (1.60) 1.300 (<LOD-.400-.00 (.425 (.300-.513) .600) .468 (.300-. which may vary for some chemicals by year and by individual sample.300) .400) .10) 1. bluish-white metal that is obtained chiefly as a by-product of processing zinccontaining ores (principally sphalerite.600 (.300 (.400) .400 (.600) .3.200-.70) 1.500-.300) .300) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.400) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.40 (1.10) 1.60-1.20) 1.70) 2742 2268 2085 1842 2219 2292 2716 3806 3478 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.300-.266-.600 (.386-.300) .700) .500 (.378-.400) .30 (1.600 (.400) .30) 1.403 (.00-1.gov/minerals/pubs/commodity/cadmium).20) 1.60) 1.400 (.200) .600-1.400) .200-.300-.424) * .460) .400) .40) 1. Fourth National Report on Human Exposure to Environmental Chemicals 199 .60 (1.400 (.700) .20-1.00 (.Metals Cadmium CAS No.300-.300 (.10) 1.50) 1.500-.50 (1.800) .40) 1. The predominant commercial use of cadmium is in battery manufacturing. see Data Analysis section) for Survey years 99-00.700) .300-.500 (.255) .300) .20) 95th 1.40-1.300) .235 (.300 (<LOD-. EPA.470) * .50-1.70) 1.300-.300) 75th .70) 1.40 (1.20) 1.500-.700) .400 (.300-.50) 1.40 (1.400) .S.20-1.300 (.300-.300-.400 (.80 (1. 01-02.382 (.900-1.00 (.500-.60) 1.700) .900 (.400 (.20-1.300 (<LOD-.00 (.400 (.376-.500) .500-.300) .500-.30-1.400 (.600 (.400-.300) .378 (.400 (.300) .400 (.600 (.326 (. population from the National Health and Nutrition Examination Survey.500 (. Since 2001.400) . 7440-43-9 General Information Cadmium is a soft.600) .40 (1.600-.00-1.00) .400-.00-1.400-. Important sources of airborne cadmium in the environment are burning fossil fuels such as coal or oil.70) 1.300-.20) 1.420 (.400 (.331) .300-.700) 1.30-1.400) .30-1.200 (<LOD-.200 (. malleable.50-1.400 (.40-1.10) 1.00) .400-.30-1.600) . 0.500-. Blood Cadmium Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U.00 (.500 (.500) .20-1.20-1.337) .600 (.00 (.362-.20) 1.30) 1. and 0.10 (1.361-.200 (.00-1.600) .400) .400) < LOD .600) .200) .400) < LOD < LOD < LOD .00-1.20-1. and 03-04 are 0.400) .300) .296-.

265 (.607) .265) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.519) .160) .510-. 01-02.890 (.100-.270 (.192-.150-.559 (.01-1.210) .295) .390 (.24) 1.806) .430) . however.72) 1.836-1.160 (.980 (.177-.220-.366-.06-1.918-1.249) . zinc.227 (.733) .481) .184-.206 (.810-1.450 (.220) Selected percentiles ( 95% confidence interval) Sample 95th 1.261-.51 (1.10 (1. an inducible metal binding protein.640) .181 (.109-.366) .067-. a factor that may contribute to the higher absorption of cadmium by women (Diamond et al. rice.17 (.20 (1. ingestion through food is the largest source of exposure.06.200 (.52 (1.919) .130 (.02-1.255) .12 (.310 (.13 (.390-.17) .440-.277 (.545 (.452 (.221) .200-.148-.22 (.220 (.261-.519) . 2001).960 (.390-.202-.817 (.253-.270 (.237-.251) .189-.456-. 200 Fourth National Report on Human Exposure to Environmental Chemicals .077 (.148) . and various seeds.03) . whose body burdens of cadmium can be approximately twice that of nonsmokers.610) .203) .210 (.22 (1. The gastrointestinal absorption of dietary cadmium is about 5% in adult men and 10% or higher in women (Diamond et al.262) .206) .730-.633-1.82) 1.450 (.226) Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 * .980) .20 (1. About one-third to one half of the total body burden accumulates in the kidney tissues (Nordberg and Nordberg.272-.713) .17 (.210 (.493-.316 (.960) 1. With chronic exposure.890-1.700-.135-.190-.302 (.989-1.858 (. including many food crops such as cereal grains.109 (.480) .351-.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 .285-.170-.381-.354) .167-.141 (. The estimated half-life of cadmium in the kidney is from one to four decades (ATSDR.433-. 1994).680 (.38) 1.209 (.134) .875) .963-1.479) .310) .34) 1.48 (1.705-.107-.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 .220) .28 (1.733-.440 (.189-.240-. 2003).36) 1.232 (.387) .972 (. wheat.28-1.800 (.263) .892-1.886-1.233) .530 (.232) .25 (1. calcium..700-.393-. **All results are corrected for molybdenum oxide interference in the ICP-MS method.290-. cadmium accumulates in the liver and kidneys where it is bound to metallothionein.336) .394-.06.238-.870) .977) .38) 1.187 (.855-1.121 (.763-.329 (.233) .199 (.175 (. 2003.208-.813 (.193 (.202 (.239 (.238) . 0.766 (.200-.299) . 2003).633 (.366-.430-. see Data Analysis section) for Survey years 99-00.151-. 2003).300) .372) .289-.234 (.12-1.980-1.260-.201 (.447 (.175 (.230) .458 (.211-.15) ..20 (1.530) .47) 1.240) .191-.06-1.207-.247) .300 (..320) .067-. 1999.892 (.191-.717-.15) 1.20) 1.078 (.800-.101) .160-.281 (.753-.06.13-1.222) .32 (1.135 (.114-.07-1.246) .83) 1.476-. Renal tubular and glomerular damage.189) .30-1.507) .322 (.219 (.180 (. copper) and protein.170-.210 (.243-.210) .01) . and 0.092) .440 (.061-.260-.01 (.540) .990) .57) 1.120 (.. Cadmium in soil is absorbed by plants.192-.623) .229) .17 (. and 03-04 are 0.20-1.843-1.445 (.25) 1. Cadmium absorption may be increased with iron deficiency (Berglund et al.817 (.74) 1.790 (.112-.282 (.41 (.980) .257-.470-.160) .169-.350 (.204 (.475 (.230) 75th . respectively.150) .313) . Kikuchi et al.** Survey Geometric mean (95% conf.551 (.210 (.848 (.412) .178-.165-.490) 1.43) 1.211 (.482) .490) .157) .306 (.400-.686-.818 (.219 (.257) .875 (. To a lesser extent.860) 1.500) 90th . Urinary Cadmium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.550 (.820 (.28) 1.330-.090) .220-..362) .230 (.492 (.219 (.388-. population from the National Health and Nutrition Examination Survey.126) .214-.284) .09-1.820-1.308) .196-. The kidney is a critical target and shows the earliest sign of cadmium toxicity.423-.326) .229-.090) .210 (.170 (.06) .110-.426 (.223 (.283 (.171-.183-.520-.466 (.255) .241) .04 (.157-.Metals 2000).153-..191 (.115-.260 (.748-1.231) .279 (.216 (.360) .940-1.26) 780 683 614 546 667 717 760 1132 1070 Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 03-04 Limit of detection (LOD.15 (. Inhalation of cigarette smoke is a predominant source of exposure in smokers.061 (<LOD-. potatoes.539) .229) .255) .886) .S.820) 1.065-.400-.714-1.226) .280 (.235) . Diamond et al.081) .087-.04 (.128 (.092 (.195-.580) .273 (.38) . Cadmium is absorbed via inhalation and ingestion.790 (.190-.551) . individual values vary and are affected by factors such as dietary intake of essential nutrients (iron.700-.589 (.173) .13) .136) .38) .445 (.596) .198) .839 (.462 (.193-.060-.19) 1. drinking water is a source for cadmium intake.077 (.980-1.200 (.455 (.26) size 2257 2690 2543 Total years 99-00 01-02 03-04 50th .194-.498-. Horiguchi et al.179-.140 (.221 (.190-.500) .249-. interval) .880) . For nonsmokers who are not exposed to cadmium in the workplace.436-.203 (.510) . 2004a.080 (.339) .741-1.327 (.

181) ..154 (.104) .185) .381-.828) .123-.667) .917 (.191 (.382-.166 (.182) .607) ..178-.08) .136-. Staessen et al.441-.199-..446) .444-.270 (.278) .071 (.183 (.06 (.281) .146-. 1999). At lower environmental exposures.168-.168-.331 (.261 (.086 (.687 (.350) . population from the National Health and Nutrition Examination Survey.083-. 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.647-.100 (.173-..470) . **All results are corrected for molybdenum oxide interference in the ICP-MS method.283 (. two studies in Japan did not find an association between cadmium in urine and renal biomarkers (Ezaki et al.084-. 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.091 (.622 (.09 (.242) .084 (..085 (.690-.190 (.338 (.962) .238-. 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.200 (.308) .210) .13) .144-.205 (.412 (.137-.826-1.473 (.678 (.531 (.280 (.813-.163) .559-.219 (.101) .316) . During the 1950’s and 1960’s.156 (.827) .159 (.826-1.479 (.093 (.07) .078-. 2002.795) 1.221 (.414 (.311) .288-. can result from high dose chronic exposure.293-.630-.238) .183) .S.414-.431) .07 (.05) 1.232) .304) . 1999).591 (. Horiguchi et al.929) .691-.178) .426-.210 (.296 (.17) .792 (.631) .219) Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 * .352) .131-.051-.096) .107) .098) .38) .909-1.157-.147 (.304-.091) .240) .227-.136-.135) .289) ..282 (.204-.122 (.184-.856 (.239-.08) 780 682 614 546 667 717 760 1132 1070 Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 03-04 * Not calculated: proportion of results below limit of detection was too high to provide a valid result.12) 1.159 (.668-.078 (.212 (.364) .267 (.340) .140-.261) .075 (<LOD-.833-1.234 (.02 (. 1996.162 (.789 (.423 (.830) .481 (.377-.176 (.289) .16) 1.440) .708-1.719 (.865 (.206-.225) .472) .438-.273 (.404) .415) .198) .181 (.170-.518) .818) .500-.666-.097) .516-.202 (.163 (.696-. Jarup et al. Olsson et al..769 (..533) .538) .536 (.215 (.219 (. Noonan et al.250) .222-.226) 75th .432 (.551) .184) .784) .884) .740 (.085-.137 (.175 (.247-.111-.303) .210 (.177) .940 (.063-.253 (.421 (.150-.300-.335 (.220 (.690-.094) . However.297) .194-.718 (.156-.04) size 2257 2689 2543 Total years 99-00 01-02 03-04 50th .170 (.438) 90th .224 (.221-.687-.16) .678-.906) .225) . 1999).090 (.190 (.507-.783) .725-1.806-1.228-.067-.501 (.106) .168 (.261-.440) . 2002.174-.653) .263 (. Fourth National Report on Human Exposure to Environmental Chemicals 201 .077-.181 (.545) .207) .931 (.201-.247-.292) .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 .234-.281) .917) .491-.645-. 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.185 (.208-.112) .189-.873 (.950) .754) .288 (.674-1.143) .197-.998) . a condition known as “itaiitai” (“ouch-ouch”) affected postmenopausal women living in a cadmium-polluted region of Japan.191) .209) .184-.288) .818) .255-.154-.433-.156) .175 (.218) .693 (.418-.157-.686 (.175-.216-.143-.253) .240) .850) .** Survey Geometric mean (95% conf.663 (.404 (.876-1.10) 1.234) .336-. most often a result of occupational exposure (Roels et al.252 (.856) .560-.274) 1.562-.182) .418) .757 (.263-.130-. 2000.802 (.839) .767) .783 (.199 (.321) .387-.209) Selected percentiles ( 95% confidence interval) Sample 95th .325 (. 2004b).Metals manifested by irreversible proteinuria and progressive reduction in glomerular filtration rate.235) .700 (.267 (.208 (.343-.232) .00 (.487 (.256-.614) .192) .729 (.979 (.075-. interval) .850) .147-.140-.919 (. 2003.779 (.161-.318 (.716-.650-.690 (.241) .233 (.316 (.091 (.617 (.211 (.537-.813-1. 2002.940-1.182) .074-.266-.398-.434 (.126 (.229) .223) .247-.874-1.688-.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 .700) ..387 (.147-.449) .245 (. 2004).423-.308 (.716) .113-. 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.00 (.176 (.767 (.268 (.191-.727-.329 (.388-.382) .148 (.830-1.104) .196 (.541) .236-.985 (.143-.757) .490 (.484 (.722-.266) .181-.391-.941 (.123-.476) .173 (.207-.187-..927-1.171-.187) .158-.470) .712 (.

Ezaki et al.e. The 95th percentiles for cadmium levels in this Report were less than the OSHA standards for both blood cadmium (5 mg/L) and urine cadmium (3 mg/gram of creatinine). 2005). Biomonitoring Information Blood cadmium reflects both recent and cumulative exposures.. 2003...cdc. People who are occupationally exposed may have blood and urine cadmium levels that are higher than those of the general population. Wennberg et al. Staessen et al. data (CDC. Waalkes (2003) provides an overview and summarizes potential mechanisms for carcinogenicity. For NHANES 19992000.Metals greater urine cadmium levels may have an increased risk for bone fracture and diminished bone mineral density (Alfven et al.. Wilhelm et al.S. Information about external exposure (i. 2004b. 1996).. 2002).. 2002) and length at birth (Nishijo et al.. 2002. urinary cadmium reflects both cumulative exposure and the concentration of cadmium in the kidney. 2003.. In the typical environmental exposure... Salpietro et al... 2004b). 2005.. 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. Becker et al.atsdr. 2005. Staessen et al.. 2003. 2002). Becker et al. Staessen et al. 2003).. Cadmium can produce lung. 2006). Olsson et al. 2000. Becker et al. has resulted in severe. 2003. Horiguchi et al..26 and 3. 2005.. Creatinine-corrected urine cadmium values in U.. 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.gov/ toxpro2. Occupational standards are provided here for comparison only. Both IARC and NTP consider cadmium a human carcinogen. decreased bone density was correlated with mean urinary cadmium levels of approximately 1 mg/gram of creatinine (Staessen et al... Workplace standards and guidelines for air exposure to cadmium have been established by OSHA and ACGIH. 2003.. Biomonitoring studies on levels of cadmium provide physicians and public health officials Fourth National Report on Human Exposure to Environmental Chemicals . In adults aged 60 years and older. Women had higher blood and urine cadmium levels compared to men of similar ages.. intermediate in former smokers and lower in never-smokers (Becker et al.. blood cadmium was also slightly higher in Mexican Americans and participants 20 years and older (CDC. Finding a measurable amount of cadmium in blood or urine does not mean that the levels of cadmium cause an adverse health effect. However. 1999).. with peak values observed in the fifth to sixth decades (CDC. 2005. Mannino et al. respectively.S. Chronic inhalation exposure to cadmium particulates was associated with changes in pulmonary function and chest radiographs that were consistent with emphysema (Davidson et al. Zhang et al. 2000. Olsson et al. Blood cadmium levels are about twice as high in smokers compared to nonsmokers (Becker et al. Suwazono et al. 2002. 1996. In postmenopausal women. 2000. 2006).. 1999).1 mg/L (Alfven et al. 1988). Friedman et al. study subjects living near a former zinc smelter were similar to those from an unexposed community and to those in this Report (Noonan et al.html. Horiguchi et al. maternal blood or maternal urine and birth weight (Nishijo et al. Wennberg et al. Workplace exposure to airborne cadmium particulates was associated with decreases in olfactory function (Mascagni et al. Small epidemiologic studies have noted an inverse relationship between cadmium in cord blood. respectively. Surveys of populations not known to have increased cadmium exposure have reported similar urine and blood levels (Becker et al. Several studies of populations residing in areas with higher cadmium soil concentrations or with frank cadmium pollution have reported mean blood and urine cadmium levels considerably higher (as much as 10 times higher) than control groups or representative U.46 mg/gram of creatinine) (Ezaki et al. 2004.... Noonan et al. environmental levels) and health effects is available from ATSDR at: http://www. 2004. Jarup et al. Ezaki et al. 2002).. In this Report the urinary and blood cadmium levels at the 95th and 90th percentiles. as may occur from welding cadmium-alloyed metals.. and drinking water and environmental standards have been established by U. Blood and urine cadmium levels are typically higher 202 in cigarette smokers. 2002). Olsson et al. CDC.. Moriguchi et al. potentially fatal pneumonitis (Fernandez et al. 2004. 2002. 2002). 2006...S. not to imply a safety level for general population exposure. Acute and heavy exposure to airborne dusts and fumes.... 2003. 2000). 2004). 2006... approached these values associated with subclinical changes in renal function and bone mineral density. 1999. EPA. 2002. Further research is needed to address the public health consequences of such exposure in the United States.. Jin et al. Jarup et al. pituitary gland and kidney tumors in animals and has been associated with lung cancer in humans in occupational epidemiologic studies. 2002. Komaromy-Hiller et al.. the risk of low bone mineral density increased by nearly three-fold when the blood cadmium exceeded 1.. 2002. Animal studies have demonstrated reproductive and teratogenic effects.. 2004.

Fukui Y. Stock AL. Int J Hyg Environ Health 2003. Chislovska NV.24:717-724. J Occup Health 2003. et al. Greves HM. Uemura T.59:194-8. Akesson A. Holguin F. 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. Fourth National Report on Human Exposure to Environmental Chemicals 203 . population. Kumagai N. 196:114-123.html. Ezaki T. Mucha A. Toxicological profile for cadmium update. Persson B. Taylor AJ. Komaromy-Hiller G. Alfven T. Environ Health Perspect 1994. Ikeda Y.Metals with reference values so they can determine whether people have been exposed to higher levels of cadmium than are found in the general population. Takebayashi T. et al. 1999 [online]. et al. Chiappino G. and dietary predictors of elevated blood cadmium levels in Ukranian children: Ukraine ELSPAC group. Jarup L. Nerbrand C. Schulz C. Sasaki S. Costa R. Occup Environ Med 2000. 102:10581066. Horiguchi H.59:497]. et al. Environ Res 2006. Vahter M. Moriguchi J.148(1-2):11-20. Intestinal absorption of dietary cadmium in women depends on body iron stores and fiber intake. Lancet 1988. Berglund M. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. et al. Tsukahara T. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Davison AG. Nermell B.gov/toxprofiles/tp5. Tsukahara T. Wang H.66(Pt A):2141-2164. Fatal chemical pneumonitis due to cadmium fumes. Uptake of cadmium in meals from the digestive tract of young non-smoking Japanese female volunteers. Agency for Toxic Substances and Disease Registry (ATSDR). Oguma E. Howerton K. a1-Microglobulin as a promising marker of cadmium-induced tubular dysfunction. Cadmium fume inhalation and emphysema. Jones RL. 2005. Oguma E. Elinder CG. Neurotoxicology 2003. Comparison of representative ranges based on U. Bo M. Ash KO. Seiwert M. No clear-cut evidence for cadmium-induced renal tubular dysfunction among over 10. Kaus S. Zhu G. Vahter M. Dietary exposure to cadmium at close to the current provisional tolerable weekly intake does not affect renal function among female Japanese farmers. Ukai H. Lancet 1999. Serra J. Lukyanova EM. Thayer WC. Consonni D. Lidfeldt J.cdc. Ye T. Renal effects of low-level environmental cadmium exposure: 5-year follow-up of a subcohort from the Cadmibel study. Savage-Brown A. Palomar M. Becker K.76:186-196. Environ Res 2004b. Lison D. Fukui Y.000 women in the Japanese general population: a nationwide large-scale survey. 4/8/09 Alfven T. Int Arch Occup Environ Health 2003. et al. Environ Res 2004. Choudhury H. Hellstrom L. Environ Health Perspect 2005. et al. Comprehensive study of the effects of age. Mascagni P. Sanz P. 206:15-24. et al. Kaus S. Seifert B. Toffoletto F. Lundh T.13(11):1627-1631.S. Schulz C. References Akesson A. Ikeda Y.1(8587):663-667. Jarup L. Urinary cadmium levels predict lower lung function in current and former smokers: data from the Third National Health and Nutrition Examination Survey. Miyamoto K. Osteoporosis and renal dysfunction in a general population exposed to cadmium in China. Fayers PM. Nomiyama T. J Toxicol Environ Health 2003. Sasaki S.57:668-672.205:297-308.46:372-374.S. Darbyshire J. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Seiwert M. Miyamoto K. Clin Chim Acta 2000. Available at URL: http://www. Kundiev YT. Ezaki T. iron deficiency. Thorax 2004. Bernard A.96:353-359. diabetes mellitus. Venables KM. Occup Med 1996. Okamoto S. Bregante G. Atlanta (GA). environmental. Cadmium and lead in blood in relation to low bone mineral density and tubular proteinuria. Furuki K.atsdr. Grubb A. Anthropometric. Horiguchi H.95:20–31.45:43-52. et al. Friedman LS. Jin T. Toxicol Lett 2004. Olfactory function in workers exposed to moderate airborne cadmium levels. ShkiryakNizhnyk AZ. Int J Hyg Environ Health 2002. Diamond GL. Bellerup P. Buchet JP. Pickering CA. Furuki K.102:83-89. Hotz P. Carlsson MD. Krause C. Pharmacokinetic/ pharmacodynamics (PK/PD) modeling of risks of kidney toxicity from exposure to cadmium: estimates of dietary risks in the U. Mannino DM. Lepom P. Nordberg G. Machida M. Lauwerys R. et al. Toxicol Appl Pharmacol 2004a.354:1508– 1513. Gadea E. et al. Dekio F.110:699-702. Machida M.296(1-2):71-90. patient population and literature reference intervals for urinary trace elements. Fernandez MA. Tubular and glomerular kidney effects in Swedish women with low environmental cadmium exposure. and cadmium burden on dietary cadmium absorption in cadmium-exposed female Japanese farmers. Becker K. possibly better than b2microglobulin. Environ Health Perspect 2002. Moriguchi J. Kikuchi Y. Centers for Disease Control and Prevention (CDC).

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although cesium was generally of low toxicity when given to animals.90) 9.4-13.22-4.1) 10. and 03-04 are 0.8) 9.84) 8.25) 4.4 (9.03 (4.57-5.64-5.72) 4.62 (5.50 (4.0-15.1 (11.71 (8.99) 7. semiconductors.95 (3.0 (9.01) 7.59-5.8) 9.81) 9.34 (4.26 (3. and cardiac arrhythmia (ATSDR.4 (9.70 (6. Little is known about the health effects of this metal.60 (7.40-5.20-5. photographic emulsions.13 (8.0-13.00-8.14.60-12. and clay.10 (6.49 (4. the body half-life is estimated to be 70-109 days based on 137Cs exposures.00) 6.70 (8.60-5.63-4.30-5.84-9.64-10.47-4. 0.30-10.90-10.97 (7.3) 9.39-4.60-6.25 (3.33 (6. nausea.3) 10.66 (7.73-11.13-8.4) 10.08 (7.24) 4.8 (10.52) 7.40) 5.30) 7.20) 4. Inorganic cesium compounds are used in photomultiplier and vacuum tubes.7) 10.60) 7.88 (8.6 (11.1-12.27) 4.56 (4.8) 12.6 (9.62) 4.50 (4.87 (4.00) 7.91 (7.49 (5.7 (9.43 (5.S.5) 12.9 (11.5 (8.6 (9.2 (9.00 (7.10 (8.35 (4. Case investigations of ingestions of large doses of cesium chloride have reported decreased appetite.90 (4.35-5.10-8. and high-power gas-ion devices.4 (10.3 (8.90-12. Workplace guidelines for cesium hydroxide are available from ACGIH and NIOSH.0) 12.3 (8.3) 10.80-10.05) 5.94-4.05) 5.2-13.87 (4.20-7.13 (5.2.89-5.60-7.56 (4.40-11.4) 11.6) 1226 1335 1281 1238 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 4.17 (6.25-5.42) 7. 7440-46-2 General Information Cesium is a silver-white metal that is found naturally in rock.71-8.02 (4.90) 5.12-5.20) 5.42-7.39) 7.40 (4.08-5.13 (7.80-10.59-5.1) 9.5-13.9 (11.68 (7.08) 7.29) 4.5-14.6) 10.12) 5.2-14.7 (8.59-5.90-10.09) 5.0) 11.26-11.71 (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 4.56-11. However.91-8.9 (10.81) 4.53-11.16-6.3-15.7 (9.70 (4.98 (7.5-14.0) 11.08 (6.4) 10.0) 9.0) 10.00-4. Fourth National Report on Human Exposure to Environmental Chemicals 205 .90) 4.0) 12. cesium hydroxide is corrosive and irritating at high concentrations.70 (9.16-6.77 (9.2) 11.26) 4.5) 9.26) 7.64 (4.2-13.23) 9.86 (7.20 (6.0 (10.87 (4.03 (4.04 (4.3) 10.9) 11. For absorbed cesium salts.3) 10.0) 12.36 (6.00-8.74 (4.95-4.84 (4. see Data Analysis section) for Survey years 99-00.22 (4.59 (5.80 (4.90) 7.00) 4.30 (6.29 (4.70 (5. diarrhea.70 (8.3-13.89) 5.80 (8.89) 4.4) 12.33-5.8-13.50) 5.50) 9.80-10.27-5.80-6.12 (4.70) 5.69-6.87) 5.87-7.53 (6.43-8.40-11.46) 7.61-6.61) 7.03-4.64) 4.04) 7.36) 3.97) 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 4.10 (6.94 (4.82-4.71) 4.7) 10. and as polymerization catalysts. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.80 (8.83-4.77-8.64) 5.10 (8.70-8.37) 7.55-11.80) 7.47-8.1 (9.05-5.23-4.80 (4.20-4. Human health effects from cesium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.38) 5.96 (6.2) 12.99-11.81-14.Metals Cesium CAS No.50 (7.95) 5.01-8. scintillation counters.08-5.32) 4.6 (11.60-7.94) 4.70-5.7 (11.00-10.10-9.84) 5.90-10.97-7.8) 12.80 (8.73-5.30 (6.9) 12.7 (10. population from the National Health and Nutrition Examination Survey.81 (4.1-13.1 (10.60-6.21) 90th 9. infrared lamps.33 (5.2-13.40-5.80-11.67 (4.40-7.93 (4.21 (4.54) 4.9 (11.62 (5.86-11.17) 4.97) 4.59) 7. respectively.37) 5.42) 6.10-5.79 (4. Radioactive 137Cs has been used medically to treat cancer.40) 5.40-5.50-7.05-5.7 (9.63) 6.45-5.40) 7. interval) 4.49) 4.60) 7.99) 9.52-9.74-5.70 (6.1) 11.81) 4.80 (4.55 (7.60) 5.2 (9.70) 7.20) 7.83) 6.9 (11.60 (8.72-7.5-16.4) 9.45-8. 01-02.7 (10.7 (10.6 (9.35 (4.17-6.9) Total 4.55 (4.49) 75th 7.7) 884 683 618 568 667 723 821 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.70) 5.00-9.44 (8.8 (10.34) 9.6) 11.98 (7.71-9.07-11.82) 5.1-12.3-13.86-12.8 (11. soil.50 (6. Most human exposure to cesium occurs through the diet.68) 9.4) 12.3) 12.32-5.5) 10.20 (4.15-8.56) 5.7-14.27 (7.31-8.8) 11.07) 4.99-11.9 (10.8) 12.6 (9.9) 8.99-6.90) 5.36 (3.90-12.4) 95th 11. and 0. Whether cesium compounds are carcinogenic is unknown.84-5.20-8.77 (9.14 (4.20) 8.76-6.50 (4.40-5.5 (10.1) 11.8) 11. 2004).12-11.30) 5.32 (3.14.7) 11.90 (6.10-7.74) Selected percentiles ( 95% confidence interval) 50th 4.80-13.92-13.1) 9. Urinary Cesium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.01-6.71-5.09-5.94 (4.64) 5.54-11.63 (4.90-8.2-12.7) 11.77 (4.

70) 7.47 (4.56) 4.44 (8.42 (4.2 (8.36-6.91-7.14-6.90-3.18-7.85) 5.17) 4.54 (4.15 (7.2) 11.84-9.66 (6.58) 8.13 (3.79) 4.70) 6.35-11.95) 8.60 (5.79) 9.42-4.00 (8.30-4.48) 90th 7.50) 8.4) 10.73 (3.77 (4.12 (3.85) 4.08-3.87-4.77) 4.25) 4.42 (5.08) 4.24 (3.33 (5.27 (6.96-4.65 (6.96-4.63 (7.26 (3.28) 7.68 (4.56) 4.30 (7.59-8.80) 6.30) 10.29) 5.20-4.39) 5.Metals Biomonitoring Information Urinary cesium levels reflect recent exposure.18 (7.88-10.98) 5.42-6.59) 4.54 (5. 2005.08 (6.39 (5.43) 8.17) 9.S.98 (7.14) 4.65-3.10 (3.00-5.53) 3.16-5.72-5.16) 5.3 (9.20-8.15-11.03) 5.97-4..93-7.43 (3.41) 4.90 (7.13-9.56) 3. Urinary Cesium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.98) 5.07) 8.64 (8.58-5.91-6.68-11.87 (5.3) 9.S. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.29) 4.91-9.77-5.43-11. Urinary cesium levels were similar in a group of forest fire fighters and residents living near the fire area (Wolfe et al.41-7.99) 4.41 (5.46 (8. Komaromy-Hiller et al.05) 6.09) 8.47) 4.00) 6.21-3.90-8.87) 5.41) 9.73-4.16-8.95 (3.5) 9.83) 8.81 (4.96) 4.95) 10.06) 4.3 (8.83-7.45-6.99-9.05-3.24-4.89-4. population results shown in this Report (Alimonti et al.72 (4.14-4.98 (6. Minoia et al.51) 4.68) 4.91) 4.05-4. 2004).9) 10.40-5.00-10.20-4.64 (4..22-11.57) 3.34 (5.50 (6.76-6.82-4.35) 3.67) 5.56 (4.84-7.95 (5.31 (4.86 (4.99 (3.47) 6.84-7.54 (3.51 (7.19-6.03-5.30) 10.74) 3.43 (4.37-3.10-4.48) 7.93-9.74 (4. population.11 (5.84-11.7-12.87) 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 5.38 (3.02 (5.04) 5.55 (3.43 (4.67 (6.06 (3.8 (9.12) 3.75 (7.95) 4.50) 4.3) 1226 1334 1281 1238 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 3.02-4.19-3.08 (3.63 (4.46 (7.56-10.51 (3.50) 4.55) 4.44-5..82) 7.10 (5.3-15.97) 8.13-9.0) 7. population from the National Health and Nutrition Examination Survey.44 (4.9 (10.40) 7.88-4.39) 8.11 (5.55-5. Using clinically submitted specimens.71) 6.28 (4.2 (8.74-11.35 (3.09 (4.78) 4.25) Selected percentiles ( 95% confidence interval) 50th 4.66-6.94) 7.37) 4.52-5.10) 7.05-3.64) 9.27 (8.67 (5.18-6.41 (8.8) 5.08) 4.30-4.08 (5.06 (5.43 (8.08) 3. (2000) found urinary cesium levels that were slightly lower than those reported for the U.28 (5.63-6.78) 4.47) 7.95-12.20) 5.75-11.00-9.66 (5.22) 6.84-9.99-4.40) 6.85-4.04-5.14 (6.14-7.21-5.36-10.41 (4.65-4.50 (7.79-5.48-6.63-6.60-10.77 (6.63) 6.33-3.50 (5.27-4.05 (4.92 (5.22 (3.72) 4.47) 6.29-3.5) 7.54 (4.61 (7.27-6.71 (7.74) 75th 5.60 (3.91 (5.58 (6.3 (10.35 (4.15-4.53 (6. and were also roughly similar to those in this Report.31-4.24-10.12-6.42-4.60-20.20-4.96) 4.38) 10.05) 3.1) 11.79 (5.03) 6.51 (3.50) 4.26-6.36-3.17-4.44-9.33 (5.68) 3.27 (6.58 (4.35-7.96 (4.94 (5.45 (4.15) 95th 8.51 (4.07-4.78 (3.29) 4.43-6.74 (5.64-6.66 (5.04) 6.90-8.41-4.3) 11.44) 3.31 (4.6 (9.07) 8.21-4. 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.91) 5.63 (6. Two small studies of European populations reported urinary cesium levels similar to U.08-7.38-7.0 (7.6) 6.47 (7.16-8.91 (5.30 (4.03-6.2) 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 3.17 (6.09) 4.5 (9.06) 5.0) 884 682 618 568 667 723 821 1132 1074 Non-Hispanic blacks Non-Hispanic whites 206 Fourth National Report on Human Exposure to Environmental Chemicals .91) 5. Finding a measurable amount of cesium in the urine does not mean that the levels of cesium cause an adverse health effect.46-4.64) 5.00-8.18) 8.46) 6.61-3.77 (7.78 (3.75 (6.62-8.62) 5.76-9.95-6.97-5.38-12.S.7) 10.64) 4.21 (2.38 (3.9 (9.7) 10.58) 3.04-11.81 (4.8) 6.10 (3.00-4. interval) 4.51 (4.30 (3.28) 8.31-6.60) 3.49) 3. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.46-8.00-5.99-9.6 (9.01-8.83-6.50-5.33-8. 1990).13) 7.07 (5.27) 4.29-3.5) 9.14) 4.92) 3.23 (7.79) 6.8) 10.68) 6.53) 6.53 (4.70 (7.26 (4.0) Total 4.

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

24 (1.465) .22-1.502) .820 (.371 (.420) .380 (.379 (.47 (1.790 (.410 (.750 (.352 (.900-1.59 (1.310 (.47) 1.290-.580 (.450) .370-.393-.620-.640) .450-.430) .520 (.740 (.47) 1.394) .450-. Cobalt occurs naturally in airborne dust.660) .800) . 01-02.01-1.700) .550-.570-.336-.50 (1.68 (1.930) .65) 1.45 (1.04-1.32 (1.48) 1.316-.980) .75 (1.830-1.460 (.690 (.07 (.427-. hard metal (alloys of cobalt and tungsten carbide).410-.399) .430 (.770) .343 (.640) .340-.81) 1.17 (1.348-.590) .32-2.26) 1. varnishes.410) .890-1.270-.810) .398 (.07. hard metal or in combination with other elements.700) .20 (1.359 (.03-1. steel-belted radial tires.870-1.12) 1. industry is imported or obtained by recycling scrap metal that contains cobalt.460 (.294 (.920-1.03) 1.900) .452 (.327-.980-1.670 (.23-2.04-1.420) .17 (1.890-1.590 (.01 (. shiny.410-.463-.500) .32) 1.510) 1.319) .950 (.369 (.660-.370 (.870 (.28 (1.428-.21) 1.480 (.364-.610) .350) 75th .06-1. 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.29 (1.610-.410 (.581) .430 (.338-.650-.16 (1.570) .09) .790) .500 (.870 (.487) . and 0.300-.73) 1.940-1.13) 1. It is emitted into the environment from burning coal and oil and car and truck exhaust.630-.22 (1.900-1.380 (.372) .06 (. Cobalt compounds are used as catalysts in producing oil and gas.940-1.730) 1.374 (. diamond-polishing wheels.750-.270-.670 (.840) .590-.600-.380 (.470 (.09 (.28 (1.418 (. 208 Fourth National Report on Human Exposure to Environmental Chemicals . Among its many uses are manufacturing superalloys used in gas turbines in aircraft engines.08. and soil.760 (.36) 1.430-.690-.360-.390 (.460) .350-. The cobalt used in U.890) .99) 1.900) .390) .375 (.16 (1.750 (.660) . Medical uses include joint and dental prostheses and radioactive cobalt in cancer chemotherapy.515 (.710 (.540-.348-. Cobalt is used as a drying agent in paints.431) .710) .523) .560 (.410 (.800-.26) 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.570-.17 (.01-2.39) 1.370-.810-.04) 1.950-1.08-1.860 (.22) 1. blue-colored pigments.520-.270-.S.S.520-.583) .440-.03) .480-.07.01 (.450) .340) . and magnetic recording media.06 (.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 .540) 1.880 (.810) .313) .520 (.680) .50) 1.419) Selected percentiles ( 95% confidence interval) 50th . automobile airbags.820 (.320 (.16-1.16) 1.47 (1.435 (.450) .620-.680 (.850) 1.16-1.890) 95th 1.15 (1.540-.56) 1.417) . Cobalt compounds are also used in manufacturing battery electrodes.310-.390 (.461 (.04 (.520-.379 (.308-.580 (.480 (.550) 90th .410-.28-2.305-.430 (.519 (.330 (.44) 1.710) 1.05 (. population from the National Health and Nutrition Examination Survey.390-.414) .330) .520 (.404) .800-. and inks.630 (.339 (.750 (.09 (.370) .650 (.14) .16) 1.460) . 0.400-. It is also a component of porcelain enamel applied to steel bathroom fixtures.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 .370-.900) .570 (.850-1.53) 1.950 (.431) .301 (.28 (1.680) .285 (.280-.454 (.880-1.930 (.333-.740-.820 (.25-1. see Data Analysis section) for Survey years 99-00.469-.07-1.03) 1.670 (.910-1.890-1.640) .550 (. and kitchenware.26) Total .07-1.05 (.334) .380-.520) .24 (.540-.950) . 7440-48-4 General Information Cobalt is a magnetic element that occurs in nature either as a steel-gray.03 (.330-.73) 1227 1335 1281 1238 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .350 (.02-1.470) .12) 1. respectively.590-.410 (.530-.850-1.316 (.60 (1.450) .340-.52 (1.543) .26-1.390 (.670-.540-.331-.690-.530 (.355-.600) .410) .360-.650 (.416) .380-.67) 1.33-1. seawater.434 (.398) . and fertilizers.367 (.32 (1.37-1.920) 1.64) 1.610) .760) .620) .960-1.340) .680 (.490-.520) .499 (.300 (.81) 1.05) 1.92) 1.32) 1.570) .460-.333-.48) 1.350-.610 (.790-. and in synthesizing polyester and other materials. Usual human exposure is from food sources.410 (.291-.360-.670-.00) .04-1.930-1.850) .740-.340 (.600 (.580 (.520-.26-2.259-.350-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.03 (.530) .388-.377-.950-1.23) .19) .564) .373) . interval) . and 03-04 are 0. large appliances.16 (.496) .08) .17-1.Metals Cobalt CAS No.15-1.405-.373-.14-1.620-.520 (.42) 1.386) .940 (.460) .430) .424) .630 (.490-.420 (.33 (1.46 (1.

632-.829) .513 (.313-.700 (.278-.294-.689 (.634-.606 (.449) .505) .259) . 1979).04-1.857-1.49) 1.829-1.753) 1.343-.00 (.824 (.938-1.679-.523 (.990) .328) .327 (.760-1.435 (.387) .534-.275-. Lung retention of relatively insoluble cobalt compounds such as cobalt oxide may be prolonged.257-.343 (.630-.400 (.407) .259-.391) Selected percentiles ( 95% confidence interval) 50th .394) .630-.844 (.334) .349) .293 (.598 (.728 (.554 (.581) .333-.275-.60) 1.361 (.278 (.03-1.407 (.554 (.23 (1.691 (.847) .471 (.548 (.963) .861-1.00 (.495 (. A portion of cobalt retained for long periods is concentrated in the liver.786-.277-.744) 1.911-1.479-.10-1.279) .513) .757-1.638-1.04 (.29) .833-1.378-.707) .306 (.708) .54) 1.475 (. Smith et al.753-.248-.83) 1.838 (.917) .611) .243-.515 (.442-.471-.479) .522) .274-. interval) .348) .756 (.368 (. Recent inhalation exposure to soluble cobalt compounds can be monitored by measuring cobalt in urine or blood (Lison et al.457 (.239-.396) .290 (.296-.331-.488) .27) 1.550-.333-.326-.781-1.560-.543) .290 (.50) 1.362 (.455 (.938) .694) .750) .06 (..738 (. 2003).487-.537 (.895-1.457-.282-.785) .12 (.378 (.392 (.462) .683-.352) .964 (. Exposure in the workplace may come from electroplating.16 (1.750-.355) .861 (.304-.850 (.14 (.300) .952 (.386 (.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 .727 (.417) .280-.272-.10) .73) 1.821-3.333 (.27) 1.850-1.781) 95th 1..955) .301-.425-.324) .408 (.352 (.361-.673-.792 (.11-1.353 (. 1972).534 (.296) . Cobalt constitutes 4% by weight of vitamin B-12 (cobalamin).384) .313-.929) . in the feces.600-.737 (.00-1.481) 90th . Urinary Cobalt (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.396) .449-.316 (.329 (.35) .353-.434-.736-.55) .279 (.774 (.60) 1. 1994).895-1.426 (.463-..310) .372) .50) 1.16 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.503-.533 (. and to a lesser extent.271 (.428-.313-.298 (.16 (.12-1.234 (.393 (.268 (.10 (.611) .804) 1.247 (.471-.574-.644 (.647) . Workplace standards and guidelines for external air exposure to cobalt and several of its compounds have been established by OSHA and ACGIH.368) .667-1.306) 75th .467-.500-.257 (.513-.Metals fabricated from cobalt alloys (Lhotka et al.608 (.419) .. Elimination reflects a multi-compartmental model dominated by compartments with half-lives on the order of several hours to a week.289) .248-.740-1.337 (.317 (.03 (.476-. cobalt is excreted predominantly in the urine.314 (.15 (.369 (. Cobalt is absorbed by oral and pulmonary routes.36) 1.339-.378-.297) .313 (.250) .30 (1.291 (.304) .660-.29 (1. with pulmonary clearance half-lives of from one to two years (Hedge et al.595) .487-. an essential human nutrient.362) .609) . 1994.256-.417 (.28) 1.960 (.324-.402 (.879-1.378-.281) .409) .563-.433) .626-.16) .36) 1.13) 884 682 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Fourth National Report on Human Exposure to Environmental Chemicals 209 .667-1.02 (.313-.932-1.286) .444 (.438) .983-1. refining or processing alloys.542 (.00 (.599) .361-.290 (.309) ..955) .358 (.851 (.381) .215-.391 (.562) .25 (.435-.949) .508-.990-1.302-.872 (. but with a minor fraction (10-15 %) exhibiting a half-life of several years (Mosconi et al.380-.00) .25 (.792-1.848 (.404-.237-.33) .335 (.09) 1.44 (.368) .704-.582-.303-.830 (.777-.17) .975 (.259 (.388 (.728) .529 (.963-1.362-.344-.963-1.50 (1.S.342-.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 .640) .323) . 1972).376 (.733-1.15) 1.29 (1.325) Sample size 2465 2689 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 ..337) .251-.361 (.352 (.821 (.329-.33) 1.00 (. population from the National Health and Nutrition Examination Survey.523 (.593) .365) . respectively.983) . A nutritional requirement for cobalt other than that contained within dietary cobalamin has not been established.319-.388 (.452-.585) .500 (.662) .365-.328 (.10) Total . or using diamond-polishing wheels that contain cobalt metal.382-.57) 1.615) .963) .738 (.703-.669) .898 (.468) . Human studies with 60Co administered as soluble cobalt chloride have reported oral absorption ranging from approximately 1 to 25 % (Smith et al.313-.393-.19) . using hard metal cutting tools.333-.297-.363) .594) .29 (1.360) .616-.562) .328 (.905) .552 (.635 (.11-1.35) 1.591 (. Once absorbed and distributed in the body.282 (.273 (.421) .425) .346 (.561) .24) .976 (.457) .439) .700 (.429) 1.327-.29) 1.00) .723 (.301) .937 (.547 (.842) .500-.900-1.469-.461) .826-1.

html. Smaller population surveys of European adults reported urinary cobalt levels that were roughly similar U. 1988). 1985.. population (CDC. Krause et al.50(13):95-104. Cobalt compounds elicited numerous genotoxic effects in both in vitro and in vivo assays (De Boeck et al..49:56-67.43(4):299-303. Toxicol Sci 1999. Case reports have also suggested a link between occupational cobalt exposure and cardiomyopathy (Jarvis et al.. Exposure to soluble cobalt salts will produce proportionately higher urinary levels because they are absorbed better. Alexandersson R. Information about external exposure (i.. The respiratory Fourth National Report on Human Exposure to Environmental Chemicals ... Shirakawa et al.. Information about the BEI is provided here for comparison.Metals Toxic effects of cobalt have been encountered in workplace settings. Sci Total Environ 1994. 2006. A subclinical decrease in thyroid production was observed in a study of cobalt production workers (Swennen et al. Cobalt compounds appear to stimulate erythropoietin production and were formerly used in the treatment of anemia (Goldberg et al. although substantial occupational exposures have produced elevated urinary levels for many weeks. Grumbein SL. Linnainmaa and Kiilunen. Atlanta (GA). 2005. 1972). 2005. Finding a measurable amount of cobalt in the urine does not mean that the levels of cobalt cause an adverse health effect.gov/toxpro2. Centers for Disease Control and Prevention (CDC). Lauwerys and Hoet.cdc. Thomassen et al. a distinction is made between soluble and insoluble (oxides and metallic) cobalt (Christensen and Poulsen.53:395417.. 2005 [online].gov/ exposurereport/. 1989). IARC has classified cobalt metal with tungsten carbide and other soluble cobalt salts as possibly carcinogenic to humans. 2003). 1992). Cobalt-beer cardiomyopathy. 1988). Haseman JK. The ACGIH biological exposure index (BEI) for inorganic forms of cobalt (except insoluble cobalt oxides) is 15 mg/L.. 1994).. The extent to which cobalt exposure alone causes interstitial lung disease is unknown (Linna et al. 210 2006. usually in combination with tungsten carbide (Cugell et al. 4/3/08 Christensen JM. has been associated with exposure to dusts that contain cobalt. 1994.. MacDonald et al. Correlations between air exposure levels and urinary cobalt levels in hard metal fabricators are well documented (Ichikawa et al.atsdr. Arch Environ Health 1988. Inhalation toxicity and carcinogenicity studies of cobalt sulfate. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Dunstan et al. 1993). et al.e. Third National Report on Human Exposure to Environmental Chemicals. Pharmaceutical preparations of cobalt used in the past as hematinics were associated with the development of overt hypothyroidism (Kriss et al. References Alexander CS.. Bucher JR.. 1998). Persons with occupational exposure to cobalt often have urinary cobalt levels that are many times higher than those of the general population. A 1982-1992 surveillance programme on Danish pottery painters. biological levels and health effects following exposure to soluble or insoluble cobalt compounds in cobalt blue dyes. Occupational exposure to cobaltcontaining dusts has caused occupational asthma (Pisati and Zedda. 2001. “Hard metal” disease. 1999).. Small studies of patients with hip replacements using metal alloy prostheses reported increased urinary cobalt concentrations. 2001. White and Sabbioni. 1993). not to imply that the BEI is a safe level for general population exposure. Am J Med 1972.. 1955).S. Lison et al. Lisi. 2001).. 2001.. Blood and urinary concentrations as estimators of cobalt exposure. Cobalt was once added as a foaming agent to beer. Urinary measurements mainly reflect recent exposure. Poulsen OM. 1990). Roycroft JR. Biomonitoring Information Urinary levels of cobalt decline rapidly within 24 hours after exposure ceases (Alexandersson et al. Biomonitoring studies on levels of cobalt provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of cobalt than are found in the general population. Swennen et al. 1994. population results in this Report (Kristiansen et al. A clinical and pathological study of twenty-eight cases. 2003) and produced lung cancer in rats and mice after chronic inhalation (Bucher et al. Morgan WKC. Sills RC. Cobalt compounds are a recognized cause of allergic contact dermatitis (Dickel et al.S. 2003. 2003. 1997). Rubin A. 1997. Perkins DG. 1998). Available at URL: http://www.cdc.... environmental levels) and health effects is available from ATSDR at: http://www.... Daniel et al. Cugell DW. Iavicoli et al. an interstitial lung disorder with findings that range from alveolitis to pulmonary fibrosis. with mean levels that were about 15-20 times higher than in the general U. For workers exposed to cobalt in the air. An industry-wide study of hard metal workers in France observed an increased mortality from lung cancer (Moulin et al. Hailey JR. and this caused outbreaks of cardiomyopathy among heavy drinkers in the mid-1960’s (Alexander et al...

Occup Environ Med 2001. Mosconi G. Fourth National Report on Human Exposure to Environmental Chemicals 211 . Uitti J. Schaller KH. Roto P. Szekeres T.216:253-270. Zedda S. Cobalt and antimony: genotoxicity and carcinogenicity. Linnainmaa M. Pradhan C. Sci Total Environ 1997.148:241-248. Lauwerys RB. Robinson C. Long-term clearance of inhaled 60Co. Lasfargues G. Goto S. Lauwerys R. Exposure assessment in the hard metal manufacturing industry with special regard to tungsten and its compounds. Zhuber K.242:1412-1415. Jarvis JQ. Shirakawa T. Lhotka C. Oksa P. Occup Environ Med 1994. Cobalt excretion in urine: results of a study on workers producing diamond grinding tools and on a control group. Kusaka Y.88(4):443448. Br J Ind Med 1993. Bacis M.204:147-160. McMinn DJ. Ichikawa Y. Co-sensitivity between cobalt and other transition metals. Sabbioni E. White MA. Molders J.95:29-37.22:359367. J Bone Joint Surg Br 2005. Thomassen H. Outcome of occupational asthma due to cobalt hypersensitivity. et al. J Occup Med 1992. Metal-on-metal versus polyethylene in hip arthroplasty: a randomized clinical trial. Cobalt cardiomyopathy.44:124-132. Respiratory health of cobalt production workers. Swennen B. Lison D. Lauwerys R. Buchet JP. Fujimura N. Gross RT. 3rd ed. Cleland D.150. Vitali MT. Wild P. Sci Total Environ 1998. et al. a study of 13 elements in blood and urine of a United Kingdom population. et al. Schank M. Occupational asthma from cobalt sensitivity in workers exposed to hard metal dust. Biological monitoring of workers exposed to cobalt metal. Kriss JP. Thabe H. Unwin P. Dunning SP. Kuska Y.” Contact Dermatitis 2001. J Rheumatol 2001. Smith T. Sci Total Environ 1994.20(1):25-31. J Orthop Res 2003. Edmonds CJ.87(5):628-631. Zobelein P. Swennen B.48:172-173. Clin Orthop Relat Res 2003. Metal ion levels after metal-on-metal proximal femoral replacements: a 30-year follow-up. Hammon E. Heki S. Kristiansen J. Sanghrajka AP. Laippala P. Blunn G. Hypothyroidism and thyroid hyperplasia in patients treated with cobalt JAMA 1955.(1-3):133-139. Kirsch-Volders M. and hard metal dust. Dunstan E. cobalt salts. Alessandrelli M. Sabbioni E.150(1-3):167-171. Hedge AG. Palmroos P. Peltier A. Industrial Chemical Exposure: Guidelines for Biological Monitoring. et al. Bourne RB. Lison D. Goto S. et al. Iversen BS. 2001. Linna A. salt. Angerer J. Contact Dermatitis 2003. Christensen JM. Goldberg MA.406:282-296. Radulescu M.69(3):193-200. Meyer zum Buschenfelde K-H. et al. Weber A. Kraus T. 1985. Cresti R. Dickel H.50(9):835-842. Moulin JJ. Hoet P. Science 1988.34:620-626. Urinary cobalt as a measure of exposure in the wet sharpening of hard metal and satellite blades. Tilley S. Salama A.58(10):631-634. Daniel J. Regulation of the erythropoietin gene: evidence that the oxygen sensor is a heme protein. Zweymuller K.36:732-734. Meier R. Buchet JP. Toxic trace element reference levels in blood and urine: influence of gender and lifestyle factors. Salvatori S. De Boeck M. Int Arch Occup Environ Health. Romazini S. Falcone G.533:135-152. Barnaby CF. Hoher T. Schramel P. A report of two cases from mineral assay laboratories and a review of the literature. J Trace Elem Med Biol 2006. Stanescu D.51(7):447450. Int Arch Occup Environ Health 1997. Four-year study of cobalt and chromium blood levels in patients managed with two different metal-on-metal total hip replacements.45:246-247. Kiilunen M. Ghat IS. Cannon SR.55(4):269-276. Sci Total Environ 1994. The effect of the diameter of metal-on-metal bearings on systemic exposure to cobalt and chromium. Biological monitoring of cobalt exposure based on cobalt concentrations in blood and urine. Cobalt-specific T lymphocytes in synovial tissue after an allergic reaction to cobalt alloy joint prosthesis. Health Phys 1979. Bunn HF. Bozec C. Mutat Res 2003.Metals effects of cobalt. Occupationallyinduced “isolated cobalt sensitization. X.150:177-183. Leghissa P. McCalden RW. Ziaee H. Iavicoli I. J Bone Joint Surg Br 2006. Health Phys 1972. Arch Intern Med 1990. The release of metals from metal-onmetal surface arthroplasty of the hip. Weyher I. Carnes WH. oxides. Pisati G. Lison D. Lung cancer risk in hard-metal workers. Sabbioni E.21(2):189-195. Lisi P. Thakker DM. and cobalt metals. Kato M. Diepgen TL.28(5):1121-1128. Epidemiological survey of workers exposed to cobalt oxides. Am J Epidemiol 1998. Steffan I. Absorption and retention of cobalt in man by whole-body counting.157:117121. DeSantis V. Am J Ind Med 2003. Rorabeck CH. Boca Raton (FL): Lewis Publishers. Chess DG. Trace element reference values in tissues from inhabitants of the European Union. HoffmannB. MacDonald SJ. Chest 1989.

00 (1.14-1.39) 1. 0.00) 3.89) 1. 7439-92-1 General Information Elemental lead is a soft.40-1. lead was added to gasoline and residential paints and used in soldering the seams of food cans.40-2.00-1.00 (4.20) .68-1.90-4.00 (1. and 0.65 (1.20-3.60 (1. leaded glass.20) 4.96-2.50-2.00) 2.40) 3.50 (4.80-3.30 (2.50-5.75-2.45 (1.20 (3.40-2.50-5.20 (1. the main source of lead exposure for the general U.10-1.12-1.Metals Lead CAS No.80 (4.30) 2.52 (1.40 (1.70) 2. 212 Fourth National Report on Human Exposure to Environmental Chemicals .30 (1.70) 1.20-2.00) 1.43-1.40-5.80-4. In the past.22 (1.10-2.75-1.30) 5.10-8.50 (1.60) 1.70) 3.70-1.62) 1.70-6.20 (3. malleable.90-2.00 (4.10-3.60) 5.10 (3.49-1.20) 3.00-1.51) 1.90) 1.39-1.50-1.25 (1. brass.90-2.50) Sample size 7970 8945 8373 Age group 1-5 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 2.40-1. such as lead phosphate and tetraethyl lead.62 (1.60 (3.90 (3.50-2.60) 1.20 (3.50) 1.30-2.70 (1.36-1.30 (2.00) 2.90-4.50) 1.70 (5. ceramic glazes.45-1.3.55-1.90-4.50) 75th 2.30) 1.40-4.60) 3.48) 1.50) 2.80) 3.10-2.66 (1.80-2. respectively.50 (2.30-1.69) 1.70-1.70 (2.900 (.70 (3.30-1.55-1.83 (1. Before the 1980’s.93-2.60 (2.40 (4.80 (1.60 (2.80) 1.70 (1.90 (1.40-1.40-3.10-6.62-1.30) 2.10-2.S.900 (.50-4.90-6.60) 4.56 (1.00) 1.87 (1.30-1. solders.986) .50 (3.70 (1.50 (2.80) 1.50) 5. Lead has a variety of uses in manufacturing: storage batteries.60) 5.899-.60) 2.78 (1.878-1.50 (2. Aerosolized lead is either inhaled or ingested after it is deposited on surfaces and food crops. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. Since lead has been eliminated from gasoline.20) 2.10) 5.60) 2.25 (1.30-2. and 03-04 are 0.80 (5.43 (1.90 (3.S.30 (2.70 (1.90) 5.80 (4.60 (2.80) 1. population was aerosolized lead emitted from combustion engines that used leaded gasoline.20) 5.90-4.60) 1.90) 3.00-2.10-1.80 (3.10) 3.90) 2.70) 4.80-4.50-1.20) 4.50-2.60-1.30 (2.71-1.43) 1.00) 2.10) 1.34-1.50) 4.40) 2.80-3.37-1.10) 3.60-2.60 (1.80 (1.60 (1.80-3.20-3.60 (1.40 (2.30 (1.10) 2.09) 1.50-1.32-1.30 (4.80 (5.00) 2.40-6. Lead was used in plumbing for centuries and may still be present.30-1.70-1.10-2.75 (1.60 (3.25) 1.80 (2.70) 1.69 (1.60 (4.20 (1.70) 4.60 (1.28.40-1.60 (2. dense.10) 4.90) 3.70 (2.30 (2. metal alloys (e.95) 1.00 (6.20 (4.10) 3.10) 1.20 (1.40) 1.70) 3.50-6.72) Selected percentiles ( 95% confidence interval) 50th 1.60) 4.30-2.30-4.40 (1.70) 4.20-3.50-3.66) 1.70-3.00-4.50) 3.40 (2.90) 2.80 (1.90 (3.10-4.90 (1.60 (3.60) 4.90 (3.00) 6.60) 2.30-1.91) 1.800-1.80) 3913 4339 4132 4057 4606 4241 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.20-6.00-5.20 (2.20-1.90) 2.30-2. ammunition. and for radiation shielding.77 (1.10-1.00) 1.80) 2.80-5.50 (1.52-1.60-6. 01-02.00-4.70) 4.32-1.70) 1.70-5.20) 3. plastics.20 (3.90-2.37 (1.60-2.30-6.86) 1.40 (1.81) 1.17) .40 (3.51 (1.10-2.40-1.30 (4.00) .30-1.60) 3.10-3. bronze).75) 1.60) 2.80) 1.40) 2.60-4.60-1.942 (.40) 1.30) 2.60) 1.60-3.00) 5.31) 1.40-3.10-6.80 (2.00) 4.52-1.50-1.10-3.20 (3.g.02) 1.50-3.90) 2.20 (1.87) 1.20-2.60 (3.80 (1.40) 4. Elemental lead can be combined with other elements to form inorganic and organic compounds.10-3.60) 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 2.20 (3.20) 3.01 (1.60) 3.80) 2.10 (2.30 (4.19 (1.20 (1.90-3.40-2.40) 2.30) 95th 5.00) 3.23 (1.10 (4.60) 4.69) 1.00 (5.50 (1.55 (1.30 (1. blue-gray metal that occurs naturally in soils and rocks.80) 2.30 (1.50) 7.10) 2.80) 1.90 (2.04-1.60 (2.90) 2.46 (1.69 (1.80 (2.10) 1.90 (2.60) 2.10 (1.30) 2742 2268 2085 1842 2219 2293 2716 3806 3478 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.40) 1.60-1.50-4.20-3.30 (3.43) 1.40 (5.60) 1.10 (2.900-1.14-1.00-6.80 (1.00) 1.70-2.00) 1.90) 1.60-1.70-4.60-4.80 (1.50) 1.40) 2.60) 3.70) 3. see Data Analysis section) for Survey years 99-00.00-4.70-2.70 (2.40-1.50-1.50 (1. antique-molded or cast ornaments.50) 1.50 (2.80-3.30 (2.60 (1.10 (2.50 (2.20-1.20 (3.10-4.50) 2.3.80) 2.40) Total 1.40-3.43 (1.00 (3.90-2.40) 5.53) 1.60 (1.20) 90th 3. adult lead exposures tend to be limited to Blood Lead Geometric mean and selected percentiles of blood concentrations (in µg/dL) for the U.60 (2. interval) 1. Lead is most often mined from ores or recycled from scrap metal or batteries.20 (2.90) 1.40 (1.30 (2.50-2.80-4.14-1.40-6.90 (4.50) 5.20) 3.946 (.20-4.36-1.10 (1.10-2.70) 1.50 (4.90 (3.20) 1.70) 1.10 (1.37 (1. population from the National Health and Nutrition Examination Survey.00) 4.30-5.50 (3.00 (2.50) 4.36) 1.70-2.70 (3.

70-2.78-2.800 (.700-.710-.10-3.636 (.40-1.33-2.40) 2.900) .20 (1.931) .59) 1.72) 1.900 (.20) 1.60-3.680-.710-1.80) 1.60 (1.30) 1.10 (.44-2.579-.600 (.10 (1.20-2.52-1.70) 1.80) 2.10 (1.80) 2.700-.35 (.753 (.70-3.731 (.900 (.14 (1.923 (.960 (.S.40 (1.700 (.70) 1. lead-contaminated dust in indoor firing ranges.60 (1.785) . population from the National Health and Nutrition Examination Survey.40) 2.20) .60-1.810-1. dust.06) .75) 3. CDC.22) 1.600) .80 (2. 2000).40-5. bullet fragments retained in human tissue.50 (2.752 (.40) 2.64) 2.500-.10-5.75) 4.86-2.815 (.80-3..29 (2.90-2.30-1.70) 3.78-2. Approximately half of the absorbed lead may be incorporated into bone.700-.20 (1.535-.00 (1.20 (1.60-2.20 (1.90-3.23) . and 03-04 are 0.955-1.560-.70 (2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. Less common sources of incidental or unique lead exposure are numerous: lead-glazed ceramic pottery.680) .10-1.641-.690) 75th 1.800 (. stained glass framing.30) 2.840 (.10) .50) 1. 01-02.40 (2.900) .30-1.60 (2.30) 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 1.40) 1.40-1.600-. However.833-1.30) 1.700 (.800 (.90) 2.556-. Children may also be exposed to lead brought into the home on the work clothes of adults whose work involves lead.730 (.800) .651) . lead-containing folk remedies and cosmetics.808 (.589-.848 (.20-1.29) 2.701) .70) 1.20-1.1.10-1.50 (1.50) 2.30-2.90 (2.800) . 2007.30) 2.33.30 (2.50-1.30) .573 (.Metals occupational (e.680-.20-1.80) 3.90-2.00) .00-2.605) .800) .960-1.52-1.40) 2.11 (1.900) .70 (1.30) 1.628) 1.20 (2.50) 3.30 (3.14-1.600-.09) 1.00-2. Small amounts of environmental lead also may result from burning fossil fuels (ATSDR. absorbed lead is bound to erythrocytes and then is distributed initially to multiple soft tissues and eventually into bone.620) 1.30 (1. pewter utensils and drinking vessels.52 (1.40) 3.00 (2.766 (.50 (2.90 (1.10) .820-1.03 (1.49 (1.60) 2.20) 1.600-.50) 2. battery and radiator manufacturing) and recreational sources.21 (2.800-1.20 (1.10) 2.590 (.640 (.10 (1.90) 2.940 (.553-.00 (1.90 (2.90-2.600-.g.970-1.900-1.82 (1.40 (2.40-3.40) 1.50-2.60-2.540-.700 (.695 (.00) 2.50-2.50) 1.745-. or after soluble lead compounds are ingested.90 (1.31 (1.700) .78-2.70 (2.30-3.51) 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.857) .40-2.773) . Fourth National Report on Human Exposure to Environmental Chemicals 213 .11) 2.915-1.610 (.04-2.90-3.50-2.718) .900) .73 (1.579-.40 (1.795 (.10-1.50 (2.00-1.19 (1.800-.20 (1.850 (.10 (.40) 1.90 (1.800 (.700 (.91) 2.580-.700) 1.40 (1.828) Selected percentiles ( 95% confidence interval) 50th .20) .833 (.20) .941) .540 (.60 (1.80) 2.600) .59-2.960-1. and 0.625-.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 1.800) .24-1.32 (1.749) .900) .738) .80) 1.07 (.990) 1.674) 1.90) 2.506-.70) 2.10 (.07-1.33 (2.40 (1.591 (.30-5.10 (1.900 (.13-3.10-3.80-2.30) 2.700-1.990) 2.18-1.20 (2.00) .570-.70 (2.40-1.80) 3.50-3.82 (2.66 (2.526-. older plumbing systems with leaded pipes or lead soldered connections.650) 1.02 (.616) .04 (.40 (2.90) 1.30) 1.600 (.80-2.691-.90-4.558 (.20 (2.00) .97) 4.600-. 0.23-4.31-3.900-1.910-.00 (.800) .20) . and contact with soil.595-.00) 1.862) .00-2.80 (1.1.80) 2.661-.900-1.625 (.00) .822-1.50) 1.00) 2.700-.13) .688 (.62-4.00-1..900) .86) 95th 2.40-1.00-1. see Data Analysis section) for Survey years 99-00.27 (1.41) 2.986) .572-.630 (.10) 1.60-3.480-. In the blood.900-1.708-.20) 1.80) 2.12) 90th 2.10-1. which is the site of approximately Urinary Lead Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.30-1. the primary source of exposure in children is from deteriorated lead-based paint and the resulting dust and soil contamination (Manton et al.800-1.564 (.800-.642 (.10-3.604 (.27) 1.04) 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 .80 (1.700-.00 (1.30-1. Lead is absorbed into the body after fine lead particulates or fumes are inhaled. Absorption of ingested lead can be as much as five times greater in children than adults and even greater when intakes of dietary minerals are deficient.04 (.920 (.10-1.40) 1.90-2.700 (.10) 2.70) 3.620 (. 1991). respectively.70 (2.00 (1.14 (1.935) 1.40 (1.80) 1.20 (3.62) Total .17 (1. or water contaminated by mining or smelting operations.86 (1. interval) .640-.89) 2.818) .02) 1.790 (.613) .30) 1.671-.637-.659 (.660) .90 (2.700 (.04) .20-2. imported children’s trinkets and toys.729-.03-2.60 (1. lead-based painted surfaces undergoing renovation or demolition.40 (2.40) 1.86) 1.757-.50 (1.920 (.677 (.66 (2.

725) .667) .971 (.790) .61) 1.990 (.800-.46 (2. Lead can cross the placenta and enter the developing fetal brain.693 (.677 (.841-1.621 (.679) 1. 2003.04-3.10 (.94-2.608 (.461) .701) .55 (1.946-1.742) Selected percentiles ( 95% confidence interval) 50th .07 (.06) .828-1.535) . Lead is cleared from the blood and soft tissues with a half-life of 1 to 2 months and more slowly from the skeleton.702-.655) 75th 1.962 (. with a half-life of years to decades.710) .938-1.639) .53) 1.55 (1. hair.70 (1.587-.559-.64) 95th 2.571-.45 (1.78-4.933-1.571-.635 (.03) 2.08-2.49 (1.469 (. and through binding to ion channels and regulatory proteins.68 (1.508) .561-.11 (1.721 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.71 (1.92) 2.22) .734) .85 (1. 1993.667-.673) .920-1.40-1.36-2.617-.03) 1. 1995).510-. 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.48 (1.56-2.51) 1.22) 1. and nails (Leggett. In 1991.38 (2.17 (.12-1.933) .603-.43 (1.742) .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 .56 (1.618 (.72-2.89-5.681-.75-2.31 (1.992-1.04) 2.78 (2.601-.07-1.09) 1.604-.654) . BLLs and associated toxic effects differ in children and adults.725) .900 (.17-1.03 (.793-1.63) 1.698) .652 (.39-1.10) 1.46 (1.988 (. through the inhibition of certain enzymes. kidney injury.28) 2.98 (1.708 (.61) 3.61) 1.87) 1.88-2.917-1. Additional mechanisms include generating reactive oxygen species and altering gene expression (ATSDR.22) 1.47 (2.781-1.66) 2.623 (.69 (1.432 (.404-.01) .11-1.09-1.639 (.632 (.679-. based on prospective population studies.28-1.648 (.926 (.720 (.29 (1.746) .722 (.62) 2.59-3.702) .82) 1.65-2.03) 2.707 (.31 (2.638 (.96 (1.61) 1.718) 1.85-2.88) 2.02) 1.758) .83) 1.03) 1.812-1.72-2.97 (1.67-4. with lesser amounts eliminated via the feces.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 .667-.62-3.05 (.79 (1.09-1.50-2.33-1.83 (2.810 (.44) 1.28) .24 (1. Staessen et al.64) 2.18) 2.605-.07) .15) 1.914 (.992-1.14 (1.603 (.97) 1.43 (2.796-1.623 (.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 .19) 1.659-.0) 3.34-1.593 (.633 (.828) .380-.914-1.730) 1.541-. 2007).765) .85-2.655) .00 (..676) .644) .56) 3.375 (.41-1.592-.763) .657) 1.918 (.03) .753) .774 (.755 (.688) .701 (.43) 1.870 (.709 (.853-1.696 (.981-1.625 (.677) .588-.686) .11 (1..722 (.06) 1. encephalopathy.41 (1.71-2.662) 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 1.914 (.862-.00 (1.88 (1.06 (1.400) .11) 1.594-.608-.20) .569 (.938 (.56-3. 2004.64-2.668-.529-.718) .77) 2.603-.63) 4.51 (1.670) 1.03) .47 (1.50-1.720 (.11) .37-1. O’Flaherty. Schwartz.882-1.404 (.85) 1.03) 90th 1.19-5.607-.428) .739) .342-.703) .957-1.43-1.18) 1.655-.677-.50) 1.88) 2.38 (2.615 (. CDC. and iron.579-.03 (.Metals 90% of the body lead burden in most adults.31) 1.31 (1.551-.698) . seizures. 1991.11 (.03 (.73-2.64 (1.98-2.41) .609 (.15-3.671 (. Large amounts of lead in the body can cause anemia.940 (. Equilibrated blood lead levels (BLLs) after chronic intake are associated with certain toxic effects.658 (.52) 1.682) .963-1.65 (1.S.645-.50-2.408-.588-.702) .66 (1.89-2.641 (. interval) .683-.08) .436) .94 (1.615 (.918-1.35) 2.644 (.05-1.52 (1. 1995.09-1.606-.460-.97-18.02-1.05-1.893) .25-1. The skeleton acts as a storage depot.20) .975-1.38 (2.27 (1.05 (1.06 (.73) 2.00 (1.72) .61) 1.44 (1.14) 1.594-.08) .700-.15) 1. and paralysis.492-.898) .26) Total .33) 1. 1996).20-3.22-2.876-1.50-2.10 (1.37-1.586-.00 (1. and approximately 40 to 70% of lead in blood comes from the skeleton in environmentally exposed adults (Smith et al.98) 2.18) 1.11 (.712 (.887 (. Nash et al.977) 1.18) .22-1.47) 1.03-2.612-.50 (1.997-1.97) 1.383-.79) 1. For instance.681-.404 (.74 (1.75 (2.58) 1.62-1.62-2.53-1.838) .31) 1.622 (. 1993). zinc.44 (1.15-2.23 (1.25-1.496 (.86 (1.79) 2. Approximately 70% of lead excretion occurs via the urine.988-1.00) .33) 2.645-.43) 2.979 (.649 (.639 (.583-. BLLs near 10 µg/dL can affect blood pressure in adults and neurodevelopment in children (Bellinger. The toxic effects of lead result from its interference with the physiologic actions of calcium.15-2.26) 2.01 (..851) . abdominal pain. population from the National Health and Nutrition Examination Survey.33 (1.88) 1.18 (1.639 (.731-.66 (1.03 (1. scant amounts are lost through sweat.

cdc. 1999).. For example.75 µg/dL in U. 1996. the geometric mean BLL was 3. adults in the 19992000 NHANES sample (Apostoli et al. 2003. 1999). 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. seizures. including minority race or ethnicity. the national prevalence rate for adults with BLLs 25 mg/dL or higher was 7. reduce sperm count.. Temporal declines in children’s BLLs have been found in other developed countries (Wilhelm et al. A general population survey of adults Germany in 1998 reported a geometric mean blood lead concentration of 3... Biomonitoring Information Blood lead measurement is the preferred method of evaluating lead exposure and its human health effects..Metals µg/dL or higher as the level of concern in children. The U. Surveillance data reported by U. the prevalence rate has declined annually since 1994 (CDC. 2007). and low family income (CDC.6%) were lower than those from NHANES 1991-1994. though there is greater individual variation in urine lead than in blood and greater potential for contamination.. Staessen et al. 1984.gov/toxpro2.. BLLs reflect both recent intake and equilibration with stored lead in other tissues. adult residents.. 2006). 1995. More recently. lead in women may be associated with hypertension during pregnancy..6% in NHANES 1988-1991 to 1.3 million children tested had BLLs of 10 mg/dL or higher (http://www. At low environmental exposures. A general population survey of adults in Italy tested in 2000 found BLLs slightly more than double those reported for U. Information about external exposure (i. 2006).. 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. IARC considers inorganic lead compounds probable human carcinogens. Pirkle et al. Muntner et al. usually with BLLs greater than 40 mg/dL. 2001). 2005b).. may alter sperm morphology. 1998). and organic lead compounds not classifiable with respect to human carcinogenicity.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.g. 2005b. Borja-Aburto et al. with overt encephalopathy. Bellinger 2005.gov/nceh/lead/surv/database/State_ Confirmed_byYear_1997_to_2006. Jones et al (2009) showed that the prevalence of BLLs of 10 µg/dL or greater decreased from 8.xls).. subtle or nonspecific neurocognitive effects have been reported at BLLs as low as 20-30 µg/dL (Mantere et al. which is an 84% decline. 1996. Recent studies have suggested that neurodevelopmental effects may occur at BLLs lower than 10 µg/dL (Canfield et al. 1991. Urine levels may reflect recently absorbed lead. Overall.. 1995) and associations between increased bone lead concentrations and blood pressure (Hu et al.07 µg/dL (Becker et al.atsdr. 2005a).4% of children had BLLs of 10µg/dL or higher (CDC. 2000). and peripheral neuropathy generally occurring at much higher levels (e. residing in housing built before the 1950’s. Workplace standards and guidelines for lead exposure and monitoring have been established by OSHA and ACGIH. High dose occupational lead exposure. The Adult Blood Lead Epidemiology and Surveillance program has tracked BLLs reported by states for mostly for occupational but also for non-occupational exposure in U. adults in the 1999-2000 NHANES sample. environmental levels) and health effects is available from ATSDR at: http://www. premature delivery. Fourth National Report on Human Exposure to Environmental Chemicals 215 . In occupationally exposed adults. 2002a).html.5 per 100. A decrease in BLLs is evident also in adult NHANES results reported over past decades (CDC. when the geometric mean BLL was 2. Many animal studies have established the multiple neurotoxic effects of lead (ATSDR. 1994).. Korrick et al. particularly in the skeleton. CDC. Data submitted through state public health programs from 2006 showed that 1.0 µg/dL in females (Soldin et al. approximately 11. and decrease fertility (Alexander et al.. both the geometric mean (1. Schwartz et al.S.S. NTP considers lead and its compounds reasonably anticipated to be human carcinogens. 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... 2009). urban residence.S.000 adults.cdc. BLLs greater than 10 µg/dL continue to be more prevalent among children with known risk factors.21% of approximately 3. almost double the geometric mean of 1.9 µg/dL) and percentage of children with BLLs greater than 10 µg/dL (1. Telisman et al.. Both drinking water and ambient air standards for lead have been established by the U. Schwartz. 2002). and spontaneous abortion (Baghurst et al. 2000). EPA.S. Low level environmental lead exposure may be associated with small decrements in renal function (Kim et al.e. Lanphear et al.4% in NHANES 1999-2004. 1987. Payton et al... Jones et al. 2003). 2003. respectively..2 µg/dL in males and 3.. adult population has similar or slightly lower BLLs than adults in other developed nations (CDC. higher than 100-200 µg/dL).S. In NHANES 1999-2002 in children 1-5 years old.S. 1996. However.. 2002. 2003.7 µg/dL and 4.

Ronchi L. 4/14/09 Centers for Disease Control and Prevention (CDC). Toxicological profile for lead. Lanphear BP.htm. Bellinger D. Rotnitzky A.89:330-335. Becker K. Checkoway H. doi:10. Available from URL: http://www. The Port Pirie cohort study: lead effects on pregnancy outcome and early childhood development. Bellinger D. Int J Hyg Environ Health 2002. 4/14/09 Centers for Disease Control and Prevention (CDC). Sparrow D. Farias P. Kim R.205:297-308. Preventing Lead Poisoning in Young Children. JAMA 1996. Ganzi A.cdc. JAMA 1996. Angle CR. 1999-2002. Atlanta. Wigg NR.htm. IARC Monogr Eval Carcinog Risks Hum 2006. Robertson EF. N Engl J Med 2003. Leggett RW.8(3):395-401. 2005b.275:1177-1181.115:521-529. Semen quality of men employed at a lead smelter. Centers for Disease Control and Prevention (CDC).cdc. Seiwert M. Atlanta (GA). Blood lead and chronic kidney disease in the general United States population: 216 Fourth National Report on Human Exposure to Environmental Chemicals . Third National Report on Human Exposure to Environmental Chemicals.287:1-11. Intellectual impairment in children with blood lead concentrations below 10 µg/dL. 2003-2004.82:60-80. Schulz C. van Netten C. Hernberg S. Available at URL: http://www. Inorganic and Organic Lead Compounds. Stanek KL.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. Speizer FE.87:1-471. Sci Total Environ 2002.cdc. gov/mmwr/preview/mmwrhtml/mm5420a5. 4/14/09 Centers for Disease Control and Prevention (CDC). et al. Jusko TA. Kaufman JD. Hertz-Picciotto I. Pediatrics 2004. Adult blood lead epidemiology and surveillance—United States.26:359-371. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans.123:e376-e385. Hu H.55(32):876-879.atsdr. Baj A. Age-specific kinetic model of lead metal in humans. Neurotoxicol 1987. Ewers TG. Vupputyuri S. The relationship of bone and blood lead to hypertension. Reese YR. Roberts RR. Cory-Slechta DA. Hänninen H. Environ Res 2000. Recommendations from the Advisory Committee on Childhood Lead Poisoning Prevention. Scand J Work Environ Health 1984. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Korrick S.275(15):1171-1176. Mantere P. Jacobson SW. Payton M. Manton WI. Sparrow D. Krause C.1542/peds:2007-3608. Korrick SA. Cognitive deficits with blood lead concentrations < 10 µg/dL in US children and adolescents. Blood lead reference values: the results of an Italian polycentric study. Wager C. Aug 2007 [online]. Neri A.htm.113(4):1016-1022. Hu H. Coresh J. Aro A.cdc. A prospective follow-up study on psychological effects in workers exposed to low levels of lead. Available at URL: http://www.348:15171526.html. Bavazzano P. et al. Acquisition and retention of lead by young children. Am J Epidemiol 1999. Vimpani FB. References Agency for Toxic Substances and Disease Registry (ATSDR). Cox C. Brody DJ. Caldwell KL. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Pirkle JL. Luukkonen R. et al. Blood lead levels measured prospectively and risk of spontaneous abortion. Lead.htm. Pediatrics 2009. Hu H. et al. Rios C.gov/nceh/lead/publications/ books/plpyc/contents. Canfield RL.cdc.gov/toxprofiles/tp13. Am J Public Health 1999. 2005. Birth Defects Research (Part A). Auinger P. Baghurst PA.gov/mmwr/preview/mmwrhtml/ mm5532a2. Public Health Rep 2000.gov/nceh/lead/ CaseManagement/caseManage_main. Available at URL: http://www. Blood lead levels—United States. Dietrich K. Trends in blood lead levels and blood lead testing among US children aged 1 to 5 yeas. et al. MMWR Morb Mortal Wkly Rep 2005a. 4/14/09 Alexander BH. Ga.54(20):513-516. Atlanta (GA). Neurodevelopmental effects of postnatal lead exposure at very low levels. Lead and hypertension in a sample of middle-aged women. Rojas LM. Weiss ST. Hunter DJ. Available at URL: http://www. 1991 [online]. Cox C. Muntner P. Weiss ST. A longitudinal study of low-level lead exposure and impairment of renal function: the Normative Aging Study. Meyer PA.150(6):590-597. Managing Elevated Blood Lead Levels Among Young Children. Rotnitzky A. Lepom P.101(7):598-616. MMWR Morb Mortal Wkly Rep 2006. Jacobson JL. Kaus S. Apostoli P. 2002 [online]. CDC.53:411-416. Muller CH. Lanphear BP. Teratogen update: lead and pregnancy. Environ Health Perspect 1993. 4/14/09 Centers for Disease Control and Prevention (CDC).73:409-420. 1988-2004. Occup Environ Med 1996. Jones RL. Blanco J.10:43-50. Neurotoxicol Teratol 2004. Homa DM. McMichael AJ. Henderson CR. Batuman V. Borja-Aburto VH. Chiodo LM. Kuehnemann TJ.

Hanak B. and tibia lead with neurobehavioral test scores in South Korean lead workers. Lee GS. Weiss ST. Soldin SJ. Roels H. Brody DJ. Lead. Amery A. Cvitkovic P. and hypertension in perimenopausal and postmenopausal women. Payton M. Smith DR.9:303-327.S. Gunter EW. O’Flaherty EJ. Gavella M.289(12):1523-1531. Pizent A. 50:31-37. Sparrow D. cadmium. Osterloh JD. Association of blood lead.Metals results from NHANES III. population to lead: 1991-1994. Schwenk M. Revised and new reference values for arsenic. Blood lead concentrations in children: new ranges. Wilhelm M. Sherwin R. blood pressure and cardiovascular disease in men. Use of endogenous. zinc. Schulz D. Telisman S. Kinetics of lead disposition in humans. Am J Epidemiol 1994. Lustberg M. IV. Staessen JA. Magder L. et al. and mercury in blood or urine of children: basis for validation of human biomonitoring data in environmental medicine. stable lead isotopes to determine release of lead from the skeleton. Pirkle JL. Schwartz J. Schwartz BS. and copper in men. Jurasovic J.327:109-113. Toxicol Appl Pharmacol 1993.104(1):60-66. Soldin OP. Hickman T.209:301305. Rubin R. Lee SS. blood pressure. Blood lead. Lee BK.118:16-29. et al.108(1):45-53. Am J Epidemiol 2001.140:821-829.63:1044-1050. Low-level lead exposure and renal function in the Normative Aging Study. Lauwerys RR. Kaufmann RB. Fourth National Report on Human Exposure to Environmental Chemicals 217 . Hwang KY. Exposure of the U. Environ Health Perspect 1998. Nash D. Semen quality and reproductive endocrine function in relation to biomarkers of lead. Clin Chim Acta 2003.153(5):453464. Kaufmann R. J Hum Hypertens 1995. cadmium. Paschal DC. Environ Health Perspect 2000. Rocic B. lead. Flegal AR. dimercaptosuccinic acidchelatable lead. Physiologically based models for bone-seeking elements. Arch Environ Health 1995. Int J Hyg Environ Health 2006. JAMA 2003. Environ Health Perspect 1996. Stewar WF. Low-level lead exposure and blood pressure.106:745-750. Hu H. Kidney Int 2003.

00) .490 (. mercuric chloride).900 (. an organic form of mercury. elemental mercury is used in rituals practiced in some Latin American and Caribbean communities. phenylmercuric acetate) or topical antiseptics (e.00) 3. Kingman et al..703-.80 (1.20-4.40-1. have often required public health intervention (Zeitz et al.90 (1.g.40-1.600) 1.40 (3.50-2.70 (1.655-. and is distributed to most tissues. The kinetics of the different forms of mercury vary considerably.50) 5. Atmospheric elemental mercury can be deposited on land and water. with the highest concentrations occurring in the kidneys (Barregard et al.797 (. The ingestion of methyl mercury.. Inhalation of elemental mercury volatilized from dental amalgam is a major source of mercury exposure in the general population (Halbach.00) 1.776 (.574) .753-1.20) 2.30 (2.00 (.20-4.30-4.60) 1. Inorganic mercury compounds such as mercuric oxide are used in producing batteries and pigments and in synthesizing many organic chemicals.700 (. to form inorganic mercury compounds or salts.979 (.60-6. constitutes the main source of dietary mercury exposure in the general population.50-1.500-. population from the National Health and Nutrition Examination Survey. silver-white liquid (quicksilver) obtained predominantly from the refining of mercuric sulfide in cinnabar ore. 1980.886) .30) 3.70 (4.418-.60-6.00 (.80 (1. sulfur.90 (4.S. electrical lamps.80) 4. may contain inorganic mercury.500 (.400-.g.90 (1.30) 5.300 (.g.70) 911 856 2081 4525 03-04 03-04 . 1993).30 (1. Some cosmetic skin creams from countries other than the U. 2007). Other major uses include electrical equipment (e.672) .00 (.40) 1.860-1. which create an episodic potential for volatization and inhalation of mercury vapor.10) .919) .900) 1.40-2.814 (.02) .60) 2085 2293 3478 Limit of detection (LOD.00 (2.500 (.700-.80) 1.30) 3.563 (.Metals Mercury CAS No.90) 95th 4. 1999 .30-2. see Data Analysis section) for Survey year 03-04 is 0. synthetic organomercury compounds were once used in pharmaceutical applications..800-1.50) 1.90) 90th 3.00) 4. interval) .700-.70 (3.800-1.50-3.60-3. or oxygen. thermostats and switches). and organic forms. Metabolism of mercury by microorganisms in aquatic sediments creates methyl mercury.20 (2. water can be contaminated by the direct release of elemental and inorganic mercury from industrial discharges.60) 1.800 (.300) .400-.50) 4.400 (.903) Selected percentiles ( 95% confidence interval) 50th ..484) . thermometers.60 (1. it is oxidized in Total Blood Mercury—2003-2004 Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U.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 .S.90) 3. IARC. 2002).40 (4.40 (3.600 (. solid-waste incineration.30-5.70 (1. thimerosal.900) 75th 1.30) 4132 4241 03-04 03-04 03-04 .500-. and mercury compounds are still used as preservatives (e.00 (2.363-.700-. 218 Fourth National Report on Human Exposure to Environmental Chemicals .00-5.00-1.30) 1.700-.30-6.40-3.700) .00 (.700) .60-2. merbromin).714-.10-3.877 (. sphygmomanometers and barometers...40-2. Also.00) 1.900) 1. inorganic.500) . Accidental spills of elemental mercury.2.800 (. Hursh et al.419 (. In addition. Inorganic mercury exists in two oxidative states (mercurous and mercuric) that combine with other elements.781 (.689-. 1998.372) .00 (1.800 (.70-2. Survey years 03-04 Geometric mean (95% conf. Elemental mercury is used to produce chlorine gas and caustic soda for industrial applications.50) 2.800-1.90-3..700-.285-. and dental amalgam..80) 3.300-.40 (4.00 (2.800-1.80 (1. After elemental mercury is absorbed.40) 3. Woods et al.30) 1. such as chlorine (e.60 (1. Imported folk and alternative medicines occasionally are contaminated with inorganic mercury..g. elemental mercury is absorbed mainly by inhaling volatilized vapor. and mining and smelting. Apart from methyl mercury.900) .800-1. 7439-97-6 General Information Mercury is a naturally occurring metal that has elemental (metallic). which can bioaccumulate in aquatic and terrestrial food chains. Elemental mercury is released into the air from the combustion of fossil fuels (primarily coal). 1994.800 (. predominantly from fish and other seafood. Elemental mercury is a shiny.20-3.60-5.927) .60 (2.900) 1.326 (. Poorly absorbed from the gastrointestinal tract.12) .80 (3.472-.

The half-life of inorganic mercury in blood is similar to the slow-phase half-life of mercury after inhalation of elemental mercury. 1999-2002.300) .30) 3.20 (.500-.300) .40-1.269-. 1992). Vahter et al.541-.307 (. interval) Selected percentiles (95% confidence interval) 50th .70 (1.10 (1.377) .300) .70-5..90 (4. Sandborgh-Englund et al. The slow-phase half-life may be several weeks longer in persons with chronic occupational exposure (Sallsten et al.343 (.800-1.200-.10 (1.73) 1.700 (. 1994). 1993).60 (2.200 (.90) 90th 1. 1992 and 1999.10) .300) .40 (1..00 (2. and peak urine levels can lag behind peak blood levels by days to a few weeks (Barregard et al.900 (. 1971).697-.60 (3.200-.30 (1.30-5. a measure of accumulated dose (Cernichiari et al.299-.256-.60) 3.90 (1.10 (.10 (1.. Suzuki et al.00) 1.833 (.06 (.00 (2. 1994. Smith and Farris.50) 2.50) 95th 2. Fourth National Report on Human Exposure to Environmental Chemicals 219 ..300 (.00-2.30) 1.800 (.500-.700 (.374) .700 (.60 (3.800 (.. 2004.200-..407) .80-3.S..297-.265-.50 (1.00-3.70-3.738-. 1996).900 (.500-1.50-2. with most elimination occurring through in the feces (Sherlock et al. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.50) 3.00) 1. Miettinen et al.01) ..200-.40) 5.80 (1.300) .00 (1. 1975.800) .800) 1.50-3. Lesser penetration of inorganic mercury occurs through the bloodbrain barrier than occurs with either elemental or methyl mercury (Hattula and Rahola.90 (3.20) 1.824) 1.. Excretion occurs by renal and fecal routes.0) 4.50) 1. 1998). National Health and Nutrition Examination Survey. excretion of mercury occurs predominantly through the kidney (Sandborgh-Englund et al. Mercury levels in the cord blood are higher than in the mother’s blood (Stern and Smith.317 (.329 (.70) 4.820 (.475) .00) 6..200-.400-..40) 1.20-3.500 (.10 (.300 (.377 (.50 (2.00) 2.70-3.395) . Less than 15% of inorganic mercury is absorbed from the human gastrointestinal tract (Rahola et al.00) 7.20-3.200 (.300 (.00 (2.3) 4.700 (.Metals the tissues to mercurous and mercuric inorganic forms.00 (3.60 (1.90) Sample size 705 872 318 432 387 440 1709 1928 Age Group 1-5 years (females and males) Females Males 16-49 years (females only) 99-00 01-02 99-00 01-02 99-00 01-02 99-00 01-02 .30 (. thereafter.300 (.00-1. After exposure to elemental mercury.30-6..20) . 1969.800) 1.80 (3.20 (2.40-2.70-6. 1984. population.800-1.40 (1.80) 1.90) 3.726-1.. 1990).70-5.30 (1. 1992.06-1.667 (.30) 1.700-1.60) 1.268-..900 (..600 (.50) 1. 1991.10) . 16-49 years) Mexican Americans Non-hispanic blacks Non-hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 . 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. Human pharmacokinetic studies indicate that methyl mercury declines in blood and the whole body with a half-life of approximately 50 days.700-.14 and 0.944 (.500-.10 (3.30 (1.200-.90 (4.500 (.90) 2. 2003).900-1. 1994) and then undergoes slow dealkylation to inorganic mercury.800) .80) 579 527 370 436 588 806 Limit of detection (LOD.800 (.871-1. 1999). Myers et al.800) 75th .70 (1. 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.60) 2. Jonsson et al.90) 2.. 1973).600) . Inorganic mercury and methyl mercury are distributed into human breast milk in relatively low concentrations.00) . Geometric mean Survey years (95% conf... Transplacental transport of methyl mercury and elemental mercury has been demonstrated in animals (Kajiwara et al. 1996.60 (1.10 (5.27) .30-3.700) 2. Vimy et al. and a useful marker of exposure in epidemiologic studies (Grandjean et al.940) Race/ethnicity (females.800-1.30-6.90) 5.700-.70) 1.00) 4.318 (. and the newborn’s levels decline gradually over several weeks (Bjornberg et al..60 (1.600) .500-. 1995.00-2. 2003).70) 4.20) .60) 1..900-1.70 (1.14.40-2.02 (.20-2. 2005).664-1.90 (1. McDowell et al..50-12. 1998).23) .30-4.40) 2. The fraction of methyl mercury absorbed from the gastrointestinal tract is about 95% (Aberg et al.20-3.825-1.500-.300) . for both acute and chronic exposures.919) .10-1.700-1.30-6. Methyl mercury enters the brain and other tissues (Vahter et al.30-4.30-2.7) 4.20-11.00-6.369) 1.30-11.35 (1. Smith et al. urinary mercury levels decline with a half-life of approximately 1-3 months (Roels et al. Methyl mercury is incorporated into growing hair..29) .00-2.10) 1. 1993).10-3.

700-. Large amounts may cause irritant or corrosive effects on the gastrointestinal tract (Sanchez-Sicilia et al. 1970. and progressive constriction of the visual fields. pain in the extremities. At levels below those that cause acute lung injury... Survey Geometric mean (95% conf. hearing impairment.. 1996). 2000.Metals may be more efficient for inorganic mercury (Grandjean et al.. < LOD means less than the limit of detection.800) .600) . and cerebral palsy (NRC. gingivitis. overt signs and symptoms of chronic inhalation may include tremor. Sakamoto et al. 2003).800) 792 842 2060 4453 03-04 03-04 * * < LOD < LOD < LOD < LOD . Smith et al. high-dose exposure to elemental mercury vapor may cause severe pneumonitis.600) .. * Not calculated: proportion of results below limit of detection was too high to provide a valid result..500 (<LOD-. typically after a latent period of weeks to months.600-. which may vary for some chemicals by year and by individual sample. and pinkish discoloration of the hands and feet (Tunnessen et al. insomnia..500-.600) .700-..600-.600-. irritability. 1993). dysarthria.800) 4015 4132 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD . sensory impairments. hypertension.700 (. Rissanen et al. and sleep disturbance (Bidstrup et al. ataxia. 220 Fourth National Report on Human Exposure to Environmental Chemicals . Bellinger et al. causing parasthesias.600 (. 2006. Rice.700 (. anorexia.. 2004).500 (<LOD-. Salonen et al. 1987).. 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. Overt poisoning from methyl mercury primarily affects the central nervous system.600-. maculopapular rash.600) .700 (.. Smith et al. In recent epidemiologic studies. cerebellar ataxia.800) .600) . Sakamoto et al..S.... 2004. Factor-Litvak et al. 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. 1995.500-.. see Data Analysis section) for Survey year 03-04 is 0. and a drinking water Inorganic Blood Mercury Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U.500) . dysarthria. Stern 2005.700 (.700-. Mercury levels in breast milk also decline in the weeks after birth (Bjornberg et al.500-.600 (. 2005).600 (. 2004).600) * 03-04 03-04 03-04 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . and neurocognitive and behavioral disturbances.600 (.600) .700) . Acrodynia is a sporadic and predominantly pediatric syndrome historically associated with calomel (mercuric oxide) in teething powders and occasionally other inorganic forms of mercury. Although recent investigations have suggested a possible link between chronic ingestion of methyl mercury and an increased risk for cardiovascular disease.500-. Vupputuri et al. short-term memory loss. 1998. 1963). population from the National Health and Nutrition Examination Survey.500-.42.700 (. depression.. The constellation of findings may include anorexia.. 2000).500-. 2002. particularly irritability.600) . DeRouen et al. 1951.500-. Workplace standards for inorganic mercury exposure have been established by OSHA and ACGIH. 2000.500 (.600) . 2006. 2004.500-. High-level prenatal exposure may result in a constellation of developmental deficits that includes mental retardation. Once absorbed. limb deformities. Inorganic mercury exposure usually occurs by ingestion. Drexler and Schaller. 1995. fatigue.600 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th .700) size 8147 Total Age group 1-5 years 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th 90th .600 (. altered physical growth. Occupational exposure to elemental mercury vapor has been associated with subclinical effects on biomarkers of renal dysfunction (Cardenas et al. 2005. the existence of a causal relation is unresolved (Chan and Egeland.700 (.600 (. Oskarsson et al.500 (. 1983). Low-level exposure from dental amalgams has not been associated with neurologic effects in children or adults (Bates et al.600) .500-. the most prominent effect is on the kidneys where mercury accumulates and may lead to renal tubular necrosis.600 (. Acute.700) 2007 2240 3406 Limit of detection (LOD.

33 (2. These distinctions can help interpret mercury blood levels in people.534) . 2009).07 (. Mahaffey et al. environmental levels) and health effects is available from the U.840-1. total blood mercury increased with age.88) 287 722 1529 03-04 03-04 .840) 1.23) .360-. A cohort of 1127 U. military veterans (mean age 52. EPA.26 (1.408) .400 (.530) . interval) .430 (.18) 2.960 (. 2003).480 (. et al. 2000).476 (.700-1.52) 2.atsdr.330-.00) 1. 2006).01 (. who participated in a 1998 representative population survey (Becker et al. adult women in several ethnic subgroups (Hightower et al.370) .66) 3.441 (.530) .330 (. Kingman et al.304) .54 (2. Clinically observable signs of ataxia and paresthesias may occur when blood mercury levels increase to approximately 100 µg/L after methyl mercury poisoning.99-6.65) 1.14.700 (.870-1. 2003).76-4. Survey years 03-04 Geometric mean (95% conf.420 (.382-. Schober et al. 1998). total blood mercury levels declined slightly in non-Hispanic black and Mexican American children.. Grandjean et al. Fourth National Report on Human Exposure to Environmental Chemicals 221 ...67-2.gov/mercury and from ATSDR at: http:// www.530-. Urine mercury levels increase as more occlusal surfaces of teeth are filled with mercury-containing amalgams (Becker et al. the total blood mercury concentration is due mostly to the dietary intake of organic forms.30) 3.463) . IARC considers methylmercury to be a possible human carcinogen and elemental and inorganic mercury to be unclassifiable with regard to human carcinogenicity.85-2. Benes et al. slightly higher total blood mercury levels were found in U.890 (.413-.770-1.96 (1.63-2.19 (1.55 µg/L. and increased slightly in non-Hispanic white children (Caldwell.29) 1..61) 1.405-..940 (.24 (2.549) ..396-.96 (1.93 (1.460) .330-. aged 18 to 69 years..9 years). (2000) studied 1216 blood donors in the Czech Republic (896 men and 320 women.580) .509) .Metals standard for inorganic mercury has been established by U. the median concentration of blood mercury was 0.78 µg/L for adults and 0.09 (2.406-.8 years. In Germany the geometric mean for blood mercury was 0. 2001.46) 3.430) . Information about external exposure (i.930-1.358 (.610-1.. range 40 years to 78 years) had an average total blood mercury concentration of 2. although non-Hispanic black females had higher levels than non-Hispanic white or Mexican American females.68 (2.S.520) .495 (.76-3.60-2.840-1.254 (.440 (.555) ..90) 2.420 (. Urinary mercury consists mostly of inorganic mercury (Cianciola et al.433 (.24) 1. particularly methyl mercury.14-2..cdc. Over the NHANES 1999-2006 survey periods.20 (1.05) 1.. Total blood mercury levels increase with greater fish consumption (Dewailly et al.290-. average age 9. and the age-related changes differed across the groups (Caldwell et al. see Data Analysis section) for Survey year 03-04 is 0.00 (.447 (.S. 1995..360-. 1997.42) 95th 3. 2002).31) 2. In NHANES 19992002..360 (.509) .442-. Urinary Mercury—2003-2004 Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.330-. 2009).e. Sanzo et al.05) 3.60 (1.460 (.39-3.23) 2. average age 33 years.46 µg/L for children. 758 children. 1998).16 (. the developing fetus may be the most susceptible to the effects of ongoing methyl mercury exposure (NRC.epa. Biomonitoring Information In the general population.03-4.67-3.28) 1.60) 619 713 1066 Limit of detection (LOD. EPA at: http://www.280-.160-.58 µg/L for 4645 adults.34-3.S.78-2.08 (1.12 (.89) 3.350-.250) .76-3.88-3.19 (2.08 (1.gov/toxprofiles.492) Selected percentiles ( 95% confidence interval) 50th . Among the three racial/ethnic groups.31) 1266 1272 03-04 03-04 03-04 .410-.870-1. However.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 .S.88 (1.480) 75th 1.13-2. total blood mercury geometric mean levels in females aged 16-49 years did not change. population from the National Health and Nutrition Examination Survey.97) 2.213-.570) .77-2.16 (1. 2001. 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.200 (.340-.14) 90th 2.416 (. These men had no occupational exposure to mercury but previously had received dental amalgams at military facilities (Kingman et al.S. During the same survey periods.313-.. From 1996 through 1998. 2004.430 (.

ACGIH recommends that the blood levels due to inorganic mercury exposure in workers not exceed 15 µg/L.964-1.333-.616) .455-.06 (.400-.498) 75th .476 (.301-.280-.376-. Survey years 03-04 Geometric mean (95% conf. Department of Health and Human Services noted that several studies have observed a modest.56) 1266 1271 03-04 03-04 03-04 .969-1. 2005).39) 1.667-1. Langworth et al.385-.508 (.875-1.25 (.12-3. Levels in U.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 .443 (.417) .455) .768 (.62 (1.391) .297 (.S.619-.208-.46-2.1 µg/L.77 (2.31 (1. 1992). Biomonitoring data will also help scientists plan and conduct research on exposure and health effects..306 (. Information about the biological exposure indices is provided here for comparison.61) 1.400) .696 (..309-.358) . representative sample of women aged 1649 years reported in NHANES 1999-2006 (Caldwell. Urinary Mercury (creatinine corrected)—2003-2004 Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.79 (1.480) .28 (.79) 1. and Italian (Apostoli et al.Metals 2000). et al.535) 1.522-.545 (. DeRouen et al.41-2. 2009).391-.343 (.365 (. 2006).588) . the urine mercury increased by approximately 0.392-.S.90) 618 713 1066 222 Fourth National Report on Human Exposure to Environmental Chemicals .463 (.88-2. population from the National Health and Nutrition Examination Survey.532 (.368) .67 (1.07) 1.21) 1.404-. reversible increase in urinary N-acetyl-glucosaminidase. 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.86) 95th 2.447 (.246-. women of childbearing age have generally been much lower than these levels (CDC. Blood mercury levels of women and children in NHANES 19992006 were also below levels established as occupational exposure guidelines (Caldwell..S.35 (1.40-1. In the study of U. Urinary mercury levels in recent German (Becker et al.87) 2.11-2.384 (.970 (.687) .13-2.63) 1.347) .587 (..S.S.800-1.307-.04-3.599) .00 (.620-.196-. 2002) adult population surveys were similar to those in a U. interval) .909 (.630) . Czech (Benes et al.76 (1.67 (1.13 (1.30) 2. and on average. The ACGIH (2007) currently recommends that urinary inorganic mercury in workers not exceed 35 µg/g of creatinine.. 2003). 1998)..06 (.65 (1.275) .00) 286 722 1529 03-04 03-04 . et al.365 (.784) 1.40 (1..486) Selected percentiles ( 95% confidence interval) 50th . among workers with urinary mercury concentrations of 25-35 µg/L or greater (Barregard et al.32-2.525 (.78-4.09) 1.11) 1.990) .652) .51-2. Urine mercury and the number of dental amalgams were correlated.00) 90th 1.464 (.32 (1.537) .88-2.485 (. An expert-panel report recently prepared for the U. 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.225-. 2009).03) 2.447-. a biomarker of perturbation in renal tubular function.23-2. 1988.44) 1..01) 2. 2006.217 (. Finding a measurable amount of mercury in blood or urine does not mean that the level of mercury causes an adverse health effect.566) .289) .276 (.255 (. mean urinary mercury was 3.362 (.54 (2. 2002)..30) 1.472-.16) 1.11) 2.455-.785-1.714-1.. not to imply a safety level for general population exposure. military veterans with dental amalgams.18-1.1 µg/L for each surface with a dental amalgam (Kingman et al.265-.88 (1.87 (1.64-2.

population.56) 3.553-.Metals Urinary Mercury−Females Aged 16-49 Years Old.97 (1.77) 1.502-.831) .699) 1. 1999-2002 Geometric mean and selected percentiles of urine concentrations (in µg/L) for females aged 16 to 49 years in the U.30 (1. 16-49 years) 99-00 01-02 .70 (2.14.596 (.520-.578-.16) 5.45-3.799) .51 (3.930) .615 (.31-1.580-.50-4.55) 90th 3.42) 2. 1999-2002.89 (2.522 (.53-3.69-3.639 (.56) 4.592 (.709) .76 (1.31 (1.10-4.25) 2.92) 4.98 (5.665) Mexican Americans Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .62 (1.723 (.57-4.685 (.18 (3.87-4.560-.14 and 0.45-2.657 (.18) 3.27 (1.47) 1.631-. 16-49 years) 99-00 01-02 .99 (3.04-10.77) 2.65) 1.00 (3.650) 1.17) 95th 5.772 (.580 (.97) 2.99) 1.47) 1.387-.62 (3.806) .774) .606 (.624-.475-.03) 1.53) 595 531 381 442 594 826 Fourth National Report on Human Exposure to Environmental Chemicals 223 .560 (.508-.10-2.54) 595 531 381 442 594 826 Limit of detection (LOD.790) .85) 4.05 (2.850-1.14) 3.91-7.68) 3.664) .706 (.656-.97) 2.91 (2.710) 1.410-.650 (.79) 3.557-.632 (.92) 2.721 (.41 (1.55-3.41 (1.665) .37) 1.45) 95th 3.32 (1.61) 1.68 (3. National Health and Nutrition Examination Survey. interval) Selected percentiles (95% confidence interval) 50th .526-.39) Sample size 1748 1960 Age group (females) 16-49 years Race/ethnicity (females.76) 2.600 (.48 (2.37 (1.710 (.13 (2.14-2.76-5.56 (1.809) .43-1.03-2.831) . National Health and Nutrition Examination Survey.569-.41-6.09-1.670) 75th 1. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. 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.09-1.21 (2.00 (2.06 (.44) 3.892) .03 (. population.23-1.28 (1.23-1.744) 1.21-3.540 (.07-2.540-.62 (4.691) .32) 2.46) 3.35) .85-3.03 (.24) 6.00) 2.68-3.99 (2.450-.724 (.59-5.45) 2.610-. Geometric mean Survey years (95% conf.22-3.686) .83-3.81-6.760 (.45 (1. interval) Selected percentiles (95% confidence interval) Survey years 50th .605-.16-5.582-.27 (2.516 (.65-4.41 (2.92) 3.97) 2.622-.637) .42-3.636-.42) 90th 2.84 (2.966) .S.27-1.38) 4.63) Sample size 1748 1960 Age group (females) 16-49 years Race/ethnicity (females.910) .824) .51) .846) .72) 1.710 (.22 (.742-1.15-1.650 (.810) . 1999-2002.05 (3.35 (1.655 (.620 (.13-4.870) .50 (1.84 (2.3) 5.07-5.719 (.45) 2.94) 1.21 (1.95 (2.79) 1.24-1.709) 75th 1.39-3.832-1.664) Mexican Americans Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .909-1.658 (.61-6.15 (2. Geometric mean (95% conf.579-.426-. Urinary Mercury (creatinine corrected)−Females Aged 16-49 Years Old.32-3.99-2.833) .46-4.07) 1.30 (2.616-.500-.30-2.50 (2.69 (1.46 (1.S.740 (.14-1.52) 3.565 (.81 (3.520-.501-.30 (2.420-.04-1.

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Orr MF. Longnecker MP. Stern AH.258(4 Pt 2):R939-945. Public Health Nutr 2001. Hall LL. Hum Toxicol 1984. Allen PV. Lind B. Zeitz P.98(1):133-142. Am J Physiol 1990. Hongo T. Schober SE. Guo S. Amurrio A. Baser M.79:786789. Kaye WE.115(10):1527-1531. Amiano P. Hislop D. The contribution of dental amalgam to urinary mercury excretion in children. Public health consequences of mercury spills: hazardous substances emergency events surveillance system. Smith AE. An assessment of the cord blood: maternal blood methyl mercury ratio: implications for risk assessment. Leitao JG. Fisher HL.2:117-131. Environ Health Perspect 2007.37:245-252. Smith JC. et al. Whittle K. Bernardo MF. Newton G.Metals Sanzo JM. Pediatrics 1987. Vorwald AJ. Vahter M.110:129-132. Vimy MJ. Matsuo N. McDowell M. JAMA 2003.40:413-419. McMahon KJ. The hair-organ relationship in mercury concentration in contemporary Japanese. DeRouen TA. Langolf GD. Smith RG.111(12):1465-1470.4(5):981-988. Methyl mercury pharmacokinetics in man: a reevaluation. Environ Res 2005. Maternal-fetal distribution of mercury (203Hg) released from dental amalgam fillings. 226 Fourth National Report on Human Exposure to Environmental Chemicals . Blood mercury levels in US children and women of childbearing age. 1993-1998. Jones RL. Sherlock J. Farris FF. Environ Health Perspect 2003. 1999-2000.289(13):1667-1674. Effects of occupational exposure to elemental mercury on short term memory. Mooney TF. Aguinagalde FX. A review of the studies of the cardiovascular health effects of methylmercury with consideration of their suitability for risk assessment. Mottet NK. Suzuki T. Blood mercury level and blood pressure among US women: results from the National Health and Nutrition Examination Survey 1999-2000. Smith JC.124:221-229. Takahashi Y. Acrodynia: exposure to mercury from fluorescent light bulbs. Toxicol Appl Pharmacol 1994. Am Ind Hyg Assoc J 1970.31:687-700. Stern AH. The kinetics of intravenously administered methyl mercury in man. Toxicol Appl Pharmacol 1996. Vupputuri S. Patil LS. Sinks TH. Estimation and validation of mercury intake associated with fish consumption in an EPIC cohort of Spain. Leroux BG. Osterloh J. Lorscheider FL. Effects of exposure to mercury in the manufacture of chlorine. Br J Ind Med 1983. Nakazawa M. Bolger PM. Woods JS. Environ Res 2005. Environ Health Perspect 2002.97(2):195-200. Most B. Imai H. Turner MD.128(2):25125-25126. Speciation of mercury in the primate blood and brain following long-term exposure to methyl mercury. Daniels JL. Tunnessen WW. Toxicol Appl Pharmacol 1994. Martin MD.48(4):221229. Dorronsoro M. Shen DD. Arch Environ Health 1993. et al. Azpiri MA. Elevation of mercury in human blood from controlled ingestion of methyl mercury in fish. Smith PJ. et al. Yoshinaga J. Friberg L. Goldberg J. Sandler DP. Topping G. Burbacher T.

7 (73.1-55.6-82.6) 93.4 (48.2 (56.4-75.5 (41.7 (50.1) 46.7-50.8 (42.6-72. respectively.6 (43.4 (34.5-65. Fourth National Report on Human Exposure to Environmental Chemicals 227 .8-49.6-55.0-110) 90.7-91.6) 71.2) 41. hydrogenation catalysts.0-56.3 (64.7-84.7) 78.9) 67.6) 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 (99.8-94.7) 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 78.0-77.1) 59.9-55.9 (52.1-44. Excretion occurs predominantly via the kidneys. molybdenum is a cofactor for three enzyme classes— sulfite oxidase.7) 86. and paints.3 (55.9) 62.4) 56.2-79.9 (78.7 (36.5 (74.5) 60. The recommended dietary allowance for adult men and women is 45 µg/day (IOM. and 03-04 are 0.0-38.5) 47..0) 55.7) 78.6) 51.3 (47.6-46.2 (49.6 (73.0) 60.7-51.3 (53.3-44.7 (44.8) 39.0-100) 63. and xanthine oxidase (Kisker et al.5 (43.5-52. semiconductor and battery industries have begun to use molybdenum.1) 35.8) 40.1 (38.2) 48.9-85.1 (34.7 (58.1 (71. 01-02.5 (67.5 (48.5-41.5-46.4-61.2 (49.3) 37.0) 62.5) 80.7) 46.3 (37.8) 48.9 (44. and the average dietary daily intake of molybdenum is approximately 100 µg/day (IOM.8 (85.5-91.1 (91.9 (33.9) 34.7 (45.8.4 (72.7 (51.8.4-52.4) 76. WHO.5) 80.3-115) 152 (120-217) 177 (142-207) 152 (141-169) 206 (150-274) 166 (147-170) 156 (135-175) 187 (146-223) 152 (134-180) 130 (119-142) 780 683 618 546 667 723 760 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limits of detection (LOD.6) Selected percentiles ( 95% confidence interval) 50th 50. More recently.8) 75.3) 90th 135 (125-146) 124 (117-130) 111 (105-118) 95th 180 (154-216) 165 (145-176) 138 (133-146) Total 45.7-73.3 (55.7-105) 69. 7439-98-7 General Information Elemental molybdenum is a silver-white.3) 85.5-124) 108 (92.4) 45.3) 47. chemical reagents in hospital laboratories.8 (67. which exert homeostatic regulation over molybdenum balance.1) 60.6 (52.7-47.3-75.3-108) 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 47.2) 53.2 (38.3-91.2-91.3 (84.8 (82.0 (81.7) 57.5-68.2) 150 (128-187) 130 (120-141) 119 (112-130) 119 (105-138) 115 (104-128) 101 (97.0-101) 82.9-83.2-53.7) 77.9-56. inks.6-42.1-59.3) 83.3 (46.4-82. and 1.6-111) 267 (159-840) 197 (161-291) 181 (138-235) 188 (146-216) 179 (155-227) 143 (130-156) 168 (143-206) 150 (130-166) 133 (119-144) 310 368 290 648 762 725 1299 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 52.2 (83.3 (79.6) 53.8) 46. 0. 2001.3) 65.0 (48.9 (32.6-96. aldehyde dehydrogenase. 2001).0-71.7-60.2-59. Molybdenum is a nutritionally essential trace element that enters the body primarily from dietary sources.9-109) 97.0-85.5.7-122) 93.0 (46. 1996).3 (73.2-59.9 (40. and in pigments for ceramics.5 (41.5) 85.0-65.2) 37.2) 52.2-37. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.0) 54.4) 49. 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.8-46.3) 41.7-96.1-88.0 (41.4) 42.4) 41.1-48.9 (37.9 (73. hard metal widely used to add strength and hardness and retard corrosion in metal alloys.2-42. 1997).7-68.0 (76.8) 44.1) 82. At a daily oral molybdenum dose of 24 µg.8-108) 87.5) 44.2-70.5-66.5-52.3 (38.6 (40. urinary excretion over six days CAS No.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 (98.4 (48.8-106) 88.0) 45.6) 71.2 (63.1-63.2 (40.4 (79.0) 97.0-53.2) 40.S.0) 39.3 (71. In humans.5 (49.1-52.6-58.7-39. lubricants.Metals Molybdenum or ore deposits.7 (37.7-41.1) 57.5 (37.4) 52.1-51.2 (55. interval) 45.9-55.7) 45.0 (43.7) 51.3-47.7 (71.1-52.9 (34.4 (80.7) 75th 84.0 (42.6-62.5 (81. see Data Analysis section) for survey years 99-00. population from the National Health and Nutrition Examination survey.2 (61.0 (42.2) 79.9-82.8-90.6 (55.3) 54.0-62.1) 126 (106-147) 109 (94. Gastrointestinal absorption of molybdenum averages 8893% for dietary intakes of 22-1490 µg/day.7-92.0) 84.6 (55. Compounds of molybdenum are also used as corrosion inhibitors.2 (69.6 (40.

1 (40.5 (36. A long term inhalation bioassay of molybdenum trioxide in mice yielded “some evidence” of carcinogenicity (NTP.4 (40.2-96.4-106) 85.5 (78.5 (83.3) 44.3-46.0) 38.7 (66.0 (74.0) 95th 144 (125-171) 130 (120-149) 120 (107-135) Total 42.1-43.3) 56.8) 79.6) 48.8-47.6-41.3) 43. the Panel on Micronutrients of the Institute of Medicine identified a no observed adverse effect level (NOAEL) of 0. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. of the ingested dose (Turnlund et al.0) 88.5 (39.9 (73.3 (37.0) 39.0 (58.1 (37.1 (33.5) 72.4-41.0-120) 85.8 (75.9-118) 91.3-115) 98.7) 53.2) 37.5 (39.0) 53.9 mg/kg/day and established a tolerable upper intake level of 0.5 (59.0-38.8-65.4-39.5-62.6-63.6-45.5 (40.4) 47.3) 61.6-61.2) 39.7) 75th 63.1-43.2 (73.4) 116 (101-126) 104 (88.2 (40.5) 60.S.9) 173 (130-243) 159 (129-170) 132 (107-158) 85.5 (65.5 (35.8 (57.4-185) 106 (94.4 (59.4 (78.1 (42.5 (80.0 (35.2) 42.9-68.5 (65.3 (83.4 (37.4 (67. 1997).5-99.1-100) 86.3-102) 122 (116-147) 123 (109-139) 118 (101-134) 310 368 290 648 762 725 1299 1559 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 40.5 (35.3 (51.3) 40. 1993).9-40.3-141) 109 (81. U.8) 38.8) 38.9) 92.1-38.9) 31.1) 37.4-42.03 mg/kg/day in humans (IOM.3) 37.Metals was 18% of the ingested dose. Based on studies finding adverse reproductive effects in rats and mice.9 (79.2-80.5-45.4-118) 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 .7 (77.6) 36.7 (30..6 (42. Biomonitoring Information Molybdenum is an essential element for health.9-87.2 (57.5 (41.2 (40.9-96.9-71.2 (43.0-46.1-67.5) 71.7-62.1 (82.9 (36. EPA.1-79.2 (69.2 (52.9-45. Human health effects from molybdenum at low environmental doses or at biomonitored levels from low environmental exposures are unknown.1 (54.6 (59.6 (57.6-76.1-81. at daily oral doses of 95 µg and 428 µg.7 (75.2-46.8) 37.9 (35.8-46.4-66. Molybdenum is generally considered to be of low human toxicity. One case-control study suggested a possible link between occupational exposure to molybdenum and lung cancer (Droste et al.6-61.2) 39.3-59.8) 39.2-41.2 (40.6 (36.1 (30.0 (80. respectively.1-112) 78.3 (37.8-118) 81.1) 40. urinary excretion over six days rose to 50% and 67%.8 (90.4) 48.7-40.5-92.7-100) 77.8) 45.4) 40.7) 45.2 (36.5 (40.5) 73.3-68.5) 90th 108 (97.3 (36.3 (53.3 (71.2-103) 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 42.2) 43.0-103) 103 (90.5 (34.8 (37.3-56.8) 62.5 (41.4) 77.6-88.3-43.1 (44.1) 101 (83.0) 36.7) 115 (93.7) 57.0-56.2-40.6) 43.1 (39.2 (33. 1999).2-47.3) 41.1-39.5 (79..9-42. but available epidemiologic data are scant. population from the National Health and Nutrition Examination survey.3-44.1-127) 90..0-46.4 (55.0-41. 1995).6-78.3) 57.9-61.8) 61.8-84.7) 41. In industry.5) 63.8-47.7-43.7) 112 (95.2) 55.4 (44.1 (38.5-119) 90. Chronic exposure to very high levels may result in higher serum uric acid levels and a gout-like illness (Koval’skiy et al.9 (64.6) Selected percentiles ( 95% confidence interval) 50th 41.5-35.9) 41.1) 43.9) 40.5-69.4-120) 101 (84.5 (38.2-49.9 (49.5 (37.1-45.1) 65.4 (53.8) 71.7-44.4) 61.0-133) 119 (88. Levels of molybdenum Urinary Molybdenum (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.6 (38.1-34.8-66.6) 39.3 (71.5 (54.5-97.7) 42.4) 89.4-107) 85.5-46.4) 44.2) 42. 2001).8-52.9) 44.5-70. and urinary levels reflect intake from all sources.0) 62.5) 214 (154-1040) 185 (165-219) 160 (129-257) 112 (78.0) 44. interval) 43.7-52.2) 58.1-41. 1961.8 (36. and clinical or epidemiologic evidence of adverse effects is limited.0) 33.5-60.6) 39.4 (56. and molybdenum has not been systematically evaluated for carcinogenicity by IARC.5-48.8-67.7-38.9-45. dust and other fine particles produced during refining or shaping of molybdenum or molybdenumcontaining alloys are inhalational pathways of exposure.2 (37.9 (39.5-50.5-44.6 (36.9 (40.1) 37.4) 60.7-93.8-42.3) 64.7) 62.1-40.6 (71.5 (50.S.9-117) 57.9 (39.3 (58.5 (37.1) 56.1-109) 89.2 (50.3-45.1 (49.4) 58.2) 38.1-39.0) 72.9) 79.8 (56.4-76.0) 39.4) 122 (107-133) 109 (99.3) 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 85.9-41.2-121) 107 (92.2-96.3 (36.2-65.2) 37.7-120) 87.9 (64.3 (55.3-52.1 (38.6-63.7-137) 129 (109-155) 112 (97.

World Health Organization (WHO). Changes of purine metabolism in man and animals under conditions of molybdenum biogeochemical provinces. EPA). Trace element reference values in tissues from inhabitants of the European Union. Finding a measurable amount of molybdenum in the urine does not mean that the level of molybdenum causes an adverse health effect.niehs. Available at URL: http://ntp. Christensen JM. Food and Nutrition Board. vitamin K. Geneva: WHO.nih. Ann Rev Biochem 1997. 56:322-327. and retention studied with stable isotopes in young men at five intakes of dietary molybdenum. 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. Van Meerbeeck JP. Molybdenum 1993 [online]. Available at URL: http://books. 1998. 16:1313-1319. Turnlund JR. Menne C. Schaub J.gov/index. Toxicology and carcinogenesis studies of molybdenum trioxide (CAS No. molybdenum. iron. Molybdenum absorption. (DC): National Academy Press. Shmavonyan DM. Inductively coupled plasma mass spectrometric determination of molybdenum in urine from a Danish population.62(4):790-796. Washington. Droste JHJ.gov/iris/ subst/0425.66:233-267. Kisker C.S. Ronchi A. 4/14/09 White MA. X. et al.S.15(2-3):149-154. Schindelin H.epa. 144-154. Molybdenum-cofactorcontaining enzymes: structure and mechanism. silicon. In: Trace elements in human nutrition and health. Sabbioni E. 4/14/09 Iversen BS. Am J Clin Nutr 1995. Third National Report on Human Exposure to Environmental Chemicals. White MA. Gatti A. and zinc: a report of the Panel on Micronutrients. White and Sabbioni. Inductively coupled plasma mass spectrometric determination of molybdenum in urine. edu/openbook. copper. Schleyerbach U. Rees DC. References Centers for Disease Control and Prevention (CDC). Minoia C. Fourth National Report on Human Exposure to Environmental Chemicals 229 . Molybdenum. Koval’skiy GA. van Sprundel MP. nickel. National Toxicology Program (NTP). Kristiansen J. J Trace Elem Med Biol 2001.S. manganese. Minoia et al.. Dietary reference intakes for vitamin A. Rapid Comm Mass Spectrom 2002. 1998).216:253-270. Peiffer GL. Sabbioni E. 4/14/09 Sievers E. 420-441.. excretion. A study of 13 elements in blood and urine of a United Kingdom population. iodine.nap. Occup Environ Med 1999.php?record_id=10026&page=420. Molybdenum in infancy: methodical investigation of urinary excretion. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Analyst 1998. chromium. population were well characterized in NHANES 1999-2000 and 2001-2002 (CDC. Sciarra G. Keyes WR. Available at URL: http://www. boron. Urinary molybdenum concentrations in infants may be slightly lower than those in other age groups (Sievers et al. 2002. vanadium. 1313-27-5) in F344 Rats and B6C3F1 Mice (inhalation studies) 1997 [online].htm.22(3):179-191. 1996. Weyler JJ. Institute of Medicine (IOM). Zhurnal Obshchey Biologii 1961. Vermeire PA. TR-462. Sci Total Environ 1998. 2001. 2001). pp. Aprea C. Occupational risk factors of lung cancer: a hospital based case-control study. Atlanta (GA). Environmental Protection Agency (U.123(1):81-85.. Turci R. arsenic. these levels were comparable to those reported for adults in smaller European population surveys (Iversen et al. Standing Committee on the Scientific Evaluation of Dietary Reference Intakes. 2005. U. 2005). Yarovaya GA. cfm?objectid=070A72C6-E9C1-AE67-4BFAB97AD0F427E8. pp.Metals in urine for the U.

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

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

3/31/08 Moore W Jr. Biomonitoring Information Urinary platinum levels reflect recent exposure. Farago ME. Angerer J. Seifert B. Kuster W. Schierl R.61(7):636-9. Environ Health Perspect 1975b.. Pethran A. Senofonte O. and in blood and urine in the United Kingdom. Schulz C. population were below the limit of detection (0. and platinum.4(1):27-36. 206:15-24.56(3):283-286. 1998).76(1):5-10. Kavanagh P. Int Arch Occup Environ Health 1997. Occup Environ Med 1998. Influences on human internal exposure to environmental platinum. Environ Res 1975a.org/documents/ehc/ehc/ ehc125. Hysell D.55(2):138-140. Wilhelm et al.70(3):205-208. 2003. Pethran et al. Hauff K. pp. et al.inchem. 2004).35:313-321. Boos KS. Part 1: monitoring of urinary concentrations.. van de Weyer C. Jankofsky M. Arch Environ Health 2001. Kaus S. Revised and new reference values for some trace elements in blood and urine for human biomonitoring in environmental medicine. 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. which elevate urinary platinum by five to twelve-fold (Begerow et al. International Journal of Hygiene and Environmental Health 2003. 2004) or less than 0. Arch Environ Health:1969. Schierl et al.01 µg/L (Becker et al. Environmental Health Criteria 125. 2000. J Expo Anal Environ Epidemiol 2003. Biomarkers 1999. Analyst 1998.. 2003. Int J Hyg Environ Health 2004.10:63-71. Herr et al.S. 1991 [online]. Cohrssen B. Wilhelm M. Nickel. et al. Seiwert M.123(3):451-454.04 µg/L) in this Report. 289-380. Kelly J. Schierl. Ensslin AS. Herr et al. Biomonitoring studies on levels of platinum provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of platinum than are found in the general population.. Stara J: Preliminary studies on the toxicity and metabolism of palladium and platinum.13(1):24-30. Patty’s Toxicology... Ruff F: Histamine release by sodium cholorplatinate. Gieler U. In: Bingham E. Blanks R. Herr CE.9:152-158.htm. Turfeld M. Gold-platinum dental restorations were correlated with increased urinary platinum concentrations.. 1998). Hysell D. Pethran A. Schierl R. Gromiec JP... German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population.org/documents/ehc/ehc/ehc125. Raab W. New York: John Wiley & Sons. Platinum concentrations in urban road dust and soil. Kazantzis G. 1999. et al. Saindelle A.htm. Neuendorf J. Biological monitoring of hospital pharmacy personnel occupationally exposed to cytostatic drugs: urinary excretion and cytogenetic studies. Uptake of antineoplastic agents in pharmacy and hospital personnel. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Campbell K. Ruff F: Platinum and platinosis. Powell CH.. palladium. Biomonitoring of traffic police officers exposed to airborne platinum.005 µg/L (Iavicoli et al. 1997. Schulz C. Urinary excretion of platinum from platinum-industry workers. Platinum-industry and precious-metal workers had urinary concentrations about one-thousand times higher than general populations (Schierl et al. Alimonti A. Grimm CH. Moore W Jr.19:685-691. 5th ed. Thornton I. Crocker W. 2001). 2003).Metals the International Programme on Chemical Safety at http:// www. Hebert R. Platinum. Stara J: Biological fate of a single administration of 191Pt in rats following different routes of exposure. Levels of platinum in urine for the U. Int Arch Occup Environ Health 2003. Several studies have shown that background concentrations in general populations were usually less than 0. Ewers U. ruthenium. Fries HG. Finding a measurable amount of platinum in the urine does not mean that the level of platinum causes an adverse health effect. Schierl R. Kulka U. Bocca B.inchem. Br J Pharmacol 1969. Parrot JL. Occup Environ Med 2004. 2003. Duneman L:Long-term urinary platinum. Petrucci F. eds. Available at URL: http://www. Rommelt H..207(1):69-73. palladium. One study found that traffic-control officers had no greater urinary platinum concentrations than office-based control subjects (Iavicoli et al. and gold excretion of patients after insertion of noble-metal dental alloys. Nowak D. Begerow J. International Programme on Chemical Safety (IPCS). Hall L. Stilianakis NI. Schierl R. osmium. Czerczak S. rhodium. 232 Fourth National Report on Human Exposure to Environmental Chemicals . References Becker K. Urinary platinum levels associated with dental gold alloys. et al. 2004. Iavicoli I. Saindelle A. Fruhmann G. Allergy and histamine release due to some platinum salts. Carelli G. Huber R.

162-.180) .410 (.340-.400) .280 (.160 (.410-.206) .202) .490) Total .460) .370) .410 (.420) .370-.310 (..220-.410-.150-.300) .390) . From these and other sources.350-.370 (.430-.430 (.500) .250-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.147-. it has not been specifically mined or refined in the United States since 1984.240) .310) .420) .280-. It is still used in relatively small amounts in pharmaceutical and electronics manufacturing.290 (.184 (.179-.430 (.220 (.350-.172) .220 (.480) .360) .420) .390-.167-.160-.320) .210 (.145-.190 (.390) .230) .200 (.470 (.180 (.230) .270 (.170-.400) 95th .550 (.02.190 (.225) .240-.390-.270 (.250-.220 (.260 (.450 (.170-.400-.190 (.370 (.250-.220) .150-.250 (.410 (.400 (.290 (.480) .190 (.290) .330) .02.520) .135-.340-. population from the National Health and Nutrition Examination Survey.440 (. and 03-04 are 0.270-.330-.450 (.200) .260-. thallium is produced in a fine particulate form that can be absorbed through inhalation or ingestion.172 (.420-.215) .640) .350-.218) .250-.Metals Thallium depilatory cosmetics. In the past.360-.180-. 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.370) .210 (.330-.390 (.310 (.200) .S.330) .187-.180-.160 (.185-.280) .400-.450 (.182-.440-.340 (.147-.290 (.175) .200) .230) .380) .410 (.157-.340-.320 (.150-.360 (.400-.220 (.170-.370 (.290-.145 (.160-.192) Selected percentiles ( 95% confidence interval) 50th .280) .210-.250-.220) .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 .270 (.260-.170 (.290) .400) .590) .450 (.350-.190-.183) .380-.171 (.440) .260-.280-.200 (.410) .480) .159 (.360-.310-.220 (.360 (. and 0.320) .181-.690) .340) .176 (.177) .460) 861 675 618 561 657 723 801 1114 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.360-.200-.250-.173-.200) .630) .390) .201 (.260 (.370 (.480) .250-.170) .360 (.460 (.430-.380 (.370 (. see Data Analysis section) for Survey years 99-00.170-.148-. 2005).400-.170) .450) .400 (.156-.380 (.290) 90th .430 (.420-. the latter being the current major industrial consumer of thallium in this country. Fourth National Report on Human Exposure to Environmental Chemicals 233 .330-.172 (.510 (.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 .440 (.430 (.370-.153-.217 (.156) .158) .420) .450 (.470) .200) . Thallium disappears from the blood with a half-life of several days.250-. Human health effects from thallium at low environmental CAS No.370-.02.180) 75th .440) .330-.410-.280) . thallium was obtained as a by-product of smelting other metals.460-.200-.400-.178) .250 (.520) .160 (.170 (.185 (.430-.500) .360-.240) .240-.350) .400) .210) .155 (.190 (. 7440-28-0 General Information Elemental thallium is a blue-white metal found in small amounts in soil and in sulfide-based minerals.200-.520 (.220) .410-.217) .200 (.270 (.173) .440) .180-.430) .270-.202 (.167 (.480) .230-.340-.450 (.270-.180 (.160 (.340) .150-.350-.330-.160 (.300 (.280 (.170 (.150-.190 (.300 (.160-.410 (.320) .370-.330-.165 (.260-.290) .133-.156) .370 (.400 (.470) .144 (.170-.290-. In addition.310 (.300) .167-.290 (.370 (.440 (.137-.170-.290 (.230 (.420) .240-.230-.330) .200 (.450 (.390-.380-.410-. In the United States.180 (.510) .140-.390-.220) .360 (.200 (.180-.400 (.183) . Elimination from the body tissues occurs slowly through urine and feces (Blanchardon et al.159 (.320-.500 (.290 (.590) .202 (.440 (. interval) .360-.500) .390) .300 (.400) .400 (.270 (.560) .290) . thallium readily crosses the placenta and also distributes into breast milk.430) .159 (.197 (.218) .470 (.490) .200) .230-.420) .197-.420-.470) .200-.239) . representing distribution into other tissues.230) .160-.220) .450 (.280 (.300) .270) .260) .188) .420) .163) .300) . however.490 (.260 (.520) .145-.150-.170-.240) . respectively.160-.300-.220) .350 (.450 (.330-.201 (.410 (.200 (.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 .390 (.196) .350 (.420-.270) .170) . 01-02.146 (. Thallium exposure occurs primarily from industrial processes such as coal-burning and smelting.420 (.260-.410-.191 (.154-.490) .350) .250) .149 (. 0.350-.147-.173) .134-.243) .330) .196) .490) .

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

Ting BG. Wiegand H. Seventy-eight percent of the urine specimens in that study contained greater than 1 μg/L. Atlanta (GA).95:89-105. Pirkle JL. A study of 46 elements in urine. Pietra R.Metals (CDC. Investigations of thallium-exposed workers in cement factories. 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. Pozzoli L. White and Sabbioni. Available at URL: http://www. Paschal DC.1 mg/m3 (Marcus.. Ewers U. Raithel HJ.113(1):47-53. Martin J-C. 2005. These urine levels are generally comparable to levels observed in earlier studies of general populations (Brockhaus et al.47(3):223-231. Paschal et al. A study of 13 elements in blood and urine of a United Kingdom population. Brockhaus et al. Dolger R. Kramer U. Trace element reference values in tissues from inhabitants of the European community I. Fourth National Report on Human Exposure to Environmental Chemicals 235 . with concentrations ranging up to 76. Int Arch Occup Environ Health 1981. Marcus RL. 1998). Finding a measurable amount of thallium in urine does not mean that the level of thallium causes an adverse health effect. blood. 7/15/09 Blanchardon E.265 people living near a thallium-emitting cement plant in Germany. 1998. Gallorini M. Centers for Disease Control and Prevention. Trace metals in urine of United States residents: reference range concentrations. Nearby residents were exposed by eating garden plants that had been contaminated by the thallium. Int Arch Occup Environ Health 1980. Investigation of a working population exposed to thallium... Buhlmeyer G..216:253-270. Sci Total Environ 1990. et al. Sci Total Environ 1998. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Soddemann H. Schaller KH.35(1):4-9. 2005) and are shown with results from NHANES 2003-2004 in this Report. Radiat Prot Dosim. Sabbioni E. Cassot G.atsdr. Urinary concentrations of 100 μg/L in asymptomatic workers (500 times higher than median levels in the U. Brockhaus A. Long term retention and excretion of 201Tl in a patient after myocardial perfusion imaging. J Soc Occup Med 1985. Jackson RJ. Schaller et al.cdc. There was no increase in the prevalence of symptoms at levels less than 20 μg/L and only a slight increase in nonspecific symptoms greater than 20 μg/L.html.5 μg/L. Minoia C.S. 1985). and serum of Italian subjects. et al. Boisson P. population) are thought to correspond to workplace exposures at the threshold limit value of 0. Valentin H. Sabbioni E. Schmidt M. X. Manke G. 1980. 2005. Challeton-de Vathaire C. Toxicological profile for thallium. Sampson EJ. Third National Report on Human Exposure to Environmental Chemicals. 1990. White MA. (1981) studied 1. 1992 [online]. Apostoli P. Morrow JC. References Agency for Toxic Substances and Disease Registry (ATSDR). Trace element reference values in tissues from inhabitants of the European Union. Minoia et al.gov/toxprofiles/tp54. Intake and health effects of thallium among a population living in the vicinity of a cement plant emitting thallium-containing dust. Celier D. 1981.48(4):375-389.76(1):53-59. Environ Res 1998. et al.

370 (.090 (. Evidence is lacking for the carcinogenicity of tungsten.107 (.270 (.060-.170 (.270 (.151) .150 (.070-. Occupational exposure is from dusts released during grinding or drilling of hard metals.560) .120-. and 03-04 are 0.250) .360-.064-. Most background environmental exposures to tungsten are from the soluble forms such as tungstate salts that may occur in drinking water.330 (. and 0.470) .130) .066-.100 (.090-.080) .160 (.180) .330) .180-.140 (.076 (.080) 75th .070 (.120-.110-.04.400-.390 (.310 (.560 (.116) .570 (.810) . Tungsten is used mainly for producing hard metals. Human health effects from tungsten at low environmental doses or at biomonitored levels from low environmental exposures are unknown.S.240 (.300-.082 (.120) .137 (.250-.800) .060 (.210) .250) .120) .380-.150 (.350-1.350) .160 (.058-.130 (.065-.00) .113 (.500 (. their illness may stem from exposure to cobalt mixed with tungsten carbide rather than to tungsten alone.130) .510-1.135) .640 (.180) .132) .096-.630) .050-.250-.160 (.210 (.093 (.073 (.410) 790 680 618 562 649 723 802 1117 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.230 (.101 (. Little information is available on the toxicity of tungsten.080 (.120-.077-.590) .53) .510 (.550) .360 (.110) .250) . and for producing ferrotungsten. and it has not been classified with respect to its carcinogenicity by either IARC or NTP.370) .230) .090-.340) . 7440-33-7 General Information Tungsten is a steel-gray to tin-white metal that occurs naturally in the earth’s crust.100) .100-.290) .400 (.062 (.070 (.430 (.210 (.110 (.081 (.830) .160-.350) .380-.340-.550) .560) .140 (.082 (.110 (.350 (.093) .620) .158 (.260) .310-.088) .076 (.200 (.068) . and as catalysts in the petroleum industry.070) .220-. see Data Analysis section) for Survey years 99-00.370-.380-.180) .160-.113 (.120) .230-.190 (.090-.073-.069) .060-.111-. respectively.060 (.490) .084 (.570 (.380 (.086 (.270-.078-.520) .100 (.420-.130) .140 (.170) .070-.050-.300 (.160-.560) .109) .095-. filaments for incandescent lamps.050-.370 (.310-.350) .320 (.110 (.550 (.069-.320-.082) .110-.04.070-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.180-.140 (.300) .300 (.123-.220 (.170) .080-.090) .071-. Urinary Tungsten Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.690) .100) .280-.180-.460 (.070 (.080) .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 .270 (.290-.340-.130 (.095-.120-.330) .082-.090-.080 (.230) .080-.380 (.510-.150-. interval) .080) .100-.060 (.420-.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 .070-.073-.204) .210 (.090) .480) Total .073) .060-.140) 90th .105) .104) .270-.290-.180 (.090) .400) .110 (.113 (. population from the National Health and Nutrition Examination Survey.160) .120) .230-.097-.170) .090-.100-.088 (.530 (.096 (.120 (.093-.130-.056-.380) .380-.430 (.670) .120) .460 (.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 .092 (.500 (.090-.620 (.190) .092) .530 (.080 (.200-.370 (.400 (.090-.070) .220) .450 (.070) .220) . 0.150) .133) .092 (.140-.120) . 236 Fourth National Report on Human Exposure to Environmental Chemicals .190-.090-.130) .290-.100 (.110) .100) .087) .090 (.460) .770 (.090) .090 (. which are used in rock drills and metal-cutting tools.180 (.360) .080 (.200) .430) .320-.070-.060-.100 (.070) .250) .320) .410-.190-.170 (.790) .410 (.650) .470 (.560) .240-.320 (.100) .190 (.430-.120-.260 (.060 (.113 (.150 (.580) .430 (.091) .084) .330-.950) .460 (.210 (.230-.190-.130-.230-.360 (.280 (. Tungsten compounds are used as lubricating agents.160 (.160-. 01-02.450-.290) .470 (. Although workers occupationally exposed to tungsten carbide may develop serious lung disease (“hard metal disease”).310) .520) .220) .062 (.065 (.620) .340-.300 (.400 (. bronzes in pigments.260-.530 (.210 (.110 (.390) .180-.060-.190-.170) .100) .074-.360 (.160 (.110-.270-.130-.300) 95th .060 (.430-.250) .056-.122) .100) Selected percentiles ( 95% confidence interval) 50th .140-.310-.800) .310-.260-.071 (.087-.500) .260 (.060-.550) .180) .330-. mainly as scheelite (CaWO4).280 (.270-.290 (.360-. which is used in the steel industry.080-.04.130-.440) .250) .050-.310-.120-.126) .160) .Metals Tungsten CAS No.470-.080 (.130) .400 (.260-.060 (.370-.490 (.470) .520) .084-.170-.101-.460) .105 (.210-.

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 .105 (.359 (.057-.158 (.555 (.091) .136 (.121 (. similar to those in this Report (Schramel et al.179-.086) .341 (.176-.258-.139 (.116 (.267) .169 (.231-..308) ..797) .065 (.Metals Workplace air standards for external exposure have been established by ACGIH and recommended by NIOSH.148 (.139) .120) .151 (.216-.059 (.073 (.154) .S.436) .075) .317-.S.077) .258 (.315-.165) .201 (.143 (.074) .278-.091 (.143-.122-.261-.096) .164 (.364 (.152-.272-.064-.105 (.180-.187) .344-.138) .174 (.054-.333) .056-.079) .360 (.063 (.255-.070 (.216-.211 (.300) .088) .099-.253-.083) .070 (.333-.284) .426) .347 (.170-.300-.554) .181 (.131-.122 (.283) .093-.081 (.081 (.329-.582) .133) .106 (.081) .28) .073 (.117 (.082) .224) .130-.(Kraus et al.080 (. In whereas the tungsten-worker group had mean urine levels a Nevada community where tungsten was measured and 35 times higher.117) .186 (.084 (.317 (.064-.108-.126-.069 (.203-.354-.176-.462) .107-.199 (.426) .146) .125) .270 (. and 2003-2004 (Paschal et al.206-.094) .083 (.138 (.063-.333 (.667) .158) .174) .453) .078 (.068-.136-.482 (.431) .148) .205-.375) .144-.083-.300-.245-.439) Total .179-.075-.308) .145 (.301) .084) .198) .150-. population.340 (.431) .465) .302-.465) .301) .200-.240-. 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. measure urinary tungsten.154) .091) .093) .075-.062 (.061-.386) .072-.339 (.161) .484 (.098-.199 (.072-.077-.065-.167-.216 (.109 (.279 (.279 (.065 (.383 (.095-.100 (.074 (.150-.063-.058-.094-.301) .080 (.065) .092) .294 (. 1997).059-. A study of 14 unexposed adults yielded values that were similar to the 95th percentiles in this Report.267-.201) .100) .108) .061-.054-.136-.237) .190) .109-.233-.124 (.317) . Nicolaou et al.081-.379 (.088) .222) . Using neutron activation analysis to 2000.082) .231 (.250 (.250 (.090-.069 (.082 (.121-.069-.079 (..071) .120) .079) .667 (.124-.055-. A were more than 900 times higher than the overall geometric nonrandom subsample from NHANES III demonstrated mean of the U.439 (.083) .098 (.130 (.063-.200-.158) .098-.286-.500) .125 (.197) .095) Selected percentiles ( 95% confidence interval) 50th .216-.333 (.116-.359 (.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 .150 (.727) .111 (.071 (.087 (.155-.071 (.167) .079) .074-.300 (.250-.169) .063-.279 (.078) .329 (.339 (.080-.197) .100) .098-.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 .414) .071) .153-.431) .538) .084 (.086) .216 (.218 (.094) .119-.071 (.079 (.136-. 2001-2002.059-.079) .139-.103-.060 (.091) .091) .459) .084) .066 (.302-.237-.392) .074-. or exposure that a control group of non-metal workers had mean levels differences.285) .066 (.067-.085 (. 1998).253 (.331-.197 (.087) .089 (.197-.167-.077) .353 (.049-.073 (. 2001).074) 75th .326) .059-.188-.358) .333-.078) .075 (.214) .412 (. interval) .605) . Workers involved in grinding operations that released tungsten metal into the air had elevated urinary levels that Levels of urinary tungsten reflect recent exposure.497 (.085-.237) .104-.217-.823) .306) .053-.215) .075) .072 (.439 (.158) . Biomonitoring Information median urinary levels were as much as 15-fold higher than median levels in the U.138 (.056-.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 .255 (.136-.880) .063 (.168 (.133) 90th .089) . population (CDC.385 (.333 (. population in the NHANES 1999-2000 slightly higher values than those found in NHANES 1999.146 (.061-.253) 95th .060-.146 (. 2003.060-.119 (.275 (.067 (.215 (.198-.333 (.184 (.381) .098) .057-.354) .287) .255 (.217-.209-. population from the National Health and Nutrition Examination Survey.452-.739) . 2005).091 (.436-1.133) .065-.333) .S. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.068 (.208-.071) .299 (.153) .078-.484) .086) .214-.075 (.071-.083 (. Patients with medically-inserted tungsten found at increased levels in drinking water.353 (.085) .293 (.122-.144 (.086-. (1987) found possibly due to methodologic.634 (.067 (.090-.080-.077-.157) .410-.265 (.073 (.167) .116) .222-.078 (.065-.

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

025-.021) .043 (.007 (.037) .015 (.012) .011) . and 03-04 are 0.114 (.008-. 235U (about 0.005-.015 (.012 (.008 (.027 (.046 (.012 (.019-. In workplaces that involve uranium mining.051) .009 (.026-.013) 90th .009-.027) . in some ceramics.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 .026-.279) .045) .031 (.026 (.013 (.017) .011-.008 (.007 (.040) .016) .016) .009) .020) .020 (.009) .009-.027 (.009-.016) .007-. It usually occurs as an oxide and is extracted from ores containing less than 1% natural uranium.008 (.018) .042 (.039) .008 (.011) .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 .016-.013 (.011 (.007) .040-.010 (.026) .065) .007-.023) .005-. including nuclear weapons. and 234U.006-.007) .011) .007-. 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.008 (.006-.021) .008 (.049) .016-.027) .007-.013-.069) .015 (. Fourth National Report on Human Exposure to Environmental Chemicals 239 .017) .009 (.006-.017-. population from the National Health and Nutrition Examination Survey.030-.012-.009) .010 (.012 (.Metals Uranium CAS No. and 0.042) .027 (.037) .033 (.008) .020-.011) .006-. 0.050) .019 (.006-.012) .010) .010) .013 (.009) .046 (.009) .026 (.046) .054) .072) .050) .005-.021 (.008 (.036-.017 (.012) .067) .008 (.015-.030) .021 (.007-.008 (.035) .010) .055 (.052 (.008 (. interval) . nuclear fuel.005-.008 (.014 (.023-.066) .037) .009) .S.006-.037 (.028 (.010-.026) 95th . the primary exposure sources for nonoccupationally exposed persons are dietary (especially root vegetables) and drinking water.041 (.023 (.016) .008-.012-.009 (.028 (.009-.013) .011 (.009-.023 (.028 (. see Data Analysis section) for Survey years 99-00.013 (.015) .037) Total .007) .006-.010 (.008-.048 (.030 (.020-.018 (.028-.021) .010) * .006 (.008-.053 (.007-. 7440-61-1 General Information Uranium is a silver-white metal that is extremely dense and weakly radioactive.012) .010 (.044 (. Since the 1990’s.014 (.008 (.021 (.007 (.036) .017) .017-.034-.011-.036 (.005.006-.009) . milling.007 (.009) .024-.037-.038) .029-.018 (.007-.036 (.006-.010) .008 (.027-.008-.016-.043) .048) .045) .007) 75th .026) .022-.053) .011-.020-.033 (.073) .009-.009-.017) .036) .008) .010-.034) .008) .039-.046 (.009 (.017-.015 (.006 (.011-.031 (.027-. Uranium has many commercial uses.007-.056) .013-.040 (. human exposure occurs primarily by inhaling dust and other small particles.008 (.031 (.009) * .032 (.006-.010) .022-.011-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.019-.033) .008 (.008) .007-.011) .040) .024 (.021-.007-. Natural uranium is a mixture of three isotopes: 238 U (greater than 99%).046-.023) .009 (.005-.009-.018) .035) .067) .017) .022-.007) . and as an aid in electron microscopy and photography.010-.027-.028-.023-.034-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.014 (.038 (.004.031 (.033-.008 (.016) .065) .011-.020-.010) .012-.039) .029 (.012 (.031-.012-.017 (.064 (.007-.012-.017-.010-.040 (.038) 340 368 289 719 762 725 1405 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .007 (.009 (.009) .049) .013 (.014 (.009) .007-.027) .016) .009) .006-.024-.007 (.007-.026 (.023-.013 (.012 (.021-.011) .009 (.018) .022 (.009 (.030 (.009) .019-.041 (.007-.006 (.027) . 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-.007 (.72%).018) .008-.063) .006 (.046 (.010 (.010) .013-.006-. respectively.016 (.020) .035-.022) .030 (.007-.008-.027 (.014 (.007-.007 (.036-.007-.158) .010-.007 (.011) .012-.088) .009) Selected percentiles ( 95% confidence interval) 50th .009 (.010) .019-.040-.008 (.127) .023 (.004.024-.018-.010-.007 (.017-.012 (.056) .011-.006-. 01-02.009-.013 (.054-.060 (.007) .031 (. or processing.007 (. DU has been used by the military in armor-piercing ammunition and as a component of protective armor for tanks.036) 883 683 618 568 667 722 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.009-.008-. Variable concentrations of uranium occur naturally in drinking water sources.014 (.015) .047 (.054) .009 (.017-.010) * .020-. Thus.009) .008) .029-.062) .007-.023) .

016) .015) .025-.007 (.007 (.007-.010 (.016-.024 (. 1992).047) . liver.006) .016) .011) .008-.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 .009) .012) .016) .019 (. Soluble forms of uranium salts are poorly absorbed in the gastrointestinal tract.006) .015-.027-.017) .027-.011) * .007 (.013 (.013 (.018 (.011-. 0.015-. which represents distribution and excretion.005 (.009-.011) .006-. 2003).026 (.012 (.017-.011 (.050 (.010-.034 (. Depending upon the specific compound and solubility.006-.009) .028-.015-.017-.007-.017) .017 (.033 (.039) Total .034-.024 (.048) .010 (.022 (.008-.015 (.006-.011-.018) .033 (.005-.030) .022-. 2005).015 (.011-.013 (.Metals impact.015 (.010) * .009 (.012 (.010-.034-.009 (.019-.029) .016) .007 (.034 (.024-.013) .025 (.019) .042-.006-.011-.007-.035 (.080) .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.008 (.010-.011-. After exposure to soluble uranium salts.024) .027-.009) .043 (. where limited absorption occurs (less than 5%).008) 75th .006-.011-.010) .019-.013 (.032) .030-.033 (.035 (.020) .007 (.017-.S.018-.006) .013-.039) .026-.006-.009-.020 (.008 (.013 (.021 (.058) .006-.007-.009) .007 (.011-.025-.010-.007-.031 (.007) . which can occur occasionally from high occupational exposure.007 (.027 (.006-.008 (.008) .050) .015) .061) .010 (.014-.007 (.004-.007 (. with much slower elimination from bone.008) .024 (.007-.033) .012 (.005-.006 (.006-.146) .014-. 240 Fourth National Report on Human Exposure to Environmental Chemicals .012 (.074) .016 (.009) .010-.015-. the shrapnel acts as a source of chronic.006-.020-.028 (.007) .038) 340 368 289 719 762 725 1405 1559 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .030 (.045 (.024-.044) .007 (.058) . kidneys.006-.007-.014) 90th .006) .014) .006-.029) .015 (..032) .007 (.019) .009-.021) .027 (.013 (.019 (.006-.011-.017 (.006 (.051) .013 (.006-.008-.008 (.024-.006-.021 (.008 (.009) .030) .018-.015-.056) .010-.014) .025-.041) .009 (.006 (.006-.028 (.012) .010) .006-.016-.009) .018-.007 (.021 (.054) .014 (.051 (.005 (.007 (.013 (.015) .013) .027) . Human health effects from uranium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.007-.007-.007 (.020 (.026) .007 (.008) .028) .010) .077) .008) .031-.008) .008-.020-. the half-life of insoluble uranium in the lungs is several years (Durakovic et al.027 (.029 (.028) .008-.026 (.006-.007-.008) .016) .042) .022) .013 (.007) .006-.019-.042) .008 (.013) . After inhalation.012) .006 (.037 (.006 (.007 (.019-..027-.006 (.039) .008-.020 (.008) .030 (.029) .019 (.010) .024) .024) .020-.039) .033 (.026 (.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 .008 (.022-.007 (. interval) . After long term or repeated exposure.029) .053) .019-.034 (.025 (.009-.005 (.048) .025-.007 (.005-. Inhaled uranium-containing particles are retained in the lungs.015) .006-.034 (.009) .017-.051) .008) .004-.006-.014) .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.005-.028) .023-.029 (.051) .012-.010) .006) .013 (.027) .006-.067) . Radiation risks from exposure to natural uranium are very low.014-.010-.010) .034 (.012 (.034) .024) .009) Selected percentiles ( 95% confidence interval) 50th .009 (.270) .007 (.005-. Health effects from uranium exposure result from chemical toxicity to the kidney.005-.018-.021 (.030-.009-.020-.005-.022-.053) .024) .008 (.016-.007 (.012 (.010-.008 (.009) * .010-.010-.009) .050) .017) .029 (.008) .100 (. the initial half-life of uranium is about 15 days (Bhattacharyya et al.025) 95th .012-.022 (.009) .016-.011 (.009) .014 (.012 (.006-.028) . about 50% of the absorbed dose is eliminated in the urine within the first 24 hours.010 (.009-. low level exposure.009 (.008) .011) ..011-.1%-6% of an ingested dose may be absorbed. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.016) . and bones can accumulate uranium with the largest amounts being stored in bones (Li et al.063) .021-. Uranium is eliminated in feces and urine.010 (.022 (.018-. In cases of retained DU shrapnel.016) . population from the National Health and Nutrition Examination Survey.005 (.008) .006-.030 (.059 (.016) .040 (.007 (.008 (.

cdc. Karpas et al. Kent (England): Nuclear Technology Publishing. and no consistent effects on multiple endpoints of kidney function were found. 2000). (May et al.. Boyd P. Finding a measurable amount of uranium in urine does not mean that the level of uranium causes an adverse health effect. 2005. Biomonitoring Information Levels of urinary uranium reflect recent and accumulated exposure. Guidebook for the treatment of accidental internal radionuclide contamination of workers. with emphasis on quality control. 1999) and other small populations have shown urinary concentrations that are similar to those in NHANES 1999-2000. References Bhattacharyya MH. Zimmerman I. Older studies have demonstrated urinary uranium concentrations that are consistent with levels in the U. Fourth National Report on Human Exposure to Environmental Chemicals 241 . and 2003-2004 (Dang et al. Workplace air standards and guidelines for external exposure to soluble and insoluble uranium compounds have been established by OSHA and ACGIH. Benedik L.. Byrne AR. 1994. Sci Total Environ 1991.. Durakovic A. 2006).e. 2002.078 μg/L (ranging up to 5. 2004). Recent studies of veterans have been conducted to examine concerns about DU exposure during military conflicts..S. although slightly increased during and after deployment. 2001-2002. 2002).011 μg/L (McDiarmid et al. Pullat VR. the geometric mean urinary uranium concentration was 0.78:143-146.066 μg/g creatinine (Gwiazda et al... 2006). soldiers who had been injured and had embedded DU shrapnel for as long as eight years. 1-49. Hamilton MM.107:143-157. 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. McDiarmid M.. Third National Report on Human Exposure to Environmental Chemicals. or wound contamination. ingestion.1992. Muggenburg BA. Health Phys 1992. Nuclear Regulatory Commission (NRC) has set an action level of 15 μg/L urinary uranium to protect people who are occupationally exposed (U.1996.S. Mil Med 2003.S. Information about external exposure (i. Breitenstein BD. In a much larger study of 446 Gulf War veterans who were concerned about past exposure to DU. Uranium content of blood. in that the levels were below their respective detection limits (Byrne et al.gov/ toxpro2. 1978).S. had a mean urinary uranium concentration of 0. Thomas RG..61 μg/g creatinine.. the median urinary concentration was 0. The U.. eds. Atlanta (GA).. A cohort of 46 U. Radiation protection dosimetry.. urine and hair of exposed and non-exposed persons determined by radiochemical neutron activation analysis. Determining the normal concentration of uranium in urine and application of the data to its biokinetics. A previous nonrandom subsample from NHANES III (n = 499) (Ting et al. 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. In: Gerber GB. Pillai KC. Hamilton et al. 2004).. 2004). Ejnik JW. the median urinary uranium concentration was 2. Drinking water and other environmental standards have been established by U. 41 (1). 28 soldiers who may have been exposed to DU by inhalation. Eighty-five percent of those levels were above the 95th percentile of the NHANES 1999-2000 population. Determination of the isotopic composition of uranium in urine by inductively coupled plasma mass spectrometry. 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. but in whom no shrapnel was embedded. Horan P. Squibb K. (Kurttio et al. Komaromy-Hiller et al. soldiers evaluated before. EPA. population. 2006).62:562-566.55 μg/L (median 0. In 17 U. urinary levels of uranium were as high as 9. Volf V. Vol. Dietz LA. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.S. 2000). 1992. pp.html. 2006. 1991.168(8):600-605. Carmichael AJ. NRC. Estimate of the time zero lung burden of depleted uranium in Persian Gulf War veterans by the 24-hour urinary excretion and exponential decay analysis..S...atsdr. Six workers in a depleted uranium program showed concentrations of 0. 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. Galletti.162 μg/L) (Orloff et al.110 to 45 μg/L (Ejnik et al. environmental levels) and health effects is available from ATSDR at: http://www. In two studies of a Finnish population with high natural uranium concentrations in their drinking water. McDiarmid et al. Centers for Disease Control and Prevention (CDC). In the same study.. In a study of 105 persons exposed to natural uranium in well water. Tolmachev et al. 2004). IARC and NTP have no ratings for uranium human carcinogenicity. et al.Metals injury associated with elevated urinary uranium levels (Kurttio et al. 2006).. during. respectively.65 μg/L). Dang HS. Stradling GN. Health Phys 2000. 2003.

Karpas Z. et al. U. Am J Kidney Dis 2006. Howerton K. Scott K. Makelainen I. Sampson EJ. Kuwabara J. Squibb K. Lewis BM.85:228-235. et al. et al. Clin Chim Acta 2000. Smith D. Health Phys 2003.110(4):337-342. Environ Health Perspect 2002. Van der Venne MT.87:51-56. Katorza E. rapid. et al. May LM. et al. Shelly T. Biokinetic modeling of uranium in man after injection and ingestion. Salonen L. Saha H. Environ Res 2004.67(8-10):697-714. Marino R.22–Bioassay at uranium mills. patient population and literature reference intervals for urinary trace elements. Comparison of representative ranges based on U. 242 Fourth National Report on Human Exposure to Environmental Chemicals . Renal effects of uranium in drinking water. Sabbioni E. Cordero S. D’Annibale L.71(6):879-85. et al. Kalinsky V. Pirkle JL. Paretzke HG. Human exposure to uranium in groundwater. Komaromy-Hiller G. Andrews WS. Squibb K. Hancock RG. Auvinen A. Metcalf S. Auvinen A. Kidney toxicity of ingested uranium from drinking water. plasma and urine and a critical evaluation of reference values for the United Kingdom population. Hamilton EI. Kurttio P.47(6):972-982.79(1):11-21. Paschal DC. Ting BG. Roiz J.44:29-40. Gwiazda RH. Englehardt SA.94:319-326.86:12-18. and inexpensive method for determination of uranium in urine and fresh water: comparison with LIF. Washington (DC): NRC. Health Phys 2004. Detection of depleted uranium in urine of veterans from the 1991 Gulf War. Hollriegl V.158:165-190.296(1-2):71-90. Lorber A. Costa R. Li WB.S. Sci Total Environ 1994. Harmionen A. Jarrett JM. U. McDiarmid MA. Salonen L. Gucer P. Oberbroekling KJ. An examination of uranium levels in Canadian forces personnel who served in the Gulf War and Kosovo.81:45-51. Ash KO. Pinto V. Mistry K. Tolmachev S. Wilson PD. July 1978. J Toxicol Environ Health A 2004. Health Phys 2002. Environ Res 1999. Nuclear Regulatory Commission (NRC) Guide 8. Noguchi H. Charp P.Metals Galletti M. Ejnik J. NRC).S. Oliver M. Uranium daily intake and urinary excretion: a preliminary study in Italy.91(2):144-153. Biologic monitoring for urinary uranium in Gulf War I veterans. McDiarmid M. Bennett LG. Health Phys 1996. Int Arch Occup Environ Health 2006. VI. Halicz L. Nuclear Regulatory Commission (U. Cremisini C. Inductively coupled plasma mass spectrometry as a simple. Pekkanen J. Health Phys 2004. Engelhardt SM. Wahl W.82(4): 527-532. Marko R. concentration and daily excretion of uranium in urine of Japanese. Saha H. Review of elements in blood. Kane R. Oeh U. Health Phys 2006. Ough EA. Radiat Environ Biophys 2005.S. Jackson RJ. Element reference values in tissues from inhabitants of the European community. Roth P. Heller J. Uranium and thorium in urine of United States residents: reference range concentrations. Karpas Z. McDiarmid MA. Kurttio P.S. Military deployment human exposure assessment: urine total and isotopic uranium sampling results. Orloff KG. Komulainen H. Biological monitoring and surveillance results of Gulf War I veterans exposed to depleted uranium.

20-11.90-11.60 (4.0 (11.70-5.40) 2.80) 3.20 (2.50) 5.70-11. laboratory analysis.75 (3.00) 3.80 (7.40-4.0 (13.80-4.90-11.90-9.40-6.0 (8.40 (4.0) 9.90) 6.70 (3.11) 4.0) 10.60) 8.00) 7.0-20.50-7.90 (5.0) 13.90-3.0 (11.40 (3.67-5.54 (3.50) 5.0 (9.70-7.70 (3.0-17.g.90-3.0) 9.56) 3.5 hours and has a small estimated volume of distribution (Crump and Gibbs.50-4.40-11.0 (11.0-23.0) 14.00) 4.90 (3.87-3.0) 11.0) 14.30-17. potassium.50 (5.80) 75th 6.10) 5.10 (6. 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. Animal and human studies have shown that perchlorate can inhibit thyroid hormone production (NAS.09) 3. and certain plants with high water content (e.40 (3.22-5.12) 3.55) Sample size 2820 2522 01-02 03-04 01-02 03-04 01-02 03-04 4. or ammonium salt.20 (5.96 (3. 2005).40) 3.89-3.00-6.65) 3.0 (11.81-16.60-7.60) 3.76) 4.0) 13.0 (11.0) 10.0 (8.0) 10.51 (3.03) 3.80-6.60 (7.0) 14.40) 3.60 (4. fabric dyeing.0) 11.90 (5.19-4.0 (11.32 (3.10) 3.10 (7. Perchlorate has been characterized as a mobile and persistent ground and surface water contaminant. It is normally found and produced as the anion of a sodium.0) 374 314 828 721 1618 1487 01-02 03-04 01-02 03-04 4. 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) 3.0-19. and reducing agents.0 (11.30-19.0) 13.21 (2.81) Selected percentiles ( 95% confidence interval) 50th 3.90-10.49-3.0) 19.50 (3. Large doses of perchlorate have been used as a medicine to treat hyperthyroidism and to diagnose disorders related to thyroid or iodine metabolism. 2001-2002 performed on surplus samples (variable unavailable of NHANES website) Fourth National Report on Human Exposure to Environmental Chemicals 243 .0-15.70-12.0) 9.0-17.90) 5.40) 6.66) 3.20-3.88) 3.10) 5.70) 3.35 (3.0-17.00) 5.01 (2.11) 3.75-3. Perchlorate is excreted unchanged from the human body with an estimated elimination half-life of about 7.29-3.0 (12.70-9. small amounts of perchlorate can form naturally in the atmosphere (Dasgupta et al. population from the National Health and Nutrition Examination Survey.S. 7601-90-3 General Information Perchlorate is an inorganic chemical containing one chlorine and four oxygen atoms.20 (8.76 (3.30) 6.08-3.40 (5.0) 1335 1229 1485 1293 01-02 03-04 01-02 03-04 01-02 03-04 4.70-3.40) 3.40-13.0) 12.0) 8.90 (2.44-4.0) 11.0 (9.20-4.20 (4..20 (2.40-4.0 (9.30 (2.10 (6.20) 4.74-3. Drinking water. but has strong oxidant properties in the presence of concentrated acids. In addition.0 (11.0 (12.30 (5.EPA.0) 9.10-11. lettuce) can be the main sources of intake for humans (FDA.S.31) 2.26 (2.0 (11.10-4.0-17.93-3.30-7.0 (8.80) 7.84) 14.68) 4.0 (9.90-9.00-6.0 (9.0) 16.0-17.93 (4.80-12.16) 3.0-18.40-5.80 (3.51 (3.20-4.60) 5.70-6.90 (4.50) 3.80 (6.0-15.0-18. 1998).20 (7.0 (11.40 (4. 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.90-6.46) 3. 2002).60-6.40) 90th 10.90 (5.0) 13.80 (3.0-18.40-7.0 (9.22 (2.30) 6. certain catalytic metals.10-11. Survey years 01-02 03-04 Geometric mean (95% conf.0) 13.40 (5. matches.80) 12. Other manufactured uses include fireworks.0) 8.S.30 (2.20) 3.0) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites 3.0) 708 617 681 652 1228 1092 Limit of detection (LOD.39-4.0) 95th 14.10 (5.80-4.Perchlorate Perchlorate (Urbansky.05.10-7.00) 3.50-11.0-14.50) 11.0 (12. 2005).93-4.0 (10.20 (6.0 (8.50-4.20 (4.50) 6. and electroplating.20-12.0) 15.0) 9. interval) 3.62 (3.38) 5.0) 9. milk.79 (2.0-17. see Data Analysis section) for Survey years 01-02 and 03-04 are 0. leather tanning. Perchlorate is stable under most environmental and physiological conditions.18-3.30-6.19 (3..50-3. Perchlorate was added to the U. and limited applications in pharmaceutics.40 (8.40 (5. 2007).0) 13.50 (8.05 (2.05 and 0.80-15.70-3.10 (2.10-12.45-4.90-12.0) 15.47-4. 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.07-4.0) 13.02 (3.70 (3.0 (12.40) 4.10) 12.80-8.30 (5.0 (8.0-29.0) 13.30-7.00-5.20) 7.

Though it produces follicular cell thyroid tumors in animal studies at goitrogenic doses.93-7.60-8.89-3.80 (4.44-6.50) 5.3-14.22-4.52 (8.0) 12.0-19.20-4.07 (2. 1999.10 (2.45) 3.82 (5.60-3.33 (7. 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.70-4.40-10.7 (11..73) 3.00) 9. However.83 (5.90-9.0 (11.97-5.15-12.46-4.33-12.20-10.33-6.34-3.80-3.93-5.0) 14.40 (3. levels.64) 5.00-2. 2005).2) 8. women with urinary levels of iodine less than 100 micrograms per day.10-3.0) 10. 2002).6) 20.30) 90th 9.41) Sample size 2818 2504 01-02 03-04 01-02 03-04 01-02 03-04 5.0 (11. menopausal status.40 (3.04-3.39-4.0) 12.4 (11.26) 4. thiocyanate.00 (4.35) 3.59) 3. urinary perchlorate at environmental exposure levels were inversely associated with thyroxine levels and positively associated with levels of thyroid stimulating hormone (Blount et al.00-3.1 (8.61-10.37 (4. dietary iodine intake. Short term human studies of the effect of perchlorate on RUI have been used for risk estimation (Greer et al.0) 4.00) 4.58) 2.26 (3.0) 6.39 (3.54 (2. it is known that maternal and congenital hypothyroidism adversely effects neurological development and decreases learning capability.71 (5.S.30-5.19-10. although iodine intake was higher than U.70 (2.00) 3.09 (7.4 (11. 2005.30 (5.20-3.30 (6.02-4.90 (7. 2006.12 (6. nitrate.99-3.21 (2.25 (3. 2005).64-3.0) 11.42 (3.61-5.3) 8. 2001.20 (7.6-17. gender.60 (3.10) 13.95 (2.0 (9.5) 8.0) 9..84) 2.43) 6.1-14.75) 3.25) 5.S.08) 3.87 (7.EPA.40 (4.40) 5.50-3.0-44.41-9..90-2.90-20. perchlorate is negative in most genotoxic assays (U. Lamm and Doemland.90-11.87) 2.35 (2.0 (9...0) 1335 1220 1483 1284 01-02 03-04 01-02 03-04 01-02 03-04 3.. NAS.3) 11..08 (3.. up to 68% RUI has been demonstrated.91) 4.47) 2.40) 3. chronicity of exposure.Perchlorate inhibition (RUI).87) 7. levels and sufficient in most participants (Tellez et al.24-2.90-3.52-9.50) 2.93) 3.96) 2.25) 5.22 (2.5 (13.60-6.44) 3.25) 5.03 (2.60) 10.0) 13.04-3.0 (8.50-9.29-6.22-4. 2005). Many factors may be important in consideration of perchlorate action on the thyroid: dose.70 (4.20 (2.4 (8.70 (2. population from the National Health and Nutrition Examination Survey. Li et al.8 (11.50) 9.20) 3. but without effects on serum levels of thyroid stimulating hormone or thyroxine (Braverman et al.0-17.4) 8. suggesting its tumorgenic effect is a result of a chronic increase in thyroid stimulating hormone indirectly resulting from iodine uptake inhibition.90 (2.20-9.0) 13. Survey years 01-02 03-04 Geometric mean (95% conf.10) 3.0) 7.50) 6.60-15.54 (3.1) 8.76 (3.90) 5.66) 3.S.4 (10.6) 12.90 (4.70-15.90 (2.80 (7. During gestation and infancy.10 (4.20 (4.32) 5.76-3.0 (8.22-6.36 (8.70-3.30) 3.60-5.00-11.20) 8.50 (3.60-5.40) 17. Steinmaus et al.60-11.1-13.70) 10.0-14.0) 12.S.24 (4.10 (1.60-11.37-13.93-5.0) 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 3.60) 8.0 (10. 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. 2007). 2005.99 (5. 2003.56-3. in a representative sample of U.10) 4.87-3.S.02) 3.67) 5.2) 8. Also. 2002. age.10 (6.56 (3.35 (4.10 (4.19-6.40 (7.4) 13.50) 95th 12. Greer et al.30 (3.50-5.0) 374 313 827 715 1617 1476 01-02 03-04 01-02 03-04 3.1-22.0 (11.05 (4.4-16.10-7.93-8. 2002. 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.29) 2. In the U.1 (11.12-2.0-14.3) 12.80-3.30-5.60-8.87 (5.3 (10.0 (9.50) 2.S.53 (2.90-15. congenital hypothyroidism is a condition for which nearly all newborn blood is screened.77 (3.98) 3.81-3.20 (3.39) 2.51-4.70) 2.18-3.g..86) 4.51 (3.30) 5.61 (5.20 (6.89 (2. interval) 3.30) 75th 5. 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.00 (6.EPA.00 (2.80) Selected percentiles ( 95% confidence interval) 50th 3.45-2. and the presence of other substances known to affect thyroid function (e.50 (6.46 (3.10) 6.70-5.09) 3. 2000).S.72 (3.0) 708 616 680 648 1227 1080 2001-2002 performed on surplus samples (variable unavailable of NHANES website) 244 Fourth National Report on Human Exposure to Environmental Chemicals .46-13. Lawrence et al. medications).0) 12.14 (2.0) 9..80 (7. U.74) 7.16-3.20-3.1-16.30-10.60) 3.

Braverman LE. Osterloh JD.11(3):295. Kirk AB.atsdr. Health effects assessment for environmental perchlorate contamination: the dose response for inhibition of thyroidal radioiodine uptake in humans. Low dose perchlorate (3 mg daily) and thyroid function. Additional information about exposure and health effects is available from the U. J Occup Environ Med 2003.html. When these NHANES 2001-2002 urinary levels of perchlorate are used to calculate daily oral intakes for the U.. Landingham CB. Erratum in: Environ Health Perspect 2005. Richman K. Tellez RT.10(8):659-663. Barnard JC. Crump KS. Neonatal thyroxine level and perchlorate in drinking water. Impact of smoking and thiocyanate on perchlorate and thyroid hormone associations in the 2001-2002 national health and nutrition examination survey. EPA reference dose (Blount et al. Washington (DC): National Academy Press. and nitrate on thyroid function in workers exposed to perchlorate long-term. Lawrence JE. Crump KS.EPA at: http://www. Page Last Updated: 05/28/2009. Sesser DE. J Clin Endocrinol Metab 2005.html and from ATSDR at: http://www.40(21):6608-6614. 2001-2002.gov/Food/FoodSafety/ FoodContaminantsAdulteration/ChemicalContaminants/ Perchlorate/ucm077653. Pirkle JL. Miller MD. Pleus RC. Pirkle JL. Skeels MR. The levels seen in NHANES 20032004 show a similar pattern to NHANES 2001-2002. Jackson WA.17(4):400-407.S. Dyke JV. et al. Lamm SH. population.110(9):927-937. Gibbs JP..gov/safewater/ccl/perchlorate/perchlorate. J Expo Sci Environ Epidemiol 2007. Erratum in: J Occup Environ Med 2004. most of the population is considered to be below the U. Abarca CR.113(8):10011008. Pino S. Finding a measurable amount of perchlorate in urine does not mean that the level of perchlorate causes an adverse health effect. Kelsh MA.90(2):700-706. May 2007. Chacon PM. Environ Health Perspect 2007. epa.46(5):509. Available at URL: http://www. Lamm S. Long-term environmental exposure to perchlorate through drinking water and thyroid function during Fourth National Report on Human Exposure to Environmental Chemicals 245 . et al. Doemland M.S. Greer SE. 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. Li FX. Food and Drug Administration (FDA). Dasgupta PK.htm. Lau EC. J Occup Environ Med 2000. Blount et al. Lawrence J.113(11):A732. Caldwell KL. References Blount BC. Steinmaus C. Valentin-Blasini L. Environ Health Perspect 2006. Daaboul JJ. Primary congenital hypothyroidism. Lamm SH.45(10):1116-1127. Lamm SH. Cross M. 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.gov/toxpro2. Perchlorate Exposure of the US Population. 2007). Perchlorate in the United States. National Academy of Sciences (NAS). Braverman LE. Also. Urinary perchlorate and thyroid hormone levels in adolescent and adult men and women living in the United States. Blount BC. Thyroid 2000. Has perchlorate in drinking water increased the rate of congenital hypothyroidism? J Occup Environ Med 1999. Benchmark calculations for perchlorate from three human cohorts. The effect of perchlorate.S. Byrd D. 2005). thiocyanate. Li Z. Compared to a previous study of pregnant women in three Chilean communities with varying perchlorate levels in the drinking water.41(5):409-411. Biomonitoring Information Urinary perchlorate levels reflect recent exposure. et al. 2005). Blount BC. Health Implications of Perchlorate Ingestion. 6/2/09 Greer MA.fda. Thyroid 2001. Rutherford GW. Valentin-Blasini L. Buffler PA. Environ Health Perspect 2005. Analysis of relative source contributions to the food chain. Howd R. Magnani B. National Research Council of the National Academies. newborn thyroid function.114(12):1865-1871. The effect of short-term low-dose perchlorate on various aspects of thyroid function. (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. Environ Health Perspect 2002. et al. and environmental perchlorate exposure among residents of a Southern California community. Osterloh JD.42(2):200-205. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.Perchlorate be unlikely to occur without overt perturbation of thyroid homeostasis. He X. Deyhle GM.. CFSAN/Office of Plant & Dairy Foods. 2005. Mauldin JP. 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. Goodman G. Pino S. Preliminary Estimation of Perchlorate Dietary Exposure Based on FDA 2004/2005 Exploratory Data. Braverman LE.cdc. Environ Sci Technol 2006.115(9):1333-1338.

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

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

It is unclear if environmentally degraded telomer products are a major source of other PFCs. and in human blood and semen (Calafat et al. The ammonium salt of PFOA has been tested at high doses in mammalian animal studies and produced altered weights of the liver.. 2005. 2003). peroxisomal proliferation. Serum Perfluorobutane sulfonic acid (PFBuS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U. Kannan et al... growth retardation and delayed sexual maturation (Kennedy et al.4. PFOA has been reported to cause liver..S. 2003a and 2004a). 2003. The PFCs often measured in human serum are listed in the table. kidney. endocrine and immune effects. the perfluoroalkyl acids (PFOA and PFOS) do not tend to accumulate in fat tissue. Survey Geometric mean (95% conf. 2005). 2004.. All sources of human exposure are uncertain. pancreas.. 1995.5 years and for PFOS. heptadecafluoro-1-decanol.. PFOS and PFOA levels in archived bird eggs from Sweden have increased thirtyfold from 1968 to 2003 (Holmstrom et al. Olsen et al. The elimination half-life of PFOA in humans is roughly estimated to be 3. but probably include dietary sources (Kannan et al. 2004). including immunologic effects and tumor induction. The liver toxicity of several PFCs is evident by vacuolization and lipid accumulation in both rodent and monkey livers (Seacat et al. PFOA (and probably other perfluoroalkyl acids) exist in the anionic state at physiologic and environmental pHs and their distribution in the body is determined. in a wide variety of marine and land animals (Kannan et al. Guruge et al. C5. C7). population from the National Health and Nutrition Examination Survey. thymus and spleen. 2005).. 2005.. U. 2006. For instance..e. Excepting PFOS and PFOA. but the relevance of peroxisomal pathways in humans is unclear (Kennedy et al. 2000. 2005). Tittlemier et al.Perfluorochemicals PFOS greater than 2000-fold over aquatic levels). the 8-2 telomer. Bookstaff et al.. 2006a. Lau et al. or effects of other PFCs. Vanden Heuvel et al.S. Some of the effects in animals may be mediated through peroxisomal proliferation. Prevedouros et al.. < LOD means less than the limit of detection. but still can have long residence times in the body.... 2004) and may be attributable to the ability of PFCs to affect intracellular lipid binding proteins. 2004. by high protein binding in plasma and other proteins. 2002. 248 Fourth National Report on Human Exposure to Environmental Chemicals . 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... there is limited information on the sources.. Unlike many organohalogen contaminant chemicals. human toxicokinetics. 2007). hepatotoxicity. 2004. may metabolize or degrade to PFOA (Dinglasan et al. Human health effects from PFCs at low environmental doses or at biomonitored levels from low environmental exposures are unknown. environmental fate. EPA. PFCs have been identified in surface coastal and ocean waters (Yamashita et al. which may vary for some chemicals by year and by individual sample. in part. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.. Keller et al. 2004)... In some cases. C6. PFOA preparations used in many studies may also contain a small percentage of other chain length perfluoroalkyl acids (i. 2005.8 years (Olsen et al. Lau et al. and in offspring. but limited observations in humans suggest that only one-fifth of the total body clearance is renal (Harada et al. 2004. approximately 4. 1990).. Taniyasu et al. and β-oxidation of lipids (Kudo et al. PFOA is mostly excreted in the urine in animal studies. 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. 1993).. 2003). 2007a). Both PFOA and perfluorodecanoic acid have been shown to reduce androgen levels in laboratory animal studies (Biegel et al. see Data Analysis section) for Survey year 03-04 is 0...

and other PFCs have not been classified as to human carcinogenicity by IARC or NTP. 2004).10) .400-1.500) . At high but non-toxic maternal doses of PFOS. thyroidal).400) . reproductive.Perfluorochemicals and testicular tumors in high dose animal testing (Biegel et al. A study of workers chronically exposed to primarily PFOA showed no biochemical evidence of hepatotoxicity or hormonal changes (adrenal.900 (. Late gestational exposure to PFOS in animal studies has also demonstrated early neonatal lethality. PFOS.500-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result..400-1.800 (.. Roughly similar levels of PFCs in serum have also been measured previously in other samples of the U.300-1. 2007a. Thibodeaux et al. Animal studies of PFOS have demonstrated weight loss. U. Analysis of the NHANES 20032004 subsample demonstrated higher levels of PFOA and PFOS in males and a slight increase in levels of PFOS with age (Calafat et al. 2007).S. monkeys. 2004.80) 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 .108 times higher than background serum levels in humans (Butenoff et al. Kennedy et al. 1992.600 (. 2003).800) 1.500) . 2003).400 (<LOD-.3.00) . Fei et al. 2003a. 2003a).700) . and changes in thyroid hormone concentrations (Grasty et al.800 (...600-2..500 (. population. 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. U. 2007b. 2003.80) 640 1454 03-04 03-04 * * < LOD < LOD . Due to marked intergender differences in the elimination of PFOA in rats and substantial differences in the half-life of PFOA in rats. Slightly higher levels of PFOS and PFOA in males than females have been noted in several other studies (Calafat et al.80) 485 538 962 Limit of detection (LOD.. 2007b).. the median PFCs values tend to be roughly similar in these age categories (Olsen et al. Harada et al. 2004a. At doses causing maternal toxicity.500-3. Cook et al.500-1. hepatotoxicity. < LOD means less than the limit of detection. developmental and teratogenic effects were demonstrated in offspring. Twelve different PFCs were measured in the sera of NHANES 2003-2004 participants...00) . Biomonitoring Information Serum levels of PFCs (particularly PFOA and PFOS) tend to reflect cumulative exposure over several years..20) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD . In comparing three separate reports on adults.400-1. development in offspring was stunted and hypothyroxinemia was observed.500) . which may vary for some chemicals by year and by individual sample.600 (. or increased cancer rates (Alexander et al. Survey Geometric mean (95% conf. PFOS.500-1.00) . 2007a. 2004.10 (. Serum Perfluorodecanoic acid (PFDeA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.400-1. 2004b).S. Olsen et al. 2003.800 (.400 (<LOD-. 2005). Two recent cross-sectional human studies observed a negative correlation of birth weight with serum levels of PFOA (Apelberg et al. 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. In such studies. population from the National Health and Nutrition Examination Survey. However. elderly and children. possibly related to lung immaturity (Lau et al.500) .400-1.300 (<LOD-.. 2005).. 2003a). Effects on serum liver enzymes in limited observational studies of human occupational exposures are unclear..800) 1.40) .. and no substantial age trends were seen within adults ages 20-69 (Olsen et al.500) 90th .00 (.10) .400-..700 (.300 (<LOD-. 2001. 2003a. PFOA. 2003).S.400-. the potential to estimate risks to humans from animal doses is uncertain.. interval) Selected percentiles ( 95% confidence interval) Sample 95th . 1999. Lau et al..300 (<LOD-.400 (<LOD-. and humans. PFOA. 2003a.50) ..900 (.S.. Olsen et al.800 (.500-1. perfluorohexanesulfonate (PFHxS). EPA. 2007. and there was no clear evidence of excess all-cause or diseasespecific mortality...500 (<LOD-1. Fourth National Report on Human Exposure to Environmental Chemicals 249 . see Data Analysis section) for Survey year 03-04 is 0.500 (.20) .10) * 03-04 03-04 * * < LOD < LOD < LOD . animal and human serum PFOA levels have been compared: serum levels associated with toxic effects in animals are 66-11.500-1. EPA.900 (. 2003. Olsen et al. 2004).600 (.

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

see Data Analysis section) for Survey year 03-04 is 1.500) 485 538 962 Limit of detection (LOD.600) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . population from the National Health and Nutrition Examination Survey. population from the National Health and Nutrition Examination Survey.300-.S.600 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.S.400 (. Fourth National Report on Human Exposure to Environmental Chemicals 251 .400 (<LOD-. which may vary for some chemicals by year and by individual sample. < LOD means less than the limit of detection. interval) Selected percentiles ( 95% confidence interval) Sample 95th . see Data Analysis section) for Survey year 03-04 is 0.Perfluorochemicals Serum Perfluorododecanoic acid (PFDoA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.900) < LOD 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD .900) < LOD .300 (<LOD-.500-.600) < LOD . Survey Geometric mean (95% conf.3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.500 (<LOD-. Serum Perfluoroheptanoic acid (PFHpA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U. Survey Geometric mean (95% conf. 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.400 (<LOD-.500) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th < LOD 90th * 03-04 03-04 * * < LOD < LOD < LOD < LOD .400) .0.300 (<LOD-. < LOD means less than the limit of detection. which may vary for some chemicals by year and by individual sample.

70) 2.60 (1.20-1.70-6.10-9.50) 6.70) 2.70-7.10) 1.600-.40) 4.689 (.00 (2.00-8.60-2.10) 1. Survey Geometric mean (95% conf.72 (1.60-7.984 (.86 (1.92 (1.10) 5.70) 1.40) 640 1454 03-04 03-04 1.50 (1.20 (1. interval) .00-1.90 (1.721-1.80) 1.44 (2.80) 5.900-1.816-1.40-1.5) 5.60) 1.60) 3.00) 1.14) Selected percentiles ( 95% confidence interval) Sample 95th 3. see Data Analysis section) for Survey year 03-04 is 0.50 (1.80-6.30) 3.20 (1.30 (2.10-9.10) 8.1) 485 538 962 Limit of detection (LOD.17 (1.90 (1.900-1.20) 1. see Data Analysis section) for Survey year 03-04 is 0.60 (1.03) 1.586-.30 (3.700 (.80-7.3 (9.00 (.10) 6.80-4. Serum Perfluorononanoic acid (PFNA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.20) .90 (1.S.10 (.835-1.70) 1.30 (1.80 (4.80-4.80-3.20 (1.30) .900 (.861 (.60-3.00-6.697-1.72) 1.70-5.834-1.S.93 (1.30 (1.00-7.90-2.05-2.5) 8.30 (2.08) 2.966 (. population from the National Health and Nutrition Examination Survey.80-3.912-1.00 (1.30 (1.70-2.852 (.60-2.10 (4.00 (1.90) 90th 5.60-4.40) 640 1454 03-04 03-04 2.50-6.80-8.80-12.90) 8.50 (6.60-2.70 (1.0) 1053 1041 03-04 03-04 03-04 1.00 (1.10 (.00-1.51) 1.54) .90 (4.900-1. Survey Geometric mean (95% conf.10 (1.60) 9.30-6. population from the National Health and Nutrition Examination Survey.12) .40 (1.90 (4.963 (.30 (6.80-7.50 (2.27) 1.20-1.80) 90th 2.60) 2.80-8.800-1.900-1.Perfluorochemicals Serum Perfluorohexane sulfonic acid (PFHxS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.90 (2.50 (6.80-2.10-5.90) 3.01 (1.10) 4.40) 1.90-19.826-1.00) 1.20 (1.60-3.91) 2.42 (1.70) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 1.70-10. interval) 1.70) 3.40-1.20-1.00 (.0) 8.04) .60-8.20-3.00 (1.40 (1.900-1.09 (.20-2.90-10.16) .20) 485 538 962 Limit of detection (LOD.60 (1.00 (5.6) 7. 252 Fourth National Report on Human Exposure to Environmental Chemicals .80) 4.40) 1.77-2.00) 2.50-6.40 (1.70) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 1.800 (.80 (1.73-2.10 (.30-12.40) 2.20) 03-04 03-04 2.87-2.40 (1.20 (6.90 (1.50) 2.90) 1.50 (1.50-10.1.50 (4.16) Selected percentiles ( 95% confidence interval) Sample 95th 8.10) 6.50 (1.900) 1.50-3.30) 03-04 03-04 .3.56-1.70 (2.90) 1.62-2.10) 75th 1.40-3.90) 1.20-1.30 (7.50 (4.30-2.17-1.70) 13.10) 1053 1041 03-04 03-04 03-04 .50) 2.80) 3.67-2.60-4.80-4.80 (1.40) .700-1.60 (6.70-2.10) 75th 3.14 (.30) 3.900 (.30 (1.30-9.30) 3.10 (4.20) 2.26) 2.20) 1.809) 1.900-1.40 (2.10) 4.20 (6.00) 3.

0-16.50-6.5) 57.0) 485 538 962 Limit of detection (LOD.1) 57.10 (3.3 (44.84-3.10 (3.1-25.2 (27.00 (5.89 (3.40-6.6-50.9) 9.90) 6.50) 4.40-14.6) 35.40-10.80) 8.70-7.30-6.2 (18.1 (24.65-4.7 (7.4-42.00) 3.11 (2.99-3.7 (43.9 (19.6) 62.5 (28.6) 9.47 (4.8-22.1-36.7-69.60 (7.0) 21.37 (2.30-11.4 (19.8-81.20-5.7) 39.60) 03-04 03-04 3.5-23.9-23.60-13.40) 90th 7.6) 42.8) 32.Perfluorochemicals Serum Perfluorooctanoic acid (PFOA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.60-9.5) 9.6 (42.90-4.5 (28.S.95 (3.20) 7.90 (7.70 (5.20) 7.4 (17.7 (35.20) 4.30 (3.60 (3.90 (5.60 (6.3) 28. see Data Analysis section) for Survey year 03-04 is 0.10) 5.96 (3.1.9 (13.8-22.60 (4.6) 18.7-33.30 (5.9) 22. Survey Geometric mean (95% conf.5-62. population from the National Health and Nutrition Examination Survey.27) Selected percentiles ( 95% confidence interval) Sample 95th 9.5-33.8-22.90 (7.3 (28.6) 7. interval) 20.85-4.3-22.40-6.60-14.5) 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 21.50-13.60-6.20) 5.7-23.91) 3.50 (4.90 (7.2 (28.4-25.80-12.10-3.35) 3.0 (27.80-9.2 (21.1) 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 4.3) 41.90-4.5) 7.1) 15.7 (13.20-4.80 (7.6 (35.60 (6.70-5.70-10.2) 30.21-3.30-8.10 (6.53) 3. Serum Perfluorooctane sulfonic acid (PFOS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.80-4.5) 19.80 (6.9 (22.0-20.70) 4.7-53.40 (6.4) 20.79) 4.3 (35.40) 3.4) 640 1454 03-04 03-04 23.0) 03-04 03-04 19.30-5.8 (45.20-9.4) 75th 30.5) 1053 1041 03-04 03-04 03-04 14.1-35.6-24.1-33.4 (23.2) 30.40) 75th 5.1-24.4) 21.4-17.5) 32.5) 8.90-12.0) 21.6 (19.50-4.6 (44.2) 45.3-61.70 (5.8) 46.9-19.9) 22.9) 27.80 (5.8 (37.6-45.7 (43.0) 23.67-4.70) 6.4.50 (3.00 (5.30) 6.0-66.00 (3.0) 90th 41.2 (16.4 (28.0) 36.6) 1053 1041 03-04 03-04 03-04 3.7 (19.3 (35.7 (35.4) 56.70) 3.9 (17.8-30.8) 27.20 (4.7-49.70-9.30 (3.2) 640 1454 03-04 03-04 4.2-57.82) 4.70-7.40) 5.30) 7.8 (34.60) 8.4 (19.20) 10.0 (20.0) 43.20 (4.1 (19. interval) 3.40 (4.3) 485 538 962 Limit of detection (LOD.27) 4.70 (3.3 (17.7-30.20) 5.60 (5. see Data Analysis section) for Survey year 03-04 is 0.50) 7.8-35.0-70.18 (3. Fourth National Report on Human Exposure to Environmental Chemicals 253 .3) 42.6) 21.30-3.80 (6.40-17.9-38.07-4.8-78. population from the National Health and Nutrition Examination Survey.5) 18. Survey Geometric mean (95% conf.S.1-52.2-22.5-21.3) Selected percentiles ( 95% confidence interval) Sample 95th 54.47-4.1 (23.2 (19.

300) .300 (.200-. < LOD means less than the limit of detection.300 (.500) .500) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .300 (. which may vary for some chemicals by year and by individual sample.300) .500) 485 538 962 Limit of detection (LOD.300) . Survey Geometric mean (95% conf.300 (. which may vary for some chemicals by year and by individual sample. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th < LOD 90th * 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .300 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th .400) 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.300-. Survey Geometric mean (95% conf.200-.200 (<LOD-.300-.4.300) .300 (.300 (.400 (<LOD-.500) .300) . see Data Analysis section) for Survey year 03-04 is 0.300 (. population from the National Health and Nutrition Examination Survey.300 (.200-.200-.200-.300 (.500) < LOD 485 538 962 Limit of detection (LOD.S.300 (.S. see Data Analysis section) for Survey year 03-04 is 0. population from the National Health and Nutrition Examination Survey.300) .300) * 03-04 03-04 * * < LOD < LOD < LOD < LOD .Perfluorochemicals Serum Perfluorooctane sulfonamide (PFOSA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.2.200-.400) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th 90th .200-.300-.200-. 254 Fourth National Report on Human Exposure to Environmental Chemicals .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.300 (.300 (.300 (.200-. < LOD means less than the limit of detection.500) .200-.300) .

10-1. Survey Geometric mean (95% conf.10-1.30) 1.70) 1.Perfluorochemicals Serum 2-(N-Methyl-perfluorooctane sulfonamido) acetic acid (Me-PFOSA-AcOH) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U. Fourth National Report on Human Exposure to Environmental Chemicals 255 .S.900 (<LOD-1.00 (.10 (1.900-1.30) .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 .30 (1. which may vary for some chemicals by year and by individual sample.30 (1.700 (<LOD-.900) 1. < LOD means less than the limit of detection.00 (.30) 1. see Data Analysis section) for Survey year 03-04 is 0.6.20 (1. population from the National Health and Nutrition Examination Survey.400 (<LOD-1. Survey Geometric mean (95% conf.600 (<LOD-1.40) 1.700) .80) 1.800) .700 (<LOD-.20-1.700 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. see Data Analysis section) for Survey year 03-04 is 0.900) 485 538 962 Limit of detection (LOD.10-1.400 (<LOD-.10) 1. which may vary for some chemicals by year and by individual sample.30 (1.10-1.800 (<LOD-.900) .10 (.50) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD 75th .20) 1. population from the National Health and Nutrition Examination Survey.700) 90th 1.700 (<LOD-.600) .900-1.00 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.700 (<LOD-2.700 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.10) .10 (.600 (<LOD-1.700) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .00) < LOD .10) * 03-04 03-04 * * < LOD < LOD .800) .300 (<LOD-1. interval) Selected percentiles ( 95% confidence interval) Sample 95th .60) 485 538 962 Limit of detection (LOD.10) 1.50 (1.10) .700) 1.700 (<LOD-.40) 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD . Serum Perfluoroundecanoic acid (PFUA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.700) 1.900-1.900-1.3.10-1.300-2.60) 640 1454 03-04 03-04 * * < LOD < LOD .90) . < LOD means less than the limit of detection.500 (<LOD-.00-1.80) 1.40) < LOD < LOD .900-1.600 (<LOD-1.10 (.80) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD .900 (.S.900-1.50 (1.600 (<LOD-.900-1.00 (.300 (<LOD-.

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1/15/06 Vanden Heuvel JP. Lau C.51(8-12):658-668. Zobel LR. Environmental Protection Agency (U.. A survey of perfluorooctane sulfonate and related perfluorinated organic compounds in water. and humans from Japan. Thibodeaux JR.198(2):231-241. Prevedouros K. U. Buck RC. Hansen KJ. Chemosphere 2004a. Lau C. et al. Burris JM. Environ Sci Technol 2003. Mandel JH. A global survey of perfluorinated acids in oceans. htm.S. Taniyasu S. Toxicol Appl Pharmacol 2004. Toxicol Sci 2002. et al. Rogers JM.74(2):369-381. Mar Pollut Bull 2005.45(3):260-270. Mandel JH. Olsen GW. and perfluorooctanoate in retired fluorochemical production workers. Ehresman DJ. Church TR. 2003. et al.1177(2):183-190. Rogers JM. Kannan K. Fourth National Report on Human Exposure to Environmental Chemicals 257 . Olsen GW. Ehresman DJ. et al. J Occup Environ Med 1999. Thomford PJ. Environ Health Perspect 2005. EPA). et al.Perfluorochemicals Kudo N. Biol Pharm Bull 2003. birds. Kawashima Y. fatty acid binding protein and peroxisomal beta-oxidation by peroxisome proliferators. Perfluorooctanesulfonate and other fluorochemicals in the serum of American Red Cross adult blood donors. Thibodeaux JR. Toxicol Sci 2003. Church TR.82(1):359.2(1):53-76.26(1):47-51.41(9):799-806. Korzeniowski SH. Burlew MM. Lundberg JK. Seacat AM. fast foods. Environ Health Perspect 2003a. and food items prepared in their packaging.40(1):32-44. Hansen KJ. van Belle G. Serum concentrations of perfluorooctanesulfonate and other fluorochemicals in an elderly population from Seattle. Sterchele PF.) Tittlemier SA. et al. (Erratum in: Environ Health Perspect. (Erratum in: Toxicol Sci 2004. 2003a. Moisey J. Pepper K. Case MT. Mandel JH. Taniyasu S. Preliminary evidence of a decline in perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) concentrations in American Red Cross blood donors. Olsen GW. Sources. Seymour C. Butenhoff JL. Seacat AM. Subchronic toxicity studies on perfluorooctanesulfonate potassium salt in cynomolgus monkeys. Stanton ME. Froehlich JW. Church TR. Richards JH. Ellefson ME. Dietary exposure of Canadians to perfluorinated carboxylates and perfluorooctane sulfonate via consumption of meat. Induction of triglyceride accumulation in the liver of rats by perfluorinated fatty acids with different carbon chain lengths: comparison with induction of peroxisomal betaoxidation.115(9):1298-1305. J Ag Food Chem 2007. Yamashita N. Olsen GW. Olsen GW. Chemosphere 2007b. Grey BE. J Occup Environ Med 2003b. Kannan K. Quantitative evaluation of perfluorooctanesulfonate (PFOS) and other fluorochemicals in the serum of children. Cousins IT.epa. Butenhoff JL.37(12):2634-2639. Epidemiologic assessment of worker serum perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) concentrations and medical surveillance examinations. fish. Grey BE. Bronson R. Barbee BD.68:105–111. Environ Health Perspect. I: maternal and prenatal evaluations. Hansen KJ. fish. Burris JM. J Children’s Health 2004b. Nesbit DJ.S. Hanari N. Reagen WK. Yamashita N.111(16):1892-1901. Historical comparison of perfluorooctanesulfonate.68(1):249-264. Toxicol Sci 2003. Butenhoff JL. Olsen GW. Mandel JH. Exposure to perfluorooctane sulfonate during pregnancy in rat and mouse. Mair DC.111(16):1900) Olsen GW. Exposure to perfluorooctane sulfonate during pregnancy in rat and mouse. Horii Y. fate and transport of perfluorocarboxylates. II: postnatal evaluation.74(2):382-392. perfluorooctanoate andother fluorochemicals in human blood. Helzlsouer KJ. Hansen KJ. Petrick G. Butenhoff JL. Butenhoff JL. Serum perfluorooctane sulfonate and hepatic and lipid clinical chemistry tests in fluorochemical production employees. Olsen GW.perfluorohexanesulfonate. Cao XL et al. Burris JM.55:3203-3210. Larson EB.gov/opptintr/pfoa/pfoara. Half-life of serum elimination of perfluoroo ctanesulfonate. Lundberg JK. Butenhoff JL. Burris JM. Biochim Biophys Acta 1993. The developmental toxicity of perfluoroalkyl acids and their derivatives. Horii Y. Burris JM. Hanson RG. Miller JP. Olsen GW.113(5):539-545. Rogers JM. Peterson RE. Available from URL: http://www. Preliminary Risk Assessment of the Developmental Toxicity Associated with Exposure to Perfluorooctanoic Acid and its Salts.54(11):1599-1611. Hanson RG. Hansen KJ. Environ Sci Technol 2006. Gamo T. Washington. 2007a. Coordinate induction of acyl-CoA binding protein. Huang HY.

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

Coldham NG.. Lovekamp-Swan and Davis. peroxisomal proliferation may not be a relevant pathway in humans (Rusyn et al. 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. Calafat AM. Sauer MJ. The monoester metabolites are thought to mediate toxic effects for some of the phthalates. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 2006).. 2007). 2007. atsdr. Kessler et al. 2006). 2000c. 2001. Food Addit Contam 2001.gov/toxpro2. Evaluation of a recombinant yeast cell estrogen screening assay.New York.nih. Jongeneelen FJ. 2004. 4/20/09 Albro PW.html). 2003.805:49-56.. 2003. Assessment of critical exposure pathways. Connor C. reducing estrogen production. 2004.gov/ reports/index. environmental levels) and health effects is also available for some phthalates from ATSDR at: http://www.45:19-25. dibutyl phthalate (DBP). 1985.cdc. Slakman AR. phthalates produced anti-androgenic effects by reducing testosterone production and. and extent of metabolite conjugation to glucuronide (Albro et al. 4/20/09 Agency for Toxic Substances and Disease Registry (ATSDR).cdc.. 2002. Cousins IT. Corbett JT. Mackay D.. which may be a pathway to the development of liver toxicity and cancers in these animals. 2004. In Staples CA (ed).. 2002). Determination of four metabolites of the plasticizer di (2-ethylhexyl) phthalate Fourth National Report on Human Exposure to Environmental Chemicals 259 . Springall C. 2004). These differences may contribute to species-specific differences in toxicity (ATSDR. 2002).. Clark K. ovarian abnormalities in the female animals (Jarfelt et al. In animals.. NTP-CERHR. gender. McDonnell DP. Anderson WA. at higher doses. 105:734-742. Automated solid phase extraction and quantitative analysis of human milk for 13 phthalate metabolites... The Handbook of Environmental Chemistry. Schroeder JL. van der Broek PH. Massey RC. Biomonitoring Information Urinary levels of phthalate metabolites reflect recent exposure to the parent phthalate diester.. 1982). 2005.html. but similar findings were not present in young Swedish men with comparable or higher median levels of urinary metabolites (Jonsson et al. Toxicological profile for di-n-butyl phthalate update [online]. 227-262. Environ Health Perspect 1997. Springer. McKee et al. Metabolism of di(2-ethylhexyl) phthalate. A biomarker approach to measuring human dietary exposure to certain phthalate diesters. testicular atrophy. and race/ethnicity (Silva et al. Albro PW and Lavenhar SR. 2001). High doses of di2-ethylhexyl phthalate (DEHP). Also. 2000b. Dirven HA.. Peck and Albro. phthalates have been shown to induce peroxisomal proliferation in rodents. Hoppin et al. 2001.html. Silvapathasundaram S.cdc.e.atsdr. and Sertoli cell abnormalities in the male animals and. 1986). Environ Health Perspect 1982. 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. at very high levels. 2000a. Rhodes et al. 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. Drug Metab Rev 1989.21:13-34. effects that may be mediated by inhibiting testicular and ovarian steroidogenesis... Matthews HB. Jordan S. References Agency for Toxic Substances and Disease Registry (ATSDR).gov/ toxprofiles/tp9. interactions with macromolecules and species differences in metabolism of DEHP. Available at URL: http://www. Hauser et al. 1982.18(12):10681074. variation also occurs in the same person during repetitive monitoring (Fromme et al. Information about external exposure (i. Castle L. The proportions of each metabolite for a given phthalate may vary by differing routes of exposure (Liss et al.Phthalates and metabolites have been tested.niehs. Available at URL: http://www.html. However.3. Part Q: Phthalate Esters. but there are known species-related differences in the hydrolysis of diester phthalates. Needham LL. Phthalate urinary metabolite levels in men evaluated at an infertility clinic were associated with several measures of sperm function and morphology (Duty et al. Vol. Variation occurs from person to person in the proportions or amounts of a metabolite excreted after similar doses (Anderson et al. J Chromatogr B 2004..atsdr. Hauser et al.gov/toxprofiles/ tp135. Herbert AR. Toxicological profile for di(2-ethylhexyl)phthalate update [online]. 2005). Pharmacokinetics. Silva MJ. Dave M. Population estimates of concentrations of specific phthalate metabolites may differ by age. pp. 2004.. Scotter MJ. efficiency of intestinal absorption. and benzylbutyl phthalate (BzBP) during the fetal period produced lowered testosterone levels.

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2004.1) 76.7-172) 103 (74.4 (31.9 (70.0) 32.3-21.4 (53.0-130) 101 (86.6) 50.2 (11.6) 37.5 (61.6) 24.1-116) 122 (93.8-41.1 (55.6 (21.2-19. People exposed to BzBP will excrete mono-benzyl phthalate (MBzP) and small amounts of mono-n-butyl phthalate in their urine.5 (67.6) 63.8) 63. residents (Blount et al.4) 129 (98.3-75.7-58.6) 14.1-38.5-36.5 (26.4) 12.7 (11.6-92.8) 33.5-14.0) 20.0 (14.1 (13.6) 67.0 (26.8-17.0) 34.8 (30.7 (13.1-16. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.4-24.4 (32.3) 13.4 (13.9 (39.6 (53.3-43.8-64.7-16.1) 13.1 (20.9) 11.8 (10.7 (70.5) 16.1-43.1-16.8-17.4) 51.4 (32.0) 70.7-170) 169 (134-198) 152 (99.9 (12.4 (68.1-35.4) 81.6 (13.9) 15.3 (12.1.8-13.6) 25.2 (10.3-82.2-33.3-18.0 (15.5) 27.2-16.7-16.9) 49. population from the National Health and Nutrition Examination Survey.3-91.9 (28. 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.6-116) 122 (102-142) 101 (85.8-35.1 (14.6-38.3.6 (66.0-85.8-98. because it is not bound to products in which it is incorporated.8 (53. 262 Fourth National Report on Human Exposure to Environmental Chemicals .4 (48.5-18.4) 98.1) 12.2-16.4 (10..9 (16.5-36.1 (58.S.3-130) 122 (88.8 (50.9) 18.5 (76. particularly male animals (McKee et al.0 (34.2) 78.5) 82.4-127) 80.3-74.2-39.0) 90th 67.8.8 (21.6) 35.5) 55.9 (21.3) 63.8) 14.4) 38.6-150) 94.8 (14. see Data Analysis section) for Survey years 99-00.9-49.2) 12.3-34.2 (47.6-43.7-16.0 (30.4 (63.9) 14.4) 71.5-25.0-106) 58.0-26.9-27. and 03-04 are 0.2) 15.4 (29.6-39.4) 14.8-14.3) 54.1-214) 166 (116-191) 145 (110-213) 88.1) Selected percentiles ( 95% confidence interval) 50th 17.4) 35. IARC considers BzBP not classifiable with respect to human carcinogenicity.9) 13.3-18.6-18.7-17.9-28.4) 33.3 (12.8 (71.5-145) 138 (106-241) 143 (127-179) 120 (99.3 (22.6) 13.6 (32. 0.1) 31.6 (13. BzBP can be released into the environment during its production and.2 (19. it can be released into the ambient air during use or disposal of the products.0 (33.9) 43.7-13.3) 37.7) 38. and 2003-2004 were generally similar those reported in U.7-25.6) 13. NTPCERHR.5) 65.3) 94.0) 24.0 (43.1 (32.8-48.3-88.6) 35.8-16.5 (55.3 (33.7-119) 99.6 (12.3-27.1-39.7-14.3) 23. Biomonitoring Information The median levels of MBzP in NHANES subsamples from 1999-2000.0 (23. 85-68-7 General Information Benzylbutyl phthalate (BzBP) is a solvent and additive used in products such as adhesives.0-55.2-155) 91. respectively.2-115) 113 (91.9-30.1) 32.4 (27.7) 40.1 (14.8) 24.4) 35.4 (53.2-20.9 (22.1-120) 52. and to a lesser extent.9-62.4 (10.1) 29.3) 13.3-125) Total 15.4-62.8-18.7 (82. vinyl tile. Food crops take up BzBP.3 (12.5 (13. and 0.8 (38.6 (13.8-14.9) 14.5) 15.5) 23.0 (55.6) 95th 103 (94.4-92.1-15.8 (80.3 (13.7) 23.3 (29. 01-02.4) 49.0 (15.5) 30.8 (86.8-72.7 (15.3 (30.S.7-35. some personal care products.2-116) 122 (102-143) 101 (84.9-87.5 (57.3-122) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.1-61.5 (27.2) 69.4) 80.3 (44.2) 33.Phthalates Benzylbutyl Phthalate CAS No.9) 12.2) 14. car care products.5-35.5) 15.5-40.2-38.0 (27.4-15.2) 66.6-132) 103 (84. can produce developmental and reproductive toxicity in rodents.5-84.1 (19.5-41.1) 68.5-33.3) 15.8 (71.1) 14.0) 23.9-190) 86.7 (51.2) 14.5-94.4 (59. interval) 15.2) 17.2) 13.1) 67.9-16.9-14.4-25.3 (29.3-12.6-72.3 (54.3-161) 99.1-15.1 (10.6 (13.8) 28.0 (11.2 (25..6) 15.9) Sample size 2541 2782 2605 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 39.2-17. 2000).2 (43.8 (12.2 (14.2 (19.4-120) 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 13.9 (11.6) 16.4) 75th 35.6 (41.7 (12. and diet is the major source for general population exposure.8-16.9-47.0) 33.4) 65. 2000).5-97.9 (12.0 (20.0 (12.2-183) 101 (78. including MBzP.5-62.1-90.1 (13.6-79.0 (30.7 (80.8 (28.6-29.6) 14.2) 22.7 (53.9 (13.2-40.8-121) 79.8-76. 2001-2002.6) 29.5) 214 (108-399) 235 (183-330) 255 (146-365) 125 (93.8-133) 89.4) 108 (96.6-92.0) 16.4-16.2-31.7-15.5 (47.6-17.5 (66.8) 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. High dose BzBP and its monoester metabolites.1-18.2) 32. sealants.7-82.

7) 19.6-26.5) 95th 77.7 (13.9-69.7-123) 77.9) 52.3-64.5-79.4) 21.6-99.8-14.5-57.6-81.7 (18.8 (10.5 (10..4) 51.8-15.6 (57.6) 53.1) 142 (99.4 (63.2) 15.5) 16.2-13.1) 35.0 (67.1) 39.9-13.2-15.7-14.7-61.9 (15.1) 12.4 (33.5 (48.0 (41.5 (56.0) 24.9) 12. population from the National Health and Nutrition Examination Survey.4) 328 393 342 752 742 729 1461 1647 1534 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 12.9) 42. 2007).4-142) 134 (116-176) 136 (85. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.5) 41.7 (55.6) 75th 25.2) 67.4-90.8-64.4) 44.5-61.6-20.2) 26.7 (54.9-13.3) 14.6) 13.4) 17.4-60.1 (11.4) 90th 50..3) 36.1 (53.1) 80.6 (30.0-27.0 (10.9) 64.8-42.3 (24.4 (25.0) 12.6 (30.5-213) 49.9-16.2-12.9 (10. Biomonitoring studies on levels of urinary MBzP provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of BzBP than are found in the general population.6 (14.1-125) 86.7-14.4-19.7 (21.5) 78.3 (15.6 (36.5-23.0 (41.8-15.0 (33.6-40.9) 24.3-38.8) 71.7 (23.7-90.3) 67.5-26.2 (40.7 (11.9) 12. and in a small sample of German residents (Koch et al.4 (69.8) 80.1 (21.0 (38.3) 89.0) 11.3) 16.0-51.0 (49.7-12.0 (12.1-79.2 (69.7-20.1 (13.9 (29.4 (21.2 (56.0 (11.5 (42.0-53.7-20.5) 23.0) Selected percentiles ( 95% confidence interval) 50th 13.1 (13.8) 13.3-16.5) 13.4 (10.7 (38.9 (15.7) Sample size 2541 2782 2605 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 40.8) 54. Hauser et al.5-58.8 (13. Finding a measurable amount of MBzP in the urine does not mean that the levels of MBzP or the parent compound cause an adverse health effect.0-15.1 (21.7 (13.7 (11.4 (34.73-12.0-90.7) 11.4 (26.3 (60.95-14.8-27.3 (13.4) 25.8 (30.8-13.3 (23.2-17.0) 15.2) 32.9 (12.4 (11.1 (41.6 (11.8 (64.9-40.7) 46.9) 11.4) 50. 2005).4) 14.4-14. 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.4) 104 (89. 2002.4-102) 70.7) 56.4) 60.6 (19.8-69.1-27.1-35.9 (51. in men attending a Boston infertility clinic (Duty et al.1 (21.0-26. 2004. 2006).3) 55.4-93.8-16.8) 68.4) 13.9 (54.3 (35.3-34.6 (24.0 (13.2) 11.0) 24. in young Swedish men (Jonsson et al.6-12.6 (22.8 (46.9) 12. 2003).8-13.8) 26.1-14.5 (12.5-58.5 (35.3) 29.9-14.6) 12.9) Total 14.1 (43.4 (11.4-14.2-15.3 (12.2-57.8-80.6) 73.5 (11. the adjusted geometric mean levels of urinary MBzP were significantly higher in several subgroups: children compared to adolescents and adults.5-31.2-13.1 (23.1 (21.5-16.1 (25.1) 23..2-49.8) 108 (75.8 (57.6) 25.4 (13.7-15...6) 58.4) 28.7-15.6) 12.1) 27.2) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 12..4-42.4-15.7 (11. In NHANES 1999-2000.4-27.5-42.9-62.6) 30.5) 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 (9.8) 53.6-15.0-48.8) 24.4-116) 73. 2002).3) 18.6 (11.3-73.7-69.5) 17.6 (11.3) 90.8) 34.9 (10.9-104) 62..0) 49.3-11.9-28.8-39.2 (41.0-109) 65.2-26.8-13.8-14.1 (19.7 (14.8) 15.8-85. A small study of African-American women in Washington.2-117) 95..8) 16.5 (10.5) 46.7) 38.1) 17.7-56.6 (51.3) 73.1 (34..3) 21.2-21.4) 12.6 (34.9-83.7-397) 70.2-51.6) 38.7-19.8-34.5 (49.9 (43.2) 11.2) 11.3) 37.0) 13.4-18.1 (46.7 (19.69-11.8 (11.3) 12.6-116) 74.8 (69.1-120) 77.8 (49.9 (24. Hoppin et al.4 (60.7-31.6-47.9-23.5) 10.8-48.8 (50.5-38.0 (12.3) 13.1) 24.4-17.7 (59.1) 24.4 (12.4-23. In an annual sample of German university students.9 (22.9 (12.2 (27.5-76.1 (9. 2004). 2003). 2007).5-26.1-12.9 (55. 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.3) 13.9 (24.4-79.9) 11.2-78.4 (74.7 (12.S.3 (39.8) 11.1-58.5) 20.8) 56.0 (62. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.9) 100 (80.7-29.2) 12. adolescents compared with adults.8) 33.6-86.8) 46.3) 13. 2005.6 (15.1 (18.4) 15.0) 60.4-99.3 (38.5-99.8) 33.9-115) 57.5 (9.8) 53. and females compared to males (Silva et al.1-12. DC reported median urinary MBzP levels that were about twice the levels of adults and females reported in NHANES 1999-2002 (CDC..8-173) 195 (121-305) 229 (99.Phthalates York City (Adibi et al.1-29.5-29. Weuve et al.5-13.5) 14.3) 14.1 (14.4 (11.1 (15.9 (39.4 (46.8-60.6-13.7-19.8 (12. median urine levels of MBzP were about one-half the median levels in NHANES subsamples from 1999-2002 (Wittassek et al.7) 25.4) 13. interval) 14.

Richthoff J. et al. Environ Health Perspect 2002. Centers for Disease Control and Prevention (CDC). Gans G. Koch HM. Internal phthalate exposure over the last two decades—a retrospective human biomonitoring study. Jacek R. Atlanta (GA). Third National Report on Human Exposure to Environmental Chemicals. Pirkle JL. Green RA. Wiesmuller GA. Barr DB. Hagmar L.html. David RM.nih. McKee RH. Hilborn ED. Duty S. Caudill SP. Rossbach B. et al. Brock JW. et al. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters.niehs. Silva MJ. 264 Fourth National Report on Human Exposure to Environmental Chemicals . Silva MJ. Duty SM. Eckard R. et al. Brock JW. Silva MJ. Hum Reprod 2007. Prenatal exposures to phthalates among women in New York City and Krakow.gov/ chemicals/phthalates/bb-phthalate/bbp-eval. Singh NP. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Int J Hyg Environ Health 2007. Needham LL. Needham LL.114(9):1424-1431. Dobler L. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Barr D. 112(5):A270]. Urinary phthalate metabolites and biomarkers of reproductive function in young men. Research Triangle Park (NC). 2005. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Butala JH.68:309-314. Helm D.111(14):1719-1722. Urinary levels of seven phthalate metabolites in the U. Reprod Toxicol 2004.210(3-4):319-333. Caudill SP. Brock JW. Koch HM.Phthalates References Adibi JJ. Environ Health Perspect 2000. Perera FP. Environ Health Perspect 2003. Phthalate monoesters levels in the urine of young children. Available at URL: http://cerhr. J Androl 2004. Silva MJ. Giwercman A. Rylander L. Levels of seven urinary phthalate metabolites in a human reference population. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. Chen Z. Baird DD.25(2):293-302.22(3):688-695.108(10):979-982.S. Drexler H.16(4):487-493. Blount BC. Poland. Weuve J. Exposure to phthalates in neonatal intensive care unit infants: urinary concentrations of monoesters and oxidative metabolites. Hu H. Environ Res 2003. Reproducibility of urinary phthalate metabolites in first morning urine samples. Calafat AM. Caudill SP. Calafat AM. Angerer J. Malek NA. Hodge CC. Ryan L. et al. Davis BJ. Monograph on the Potential Human Reproductive and Developmental Effects of Butyl Benzyl Phthalate (BBP). Meeker JD. Wittassek M. Epidemiol 2005. Hoppin JA. Jonsson BAG. Reidy JA. Sampson EJ. Ryan L. Bull Environ Contam Toxicol 2002.112(3):331-338.110(5):515-518. Camann DE. Sanchez GN. Schettler T. 2000 [online].93:177-185. et al. 4/20/09 Silva MJ. Environ Health Perspect 2006.18(1):122. Hauser R. et al. NTP-CERHR. Jedrychowski W. Environ Health Perspect 2004.

44-2.7) 14.30 (1.6) 12. Studies of children found age-related differences in urine MBP levels.19-3.40-3.80 (2. NIOSH and ACGIH have established guidelines for workplace air exposure to di-n-butyl phthalate.5) 23.6 (13.85-6. 84-69-5 General Information Dibutyl phthalates (both di-n-butyl and di-isobutyl phthalates.00) 4.25) 01-02 03-04 01-02 03-04 01-02 03-04 4.5) 25.6) 10.56 (5. see Data Analysis section) for Survey years 01-02 and 03-04 are 1.90 (4.7 (17. NTP-CERHR..30-6.20) 7.0) 9.80) 75th 5.5) 19.2 (12..0) size 2782 2605 Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 03-04 50th 2.8) 21. interval) 2.37) 6.80-5.60 (5.00) 6.3-20.55 (3.S.17 (2.20 (7.50) 2.50) 7.1) 16.00-4.96) 3.0 and 0.4) 12.4) 22.7 (9. Hauser et al.4 (20.30-13. and insecticides.5) 18.0 (13.2-14.17) 4.10) 3.10) 2.S.5-29.55) 2. 2000).5 (27..7-31.90 (4.00) 7.50-10.3-43. In addition.22 (3. 2003).4-12. CDC.2 (8.90 (3.60 (2.22) 3.5 (11.90-4. Survey Geometric mean (95% conf.20-6.6-26.40-5. pharmaceutical coatings.60 (8.Phthalates Di-n-butyl Phthalate CAS No.3-24.9) 15.80 (2.5) 14.0) 20.6 (29. When total DBP metabolites have been measured.5 (20.40-3.3) 18.1-20.1-12.2-22.60 (4.6) 17. about 65% to 80% of a dose is eliminated in urine within 24 hours.9-14.3 (11.0 (11.3 (16.10 (4.07 (3.97-7.46) 2.20 (6.50-4.3 (13.7) 15..10) 8. and also in some printing inks.30) 10.3 (16.6 (10. Koch et al. referred to as DBP) are industrial solvents or additives used in many personal care products such as nail polish and cosmetics.50) 8. 2005. in a small sample of pregnant women in New York City (Adibi et al.80 (5.40 (2. Neither IARC nor NTP has evaluated dibutyl phthalates with respect to human carcinogenicity.1) 25.1-17.6) 16.60) 3. and in a small sample of Japanese adults (Itoh et al.6-14.0) 393 342 742 729 1647 1534 01-02 03-04 01-02 03-04 2.26 (2.1 (8.91) 4.46 (2.5-24.90) 12.00-11.90-2.20-2.10-2.00-6.3-19.7-31.10 (3.70 (2.49-2.4-27.70-4.24-8.80 (3.6 (14. 2003).0-14.70 (5.6 (10. exposure to benzylbutyl phthalate (BzBP) will also result in small amounts of mono-n-butyl phthalate appearing in the urine.7 (18.82-3. Biomonitoring Information Median concentrations reported in the NHANES 19992000.50) 90th 12. population from the National Health and Nutrition Examination Survey.02) 4. they have been referred to as monobutyl phthalate (MBP).30) 2.0) 24.40-4. DBP can produce reproductive toxicity in male rodents (McKee et al.30) 10.40 (7.6-18.20 (3.0) 1371 1250 1411 1355 01-02 03-04 01-02 03-04 01-02 03-04 3. 2004.3.00 (5.0 (13. OSHA has established a workplace air standard for external exposure to DBP.3) 3.2 (11. 2007).0-18.0-38.40) 5.4 (14. 2005). 2004.6) 16.6) 17.0 (19..7-20.2-33.43) 6.50) 5.3) 33.59) 3. Compared with the median for 6 to 11 year olds in NHANES 1999-2004 (CDC.50 (3.56) 3.90-4.67 (5.4) 5.7) 18.1-25. mostly as MnBP (Anderson et al. 2001).6 (9.56-4.3 (13.40 (6.1) 22.40-9. 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.20-9.5) 18.73 (2.80-5.66) 2.00-6.0) 13.30-6.2) 5.3-18.30-11.6) 26.40 (2.3 (18.56 (3. 2005). Small amounts of mono-3-carboxypropyl phthalate are also produced from di-n-butyl phthalate.40-17.20-12.63) 3.1 (13.33 (2.6-20.5 (17. in men attending a Boston infertility clinic (Duty et al.30-2.5-16.30 (4.30) 5.71 (2.50 (6. Following oral administration of DBP to humans.7 (17. 84-74-2 Di-isobutyl Phthalate CAS No.30-7.9) 10.0-25.7) 4..10) 11.20) 4.9 (16.5 (10.50-6. 2001-2002 and 2003-2004 subsamples were similar to MBP levels reported in U.70-8.8) 677 652 703 699 1216 1088 Limit of detection (LOD.7-18.46 (3.90-7.8) 40.10 (4.94) Selected percentiles ( 95% confidence interval) Sample 95th 17.9-23..40-4.48 (2.6 (13.6 (11.81 (3. residents (Blount et al.97) 4.60-6.5) 12.97) 2.70) 5.7) 7.00-9.40 (3. Fourth National Report on Human Exposure to Environmental Chemicals 265 .80 (5.70) 3.50) 18.0) 12.10-9. 2005).00) 10.5-16.30-3.8 (9.3 (19..84) 4. People exposed to dibutyl phthalates will excrete mono-n-butyl phthalate (MnBP) and mono-isobutyl phthalate (MiBP) in their urine.72-3.30) 6..70-4.28-5.50-2. Median MBP levels in two European studies were about two to six times higher than median levels in this Report (Jonsson et al. 2000.3-30.7 (7.7 (16.20-12.5) 22.10) 9.46-5.40-12.6-34.30 (3.3-48.73-5.9 (16.10-9.68 (2.00) 4.00 (7.6 (14.90 (6.11-3.

36-2.76-3.58-4.84 (4.80 (3.1) 11.2 (10.81 (3. Between 1998 and 2003.1 (10.31 (2.0) 393 342 742 729 1647 1534 01-02 03-04 01-02 03-04 2.9-26.89) 6.33-9.28 (4.47-12.11) 5.19 (2.81) 9.22 (2. Survey Geometric mean (95% conf.59 (4. 2005).46 (2.04) 7.04) 3.1) 4.46-11. 2004).20 (2..66) 10.7-28.69) 4.0 (8. 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.73 (5.54 (2.08) 75th 4.03-7.00) 01-02 03-04 01-02 03-04 01-02 03-04 4.5-19.55-6.80-3.13-6.02-10.57 (3. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.00-7.3) 13.5) 15.4 (12.89 (3. the students’ median values for MiBP levels remained relatively unchanged.9) 12. In an analysis of NHANES 1999-2000.and gender.43) 3.74 (4.94-12.76-3.53-4.1) 10.6 (12.86) 6. 2004).38-10.66) 4.6 (15.31) 2.53-5.0) 11.09-2.8) 10.00 (3.61-3. ranging from more than one-tenth the NHANES median (Itoh et al.98 (2.69-7.85 (2.07 (2.68) 3.65 (4.6-19..15-4.1 (11.76 (3.29-8.0 (10.54 (4.75 (4.56) 5.51) 15.57-4. Weuve et al.68 (2.26-2.39) 5.32) 7.related differences in the adjusted geometric mean levels of urinary MiBP and MnBP (CDC.4) 7.05) 2.81) 4.7 (13.3 (13.89-5.52-20.36-7.7) 1371 1250 1411 1355 01-02 03-04 01-02 03-04 01-02 03-04 3.3) 28.33 (2. Over this time.0) 7.57 (3.78) 8.8-13.20-4.73) Selected percentiles ( 95% confidence interval) Sample 95th 12..78) 9.52 (2.53-3.17) 90th 8.13 (2.1) 13.8-18.5 (9.3) 16.18 (4.7) 11.9 (11.38 (6.8 (10.43) 3.75 (6.04-5.21) 10.1) 15.95) 10. up to four and 13 fold.28-13.42) 2.14 (4.6 (8.65-4.6) 13.5) 13.5 (11.00-3.35) 3.1) 677 652 703 699 1216 1088 266 Fourth National Report on Human Exposure to Environmental Chemicals .33 (3. population from the National Health and Nutrition Examination Survey.7) 10.1-24. 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.69) 6. 2005). interval) 2.8 (8.30) 2.66 (8.20 (2. to about two to fourfold higher (Fromme et al.41 (2.7) 19. 2007).6-19.4) 15.26 (2.01-2.0-18.7 (9.18 (1.03 (5.17-12.82 (4.83 (2.2-15.64-7.21 (5.99) 7.6) 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 2.67-5.2 (11.95-3.17 (2.0 (12.0) 15.. 2002.9 (9.43) 3.20-2.56-15.47-5.1) 7.31) 2.32 (7.56) 2.15) 3.37) 3.3 (17.95) 2.03-11.7 (21.30 (6.69 (2.51) 5.79 (4.20-3.. respectively.96 (3.58-3.1-15.66) 2.94 (5.81 (6.08-2.76-15.8-36.93-6.64-7. 2006).6 (8. 2007). 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. An analysis of NHANES 2001-2002 showed similar age.62 (6.82) 4.44 (3.18) 3.79-8.56-4.2) 9.02 (7.20 (7.80) 7. samples from German university students had consistently higher median urine levels of MnBP and MiBP.91-6.7 (11.11-2.86-4.8 (9.31 (7.6 (9.3) 13.1-12.32 (3.2-13.8-18.2) 8.18) 4. than adults in NHANES subsamples during the same time period.33) 3.51) 2.97-2.Phthalates for neonates was lower (by about half) and the median for toddlers was higher (by about sixfold) (Brock et al.9-40.7) 3.39-3.94) 6.11 (5.62-12.27-12.99-4.18-4.72-7.52-3.6 (10. Differences in urinary MBP population estimates by gender have also been shown (Silva et al.78-8.S.0) 3. Studies measuring urinary MnBP have reported variable median values compared to the NHANES 2001-2002 and 2003-2004 subsamples.07-5.65-11.4-16.9-16.72) 5.00-3.68) 5.64-10.84 (8.6) 11.52) 3.45) 3.54) 2.34 (3.10-5.29-3.46) 3.47 (3.88 (2.. while MnBP declined (Wittassek et al.9 (15.24) 3. Urinary Mono-isobutyl phthalate (MiBP) (creatinine corrected) Metabolite of Di-isobutyl phthalate (DBP) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U..92 (7.74-3.79-6.18-10.4) 23.2) 24.3) 18.25) 5.1-25.

8) 48.7 (43.4-31.4 (23.0 (36.1-122) 122 (104-137) size 2541 2782 2605 Total years 99-00* 01-02 03-04 50th 26.0 (31.6 (55.3 (17.5 (59.9-53.5) 17.1-20.3 (23.4 (36.3-96.0 (15.3) 36.7-116) 95.2-49.6-143) 127 (99.7) 42.4-20.7-42.7 (18.6) 38.7-91.1 (62.4) 59. respectively.2) 26.1.9 (79.0 (23.0) 120 (98.6-31.5 (29.5) 31.1-80.0 (17.1) 31.7-20.7 (22.8) 58.3-24.3-21.4-159) 107 (84.5 (28.3) 23.6) 46.4 (19.6-36.6-44.3) 24.7 (24.6 (26.4 (35.0 (78.3 (51.5 (74.1-24.8-29.3-67.9) 21.6 (19.1) 23.6 (65.8-119) 90.5) 21.5-43.4) 52.3) 40.9) 46.5-44.7) 124 (98.6 (44.7 (28.9-79.5-47.4) 64.7) 74.2) 68.3-145) 85.1 (19.7 (51.7 (70.6-37.7-127) 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. population from the National Health and Nutrition Examination Survey.6) 80.6-29.4-42.1-29.3) 26.6-40.4 (38.7-117) 118 (108-143) 93.0-21. concentrations of mono-isobutyl phthalate and mono-n-butyl phthalate were measured together and expressed as a combined value.0) 21. 01-02.2 (18.0-19.7) 92.4 (35.7-121) 97.4 (35.0 (20.4 (72.7-34.1 (51.8-165) 167 (143-197) 138 (110-184) 144 (115-168) 142 (111-161) 107 (89.1 (54.2-21.9-22.5) 34.8-123) 101 (90.1-82.9 (17.5) 65.9-33.9) 26.4.8) 23.9-101) 77.5-117) 95.7) 28.6-49.7 (38.2 (17.3-79.1) 19.0) 31.9-87.7-111) 64.2 (79.2-56.2 (58.6) 35.1) 36.2) 62.9) 71.8 (57.1) 47.6-20.5-42. see Data Analysis section) for survey years 99-00.2-32.7-24.7-34.6-48.1) 46.1 (19.5) 36.9-114) 116 (97.3-85.1 (26.1-75.0-51.5 (30.3-76.2-23.9) 18.0) 117 (104-131) 112 (84.2 (21. Fourth National Report on Human Exposure to Environmental Chemicals 267 .1 (21.4) 22.5) 26.5) 24. 1.1) 17.4-18.7-124) 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.6) 17.4 (21.5-47.8) 19.5-121) 106 (94.3 (60.1 (18.0) 30.1 (58.1 (28.0 (30.5) 85.4 (84.4) Selected percentiles ( 95% confidence interval) Sample 95th 150 (121-169) 108 (94.1) 25.5) 36.9) 75.4 (25.8-132) 95.0-73.8 (19.7) 52.3 (23.1 (36.4) 20. Survey Geometric mean (95% conf.3 (30.6 (16. interval) 24.9.6) 20.4 (71.3 (56.1-27.3-60.1) 23.2 (21.3) 21.1) 23.1 (19.2 (25. referred to as monobutyl phthalate (MBP).7 (19.8-111) 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 23.2 (20.1-51.9-22.2) 32.0) 84.5) 37.6-24.8-42.1) 30.3) 19.2-93.2) 20.8-25.3 (30.2 (75.2-24.9 (17.1-92.0 (45.2-22.0) 38.8) 75th 51.9) 36.2) 42.1 (34.0-24.3 (42.0 (18.7-53.5) 47.1-22.4-44. *In the 1999-2000 survey period.6) 71.0-24.6-33.5) 78.2) 90th 98.6 (32.2 (59.0-26. and 0.7 (18.0) 20.9-42.6 (61.7-106) 69.7 (16.5-53.2-159) 92.2 (19.0 (25.5-27.2 (74.9 (79.2-114) 73.1 (31.0) 27.1) 20.4 (35.6) 39.2) 38.S.8-22.3 (36.7-42.6) 21.1 (17.6-113) 108 (90.0-19.2-87.5) 95.3) 18.8) 62.3-40.9-92.2-33.4-26.2-63.5-60. and 03-04 are 0.8) 43.9-28.5) 40.6 (48.0-58.9 (20.5 (59.4-60.5) Age group 6-11 years 99-00* 01-02 03-04 99-00* 01-02 03-04 41.1 (41.7 (33.5) 20.7-92.4-25.Phthalates Urinary Mono-n-butyl phthalate (MnBP) Metabolite of Dibutyl phthalate (DBP) and Benzylbutyl phthalate (BzBP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.6-69.1 (19.2 (78.3 (37.0-32.6) 166 (127-279) 159 (110-290) 191 (150-243) 165 (121-227) 148 (106-185) 134 (110-158) 143 (117-161) 95.1 (16.7 (64.0 (72.9) 29.5) 19.6 (22.6-29.7-26.3-136) 137 (107-162) 119 (90.6 (90.

3-20.6-32.4 (33.1) 20.9 (64.0 (19.8) 34.0-38.1) 37.9) 19.7 (27.3 (48.6-53.2) 159 (102-263) 147 (93.3 (71.3 (21.7 (60.8-43.7-39.8 (18.5) 82.7 (57.5-142) 89.1-128) 97.9-38.9 (19.8) 17.6-74.9-100) 86.5-41.6) 24.8) 40.2 (35.0 (70.5-76.3 (42.5 (81. concentrations of mono-isobutyl phthalate and mono-n-butyl phthalate were measured together and expressed as a combined value.4-131) 81.3) 19.5-37.6) 24.5 (14.9-84.8 (16.2-106) 64.6) 31.5-21.0-17.Phthalates Urinary Mono-n-butyl phthalate (MnBP) (creatinine corrected) Metabolite of Dibutyl phthalate (DBP) and Benzylbutyl phthalate (BzBP) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.2 (83.9 (30.6) 39.4-76.2 (19.4 (17.9) 20.5-18.0) 53.0 (18.7 (28.9 (35.6-44.6) 37.0) 75.3) 35.0-92.1 (15.1 (32.2-21.4 (16.8 (22.9 (73.2-61.4) 15.3 (60.9 (39.3-49.4-47.5) 39.1) 61.0 (43.9) 30.8-23.4) Selected percentiles ( 95% confidence interval) Sample 95th 97.2 (38.1) 50.3-21.8 (33.6-139) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00* 01-02 03-04 99-00* 01-02 03-04 21.9-26.8) 13.3-23.9-105) 85.9) 14.1) 17.6 (72.9-36.4 (47.0-19.4-65.8-24.5-70.0 (52.4 (50.7-26.6) 65.7 (16.0) 55.9) 49.0) 108 (71.2) 21.4 (16.3-18.2-16.0) 28.9 (20.1-99.3-78.8-235) 137 (108-198) 88.5-30.6-23.3 (16.4 (31.4 (56.5-142) 81.8) 75th 38.1) 20.6-16.0) 35.5) 91.6-119) 63.1 (46.6 (25.4 (68.7-19.6-22.0) 59.4 (31.5 (18.3-114) 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 17.0 (69.9 (37.8 (65.9 (30.3 (24.7 (54.7-37.9-14.6 (25.0-90.2-22.6-27.2 (16.1 (29.3 (46.2-27.0) 41.2-86.9-70.2-22.0) 29.5 (18.9) 52.7 (73.6 (19.1) 42.8) 23. Survey Geometric mean (95% conf.4) 20.1-83.7) 36.0-113) 104 (83.1) 21.3-106) 74.7 (12.2-179) 84.6) 34.3 (17.7 (20.4-34.7-51.6) 23.4) 21.1-115) size 2541 2782 2605 Total years 99-00* 01-02 03-04 50th 21.6 (31.6) 83.3-40.5) 17.0 (16.6-43.9 (35.3-71.9) 28.5) 90th 68.7-78.2) 59.3) 33.8) 22.8-24.9 (56.3-21.7-21. interval) 22.3-81.9-56.5) 134 (93.5) 84.5 (30.0-47.2-18.4-72.3 (69.2-108) 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.8 (17.4 (18.9 (21.0) 26.9-68.8 (13.6-26.9) 91. population from the National Health and Nutrition Examination Survey.9) 39.6-44.1) 44.2-22.3 (55.0) 94.3 (19.2-73.7) 20.2-48.3 (17.8 (18.8) 63.8) 20.4) 53.7-80.4) 16.8) 20.4 (31.7 (81.9) 62.3) 52.4 (37.3) 19.8 (18.3) 59.2 (19.6 (29.9 (30.4) 15.3) 21.4 (45.7) 19.3-39.5 (15.8) 19.7 (19.0) 81.4 (50.6) 25.0-60.4-24.4-135) 71.0 (34.7-19.9-68.1) 53.7-42.2) 74.6) 64.6) 14.0 (27.5-22.2) 16.1-23.2) 65.8) 17.5) 21.3) 33.0 (71.4) 51.8) 17.1) 35.8 (50.4 (23.6 (27.1-21.6-28.2-28.0 (50.1-99.4-103) 117 (83.7 (60.1 (56.1 (21.2) 31.5) 60.3) 67. 268 Fourth National Report on Human Exposure to Environmental Chemicals .8 (25.7-20.8) 28.6-23.1) 22.0 (18.S.6-19.0-41.8) 30.8) 35.5 (64.6 (17.0) 25.6-50.8-32.0) 19.9) 24.7 (43.8) 34.6 (74.6-155) 91.7 (14.1 (61.7) 42.4-164) 96.6-24.7-28.3-38.3 (52.4 (17.4) 19.6-42.2-85.9-34.6 (41.6-92.1-18.4-61.0-75.0 (20.6 (57.4 (19.3) 17.3) 18.0 (26.4) 62.3 (17.5-15.5-16.3 (28.4 (53.6) 18.4 (13.3) 20.3 (52.0 (15.4 (20.9-49.3-32.3-26.2) Age group 6-11 years 99-00* 01-02 03-04 99-00* 01-02 03-04 41.0 (61.1-32.6-128) 96.5-23.1 (34.6) 38.3-17.6 (61.3 (76.9 (16.9 (58.5-64.7-23.1-62.0) 70.6-24.

Itoh H. McKee RH. Meeker JD. Calafat AM. Yoshida K. Exposure to phthalates in neonatal intensive care unit infants: urinary concentrations of monoesters and oxidative metabolites. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Massey RC. Green RA. Jacek R. Gans G.S. Perera FP. Urinary levels of seven phthalate metabolites in the U. Environ Health Perspect 2000. Epidemiol 2005. Bull Environ Contam Toxicol 2002. Bolte G. Angerer J.210:21-33. 2000 [online].Phthalates References Adibi JJ.html. Available at URL: http://cerhr. Barr D. Chen Z. David RM. Sampson EJ. Int J Hyg Environ Health 2005. Springall C. Koch HM.18(1):122. et al. Atlanta (GA). Butala JH. et al. Reprod Toxicol 2004. Drexler H. Koch HM. Dobler L.niehs. Caudill SP. 4/20/09 Silva MJ. et al.nih. Singh NP.22(3):688-695. Castle L. Barr DB. Occurrence and daily variation of phthalate metabolites in the urine of an adult population. Fourth National Report on Human Exposure to Environmental Chemicals 269 .68:309-314. Rossbach B. Anderson WA. Environ Res 2003. Reidy JA. Duty S. Brock JW.18(12):10681074. Fromme H. Third National Report on Human Exposure to Environmental Chemicals. Needham LL. Int J Hyg Environ Health 2007. Helm D. Evaluation of the effect ofa governmental control of human exposure to two phthalates in Japan using a urinary biomarker approach.112(3):331-338. Richthoff J.16(4):487-493. et al. Monograph on the Potential Human Reproductive and Developmental Effects of Di-n-Butyl Phthalate (DBP). Giwercman A. Silva MJ. Internal phthalate exposure over the last two decades—a retrospective human biomonitoring study. Koch HM. Sanchez GN. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. Hum Reprod 2007.208:237-245. Malek NA. Silva MJ.114(9):1424-1431. Masunaga S. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Food Addit Contam 2001. Schettler T. Wiesmuller GA. et al. Ryan L. Hauser R. Prenatal exposures to phthalates among women in New York City and Krakow. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. Environ Health Perspect 2004. Weuve J. Int J Hyg Environ Health 2007. Hodge CC. Rylander L. Environ Health Perspect 2006. Drexler H. Poland. Silva MJ.gov/chemicals/ phthalates/dbp/dbp-eval. Boehmer S. 2005.210(3-4):319-33. Duty SM. Hilborn ED. A biomarker approach to measuring human dietary exposure to certain phthalate diesters.111(14):1719-1722. et al. Angerer J. Calafat AM. et al. Jedrychowski W. Eckard R.25(2):293-302. Caudill SP. Research Triangle Park (NC). Urinary phthalate metabolites and biomarkers of reproductive function in young men. Wittassek M. Hu H.93:177-185. 112(5):A270].108(10)979-982. Environ Health Perspect 2003. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Brock JW. NTP-CERHR. et al. Jonsson BAG. Pirkle JL. Camann DE. Needham LL. Hagmar L. Silva MJ. Blount BC. Caudill SP. Centers for Disease Control and Prevention (CDC). The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. Levels of seven urinary phthalate metabolites in a human reference population. J Androl 2004. Phthalate monoesters levels in the urine of young children. Ryan L. Scotter MJ.

400) < LOD < LOD .400 (.300) < LOD .300 (.400-.400) 1.400 (<LOD-. In this Report.Phthalates Dicyclohexyl Phthalate CAS No.10 (<LOD-1.10 (<LOD-2.2. People exposed to DCHP will excrete mono-cyclohexyl phthalate (MCHP) in their urine.9.300 (.500 (. resins.3. Urinary Mono-cyclohexyl phthalate (MCHP) Metabolite of Dicyclohexyl phthalate (DCHP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.70) .300-.500) < LOD * * * Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1.300-. and polyvinyl chloride.500 (.400 (<LOD-. 270 Fourth National Report on Human Exposure to Environmental Chemicals . and 0.300) < LOD . Biomonitoring Information Urinary levels of MCHP are infrequently measured and the limited population-based surveys available to date have reported most levels below the limit of detection.500) 1. respectively.300 (.200-.10 (.50) .200-.300 (.400-.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 .500 (.S.700) .400) size 2541 2782 2605 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .400 (<LOD-.500) .200-. 01-02.10) .600) .300-.700) .00-3.500 (.400 (. 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.600) < LOD . including nitrocellulose.700) .500-.00 (<LOD-1. which may vary for some chemicals by year and by individual sample.400-.300 (.600) .400 (.400-.300 (<LOD-.400) 1.500 (.300-.00 (<LOD-1.00) .500 (.300-.200 (<LOD-.900-1.300-.500 (.400) < LOD 1. see Data Analysis section) for Survey years 99-00.500) 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 . population from the National Health and Nutrition Examination Survey.500 (. polyvinyl acetate.300 (.400 (.400 (.600) .400-. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.500) .50) .400 (<LOD-.70 (1.300 (.300-.300-.400 (.200-.400-.400-.500) 1.200-. 0. 84-61-7 General Information Dicyclohexyl phthalate (DCHP) is used to stabilize some rubbers.00-2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.10 (<LOD-1.400) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.500) < LOD < LOD .600 (.500) . only levels at or above the 90th percentile could be characterized.600) .20) .500) < LOD 1.70 (1.400 (. < LOD means less than the limit of detection.300-.90) .70) .500) < LOD < LOD . Neither IARC nor NTP has evaluated DCHP with respect to human carcinogenicity.500) 1. and polymers.200-.80) . Survey Geometric mean (95% conf. 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-1.600) .500 (. and 03-04 are 0.500) .

54 (<LOD-2.330 (.690) < LOD < LOD .06) .270) < LOD .390 (.500 (.610 (.82 (1.44) .770) < LOD 2.880 (.940 (.620) < LOD .450 (.54-6.170-.500) size 2541 2782 2605 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .470 (.33 (<LOD-3.510 (. Fourth National Report on Human Exposure to Environmental Chemicals 271 . population from the National Health and Nutrition Examination Survey. Survey Geometric mean (95% conf.14 (<LOD-3.53) .530) 1.770-1.480 (.500) 3.590) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .490) . interval) Selected percentiles ( 95% confidence interval) Sample 95th 3.830) 1.590 (.910 (.660) < LOD < LOD .290-.370 (<LOD-.380-.470) 3.43 (1.420-.00) .690 (.510-.10) .310-.660) .740) < LOD < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.910 (.690) < LOD 2.360-.12-1.250 (.740) .420-.530-.11) .770-1.910 (.710) .310) < LOD .410 (.00 (<LOD-3.67 (1.S.630 (<LOD-.06) .910 (.33) .16) .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.690-1.34) .420-.54) .380 (.36-1.770 (.22 (<LOD-1.53) .670-1.400-.560) 1.450 (.950 (.74) .400-.530-1.500-.630 (<LOD-.16 (<LOD-3.18) .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 .220 (<LOD-.770-1.800-1.530 (.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.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 1.05) .330 (.82) .590 (<LOD-.350-.17) .260-.790-1.240-.670 (<LOD-.

Neither IARC nor NTP has evaluated DEP with respect to human carcinogenicity. A small study of children less than 2 years old reported mean urine MEP levels that were about twice as high as levels in children (aged 6-11 years) in NHANES 2001- Urinary Mono-ethyl phthalate (MEP) Metabolite of Diethyl phthalate (DEP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.7) 71.1 (71.3 (74. deodorants..9. Workplace air guidelines for external exposure to DEP have been established by ACGIH and NIOSH.2-102) 95.S. and hand lotions.4. particularly those containing fragrances.8-111) 85.1-93.3-103) 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. soaps.4 (62. and 2003-2004 subsamples were similar to median or geometric mean levels in small samples of pregnant women in New York City (Adibi et al. Biomonitoring Information MEP levels in the NHANES 1999-2000. respectively.. 84-66-2 General Information Diethyl phthalate (DEP) is a solvent used in many consumer products. In contrast.. 2002). 2003) and African-American women in Washington. 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. Products that may contain DEP include perfumes. 2001-2002.3 (82. 272 Fourth National Report on Human Exposure to Environmental Chemicals . shampoos.9-92. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.Phthalates Diethyl Phthalate CAS No. DC (Hoppin et al.5) 81. population from the National Health and Nutrition Examination Survey. 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. 0. People exposed to DEP eliminate mono-ethyl phthalate (MEP) in their urine. colognes.3-110) 211 (160-278) 197 (159-243) 225 (187-270) 190 (164-219) 191 (171-214) 205 (176-238) 75. see Data Analysis section) for Survey years 99-00.7 (70. and 03-04 are 1.9 (61. and 0. 01-02.2. and also in men attending a Boston infertility clinic (Hauser et al.

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. 2002).0-117) 142 (119-169) 152 (126-184) 168 (141-201) 179 (161-199) 181 (164-200) 197 (174-223) 79. the adjusted geometric mean levels of urinary MEP were lower in the group aged 6-11 years than in either of the other age groups..9-110) 96. 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.7-110) 81.3-105) 87. In an analysis of NHANES 1999-2000.Phthalates 2002 (Brock et al. Finding a measurable amount of MEP in urine does not mean that the levels of MEP or the parent compound cause an adverse health effect. Analysis of NHANES 2001-2002 showed similar findings.5-113) 122 (93. population from the National Health and Nutrition Examination Survey.0-156) 140 (111-180) 150 (123-184) 154 (136-177) 160 (146-182) 177 (147-202) 165 (127-208) 177 (135-224) 180 (145-203) 364 (275-495) 330 (249-409) 363 (292-485) 390 (336-452) 419 (363-486) 512 (423-632) 341 (219-554) 512 (290-802) 470 (310-596) 879 (676-1260) 808 (590-1100) 791 (589-1080) 1010 (803-1460) 1060 (884-1320) 1230 (989-1610) 625 (400-784) 843 (512-1320) 719 (470-1330) 1760 (1000-2000) 1330 (868-1840) 1470 (987-2220) 2170 (1790-3350) 2120 (1520-2790) 2290 (1770-3200) 328 393 342 752 742 729 1456 1647 1534 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 141 (124-159) 148 (130-168) 154 (139-171) 187 (165-211) 187 (166-210) 211 (180-248) 120 (107-134) 126 (110-147) 127 (108-150) 158 (142-179) 171 (148-188) 181 (148-217) 324 (249-415) 352 (282-425) 390 (341-465) 377 (307-495) 407 (355-473) 508 (379-634) 1000 (693-1480) 1100 (839-1480) 1070 (852-1360) 822 (697-1170) 860 (712-1100) 1120 (889-1400) 1950 (1460-2900) 2120 (1490-3030) 2000 (1610-2410) 1930 (1170-3410) 1430 (1190-2010) 2250 (1440-3330) 1214 1371 1250 1322 1411 1355 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 164 (142-190) 213 (182-249) 241 (213-271) 208 (183-236) 247 (226-271) 254 (225-287) 149 (135-165) 157 (142-173) 165 (144-189) 154 (136-174) 199 (164-242) 233 (202-270) 196 (166-228) 227 (185-270) 212 (188-246) 128 (111-142) 136 (124-150) 135 (120-158) 382 (314-472) 461 (396-572) 533 (417-665) 443 (390-505) 557 (478-618) 619 (476-791) 313 (239-387) 338 (288-402) 386 (338-485) 814 (673-974) 1080 (860-1650) 1230 (956-1610) 1030 (762-1700) 1240 (961-1480) 1530 (1200-1970) 856 (655-1390) 919 (712-1160) 989 (831-1330) 1330 (974-1920) 1940 (1410-2630) 2270 (1810-3140) 1920 (1230-2590) 2090 (1550-2800) 2590 (2160-3500) 1950 (1480-2740) 1590 (1320-2170) 1920 (1400-2780) 813 677 652 603 703 699 908 1216 1088 Non-Hispanic blacks Non-Hispanic whites Fourth National Report on Human Exposure to Environmental Chemicals 273 ..S. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.9 (82.6 (77. interval) 163 (149-178) Selected percentiles ( 95% confidence interval) 50th 141 (129-157) 148 (133-162) 153 (137-177) 75th 360 (307-422) 388 (330-435) 452 (386-504) 90th 905 (753-1180) 969 (805-1180) 1110 (889-1290) Total 167 (150-185) 181 (163-202) Sample size 1950 (1670-2310) 2536 1840 (1450-2200) 2782 2040 (1640-2540) 2605 95th Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 92.6 (65. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. with adjusted geometric mean levels of urinary MEP that increased with age (CDC. 2004).2 (66. Median MEP levels found in a small sample of German residents (Koch et al.0 (66. Other population estimates also differed by sex and race ethnicity (Silva et al. 2005).5-114) 101 (87. 2003) were slightly lower than levels found in NHANES 2001-2002.. This age-related trend is opposite the direction seen for other phthalates.

22(3):688-695. et al. Perera FP. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Hauser R. Meeker JD. Urinary levels of seven phthalate metabolites in the U. Koch HM. Silva MJ. Third National Report on Human Exposure to Environmental Chemicals. Brock JW. Davis BJ.S. Atlanta (GA). population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Angerer J. Silva MJ. Hodge CC. Hum Reprod 2007. Phthalate monoesters levels in the urine of young children. Ryan L. Singh NP. Caudill SP. 112(5):A270]. Environ Health Perspect 2004. et al. Duty S. Bull Environ Contam Toxicol 2002. et al. Caudill SP. Environ Health Perspect 2003. Barr D.112(3):331-338.111(14):1719-1722. Centers for Disease Control and Prevention (CDC). Prenatal exposures to phthalates among women in New York City and Krakow. Poland. Needham LL. 274 Fourth National Report on Human Exposure to Environmental Chemicals .110(5):515-518. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. Reidy JA.93:177-185. Hilborn ED. Rossbach B. Camann DE.Phthalates References Adibi JJ. Silva MJ. Environ Res 2003. Baird DD. Malek NA. Jacek R. Environ Health Perspect 2002. 2005.68:309-314. Reproducibility of urinary phthalate metabolites in first morning urine samples. Jedrychowski W. Hoppin JA. Drexler H. Brock JW. Barr DB.

40) 8.63-4.5 (24.90-11.46) 3.5 (25.56 (2.6 (9.90-3.8 (19.50 (7.5-28.50-6. 1.3) 13.30 (3.40) 1.49 (3.90-8.3 (19. MEHP is primarily formed by the hydrolysis of DEHP in the gastrointestinal tract and then absorbed.30-11.5 (18.10-5.3) 28.40 (4.5) 31.80) 13.40) 4.9 (16.50 (8.1 (8.30-13.70 (1.6) 9.85 (3.3-64. packaging film.0 (19.92-5.60) 8.31-4.21 (2.9 (7. interval) 3. Fourth National Report on Human Exposure to Environmental Chemicals 275 .84) 3.5-27.80) 6.80 (1.7) 19.60-7.40) 75th 7.70 (1.00) 2.10) 3.10 (3.9) 18.87-2.00) 5.23) 3.27 (3.6-60.67-4.80-4.9) 13.5) 19.00-3. Peck and Albro.80 (8.10-3. Four metabolites were measured in this Report: mono-(2-ethyl-5-hexyl) phthalate (MEHP).70-2.6) 95th 23.20 (1.57 (3.41 (3.80-9.8-36. mainly polyvinyl chloride.40 (6.6) 39.84 (2. and 03-04 are 1.0-84.60) 90th 14.9 (26.9-49.15 (1.44) 4.50-3.1-29.10) 4.92-2.70-8.20 (4.7) 22.4) 13.1-27.75 (3. and 0.5 (20.70-6.16-3.0.50-6.4-20.1 (8.25-3.10-3.4-27.40 (2.70 (7. 01-02.80 (8.00) 11.50) 9. and in humans.3-25.84-4.30) 2.60) 9.9) 27.0 (21.0-18.0 (19.5 (12.4) 15.10) 8.00-3.10-11.90-4.30 (4.10) 3.7) 35.9) 15.4) 22.00-5.4-53.0 (17.20 (1.0) 328 393 342 752 742 729 1461 1647 1534 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 3.6-25.4-20.50-20.8) 17.4-42.90) 7.00 (4.19-3.1-17.40-8.10) 3.50-5.42-5.3-57.6 (41. Urinary Mono-2-ethylhexyl phthalate (MEHP) Metabolite of Di-2-ethylhexyl phthalate (DEHP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.0 (18.82 (3.7) 27.1982).9-19.8-47.1) 19.80-5.70 (3. DEHP present in medical devices and parenteral delivery systems results in the diester rather than the monoester form being directly introduced into the blood.82) 3. as glucuronide conjugates (Albro et al.8-50.5 (12.51) 4.94-3.70) 2.32 (3.70-5.80-3.20 (3.40-8. 2002.6-130) 31.70 (5.9) 5.37-4.7 (17.92) 4.30-6.50-5.2. mono-(2-ethyl5-hydroxyhexyl) phthalate (MEHHP) and mono-(2-ethyl5-carboxypentyl) phthalate (MECPP).9-29.50-14.6 (20.93) 6.9 (29.90) 1.7) 8.50-2.9.86) 2.2 (11.0) 31.5-17.5-40.70-2.70-3.69) Selected percentiles ( 95% confidence interval) 50th 3.2) 29.9 (29.9 (17.30-8.80-4.00 (5.00) 1.00) 3.98) 2.50 (7.1) 22. DEHP is metabolized to more than 30 metabolites which are rapidly eliminated in urine.34 (2.1) 25.1-17.50-11.0) 35.0 (14.90) 4.0-19.5) 23.10) 2.10) 2.40) 11.70-5.0-18.80 (4.61 (3.9 (13.50 (2.10-4.Phthalates Di-2-ethylhexyl Phthalate CAS No..40-12.96) 4.4) 5.80-8.00) 9.1-48.07-4.3 (24.57-7.70 (3.9-55.91-3.54) 4.75-4.42) 3. 1989.70-4.00 (7.90 (3.5 (18.9-57.00) 2. and blood product storage and intravenous delivery systems.10 (4.79) 2.5-28.7) 6.30 (6.0) 23.10-5.5) 32.2) 23.50) 4.3