2009

Fourth National Report on Human Exposure to Environmental Chemicals

Fourth National Report on Human Exposure to Environmental Chemicals

2009

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

Contents

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

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

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

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

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

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

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

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Introduction

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

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

Fourth National Report on Human Exposure to Environmental Chemicals

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3-Dichlorobenzene (m-Dichlorobenzene) 1.2'.5-Dimethylfuran Ethylbenzene Hexachloroethane Methyl-tert-butyl ether (MTBE) Nitrobenzene Styrene 1.1.4'.4.4’.html.2'. Table 1.2’.2-Tetrachloroethane Tetrachloroethene Tetrachloromethane (Carbon tetrachloride) Toluene 1.5.5'.2'.5'-Tetrachlorobiphenyl (PCB 49) 2.5-Pentabromodiphenyl ether (BDE 99) 2.4-Tribromodiphenyl ether (BDE 17) 2.2-Dichloroethane (Ethylene dichloride) 1.1.4.4.6-Heptabromodiphenyl ether (BDE 183) 2.5'-Tetrachlorobiphenyl (PCB 44) 2. 2009 Acrylamide Adducts Acrylamide Glycidamide Total and Speciated Arsenic Arsenic.2'. 75 new chemicals are added for the 2003-2004 survey period and are listed in Table 1.cdc.3'.2'.4.4'.3.4.2'.4.4.3. Paradichlorobenzene) 1.3-Tetramethylbutyl] phenol) Triclosan (2.3.and p-Xylene o-Xylene 2 Fourth National Report on Human Exposure to Environmental Chemicals .1.5.4.4'.2. Total Arsenic (V) acid Arsenobetaine Arsenocholine Arsenous (III) acid Dimethylarsinic acid Monomethylarsonic acid Trimethylarsine oxide Disinfection By-Products (Trihalomethanes) Bromodichloromethane Dibromochloromethane (Chlorodibromomethane) Bromoform (Tribromomethane) Chloroform (Trichloromethane) Environmental Phenols Benzophenone-3 (2-Hydroxy-4-methoxybenzophenone) Bisphenol A (2.6-Pentabromodiphenyl ether (BDE 100) 2.2'3.5'-Hexabromodiphenyl ether (BDE 153) 2.4’.4'-Tribromodiphenyl ether (BDE 28) 2.6'-Decachlorobiphenyl (PCB 209) Perchlorate Perfluorinated Compounds Perfluorobutane sulfonic acid (PFBuS) Perfluorodecanoic acid (PFDeA) Perfluorododecanoic acid (PFDoA) Perfluoroheptanoic acid (PFHpA) Perfluorohexane sulfonic acid (PFHxS) Perfluorononanoic acid (PFNA) Perfluorooctane sulfonamide (PFOSA) Perfluorooctane sulfonic acid (PFOS) 2-(N-Ethyl-Perfluorooctane sulfonamido) acetic acid (Et-PFOSA-AcOH) 2-(N-Methyl-perfluorooctane sulfonamido) acetic acid (Me-PFOSA-AcOH) Perfluorooctanoic acid (PFOA) Perfluoroundecanoic acid (PFUA) Phthalate Metabolite Mono-(2-ethyl-5-carboxypentyl) phthalate (MECPP) Polybrominated Diphenyl Ethers (PBDE) and Polybrominated Biphenyl 2.4.3.2-Dichloroethene Dichloromethane (Methylene chloride) 1.6.4.1.2-Trichloroethane Trichloroethene (Trichloroethylene) m.4'-Tetrabromodiphenyl ether (BDE 47) 2.2-Dichloropropane 2.2'.4.4'.2-Dichloroethene trans-1.4'.What’s New in this Report What’s New in this Report In this Fourth Report.5.1-Dichloroethane 1.1-Dichloroethene (Vinylidene chloride) cis-1.5’.2'.2-bis[4-Hydroxyphenyl] propane) 4-tert-Octyl phenol (4-[1.1-Trichloroethane (Methyl chloroform) 1.4’-Trichloro-2’-hydroxyphenyl ether) Non-dioxin-like Polychlorinated Biphenyls 2.2-Dibromo-3-chloropropane (DBCP) Dibromomethane 1.2'4.4'-Tetrabromodiphenyl ether (BDE 66) 2.4.2'.4'-Pentabromodiphenyl ether (BDE 85) 2.3’.5.gov/exposurereport/chemical_selection.4-Dichlorobenzene (p-Dichlorobenzene.6'-Hexabromodiphenyl ether (BDE 154) 2.2-Dichlorobenzene (o-Dichlorobenzene) 1.5'-Hexabromobiphenyl (BB 153) Volatile Organic Compounds (VOCs) Benzene Chlorobenzene (Monochlorobenzene) 1. The process for selection is described at http://www. Chemicals reported for the first time in the Fourth National Report on Human Exposure to Environmental Chemicals.

Some results reported previously have been changed or removed due to improvements in analytical measurement or recognition of an analytical issue (e. Data for other pesticides are included only for 1999-2000 and 2001-2002.g. Percentiles for all three NHANES survey periods (1999-2000. Explanations for each change are provided in Appendix B. 2003-2004 data for the organochlorine pesticides and the dialkyl phosphate organophosphorus insecticides are included in the Report. 2003-2004) have been re-computed by use of this improved procedure. urinary 2.5-dichlorophenol for the 1999-2002 survey periods.. Details of this procedure are provided in Appendix A. and polycyclic aromatic hydrocarbons (PAHs) for one or more of the 1999-2002 survey periods.4-dichlorophenol and 2.g. five results that all have the value 90. and these data will be included in the next release of the Report.. 2003-2004 data for these other pesticides will be provided on this website as soon as they are available. 2001-2002.1). Affected analytes were serum beta-hexachlorocyclohexane for the 2001-2002 survey period. the presence of an interference) that produced results of inadequate quality. Fourth National Report on Human Exposure to Environmental Chemicals 3 . Only slight differences should be noted when one compares the recomputations to previous releases of the Report.What’s Different in this Report What’s Different in this Report The Fourth Report uses a new procedure to estimate percentiles when the percentile estimate falls on a value that is repeated multiple times (e.

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

Serum levels reported per gram of total lipid reflect the amount of these compounds that are stored in body fat.gov/nchs/nhanes/ nhanes2003-2004/analytical_guidelines. Urinary levels are expressed both ways in the literature and used for different purposes. Acrylamide and glycidamide adducts are expressed as the picomoles per gram of blood hemoglobin to which the adduct is bound. Laboratory measurements underwent extensive quality control and quality assurance review. For example. This design does not permit straightforward analysis of exposure levels by non-targeted strata such as locality. Useful unit conversions are shown in Table 2. results are given for the total population as well as by age group. Data were analyzed using the statistical software package Statistical Analysis System (SAS) (SAS Institute Inc. if one person has consumed more fluids than another person. non-Hispanic black.cdc. including the lipid in serum.S. sample weights must be used to adjust for the unequal probability of selection into the survey. The geometric mean is influenced less by high values than is the arithmetic mean. levels are presented two ways: per volume of urine and per gram of creatinine. serum. Other racial/ethnic groups are included in estimates that are based on the entire population sample. proximity to sources of exposure. 2001). Age groups are as described for each chemical in each data table. Geometric means were calculated by taking the log of each concentration and then computing the weighted mean of those log-transformed values using SUDAAN software. micrograms per liter). population. Table 2. Census Bureau estimates of the U. References for the analytical methods used to measure the different chemicals are provided in Appendix C. Other mostly non-lipophilic chemicals measured in serum are expressed per liter of serum (e. the measurement of quality control samples in each analytical run to detect unacceptable performance in accuracy or precision. Levels per gram of creatinine (i. furans. Sample weights also are used to adjust for possible bias resulting from nonresponse and are post-stratified to U. Gender is coded as male or female. multistage. and race/ethnicity as defined in NHANES. serum. Units of measurement are important. his or her urine output is likely higher and the urine more dilute than that of the other person. Serum levels per whole weight of serum are also included to facilitate comparison with studies investigating exposure to these chemicals and reported levels in these units. creatinine corrected) adjust for urine dilution. or graphite furnace atomic absorption spectrometry.e. inductively coupled plasma mass spectrometry. 2002) and the statistical software package SUDAAN (SUDAAN Release 8. Units of Measurements and Abbreviations Unit liter deciliter milliliter gram milligram microgram nanogram picogram femtogram Abbreviation L dL mL g mg µg ng pg fg Value 10 liters -3 10 liters 10 grams -6 10 grams -9 10 grams -12 10 grams -15 10 grams -3 -1 Geometric means: A geometric mean provides a better estimate of central tendency for data that are distributed with a long tail at the upper end of the distribution. Other racial/ethnic groups are sampled. Units: For chemicals measured in urine. stratified. but the proportion of the total population represented by other racial/ethnic groups is not large enough to produce valid estimates. For dioxins. and urine were based on isotope dilution mass spectrometry. including tolerance limits for operational parameters.. or region. and verification of traceable calibration materials.Data Sources and Data Analysis metabolites in blood. or urine levels for each environmental chemical. or by use of particular products. generally conforming to those most commonly used in biomonitoring measurements. The Report presents descriptive statistics on the blood. PCBs. These compounds are lipophilic and concentrate in the body’s lipid stores. Ninety-five percent confidence intervals around this Fourth National Report on Human Exposure to Environmental Chemicals 5 . Guidelines for the analysis of NHANES data are provided by NCHS at http://www. race/ethnicity is categorized based on the sample design as Mexican American. serum levels are presented per gram of total lipid and per whole weight of serum.. Statistics include unadjusted geometric means and percentiles with confidence intervals. gender. 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. In each table.g. state. and organochlorine pesticides.0. This type of distribution is common in the measurement of environmental chemicals in blood or urine. Results are reported here using standard units.htm. and nonHispanic white.. Data Analysis Because the NHANES is a complex. For these analyses.S. SUDAAN uses sample weights and calculates variance estimates that account for the complex survey design. seasons of the year. probability-cluster design.

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

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

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

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

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

6) 90th 141 (124-155) 03-04 03-04 03-04 03-04 03-04 03-04 03-04 59..4 (54.6-108) 61. in permanent press fabrics. 2004). and well below doses known to cause nerve damage or carcinogenicity in animals..8 (57.2 (75. EPA.3-71. glycidamide.9-105) 86.0 (53.8 (52. 2004. 2005).7 (63.2-59. In the general population.4-83.6-61.3) 70.6) 50. Fennell et al.3 (53.1 (73.1-64.6-65. acrylamide is synthesized and used in the production of polyacrylamide polymer.Acrylamide Acrylamide CAS No.8-55.2) 57.1 (52..2-70.6) 90.7) 54. are heated at temperatures used for frying and baking.4 (53.6 (56.2 (58.7-64. interval) 61. 217 million pounds of acrylamide were produced commercially in the U.2-114) 163 (147-191) 96.4) 57.4) 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. and peripheral neuropathy following chronic Acrylamide Geometric mean and selected percentiles of hemoglobin adduct concentrations (in pmol/g hemoglobin) for the U. 2006. mineral processing. Recently.S.1 (83.7 (58.7) 96.4 (54. 79-06-1 General Information Acrylamide is a small organic molecule existing as a white crystalline powder in its pure state.2-118) 98. and is either metabolized to the reactive epoxide.3) 63.0-108) 152 (139-175) 126 (111-142) 108 (86.9) 75. Elimination occurs mainly in the urine as mercapturic acid conjugates. the main source of exposure is from the diet.4 (59. ocular and dermal irritation from direct contact with acrylamide containing materials.2-93. and binding agents.S.0) 85.5-85.S. drinking water.0 (67.4) 57.1) 46. 2005).1) 53.S. (NTP-CERHR.9 (69.6 (51.0 μg/kg for adults (FAO/ WHO.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. but can covalently bind to form adducts with proteins. 2005).6 (81.3-2.0-58.1 (88.3) 86.9 (60.6) 71. Animal studies indicate that acrylamide is well absorbed.7 (65.9) 57.3 (55. pulp and paper production.9 (54.9) 63.7-64. and an average daily intake is estimated as 0.2 μg/kg/day (U.5 (79.9) 58. 2002).0) 57.6) 73.8 (91. although additional exposures from cosmetic products could add a similar amount (NTP-CERHR.0.5-80.6-66. acrylamide has produced upper airway irritation following inhalation of high levels.5 (52. Polyacrylamides are useful water-compatible polymers used in water treatment.4-60.1 (47. FDA. but are generally above the U.5) 66. Smaller scale applications of polyacrylamides include additives to paperboard used for food packaging.1-64.9-52. and cosmetics (NTP-CERHR. it was discovered that acrylamide is formed when starch-rich foods. Acrylamide is not thought to accumulate in the body at environmental doses. soil conditioners. and from dermal contact with products that contain residual acrylamide. and in the synthesis or compounding of dye materials.6-75. population from the National Health and Nutrition Examination Survey.4-89.5 (44. gels. 2005).1-57.4-76.5) 58.4 (51. FAO/WHO. in some sealing grouts.2 (62. or to glutathione conjugates (Calleman et al.7) 73.7) 58. 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. People may be exposed to acrylamide from foods.0-49.0-66.1-61. widely distributed in tissues. as an absorbent in disposable diapers.2-91. Survey Geometric mean (95% conf.7 (55.0 (69.4) 100 (89.1) 55.1) 101 (95. environmental releases of acrylamide can enter aquatic systems and soils where it degrades within days and does not bioaccumulate (U.8-57.2) 57. Tareke et al. and in some cosmetics. 2006). EPA reference dose of 0. see Data Analysis section) for Survey year 03-04 is 3. smoking.8 (81. In humans.2-77. In 1997.2-67.0 (57. such as potatoes and some grains. 1994). 2005.1) 62.7-60. Commercially.4-60. 1990. Natural substances in the food are converted to acrylamide.7) 75th 79. Fourth National Report on Human Exposure to Environmental Chemicals 11 . 2005). EPA.0-115) 156 (120-203) 146 (129-163) 149 (125-179) 218 (172-271) 197 (172-223) 1792 1874 2994 Limit of detection (LOD. Estimated intakes in children are about twice that of adults (DiNovi and Howard.S. Since acrylamide has limited volatility and high water solubility. These estimated intakes are hundreds of times lower than occupational exposures.9-61.5 (74.6-104) 82.

.9-64.2 (56. Vesper et al.4 (56.. population from the National Health and Nutrition Examination Survey.. U. 2005. 2005. 2006).4-65. 2005. 2005).7-62.9) 87.5-64.. 2004.. male germinal cell injury. 2006). Several of these studies have shown that smokers have adduct levels that are three to fourfold higher than non-smokers.5) 71. Schettgen et al.4) 83. uterine.0-93. and other sites) (FAO/WHO. 2006.7 (57. 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. respectively) are markers of integrated acrylamide exposure over the preceding few months.5 (56.S. 2005. 2008).7) 61. In addition.3) 59.0-103) 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 64.4 (81.0) 118 (103-126) 121 (112-134) 113 (94. Puppel et al.S. to increase the unscheduled synthesis of DNA in tumor susceptible tissues (Klaunig et al. 2009). see Data Analysis section) for Survey year 03-04 is 4. gov/iris/ and from the Food and Agriculture Organization of the United Nations and WHO at: http://www.. most non-smokers had levels less than about 100 pmol/gram hemoglobin. 2005). interval) 59..9-76. Survey Geometric mean (95% conf.8-48.2) 55.0 (70.0 (52.4 (61. and to increase DNA reactivity when glutathione availability is reduced (Klaunig et al. 1997.0) 94.2 (72.4) 53.6-62..epa.4-103) 79. Younger children may have slightly higher levels possibly due to increased intake of acrylamide-containing foods relative to body size (Dybing et al. altered gene expression in testicular tissues (Yang et al.2) 87.4 (51. probably through its epoxide metabolite.7 (87.9 (57.2 (63.7 (61.1-60. 2006) have been demonstrated after acrylamide dosing. Animal studies have shown that acrylamide can cause nerve damage (neuropathy).3 (56. 2005. Puppel et al. 1997.1 (82.9) 65. Glycidamide Geometric mean and selected percentiles of hemoglobin adduct concentrations (in pmol/g hemoglobin) for the U.9-138) 143 (130-159) 96.9 (58.2-91. dominant lethality). U..3) 85.1) 56.7 (84. Axonal degeneration..8-61. Additional information is available from U.1 (66. 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.1 (56.1-62..7-86. 2005). 2002. Acrylamide is clastogenic and can produce dominant lethal mutations. Biomonitoring Information Acrylamide and glycidamide hemoglobin adducts (AHA and GHA.8 (51.6 (66. levels of AHA adducts decline but may remain detectable for several months (Hagmar et al.7-64.1 (57. glycidamide (NTP-CERHR.5 (83.5-92. Glycidamide has been shown to react with DNA (Doerge et al.5) 75th 85.. 2004).S. 2005.6-64.5) 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.9) 75..1 (70.4) 46. Adducts are formed when either acrylamide or glycidamide react to form a permanent covalent bond with hemoglobin in the blood.5 (42.2-68.7) 60.3) 59.int/ ipcs/food/jecfa/summaries/summary_report_64_final.2-90. AHA levels have been shown to increase with dietary intake (Hagmar et al.2) 65.4-59. Vesper 2005) and smoking (Bergmark. Hagmar et al. 12 Fourth National Report on Human Exposure to Environmental Chemicals . 2005.. and cancer (mammary.0-62. scrotal.8) 60. 2005) and sperm DNA adducts (Xie et al.1-70.1) 62.7) 74.8-49.5) 90th 130 (120-141) 03-04 03-04 03-04 03-04 03-04 03-04 03-04 71.9) 59. thyroid.9-78. Schettgen et al. presynaptic nerve terminal binding (LoPachin.3-78.6 (90. EPA at: http://www. reproductive effects (reduced litter size. EPA. EPA.Acrylamide occupational exposures.0.5-66. Maniere 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. 2003. After exposure ceases..6-90.4-98.7) 90.S. 2001)..9 (81.5-94. Klaunig et al. 2008). 2002.4 (57. 2005.3) 59. 2005). fetal death. IARC classifies acrylamide as probably carcinogenic to humans.0 (80.1-56.5) 87. Mucci et al.1) 60. 2005. NTP-CERHR. 2005) have been demonstrated in animals. although different analytic methods can affect results. adrenal.who. 2005.9-62..8) 45. 2005.pdf.5 (59....0 (75.9-77. Rice.8 (44.4 (90.3-101) 95. and neuronal DNA reactivity (Doerge et al.

2001. Mucci LA. Determination of hemoglobin adducts in humans occupationally exposed to acrylamide. 2/3/09 Klaunig JE. 1999). Paulsen JE. Fennell TR. Twaddle NC. Aprea P. AHA levels were several fold to several hundredfold higher than levels in non-exposed non-smokers (Bergmark et al. DNA damage and DNA adduct formation in rat tissues following oral administration of acrylamide. Chem Res Toxicol 1997 Jan.27(4):219-226. Available at URL: http://www. Mutat Res 2005. In another study. Wilson KM.pdf. Duale N.nih. Joint FAO/WHO Expert Committee on Food Additives. Calleman CJ. Kamendulis LM. July. Toxicol Sci. Churchwell MI. Costa LG. 2009 Jan 8. Nordander C. Chem Res Toxicol 1990. Mutat Res 2005. Becher G. Axmon A.580(1-2):119-129.580(1-2):157-165. and Research Strategies. 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.Acrylamide In occupational settings. 2004 Acrylamide in Food Workshop: Update Scientific Issues. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Farmer PB. et al. Wirfalt E. Differences in hemoglobin adduct levels of acrylamide in the general population with respect to dietary intake. Uncertainties. February. Toxicol Appl Pharmacol 1993.. et al. References Bergmark E.126(2):361-371. NIH Publication No. Zhang S. Summer SCJ. Acrylamide is metabolized to glycidamide in the rat: evidence from hemoglobin adduct formation.120(1):45-54. Churchwell MI. He F.580(1-2):131-141. Food and Drug Administration (FDA).html#u1004. Mutat Res 2005.. 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. Tian G. Italy. Snyder RW. Acrylamide intake through diet and human cancer risk. Paulsson B. Spicer R. 8-17 February 2005. 054472. Hagmar L. Magnusson AL.. Mechanisms of acrylamide induced rodent carcinogenesis. Burgess J.fda. Food Chem.niehs. Biomarkers of human exposure to acrylamide and relation to polymorphisms in metabolizing genes. Toxicol 2005. Godard T. Acrylamide neurotoxicity: neurological. gov/~dms/acrydata. Guffroy M. Laurentie M. Fennell TR.who. DNA adducts derived from administration of acrylamide and glycidamide to mice and rats. Human exposure and internal dose assessments of acrylamide in food. Center for the Evaluation of Risks to Human Reproduction (NTP-CERHR). Hagmar et al. 2001). Bjellaas T. [Epub ahead of print] Dybing E. Calleman CJ. The Updated Exposure Assessment for Acrylamide. 2005.int/ipcs/ food/jecfa/summaries/summary_report_64_final. et al. Bergmark E. Doerge DR. Chicago. Granath F. Available at URL: http://www. Relationships between biomarkers of exposure and neurological effects in a group of workers exposed to acrylamide.gov/chemicals/ acrylamide/Acrylamide_Monograph. Bridson WE. Illinois. Monograph on the Potential Human Reproductive and Developmental Effects of Acrylamide. Wu Y.10(1):78-84. Toxicol Sci 2005. Tornqvist M. smokers and nonsmokers. et al. J Agric Food Chem 2008. Adv Exp Med Biol 2005. Available at URL: http://cerhr. Doerge DR. Bergmark E. Beland FA.cfsan. 1994)..561:21-37. Haugen M. Rosen I. Malmberg B. 6013-6019. Metabolism and hemoglobin adduct formation of acrylamide in humans. Health effects of occupational exposure to acrylamide using hemoglobin adducts as biomarkers of internal dose. 64th Meeting: Summary and Conclusions (FAO/WHO). et al.561:49-62. Kautiainen A. da Costa GG.pdf. Bruze M. DiNovi M and Howard D. 1993. symptoms of numbness or tingling in the extremities did not occur in exposed workers whose AHA levels were below 510 pmol/gram hemoglobin. Perez et al. Calleman CJ.56. National Toxicology Program.3:406-412.85:447-459. Scand J Work Environ Health 2001. Costa LG.43:365–410. Andersen M. 2006. morphological and molecular endpoints in animal models. and 39% of workers with levels above 1000 pmol/gram hemoglobin had these symptoms (Hagmar et al. Hemoglobin adducts of acrylamide and acrylonitrile in laboratory workers. 2004. smoking habits and gender. 2/3/09 Perez HL. 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. Maniere I. Bergmark E. McDaniel LP. Yang JS. Alexander J. LoPachin RM.Toxicol Appl Pharmacol 1994. 2/3/09 Hagmar L. April 13-15. Rome. Osterman-Golkar S. Adv Exp Med Biol 2005. He F. Tornqvist M. Survey data on acrylamide in food: individual food products. Simultaneous analysis of hemoglobin adducts of acrylamide and Fourth National Report on Human Exposure to Environmental Chemicals 13 .. CFSAN/Office of Plant and Dairy Foods. Cheong HK.

Mutat Res 2005. Acrylamide. Pilot study on the impact of potato chips consumption on biomarkers of acrylamide exposure. Chae C.580(1-2):3-20. Rice JM.56(15):6046-53. et al. 2/3/09.S. Toxicol Lett 2006. Environmental Protection Agency (U. Ding X. Angerer J. Schettgen T. Rydberg P. Licea-Perez H. Int J Hyg Environ Health 2003. Fu D. A first approach to estimate the internal exposure to acrylamide in smoking and non-smoking adults from Germany. Washington (DC). Office of Pollution Prevention and Toxics. a carcinogen formed in heated foodstuffs. Hemoglobin adducts of ethylene oxide. revised 1/3/06. Drexler H. Liu Y. 1994.163(2):101-8. Gray JG. Int J Hyg Environ Health 2004. Lee SH. J Agric Food Chem 2008.epa. Liu K.htm. Marko D.txt.580(1-2):71-80. The carcinogenicity of acrylamide. Adduction of biomacromolecules with acrylamide (AA) in mice at environmental dose levels studied by accelerator mass spectrometry. Myers GL. Cross-sectional study on acrylamide hemoglobin adducts in subpopulations from the European Prospective Investigation into Cancer and Nutrition (EPIC) Study.S. Han DU.50(17):4998-5006. Xie Q. Schettgen T. Angerer J. Meyers T.epa. Adv Exp Med Biol 2005. acrylonitrile and acrylamide-biomarkers in occupational and environmental medicine. Toxicol Lett 2002.207(6):531-9. Toxicological effects of acrylamide on rat testicular gene expression profile.Acrylamide glycidamide by gas chromatography-mass spectrometry. Tareke E. Schettgen T. Jin Y. Rossbach B. Determination of haemoglobin adducts of acrylamide and glycidamide in smoking and non-smoking persons of the general population. Choi JH. Eriksson S.S. Mutat Res 2005 Feb 7. Ingham L. Fueller F. DNA strand breaking capacity of acrylamide and glycidamide in mammalian cells. Tjønneland A. Weiss T. U. Lee MH. propylene oxide. Yang HJ. EPA). Sun H. Ospina M. Smith A. Available at URL: http://www. EPA). Broding HC. Rapid Commun Mass Spectrom 2006. Letzel S.206(1):9-14. U. Tornqvist M. Available at URL: http://www. Analysis of acrylamide. Reprod Toxicol 2005. et al.gov/iris/subst/0286.20(6):959-64. Han CH.S.134(1-3):65-70.274(1):59-68. Puppel N.561:89-96. Benetou V. Hallmans G. Environmental Protection Agency (U. Drexler H. Ospina M. Slimani N. Chemical Summary for Acrylamide. Vesper HW. Integrated Risk Information System (IRIS). Angerer J. Karlsson P. September. 14 Fourth National Report on Human Exposure to Environmental Chemicals .gov/chemfact/s_acryla. Meyers T. Anal Biochem 1999. 2/3/09 Vesper HW. J Agric Food Chem 2002. Drexler H. Tjaden Z. Vesper HW. Kutting B. Agudo A. Automated method for measuring globin adducts of acrylamide and glycidamide at optimized Edman reaction conditions.19(4):527-34.

060 (..080) < LOD . 486-56-6 Metabolite of nicotine (a component of tobacco smoke) General Information Tobacco use is the most important preventable cause of premature morbidity and mortality in the United States.167 (.145) .071) .70-2.059-.960-1.45) 1.48-3.190-.110-.139) * .160 (.058 (.950 (.080-.050-.50-1.93) .770) .17 (1.090-.310-1.480-1.09-2.18-3.580-1.163) .S.68) .Cotinine Cotinine CAS No.140-.900-1.14) .312) .570-1.059-. Persons exposed to secondhand tobacco smoke (environmental tobacco smoke [ETS]) may have adverse health effects that include lung cancer and coronary heart disease. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.061) < LOD .77 (2.080 (.02 (.160 (.108) * .540 (.00) 1.054 (.65 (1. and 03-04 are 0.163 (. and 17% had an LOD of 0.350 (.200) 1.213) .087 (. and exacerbated asthma (U.32-2.110-.090-.360) .12) 1.43 (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.110) .120) .073) < LOD .21-1.500 (.22) 2789 3152 2937 3210 3667 3383 Females Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 * .060 (<LOD-.068) .310-1.89) 1.104-.39 (1. acute respiratory infections. stroke.210 (.137 (.28-1.063) .062 (.580 (.220-.19) 1.540-. DHHS.42-4.052 (<LOD-.920 (.175 (.19) . and more than 50 compounds present in ETS are known or reasonably anticipated to be human carcinogens (NTP.34 (1.308 (.20) .142-.17 (.520 (.506 (.124 (.44 (1.190-.15 (2.040 (.066-.32) 1. ** In the 2001-2002 survey period.14-1.910-1.060 (.198) * .050 (<LOD-. cardiovascular disease.110 (. Cigarettes contain about 1.350-.070 (<LOD-. 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.50-4.180) .50) 3.164 (.850 (.120 (.77 (1.150) .83-2. maternal exposure during pregnancy can result in lower birth weight.60-2.410) .96-4.080) < LOD < LOD .087) < LOD < LOD .076-.21 (.160-.150) .01 (1.428-.23-2. ear problems. producing roughly 1–2 mg of bioavailable nicotine per cigarette (Benowitz and Jacob.85 (1. 1998). Children exposed to ETS are at increased risk for sudden infant death syndrome.30) 2.030-.068) .23 (1.088-.950-1.54) 1.05) 1.480-.44 (2.154-.120-.310) .153-.302) .120-.230 (.120 (.310) 90th 1.430-1. The smoke produced by burning tobacco contains at least 250 chemicals that are toxic or carcinogenic.030 (.620 (.770-1.62) 2.140-.084) .180 (.120 (.54) size 5999 6819 6320 Total years 99-00 01-02** 03-04 50th .047-.188) .110 (.110) . Survey Geometric mean (95% conf.21-1.63-2.20) 1.047-.300) .740-1.63 (2. 2006).053 (<LOD-.11) .070) 75th .81-2.12 (2. acute respiratory illness.057-.050-.88 (.66 (1.137-.060 (<LOD-.28) .050) .30) * .077) .050 (<LOD-.086 (.48-2.087-.20-2.050 (.997-3.68) 2.130) .57) 2. and 0.066 (.144 (.23 (.060-.68 (1. respectively. 2004).54 (1.070) .840) 3.030-.060-.S.990) .060) .20 (.180) .660) .110 (.01) 3.44) 2.625) .220) .180) .148-.84-3.080-.730 (.32-2.060-.02) 1.62 (2.600-1.99) 2.020-.09-3.015.92) 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 .180) .075 (. population from the National Health and Nutrition Examination Survey.350-.77 (1.38-2.050) .50 (1.76 (1.95) 1.40) .49) 1.110 (.26-1.78) 2.05.094) .19-2.140 (.220) .120 (.533-.040 (.00) .160 (.96 (1.70) 2.120 (.260) 1.53-4.5% nicotine by weight (Kozlowski et al.450-.S.42 (1.160) .55 (1.88 (1.050 (<LOD-. Fourth National Report on Human Exposure to Environmental Chemicals 15 .030-.740-1.280 (.570 (.580) .071 (.820) .800 (.09-3.230) . The consequences of smoking and of using smokeless tobacco products are well known and include an increased risk for several types of cancer.14) .234) .690 (.040 (.040-.04 (1.790) . < LOD means less than the limit of detection.22) 2. see Data Analysis section) for Survey years 99-00.110 (.470-.077) .20 (1.400-.30) 2.015 ng/mL.770) .180 (.320) .16) .201) . 83% of measurements had an LOD of 0.630 (.66) 1.115-.080-.505 (.111-.160) .052 (<LOD-.140 (. which may vary for some chemicals by year and by individual sample.043-.050 (<LOD-.23 (2.94) 1. 2004).630 (.187) .216 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. DHHS.96) 2.240 (.260-1.49) 1. and various other disorders (U.621-1.040-.55-2.710 (.670) .47-3.130 (.54 (1.12 (1.089) Age group 3-11 years 99-00 01-02** 03-04 .92 (1.070) .126) .193) .17) .070-.190-.05 ng/mL.79) 3.080-.197) .02) 1.35 (2.110-.53 (1.080 (.33-2.12-4.990 (.75) 1.106-.180) .726) .510 (.131 (.620-1.44) 2.39) 3.860 (.164 (.87-3.930 (.090-.370-.15) 2.99) 2.100-. emphysema.066) .66-3.630 (.

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

280:135-140. Nicotine metabolism and intake in black and white smokers. Warner K. Giovino G. Bernert JT.4:313-316.7:369-375. [online]. Metabolism of nicotine to cotinine studied by a dual stable isotope method. Pechacek TF. National Toxicology Program (NTP). Pirkle JL. 4/13/09 National Cancer Institute (NCI). cigarette smokers: the Third National Health and Nutrition Examination Survey. population to environmental tobacco smoke: the Third National Health and Nutrition Examination Survey. Mowery PD. Brody DJ. Jacob P III.57(1):79115. Tobacco related exposures.fr/ENG/Monographs/allmonos90.18:188-204.niosh. Jacob III P. IARC Monogr Eval Carcinog Risks Hum. Benowitz NL. Sweeney CT. Am J Public Health 2004. Benowitz NL.gov/library/ secondhandsmoke/. Soliman S. 4/13/09 U. Flegal KM. 4/13/09 Iwase A.pdf. 4/13/09 Perez-Stable EJ. Pharmacol Rev 2005. Available at URL: http:// cancercontrol. Schwartz SS. available at URL: http://mtn.nih. Absorption and metabolism of nicotine from cigarettes. U. International Agency for Research on Cancer. 1999. Coordinating Center for Health Promotion. Fong I.S. Filter ventilation and nicotine content of tobacco in cigarettes from Canada. Smoking and Tobacco Control Monograph 10 [online]. Int Arch Occup Environ Health 1991. Office on Smoking and Health [online] 2006. 1988-1991. The Health Consequences of Involuntary Exposure to Tobacco Smoke: A Report of the Surgeon General — Executive Summary.php. Available at URL: http://ntp. Biomonitoring data can also help scientists plan and conduct research about exposure to ETS and about its health effects. The Health Consequences of Smoking: The Surgeon General’s Report—Executive Summary. Current Intelligence Bulletin 54: Environmental tobacco smoke in the workplace. Pollack HA. Cotinine as a biomarker of environmental tobacco smoke exposure. Atlanta (GA): 2005. Hukkanen J. 1991. Third National Report on Human Exposure to Environmental Chemicals. Pechacek TF. IARC Monogr Eval Carcinog Risks Hum.291(3):1196-1203. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. National Institute for Occupational Safety and Hygiene (NIOSH). Caraballo R. Aiba M.cancer. 2004. References Armitage AK. Richter PA. Mehta NY. Coordinating Center for Health Promotion. Jacob P III. 1988-1991. Houseman TH. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans.iarc. Metabolism and disposition kinetics of nicotine. population to secondhand smoke: 1988-2002. Trends in the exposure of nonsmokers in the U. Kira S. Benowitz NL.niehs.15:302-307. BMJ 1975.56:483-493. 11th ed.S.S Department of Health and Human Services (U.Cotinine and public health officials determine whether people have been exposed to higher levels of ETS than are found in the general population. Vol 83. Available at URL: http://www. 1999-2002. Modin G. Centers for Disease Control and Prevention. Vol 38. DHHS). Decrease in the prevalence of environmental tobacco smoke exposure in the home during the 1990s in families with children. Pickett MA. Etzel RA. Summary of Data Reported and Evaluation [online] 2004. and the United States. U. Strauss WJ. Tobacco Smoke. Centers for Disease Control and Prevention. In Report on Carcinogens. Caudill SP. Herrera B. Available at URL: http://monographs. Tob Control 2006. 4/13/09 Centers for Disease Control and Prevention (CDC).63:139-43. U. Tobacco Smoke and Involuntary Smoking. Maurer KR. Environ Health Perspect 2006.114(6):853-858.cdc. Curtin LR. Ethnic differences in N-glucuronidation of nicotine and cotinine.pdf. 4/13/09 International Agency for Research on Cancer. Racial/ethnic differences in serum cotinine levels among adult U. Department of Heath and Human Services.94(2):314-320. Pirkle JL.S. DHHS). Brody DJ. Vogler GP. George CF. JAMA 1996. Herrera B. Tob Control 1998. J Pharmacol Exp Ther 1999. Jacob P. Smoke-free laws and secondhand smoke exposure in US nonsmoking adults.php. Summary of Data Reported and Evaluation [online] 1986. Schober SE. iarc. et al. National Center for Chronic Disease Prevention and Health Promotion. Available at URL: http://monographs. Exposure of the U. JAMA 1998. Centers for Disease Control. Benowitz NL. Perez-Stable EJ.surgeongeneral. Respiratory nicotine absorption in non-smoking females during passive smoking. National Center for Fourth National Report on Human Exposure to Environmental Chemicals 17 . Benowitz NL.S.275:1233-1240. Giovino GA.S Department of Health and Human Services (U. Jarvis MJ. Department of Heath and Human Services.fr/ENG/Monographs/ allmonos90. et al. Sosnoff CS. Dollery CT. the United Kingdom. Bernert JT.S. June.gov/tcrb/monographs/10/. Lewis PJ.gov/eid/rmca/critdocs/ criteriadoc/33. Epidemiol Rev 1996. JAMA 1998.S. Clin Pharmacol Ther 1994. Turner DM. Health Effects of Exposure to Environmental Tobacco Smoke: The Report of the California Environmental Protection Agency.S.gov/ntp/roc/eleventh/profiles/ s176toba. Kozlowski LT.280:152-156.

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

2002). have been reported as result of self-poisoning by ingestion or excessive dermal application.180 (. DEET can be applied to clothing and the skin to repel biting insects.120-. 2002). DEET has low acute toxicity. DEET is not a developmental or reproductive toxicant in animals (U.S.130 (.EPA at: http://www. Most reports of adverse effects from overexposure to DEET involve skin reactions (Bell et al. 2003).180 (. < LOD means less than the limit of detection.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 (<LOD-.1.140 (. DEET is not registered for use on agricultural commodities. 1998). General population exposure to DEET occurs from skin application and from inhalation of aerosol formulations.140) < LOD .N-diethyl-meta-toluamide (DEET) is an insect repellent that was first marketed in 1957.S.N. Additional information is available from U. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.449 and 0.250) < LOD . Human health effects from DEET at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 134-62-3 General Information N.100-. DEET is also used in combination with dermal sun screens (U.140) < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result. After absorption.S. About 3-8% of dermally applied DEET is absorbed. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD .140) < LOD . Urinary N.180 (. Exposure can also occur from consuming food contaminated by DEET on hands or that was sprayed nearby.120-.130) < LOD .140-.110-.130-.N-Diethyl-meta-toluamide (DEET) Geometric mean and selected percentiles of urine concentrations (in µg/L) for 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 .160) < LOD .130-.520) < LOD .110 (. 2003). Sudakin and Trevathan. 1998). 1995.S.130-.170 (.220 (.100-.100-.110 (<LOD-. DEET is metabolized via hydroxylation and dealkylation pathways and eliminated in the urine within approximately 24 hours (Selim et al. People in outdoor occupations may apply DEET more frequently or use higher concentration formulations resulting in higher levels of exposure. Neurological effects in humans. and it has not been rated by IARC or NTP with respect to human carcinogenicity. Fourth National Report on Human Exposure to Environmental Chemicals 19 .100-.epa. which may vary for some chemicals by year and by individual sample.100-. but higher DEET concentrations and different formulations may result in greater absorption (Sudakin and Trevathan.100-.gov/pesticides/.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 . Its use is recommended for prevention of several vector-borne diseases.140) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .130-.S.180) < LOD ..110 (.110 (.170 (.110 (.N-Diethyl-meta-toluamide (DEET) CAS No.N-Diethyl-meta-toluamide (DEET) N.270) 688 678 518 700 598 956 Limit of detection (LOD. (U. DEET is not genotoxic. and they range in concentration from 4% to 100%. EPA.110 (<LOD-. population from the National Health and Nutrition Examination Survey.210 (.240) < LOD .560) < LOD .S. One survey detected DEET in 74% of sampled streams in the U..EPA.150) < LOD . Survey Geometric mean (95% conf.130 (.190) < LOD .110-. (Kolpin et al.130) < LOD . There are over 225 insect repellents brands containing DEET.130 (. 2005).EPA.. including seizures and encephalopathy.

190 (.640 (.93) < LOD . Urinary levels of DEET were characterized only at the 90th and 95th percentiles of the U.320 (.440) < LOD ..270) < LOD .290-.N.390-. 2007). representative subsamples from NHANES 2001-2002. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD .350-.190-. DEET was detected in 10% of 60 Latino children in eastern North Carolina farm worker households (Arcury et al.370-.230-.250-.270 (.330 (.350) < LOD .480 (.410 (.150-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.150) < LOD .240) < LOD .270 (<LOD-.190 (.250 (.250) < LOD . Urinary N.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 .690 µg/L were measured in eight park employees who applied 71% DEET once a day (Smallwood et al.190 (<LOD-.140-. the limit of detection was lower than for the NHANES 1999-2000 survey period (CDC.280 (.230) < LOD . Urinary DEET levels as high as 5.300) * * 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 .200 (.350) < LOD .630) < LOD . Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 2005).240-.230-.S.300 (.330 (.370) < LOD .410 (. Survey Geometric mean (95% conf. population from the National Health and Nutrition Examination Survey.410-.N-Diethyl-meta-toluamide (DEET) Biomonitoring Information Urinary levels of DEET reflect recent exposure.170-.500) 480 580 672 828 825 1126 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . 20 Fourth National Report on Human Exposure to Environmental Chemicals .500 (.490) < LOD .270-.S.320) < LOD . Finding a measurable amount of DEET in urine does not mean that the level of DEET causes an adverse health effect.130 (<LOD-..N-Diethyl-meta-toluamide (DEET) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.550) 688 678 518 699 598 956 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.280-1. 1992).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 . 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. In this survey period.

Thurman EM.16(1):10-13. Quandt SA. Centers for Disease Control and Prevention (CDC). Environ Sci Technol 2002.115(8):1254-1260. Meyer MT. N. 1999-2000: a national reconnaissance. Diethyltoluamide (DEET).41(6):831-839. Fundam Appl Toxicol 1995. Atlanta (GA). Page BC. DeBord KE. Toxicity and Exposure Assessment in Children’s Health. 1-118. and excretion of N. Environmental Protection Agency (U.S. Osimitz TG.N-Diethyl-meta-toluamide (DEET) References Arcury TA.gov/oppsrrd1/REDs/0002red. Available at URL: http://www. Environ Health Perspect 2007. hormones.N-diethyl-mtoluamide insect repellents reported to the American Association of Poison Control Centers. Third National Report on Human Exposure to Environmental Chemicals. Zaugg SD. Veltri JC.36(6):1202-1211. Bell JW. Lowry LK. Pesticide urinary metabolite levels of children in eastern North Carolina farmworker households. pp. Int J Toxicol 2002. Sudakin DL.epa.N.N-diethyl-mtoluamide following dermal application to human volunteers. and other organic wastewater contaminants in U. Chen H. Reregistration Eligibility Decision (RED): DEET. Absorption.S.epa. Grzywacz JG.gov/teach/chem_summ/ DEET_summary. Washington (DC): U. Smallwood AW. Hartnagel RE Jr. Environmental Protection Agency (U. 2005.S.N’-diethyl-mtoluamide (m-DET): analysis of an insect repellent in human urine and serum by high-performance liquid chromatography. U. J Toxicol Clin Toxicol 2003.pdf. J Anal Toxicol 1992. Available at URL: http://www. streams. pdf. DEET: a review and update of safety and risk in the general population. Barber LB. Chemical Summary. 2005 Kolpin DW. Gabriel KL. EPA.S. Trevathan WR.25:95-100.S. metabolism.S.EPA). Barr DB. Pharmaceuticals. 1993-1997.EPA. U. et al. Selim S. Furlong ET. 4/9/09 U. Tapia J. Schoenig GP.EPA). September 1998.S.2:341352. EPA 738-R98-010. 4/9/09 Fourth National Report on Human Exposure to Environmental Chemicals 21 . 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

32 Fourth National Report on Human Exposure to Environmental Chemicals . Hum Ecol Risk Assess 2004. MacLusky. Available at URL: http://cerhr. et al. Gender differences in the levels of bisphenol A metabolites in urine. Human Health. DirectorateGeneral Health and Consumer Protection. November 26.it/DOCUMENTS/ Existing-Chemicals/RISK_ASSESSMENT/SUMMARY/ bisphenolasum325. Pyo MY. Cha SW.10:875-921.4’-Isopropylidenediphenol (Bisphenol-A) Summary Assessment Report. Yoshinaga J. Calafat AM. T. et al. Imai H. hormones. Tsugane S. Endocrinology 2008.69(22):2611-2625. Howdeshell KL. National Institute of Environmental Health Sciences. Hlywka JJ. Rubin C.gov/chemicals/bisphenol/BPAFinalEPVF112607. Yang M. Bisphenol A. Regul Toxicol Pharmacol 2002.europa. In vitro and in vivo interactions of bisphenol A and its metabolite. 2/4/09 European Commission. Caudill SP. Timms BG. Needham LL. Joskow R. Environ Health Perspect 2005. Koulova AI. Estrogenic chemicals in plastic and oral contraceptives disrupt development of the fetal mouse prostate and urethra. Han SS. J Am Dent Assoc 2006. Klinefelter GR.jrc. National Toxicology Program Center for the Evaluation of Risks to Human Production (NTP-CERHR). Twomey K. 2/4/09 National Toxicology Program Center for the Evaluation of Risks to Human Production (NTP-CERHR). Endocrinology 2004.113(4):391-395. Thomas BF. August 2001. NTP-CERHR Panel Report on Reproductive and Developmental Toxicity of Bisphenol A. Bradley S. Ye X.J. Research Triangle Park. Richter CA. Serizawa S. Weight of the evidence evaluation of low-dose reproductive and developmental effects of bisphenol A.59(4):403-408. Calafat AM. European Commission. and Hajszan. Kim JC. National Toxicology Program. Barr DB.68(1):121-146. vom Saal FS. An evaluation of the possible carcinogenicity of bisphenol A to humans. Hara K. Keimowitz AR. Barber LB. U. Urinary concentrations of bisphenol A and 4-nonylphenol in a human reference population. NTP-CERHR Panel Report on Reproductive and Developmental Toxicity of Bisphenol A. Life Sci 2001.pdf . Proc Natl Acad Sci USA 2005. NC. Leranth. niehs.. population to bisphenol A and 4-tertiary-octylphenol: 2003-2004. 2003. Needham LL. Urinary bisphenol A and plasma hormone concentrations in male workers exposed to bisphenol A diglycidyl ether and mixed organic solvents. Estimation of intake level of bisphenol A in Japanese pregnant women based on measurement of urinary excretion level of the metabolite. Pharmaceuticals. Evaluation of developmental toxicity in rats exposed to the environmental estrogen bisphenol A during pregnancy.. Ispra. Available at URL: http://ecb.S. Harazono A. Haighton LA.Scientific Committee on Toxicity. Italy. Brussels.36(6):1202-1211. Joint Research Centre Institute of Health and Consumer Protection. Sottas CM. May 22. Bisphenol A prevents the synaptogenic response to testosterone in the brain of adult male rats. Szigeti-Buck. McConnell EE. Shin HC. 5: 505-523. Available at URL: http://ec. Watanabe C.nih.pdf. 2/4/09 Fujimaki K. J Chromatogr B Analyt Technol Biomed Life Sci 2002. Cohen JT. Zaugg SD. Munro IC. niehs. Toxicol Sci 2002. Available at URL: http://cerhr. 2/4/09 National Toxicology Program’s Report of the Endocrine Disruptors Low-Dose Peer Review (NTP). bisphenol A glucuronide. 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. Biochem Biophys Res Commun 2003. Hughes C. Three-generation reproductive toxicity study of dietary bisphenol A in CD Sprague-Dawley rats. Reidy JA. Nippon Eiseigaku Zasshi 2004. Ecotoxicity and the Environment (CSTEE). and other organic wastewater contaminants in U. Rat two-generation reproductive toxicity study of bisphenol A. et al. Measurement of bisphenol A in human urine using liquid chromatography with multi-channel coulometric electrochemical detection. Kuklenyik Z.S. Available at URL: http://ntp. Thurman EM. Furukawa M. Kawamura N. Lynch BS.nih.pdf.gov/ntp/htdocs/liason/ LowDosePeerFinalRpt. Doull J. Department of Health and Human Services. Exposure to bisphenol A from bis-glycidyl dimethacrylatebased dental sealants. streams.. Tyl RW. Exposure of the U. Kim CS.149:988-994.nih. Matthews JB. September. Kroes R. Barr JR. Zacharewski TR. Ekong J. Han SY.116(1):39-44. Park S. 1999-2000: a national reconnaissance. Belgium. Reprod Toxicol 2001.145:592-603. 2008. Watanabe S. Koh WS. Barton L. Kolpin DW. Gray GM.Environmental Phenols References Akingbemi BT. K. Hanaoka T. Cunha G.14(2):149-157. Environ Sci Technol 2002. Arakawa C.102(19):7014-7019. Wong LY.niehs. Fujii S. Myers CB. Rhomberg et al.59(9):625-628.312(2):441-448. Occup Environ Med 2002. 2007. with estrogen receptors alpha and beta. Kiguchi M. 2002. Brine DR.pdf. 4. Reidy JA. 2/4/09 Ouchi K.S. Kim YH. and Hardy MP. Environ Health Perspect 2008. Chem Res Toxicol 2001. National Institutes of Health. Ikka T.780(2):365-370. Needham LL.137(3):353-362. C. Meyer MT.eu/ health/ph_risk/committees/sct/documents/out156_en. Marr MC. Calafat AM. Ema M. N.pdf . Chung MK.gov/chemicals/bisphenol/bisphenol. Furlong ET.35(2 Pt 1):238-254.

Chang SS. Kawamoto T.147(6 Suppl):S56-69. Filser JG.103(1):9-20. Endocrine mechanisms mediating effects of bisphenol A at levels of human exposure. Environ Health Perspect 2005. An observational study of the potential exposures of preschool children to pentachlorophenol. Chem Res Toxicol 2002. Fourth National Report on Human Exposure to Environmental Chemicals 33 . Nagel SC. Lee SM. III. Vom Saal FS. Morgan MK. Biological monitoring of bisphenol a in a Korean population. Kim SY. Environ Res 2007.15:12811287. and nonylphenol at home and daycare. Endocrinology 2006. Metabolism and kinetics of bisphenol A in humans at low doses following oral administration. Chuang JC. Sheldon LS. Food Chem Toxicol 2002.113(8):926-33. Colnot T. et al. Arch Environ Contam Toxicol 2003. bisphenol-A. Welshons WV.40(7):905-12. Dekant W. An extensive new literature concerning low-dose effects of bisphenol A shows the need for a new risk assessment.Environmental Phenols Volkel W. Csanady GA. Yang M. Jang JY. vom Saal FS. Hughes C. Witorsch RJ.44(4):546-51. Wilson NK. Large effects from small exposures. Lordo RA. Low-dose in utero effects of xenoestrogens in mice and their relevance to humans: an analytical review of the literature.

60-3.. and impaired spermatogenesis (e. 2000. Urinary 4-tert-Octylphenol (4-[1. 1995. Indoor and to a lesser extent. the various alkylphenols have also been used as emulsifiers and modifiers in paints. Less frequently.600-1. Disposition in humans has not been studied sufficiently.50) 1. several European nations banned the use of alkylphenol ethoxylates in domestic detergents and other uses.10) 2.500-1.300 (<LOD-.80 (1.70 (1.70 (1.g.600) .299-.000 tons of alkylphenol ethoxylates were produced annually worldwide. and some personal care products. Survey Geometric mean (95% conf. to shorter chain alkylphenol ethoxylates.600) 1. Human health effects from 4-tert-octylphenol or the corresponding octylphenol ethoxylates at low environmental doses or at biomonitored levels from low environmental exposures are unknown.g.80) 2. Nonylphenol ethoxylates are more commonly used than octylphenol ethoxylates.50) .369 (.600-1. 34 Fourth National Report on Human Exposure to Environmental Chemicals .50 (1.40) 1.Environmental Phenols 4-tert-Octylphenol CAS No. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.1.20 (1. Saito et al. including 4-tert-octylphenol.70 (1.50-2.60) 1. In 1999-2000.500) 75th .300 (<LOD-..300 (<LOD-.507) * < LOD .00) 1229 1288 03-04 03-04 03-04 * . 4-octylphenol monoethoxylate was detected in 43..50) 1.900 (.600-1. Bian et al.20-2. The alkylphenol ethoxylates enter the environment through human use of products containing them.497) * .50) 1.200-. is used to manufacture alkylphenol ethoxylates.477) .300 (<LOD-.60-3.300-.900 (..300-.900 (.400 (..10 (. and to alkylphenoxycarboxylates.20-2.50-3. Several alkylphenols.00 (1.S.80 (1.400 (.60-3. 2003.60-3.357 (. which may vary for some chemicals by year and by individual sample.500) . < LOD means less than the limit of detection.500) .500 (.20) 314 715 1488 03-04 03-04 * * .. 2000.60) .20) 2.. 2006.600-1.60-3.30 (1.10) 1.00 (. These high dose parenteral effects of 4-tert-octylphenol have included altered sex hormone levels and hypothalamicpituitary suppression. and was quickly eliminated from the blood (Certa et al. through sewage.20-2.70 (1. Octylphenols and nonylphenols can also enter the environment directly from manufacturing waste streams. did not bioaccumulate. and some of their degradation products are toxic to aquatic life.700-1.20) 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 . 1997. Katsuda et al.600) . pesticides.90) 2.3.20) 1.268-.30 (1. In the 1990s.500) . 2002). and emulsifiers. They are biodegraded to the corresponding alkylphenol (octylphenol or nonylphenol). population from the National Health and Nutrition Examination Survey.389 (.S.200-. testicular atrophy.10 (1. During the 1980s and 1990s.60) 613 652 1092 Limit of detection (LOD.2.30-2..900 (.40) 2.50) . 1996). Blake and Boockfor.300 (<LOD-. have demonstrated estrogenic effects particularly when injected at high doses in animals.20-2.5% of 139 U. 2004).10 (.. over 500. In rats. orally administered 4-tert-octylphenol was well absorbed.600) .30 (1.60-3.600-1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.900 (. Human exposure to alkylphenols and alkylphenol ethoxylates may occur through ingestion of contaminated foods (e. and through manufacturing waste streams (Warhurst. textiles.274-.40) * 03-04 03-04 03-04 .30) 2.20-2.40) 1.90) 2. 2002).. impaired steroidogenesis.400) 1. fish) and drinking water. Alkylphenols also have been used as plasticizers and antioxidants in plastics and resins.500-1. which are anionic surfactants used in detergents. industrial cleaners. outdoor air may have detectable levels of 4-tert-octylphenol and 4-tert-octylphenol monoethoxylates.30) 90th 1.30 (. altered estrus cycles and reproductive outcomes. The alkylphenols can bioaccumulate in some fish.80 (1.30 (1.40 (1. streams in 30 states (Kolpin et al.40) 2.400 (.00 (. and from contact with some personal care products and detergents. Commercial formulations of alkylphenol ethoxylates usually contain a mixture of oligomers and isomers. an alkylphenol.20-2. leading to inhalation as another potential exposure route (Rudel et al. 140-66-9 General Information 4-tert-Octyphenol. see Data Analysis section) for Survey year 03-04 is 0.30) 1.3-Tetramethylbutyl] phenol) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. and the polyethoxy chain may consist of up to 50 ethoxy units.600-1. Laws et al. Ying et al. altered neonatal sexual development.10-2.800-1.

68) 2..740 (.850 (.460 (.160-.560) .54) * 03-04 03-04 03-04 .540-1. In a small number of adult Japanese volunteers.470-1.276 (.40 (1. It is unclear if estrogenic or other effects occur in animals through oral dosing.11-2.610) .270 (.207-.65-3.470-1.00) size 2514 Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th .640-1. 2000. 2003.31-2.00 (. Tyl et al.33) 3.62 (1.Environmental Phenols Myllymaki et al.00) 2.68-2.400) .349) * < LOD . Yoshida et al. Biomonitoring Information Urinary levels of 4-tert-octyphenol reflect recent exposure..71) 2. representative subsample of NHANES 2003-2004. at lower or environmentally relevant doses (Blake et al.337-.03 (1..280-.22) .470) 75th . Sweeney et al.740 (.910 (.450) 1. 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. 2005.08) 1.15) 1.860 (.11) 2.620-1. 1999).S.890-2.00 (.41) .18-4.1.410 (.170-.60 (1.11) 1.320 (<LOD-. (2008) showed that urinary levels of 4-tertoctyphenol were detectable in slightly greater than half of the participants of the U.85 (1.270-.05-2..370 (<LOD-.269 (.81 (1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2. Survey Geometric mean (95% conf.50 (2.25) 90th 1.78 (1.25-2.00) 2.64 (.25) 2. 2004.31 (1.14) 314 713 1487 03-04 03-04 * * . 2001).300 (<LOD-. IARC and NTP have not rated octylphenol. Nagao et al. Calafat et al.20 (1.43) 1.33 (2. or their corresponding ethoxylates with respect to human carcinogenicity.53-3.380 (<LOD-.73) 2.76 (2..43) 1.260 (<LOD-.62) .43-3.03 (1. Finding measurable amounts of 4-tert-octylphenol in the urine does not mean that the levels of 4-tert-octylphenol cause an adverse health effect.78) 3.620) .550-1.270 (.59 (1.530) .67-2.29) 2.435 (. population from the National Health and Nutrition Examination Survey.10-2. 2001.62 (1.570) .24) 612 651 1091 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. nonylphenol.06 (2.420) ..03-6.3. 4-tert-Octylphenol is not considered directly genotoxic. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.02-4. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.78) 1228 1286 03-04 03-04 03-04 * . Kawaguchi et al.500-1.17 (.00) 1.36-3.770 (.96-4.450) .630-1.59) 1.3-Tetramethylbutyl] phenol) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.730-1.384) * . Urinary 4-tert-Octylphenol (4-[1.199-. 2004). Fourth National Report on Human Exposure to Environmental Chemicals 35 . the urinary concentrations of 4-tert-octyphenol were near or below the detection limit (Inoue et al.S.40-4.

Pharmaceuticals.15(6):683-692. testis size. Sweeney T.54(1):154-167. polybrominated diphenyl ethers.799(1):119-125. Xu L. Bolt HM. Biol Reprod 1997. Zaugg SD. Maekawa A. Bodman GJ. Phthalates. alkylphenols. Taya K. Fedtke N. Warhurst AM. Nicol L. Toppari J. Calafat AM. The toxic effects of 4-tert-octylphenol on the reproductive system of male rats. Onuki A. Effects of neonatal exposure to a high-dose p-tertoctylphenol on the male reproductive tract in rats.pdf. Carey SA. Ye X. Roche JF. Seto H. Exposure of the U. Fail PA. Environ Sci Technol 2003. An environmental assessment of alkylphenol ethoxylates and alkylphenols. Korn LR.foe. Boockfor FR. Anal Chim Acta 486:41-50. Irreversible effects of neonatal exposure to p-tert-octylphenol on the reproductive tract in female rats.S. Toxicol Lett 2001. Cooper RL. and sertoli cell number. Yoshimura S. Blake CA. Reidy JA. Toxicokinetics of p-tert-octylphenol in male Wistar rats. Reprod Toxicol 2004.S. et al. Brine DR. Laws SC. Blake CA. pesticides. Karjalainen M. Toxicol Sci 2000. Paranko J. 36 Fourth National Report on Human Exposure to Environmental Chemicals . Saito Y. Barber LB.36(6):1202-1211. Measurement of 4-nonylphenol and 4-tert-octylphenol in human urine by column-switching liquid chromatography-mass spectrometry. et al. Myllymaki SA. Environ Int 2002. Izumi S.14(5):325-332. J Chromatogr B Analyt Technol Biomed Life Sci 2004. Qian J. Kolpin DW. et al. Needham LL. Myers CB.207(1):59-68. Food Chem Toxicol 2006. Chen J. Yoshida M.uk/resource/reports/ethoxylates_alkylphenols. Environmental fate of alkylphenols and alkylphenol ethoxylates--a review. Nakagomi M. Ito R. Yoshimura Y. Millette CF. Estrogenic activity of octylphenol.44(8):1355-1361. Saito I. Endocrinology 2000. Indoor Air 2004. prolactin. Ferrell JM. Tyl RW. Watanabe G. Reproductive effects in male and female rats from neonatal exposure to p-octylphenol. Meyer MT.co. 2/4/09 Ying GG. Chronic administration of the environmental pollutant 4-tert-octylphenol to adult male rats interferes with the secretion of luteinizing hormone. Sakui N. Rudel RA. Taya K. 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. Inoue K. and other endocrine-disrupting compounds in indoor air and dust. et al. Environ Health Perspect 2008. hormones. Boockfor FR. Muller AM. Raychoudhury SS. Takenaka A. Environ Sci Technol 2002. Maekawa A.folliclestimulating hormone.165(3):217-226. Brody JG. Kawaguchi M. Maternal exposure to octylphenol suppresses ovine fetal follicle-stimulating hormone secretion. Marr MC. Haavisto TE. Available at URL: http:// www. Thurman EM. 1995. Furlong ET. and other organic wastewater contaminants in U. Effects of 4-tert-octylphenol given in drinking water for 4 months on the male reproductive system of Fischer 344 rats. Toxicol Appl Pharmacol 2000. Watanabe G. Reprod Toxicol 2001.121(1):21-33. Nair-Menon JU.Environmental Phenols References Bian Q. Brooks AN.30(2 Pt 1):81-95. Ono H. Song L.18(1):43-51. Indoor air pollution by alkylphenols in Tokyo.71(1-2):112-122. Williams B. Makino T.116(1):39-44. Toxicol Appl Pharmacol 2005. Two-generation reproduction study with para-tert-octylphenol in rats.37(20):4543-53. nonylphenol. Spengler JD. Wong LY. Wiegand HJ. 2003. Okada F. Katsuda S.28(3):215-226. and testosterone. 1999-2000: a national reconnaissance.141(7):2667-2673. Usumi K. Arch Toxicol 1996. Seely JC. Kawaguchi M. Infantile 4-tert-octylphenol exposure transiently inhibits rat ovarian steroidogenesis and steroidogenic acute regulatory protein (StAR) expression. Takai N. Kookana R. Inoue K. Certa H. Katsuda S. population to bisphenol A and 4-tertiary-octylphenol: 2003-2004. Wang X. Horie M. Yoshida M. Nagao T.57(2):255-266. McCoy GL. Regul Toxicol Pharmacol 1999. Camann DE. streams. bisphenol A and methoxychlor in rats.

and has also been impregnated into some kitchen utensils. and has not been considered mutagenic or carcinogenic (Bhargava and Leonard.. In animal studies.Environmental Phenols Triclosan CAS No. acne medications. In animal and human studies.. 2008). 2007). General population exposure results from dermal and oral use of products containing triclosan. but not by race/ethnicity and sex... Finding measurable amounts of triclosan in the urine does not mean that the levels of triclosan cause an adverse health effect. a process that can result in the formation of small amounts of 2. Moss et al. 2004).. Triclosan has a low bioaccumulation potential in fish. In a study of 90 U. 1988.6% of 139 U. 1996. toys. representative subsample of NHANES 2003-2004. 2002).S. 2007). 2007. 2006).. 1976.2 µg/L) of children 6-11 years of age who participated in NHANES 2003-2004 (Wolff et al. and wound disinfection solutions. Triclosan formulations may rarely cause skin irritation.S. 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. young girls. Veldhoen et al.. toothpastes. the median urinary triclosan level of 7. Biomonitoring Information Urinary triclosan levels reflect recent exposure. and medical devices.2 µg/L was comparable to the median level (8. (Sandborgh-Englund et al. 2000). 2000.. 1969). deodorants. Triclosan is not considered teratogenic at maternally toxic doses.. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.S. In the body it is conjugated to glucuronides and sulfates (Bodey et al. triclosan was found in 57. Lyman and Furia. Triclosan can be absorbed across skin into the blood stream. Some reports show endocrine effects are observed in amphibians and fish (Foran et al. It acts by inhibiting bacterial fatty acid synthesis... Fourth National Report on Human Exposure to Environmental Chemicals 37 . Human health effects from triclosan at low environmental doses or at biomonitored levels from low environmental exposures are unknown.. it has low acute toxicity.. In 1999-2000. 3380-34-5 General Information Triclosan is a phenolic diphenyl ether used for over 30 years as a preservative and antiseptic agent. In a U. 1987). 2007. Mezcua et al. mouthwashes. Triclosan has been added to soaps. it is excreted over several days in the feces and urine as primarily as unchanged triclosan (Kanetoshi et al.. Calafat et al. There is some concern that widespread use of triclosan and other biocides can alter antibiotic resistance in bacteria (Aiello et al. Triclosan can remain present in the oral saliva for several hours after the use of toothpaste containing triclosan (Gilbert et al. Calafat et al. It can be photochemically and biologically degraded.. streams sampled in 30 states (Kolpin et al.8-dichlorodibenzo-p-dioxin (Aranami et al. 2008 has shown higher levels during the third decade of life and among people with the highest household income. Triclosan enters the aquatic environment mainly through residential wastewaters. IARC and NTP do not have ratings with respect to human carcinogenicity. 2005. Matsumura et al.

2 (25.4 (32.1 (8.7) 10.82 (8.2 (13.4-163) 304 (134-566) 261 (198-317) 157 (113-380) 655 (310-890) 472 (406-522) 314 715 1488 03-04 03-04 16.8) 9.3 (9.6-20.4) 75th 43.1) 9.60 (6.20 (7.38-18.2) 12.0 (36.6-65.9) 8.4-18.4) 90th 249 (188-304) 03-04 03-04 03-04 8.8-60.Environmental Phenols Urinary Triclosan (2.S.0-73.4 (12.7) 123 (36.2-14. interval) 12.4.1) 7.6 (9.9) 32.32-14.50) 10.3.30-14.8-127) 37.10-9.6 (10.6-111) 33.1) 9.00 (4.6) 10.43-13.3-67.0) 9.8) 14.2 (10.1) Selected percentiles ( 95% confidence interval) Sample 95th 368 (294-463) size 2514 Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 9.3) 6.4’-Trichloro-2’-hydroxyphenyl ether) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.2) 13.0) 49.7) 292 (151-432) 132 (78.4) 51.9 (11.48 (8.10) 84.0-213) 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 .8 (21.29-12.55 (4.5) 13.2) 9.20-13.9 (8. see Data Analysis section) for Survey year 03-04 is 2.8-112) 30.1 (15.70-16.5-250) 574 (461-716) 380 (258-430) 1229 1288 03-04 03-04 03-04 14.50-10.6-15.90-10.3) 10.1) 11.5) 20.6) 31.9 (50.00-8.2-58.5-86.40-17.9) 75th 47.9-61.4-19.S.4) 317 (231-433) 144 (96.0-15.0 (34.7 (28.5-341) 245 (163-334) 597 (372-992) 450 (254-750) 461 (383-527) 613 652 1092 Limit of detection (LOD.2 (37.74 (5.6) 12.20-10. population from the National Health and Nutrition Examination Survey. population from the National Health and Nutrition Examination Survey.6-37.6) Selected percentiles ( 95% confidence interval) Sample 95th 461 (383-522) size 2517 Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 9.1) 13.93 (7.5) 66.45-10.0-15.4) 7.0 (11.4 (38.3) 47.21 (6.0 (26.5 (11.4 (11.5) 11.9-236) 193 (90.11-11.16 (6.3 (26. interval) 13.1) 50.3-15.48-10.4) 73.2-46.7 (14.2 (11. Survey Geometric mean (95% conf.22-10.6) 39.86-12.4.1-39.4’-Trichloro-2’-hydroxyphenyl ether) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. Survey Geometric mean (95% conf.8) 7.6-14.72-13.45 (5.3 (8.1 (45.9 (33.6 (30.7-318) 224 (186-272) 236 (115-336) 356 (169-580) 385 (308-506) 314 713 1487 03-04 03-04 13.2-58.20 (7.5-14.7 (39.40-11.1) 14.92-12.8-85.0) 65.3-31.7 (11.45-13.1) 9.0 (8.89-11.7 (9.60 (8.9) 7.0-19.3 (11.6 (12.4) 357 (225-456) 203 (87.1) 9.6-14.3-35.80 (5.6) 237 (175-294) 182 (138-217) 384 (294-506) 336 (225-480) 1228 1286 03-04 03-04 03-04 13.94 (7.8) 116 (39.2 (27.20-11.6) 90th 212 (172-241) 03-04 03-04 03-04 9.8-63.54 (8.4) 25.18 (5. Urinary Triclosan (2.

Aranami K. Arch Environ Contam Toxicol 1988. Gunderson MP.S. Fourth National Report on Human Exposure to Environmental Chemicals 39 . Environ Health Perspect 2007.115:116-121. Pharmaceuticals. Environ Sci Technol 2002. Kaneshima H. Furia T. Foran CM. Aguera A. et al. Randomized trial of a hexachlorophene preparation and P-300 bacteriostatic soaps. Mar Environ Res 2000.83(1):84. Veldhoen N. and phenols in girls. Br J Clin Pharmacol 1987. Okui T. IMS Ind Med Surg 1969. Effects of nonylphenol and triclosan on production of plasma vitellogenin and testosterone in male South African clawed frogs (Xenopus laevis). Furlong ET. Clapson DJ. 4’-trichloro-2’-hydroxydiphenyl ether. Evidence of 2. Adolfsson-Erici M. Fernandez-Alba AR. Thurman EM. Developmental evaluation of a potential non-steroidal estrogen: triclosan. Anal Chim Acta 1004.69(20):1861-1873. Levy SB. Reidy JA. 1999-2000: a national reconnaissance. hormones.66:1052-1056. Lyman FL.45 Suppl 2:S137-S147.8-dibenzodichloro-pdioxin as a photodegradation product of triclosan in water and wastewater samples.116(3):303-307. Pinney SM. Wong LY. Matsumura N. Osachoff H. Howes D. et al. Ferrer I. Benson WH. J Invest Dermatol 1976. phthalates. Gomez MJ. Leonard PA. Nagao Y. Ogawa H. Hong HC.38(4):361370. Aquat Toxicol 2006.Environmental Phenols References Aiello AE. Pilot study of urinary biomarkers of phytoestrogens.17(5):637-644. Meyer MT. The oral retention and antiplaque efficacy of triclosan in human volunteers. Ebersole R. Ye X. Williams FM. Kolpin DW.. Bhargava HN. Chelimo C. Windham G. population: 2003-2004. Photolytic degradation of triclosan in freshwater and seawater.524:241-247.4’-trichloro-2’hydroxydiphenyl ether). Britton JA. Skirrow RC. Shiratsuchi H.38(2):64-71. Hirano M. Chemosphere 2007. Williams PE. Wigmore H. and other organic wastewater contaminants in U. Ekstrand J. Consumer antibacterial soaps: effective or just risky? Clin Infect Dis 2007.50(1-5):153-156. Hernando MD. Readman JW. Calafat AM. streams. Percutaneous penetration and dermal metabolism of triclosan (2. Disposition and excretion of Irgasan DP300 and its chlorinated derivatives in mice. Barber LB.7/2.67(4):532-537. Toxicology of 2.S. Environ Health Perspect 2008. Watanabe N. Pharmacokinetics of triclosan following oral ingestion in humans. Bodey GP.24(3):209-218. Wolff MS. Gilbert RJ. Erratum in: Aquat Toxicol 2007. et al.4. Odham G. J Toxicol Environ Health A 2006. Urinary concentrations of triclosan in the U. Sandborgh-Englund G. Kanetoshi A. Ishibashi H. Katsura E. Needham LL.28(9):1748-1751.80(3):217-227. 4. Moss T. Am J Infect Control 1996. Larson EL.36(6):1202-1211. Food Chem Toxicol 2000. The bactericidal agent triclosan modulates thyroid hormone-associated gene expression and disrupts postembryonic anuran development.23(5):579-583. Triclosan: applications and safety. Teitelbaum SL. Zaugg SD. et al. Biol Pharm Bull 2005. Mezcua M. Bennett ER.

51) 1.650) 1.350 (.23 (.350 (.350) < LOD .480-2.860-2. Effects including hyperthermia.350-.890-1.10) 1.00) 1.350) < LOD . and possibly of lindane (IPCS.350-.Fungicides Pentachlorophenol inhale it or absorb it through exposed skin.350 (. with repeated or chronic exposure.350 (.70) 2. Survey Geometric mean (95% conf.60) 1. PCP is absorbed rapidly and well by all exposure routes.30 (.350 (.350) < LOD .350-.67) 1. are eliminated in the urine.350 (. PCP use in the U.350) < LOD .48 (.350 (.350 (.350-2.350) < LOD . General population exposure to PCP may occur by inhalation of contaminated air.76) 1.90) 1.83 (2.S.60) 1.350-2. 1997).78) 1.350-. herbicide.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-.62 (. the elimination half-life may be a week or more (Uhl et al.350-2.390 (.350-.54-2.350-.33) .590-1.350-.40 (.350-2.990-2. and dermal contact with PCP-treated products. Human health effects from PCP at low environmental doses or at biomonitored levels from low environmental exposures are unknown.33-2. population from the National Health and Nutrition Examination Survey.350-.350) < LOD .90 (1.350-. 1986).350) < LOD .47-3.350) < LOD . ingestion of contaminated food or water.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.350-.350-1.58-2.890 (. Human exposure to PCP has become less common. To-Figueras et al.350 (. water and sediments because of the large amounts that were produced and used historically. 1976.00 (. PCP cannot be used on wood in residential or agricultural buildings.91 (1.58-2.350-1.350) < LOD . The parent compound and conjugates.80) .350-.73 (1.350) 90th .70) . which may vary for some chemicals by year and by individual sample. and animals.500-2.350-.47-5. plants.48-2. and it is used primarily as a preservative for wood to be used outdoors (e.30) 1.65 (.30 (.390 (. has been restricted.45-2. Since 1984.350 (.g. utility poles and fence posts)..510-3. 1979).53) 482 577 681 826 831 1125 99-00 01-02 99-00 01-02 * * * * .350-.09) .18 (<LOD-1.350 (.76) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .10 (.00) 2. along with small amounts of tetrachlorohydroquinone and conjugates.10 (<LOD-1.04) 1.350 (.630 (. PCP also may be eliminated in urine as a metabolite of hexachlorobenzene.350) < LOD .94 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. air.350 (.350-.65 (.30) . Kohli et al. < LOD means less than the limit of detection.10 (1.350 (..32 (.76) .350 (.350) < LOD . interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.850-2.350) < LOD .350-.980 (.530) 1.350-1.37) . PCP is distributed to most tissues and is not extensively metabolized.350) < LOD .00) 1.350 (.S.350-2.350-.37 (.94 (1.350) .350-.90) 2.42) 973 1190 1021 1338 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * . see Data Analysis section) for Survey years 99-00 and 01-02 are 0.350-1. 2002.660 (. bactericide.25 and 0. After absorption. After a single dose.350-. Workers who manufacture or apply PCP may Urinary Pentachlorophenol Also a Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.350 (.350 (.08-3.350) < LOD .350) < LOD ..770 (. mollusicide.30) 1.350 (.5. Acute.960) 1.350) < LOD < LOD 75th .30 (1.01 (<LOD-1.350) < LOD .98 (1..510-5.350 (. In the environment. and metabolic acidosis were observed in CAS No. PCP has been detected in soils. high dose exposure to PCP can induce a hypermetabolic state and excessive heat production as a result of uncoupling mitochondrial oxidative phosphorylation.990 (<LOD-2.64) 1. PCP is eliminated over a few days (Braun et al. other polychlorinated benzenes.10) 1. PCP is degraded by sunlight and metabolized rapidly by microorganisms. hypertension.650 (. algaecide and insecticide.350 (.42) 696 680 521 696 603 951 Limit of detection (LOD.75) 2.680-1. 40 Fourth National Report on Human Exposure to Environmental Chemicals .350-.350-.50) 1.

1995). population from the National Health and Nutrition Examination Survey.470 (.00-1.19) 2.19 (1.290) < LOD .S.330-.440 (. 2003).09 (<LOD-2..19) 2.35-2.510-.490) < LOD .30) 1. 1991).06 (.900-1. Death can result from seizures and cardiovascular collapse. urinary PCP levels at the 95th percentile were approximately fivefold lower than 95th percentile values measured in a nonrandom subsample from NHANES III (1988-1994) participants (Hill et al.09-1. 2000). Among adults in the NHANES 1999-2000 subsample.S.950-1.580-.360 (.67 (1.9 mg/L. carcinogenic.51) 1.220-.730) < LOD .630 (.25-2. 2004.290-.67-3.220-.300 (.510-.400 (.560) < LOD .40) 1. chronically administered high doses of PCP were hepatotoxic.30) 1.69 (1.310) < LOD . and the FDA has established a standard for bottled water. In a small sample of U.250 (. the median and 95th percentile urinary PCP levels were approximately three times lower than comparable values in German adults (2. Urinary PCP levels at the 95th percentile in this Report are approximately half the corresponding 95th percentile values found in German adults evaluated in 1998 (Becker et al.6 and 14.830) < LOD .780) < LOD .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 .560) < LOD ..75 (<LOD-2.290-.90) 1.83 (1.240-. In NHANES 2001-2002 subsamples.40-2.html.21-2.Fungicides adults and children severely exposed to PCP through ingestion.06-3. Fourth National Report on Human Exposure to Environmental Chemicals 41 .78) 1.300 (. 1989).320) < LOD .270-.700-2.800) < LOD 1.67 (1..360-.67-2. 2003).67-3. EPA at: http://www.40) 1.500-.16-1.10-2.560-.0 mg/L. EPA has developed standards for PCP in drinking water and the environment. environmental levels) and health effects is available from the U.25-1.00-1.35) 1.57 (.13 (. 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.710-1.84 (1.75) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .16 (.430-.340-.35-2. or skin absorption.36) .cdc.EPA. 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.84-4. and adversely affected thyroid function (U. 1989).420) < LOD .320) < LOD < LOD 75th .gov/ pesticides/ and from ATSDR at: http://www.280) < LOD .e. In animals. OSHA has established an occupational standard.94 (1.99) 482 577 681 825 831 1125 99-00 01-02 99-00 01-02 * * * * .25 (1.380-.S.94 (1.00) 1. respectively) (Seifert et al.08 and 5.40) 1.gov/ toxpro2.26 (1.55) 973 1190 1021 1337 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .atsdr.79) 1.82 (1.500 (.260 (.250 (..570 (.48-2.950-1.94-3.430) < LOD .40) 1.29-3.590) < LOD .800-1.350) < LOD .52 (<LOD-1.epa. van Raaij et al.78) 1..500-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.67 (1.760 (. IARC has determined that pentachlorophenol is possibly carcinogenic to humans.06) 1.92) 1..67 (1.310-.52 (<LOD-1.95) 3.30 (. children in the 1980’s.56) 1.08) 696 680 521 695 603 951 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.950-1. Biomonitoring Information In NHANES 1999-2000 the median urinary PCP levels among children aged 6-11 and 12-19 years were as much as thirteen times lower compared to a sample of German children aged 6-14 years in 1990-1992 (4. 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.25 (1.34 (. Pentachlorophenol is not mutagenic or teratogenic.52 (1..26 (1.370 (.30-2.40) 1.84) 1.320 (.11) 2.320) < LOD ..73 (1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.18 (1.67 (1.S.990 (.920 (.610 (. inhalation.18) .75) 1.25-2. Survey Geometric mean (95% conf.850 (.650 (.19) 2.910-1.780-1.55) 1.650) 90th 1.10 (1.270-.35) 1.590-1.S.300 (. More information about external exposure (i.650 (.52) 1. The U.57 (1.82) 1.25) 1. respectively) (Becker et al.21 (.

11/30/2004. Pesticide residues in food-2002-Joint FAO/WHO meeting on pesticide residues. Sala M.18:475-481. Bragt PC.105(1):78-83.58:182-186. Seiwert M.Fungicides Finding a measurable amount of PCP in urine does not mean that the level of PCP causes an adverse health effect. 42 Fourth National Report on Human Exposure to Environmental Chemicals . Engel R. Dev Toxicol Environ Sci 1979. Schulz C. Kaus S. Cline RE. Needham LL. 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. Hill RH Jr. Phillips DL. Notten WR. Barrot C. 4/21/09 Kohli J. et al. Schlatter C. Effects of hexachlorobenzene and its metabolites pentachlorophenol and tetrachlorohydroquinone on serum thyroid hormone levels in rats.10:552-65. To T. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children. Krause C. Environmental Protection Agency (U. Shealy DB. Hill RH. Fast DM. References Becker K. Can J Biochem 1976. Head SL.S. Environ Health Perspect 1997. Gregg M. Int J Hyg Environ Health 2003. Seiwert M. The German Environmental Survey 1990/1992 (GerES II): reference concentrations of selected environmental pollutants in blood. 2002. Metabolism of hexachlorobenzene in humans: association between serum levels and urinary metabolites in a highly exposed population. Jones D. Helm D.org/documents/jmpr/jmpmono/2002pr08. The metabolism of higher chlorinated benzene isomers. PCP: Human Risk Characterization [online]. Uhl S.S. Available at URL: h t t p : / / w w w.inchem. et al. U.4:289296. Safe A.18(4):469-474. r e g u l a t i o n s . Braun WH. drinking water and indoor air. Arch Environ Contam Toxicol 1989. Pharmacokinetics of pentachlorophenol in man. available at URL: http://www. Needham LL. Becker K.71:99108. Pesticide residues in urine of adults living in the United States: reference range concentrations. Schulz C. To-Figueras J. Schmid P. Lindane. Chenoweth MB. Seifert B. hair. urine. 4/21/09 van Raaij JA. Bailey SL. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Baker S. 206:15-24. International Programme on Chemical Safety (IPCS). Rodamilans M. htm. Otero R. 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. Smith SJ. EPA). Santiago-Silva M. Hill RH Jr. Seifert B. J Expo Anal Environ Epidemiol 2000. Toxicology 1991: 67(1):107-16. Environ Res 1995. The metabolism/ pharmacokinetics of pentachlorophenol in man and a comparison with the rat and monkey. Arch Toxicol 1986. Arch Environ Contam Toxicol 1989. Holler JS. Biomonitoring data can also help scientists plan and conduct research about PCP exposure and health effects. van den Berg KJ.54(3):203-208. et al. Blau GE. Pentachlorophenol measurements in body fluids of people in log homes and workplaces. house dust.

498 (.670) 2. EPA.19 (.860 (.450 (<LOD-.14 (<LOD-3.90) .490 (<LOD-.10) . such as fruits and vegetables..40 (.580-1.970 (.466 (.370-. are antimicrobial agents used as bacteriostats. 90-43-7 General Information Ortho-phenylphenol (OPP.00-2. small amounts of OPP have been measured in human adipose tissue (Onstot and Stanley.500-2. or oral routes from residential use and by ingesting treated food or food that was in contact with treated surfaces or equipment.27 (.610-1. and as a wood preservative.570-2.80-3.33 (. sodium ortho-phenylphenate (SOPP).630) < LOD ..780) < LOD .50) < LOD .50) < LOD .508 (.91) 973 1190 1018 1339 99-00 01-02 99-00 01-02 99-00 01-02 .60 (1.480-1. however.950) < LOD .10-2.60 (1.640) < LOD . Both have been used in agriculture to control fungal and bacterial growth on stored crops.760-2.07 (.550-1.17 (.EPA.830 (.50) < LOD .20 (.50-3.493 (.60 (1.410-.570-.402-.50-2. 2002.30 (1.552 (.490 (<LOD-.696) * . OPP is still used as a disinfectant fungicide for industrial applications.20 (1.00) .610 (.590-2.645) * .364-. Fourth National Report on Human Exposure to Environmental Chemicals 43 . whereas SOPP is not volatile and is more water soluble. < LOD means less than the limit of detection.10 (1.600) < LOD . Survey Geometric mean (95% conf.20-2.389-. Workers who manufacture.890 (.540-2.23) 695 680 520 695 603 953 Limit of detection (LOD.349-. OPP is considered to be moderately toxic after acute oral doses in animal studies.EPA.80) 1.90) .60-2.600-1.600-1.890 (.30) < LOD .22) 2.50 (1.632) Selected percentiles ( 95% confidence interval) Sample 95th 2.10 (1. Most agricultural food applications have been revoked.S.3 and 0. 2006). OPP is volatile.930 (. which may vary for some chemicals by year and by individual sample.40-2.50) .490 (<LOD-.520 (.710-2.636) * .30) 1.20-3. Available evidence suggests that OPP does not accumulate in the body.600) < LOD 1. but OPP and SOPP are still used on pears and citrus (U.389-. it was used in home sanitizers for surfaces.10) 2. Both chemicals degrade within hours to weeks in the environment (U.509 (. on ornamental plants and turfs.76) 1.90 (1.50 (1.450 (<LOD-.30-7. 1989).570-1.92 (.570 (.836) * .450 (<LOD-. interval) .770 (.40-7.34) 1.50 (1. and sanitizers. OPP was detected in 40 of 60 different canned beers at concentrations in the low parts per billion (Coelhan et al. 2006).820 (.80) 1.00 (1.23) 480 577 681 827 830 1125 99-00 01-02 99-00 01-02 .28 (.90) 2.890) 1. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. General population exposure can occur via dermal.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 .50) 1.350-1.40-5.20) 2.624) * .560-8.690-1.60-3.S. 2006).30) < LOD 1.742) * . and it has limited water solubility.00 (1. fungicides.496 (.10) 1.621) * .880-2.00) .840-1. In the past. 1998).600) < LOD .20 (1. leaving the chemical residue OPP. Timchalk et al.3. population from the National Health and Nutrition Examination Survey.85) 2. inhalational.00) < LOD .03) 1.567 (.90) 1.570 (.800-3.710) 3.90 (1. Estimated human intakes have been below recommended intake limits (U.770 (.750-2.638) * .690) < LOD .30-2.390-. in paints.497 (.790) 2. or apply these chemicals may be more highly exposed than the general population.00 (1. formulate.850 (.10) 1.09) 2.50-4.740 (.10-1.370-.Fungicides ortho-Phenylphenol CAS No.490 (<LOD-.386-.490 (<LOD-.20) < LOD 1.420 (<LOD-. Cnubben et al.02) 1.61) 2.80 (2.600) < LOD 75th . OPP is efficiently absorbed from the gastrointestinal tract and through the skin. 1998. or 2-phenylphenol) and its water-soluble salt.860) * 99-00 01-02 99-00 01-02 99-00 01-02 . 2006).22 (.S.10) .10) ..433-. and it is eliminated rapidly from the body as OPP glucuronide and sulfate conjugates (Bartels et al.20) < LOD 2. Human health effects from OPP at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 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.470 (<LOD-.370-.00 (1.600-1.30) < LOD 90th 1. SOPP is applied topically to the crop and then rinsed off.88) 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.40-5.S.28-3.

Zhao et al.580-1.444 (.910-1.550) < LOD .40-13.S.650-1.343 (. 44 Fourth National Report on Human Exposure to Environmental Chemicals .610) < LOD 1. 1984. U. Dermally applied OPP was not carcinogenic in a 2-year experimental study in animals (NTP. Nakagawa et al.640-1. by possible genotoxic mechanisms (Hagiwara et al.. 1999.88-4. ortho-phenylhydroquinone and ortho-phenylbenzoquinone. 2005). Survey Geometric mean (95% conf.480-.. Additional information is available from U.17 (.28 (<LOD-4.353-.28 (2.4 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.950) < LOD . CDC.61 (2.93) . 2005).670 (.04-4.74 (1.27) < LOD .08-1.30) 480 577 681 826 830 1125 99-00 01-02 99-00 01-02 .47) .770-2. In high dose animal studies.453 (. Bomhard et al. Biomonitoring Information Urinary OPP levels reflect recent exposure.11 (.990) < LOD .900) < LOD .84 (1.17) * 99-00 01-02 99-00 01-02 99-00 01-02 . Pathak and Roy.361-.568) * . OPP or SOPP produced carcinomas of the bladder only after phase II detoxification pathways were saturated. Ito et al.750-2.910 (.43) 3.43-2.791) * .670 (.20) < LOD 3.06-5.33-2.570) < LOD 1.560) < LOD 75th .600-1.17 (. 2002.gov/pesticides/.43-2.270-. 1986).52 (.810) < LOD .96-4.08) 1.301-. 1992.96 (1.06-4.620-1.670) < LOD .26) 1.33) .590) * .00 (1.514 (.61 (.320 (<LOD-.780 (. but no neurologic. 2002). Kwok et al.46) < LOD 1.550-.385 (.410 (<LOD-.S.403-. population in the subsamples from NHANES 1999-2000 and 2001-2002 (CDC.970) 1.21-2.09-6..900-1.508) * . population from the National Health and Nutrition Examination Survey.360 (<LOD-.580) < LOD .75 (1.620-1.. OPP was not found to be mutagenic.11) < LOD 90th 1.EPA at: http:// www.93 (1. Biomonitoring studies on levels of OPP provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of OPP than are found in the general population.Fungicides anemia. 1998.EPA 2006).470) < LOD .43 (1.08-2.455-.59) 1.291-.750 (.61 (1.51-3.420 (<LOD-.EPA 2006).248-. and it has classified OPP as not classifiable with respect to human carcinogenicity.484) * .44 (1. Volunteers exposed to 0.311-.38) 1.12) < LOD 1.840 (.58) 2.. Finding a measurable amount of OPP in urine does not mean that the level of OPP causes an adverse health effect.860 (. 2000. 1997.558) Selected percentiles ( 95% confidence interval) Sample 95th 2.980 (.64 (2.510 (<LOD-.550 (.78 (2.69 (1.666) * .11-1. These metabolites may induce carcinogenicity via nongenotoxic regenerative hyperplasia of the bladder (Appel.S.473) * .01) 1.690 (.410 (<LOD-.06 (1.510-.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 .S.62) .. Brusick.500) < LOD . Urinary ortho-Phenylphenol (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. 2005.38-3.29) 1.89 (1.12-2.32) 3.59) .17) 2.81) 1. U.91) 695 680 520 694 603 953 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.810-1..4) 3.02 (.93) 1. reproductive.38) 2.18) 2.31) < LOD .329-.epa.91 (1.38) 973 1190 1018 1338 99-00 01-02 99-00 01-02 99-00 01-02 ..24-2.880-1.800-1. 1984.0) 1.97 (2.496 (. or.470 (<LOD-. or developmental toxicity was observed (Bomhard et al.86 (1.S. Smith et al. interval) . Detectable levels were seen in over half the U.440 (.780-14.32) 1.53) 1.382 (.560-2.940-2. Murata et al.460-. less likely..07) 2.380 (.860 (.11) 4.25-6.93) . 1993. IARC has classified SOPP as a possible human carcinogen.96 (1.75 (1.96) 1.00 (.21) 1.11 (..656) * .980 (<LOD-1.29) 1. 2002.420 (<LOD-.24-2.910 (<LOD-1.09 (1. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.21 (.09-3.13) 1.05-2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. leading to production of two metabolites. 1999.750 (.

Eastmond DA. Shirai T. Determination of orthophenylphenol in human urine by gas chromatography-mass spectrometry. Nakagawa Y. Drugs. Oxidative damage to cellular and isolated DNA by metabolites of a fungicide orthophenylphenol.niehs. Freyberger A. Atlanta (GA). Hakkert BC. U. Selim S. Bormett GA.159(1):18-24. Gierthy J. Toxicol Appl Pharmacol 1999. et al. Inoue S. Vogel JS. Moldeus P. Comparative metabolism of orthophenylphenol in mouse.pdf. U. Turteltaub KW. Bartels MJ. Cnubben NH. 2006. Kawanishi S. Shibata M. Fukushima S. Eadon G.286(2):309-319. Third National Report on Human Exposure to Environmental Chemicals. Available at URL: http://www. Office of Toxic Substances.35(2 Pt 1):198-208. Sangha GK.74(2):61-71. Sangha G. Leser KH. Timchalk C. Detection and characterization of DNA adducts formed from metabolites of the fungicide ortho-phenylphenol. McNett DA. Richter M.gov/ntp/htdocs/LT_ rpts/tr301. March 1986. Cano M. In vivo genotoxicity of sodium orthophenylphenol: phenylbenzoquinone is one of the DNA-binding metabolite(s) of sodium ortho-phenylphenol.50(11):3351-3358. Available at URL: http://ntp. Regul Toxicol Pharmacol 2002.(56):399-407. Long-term toxicity and carcinogenicity study of sodium o-phenylphenate in B6C3F1 mice.54(16):5731-5735. Roberts AL.32(6):551-625. Coelhan M.EPA). Xenobiotica 1998. Tayama S. Dose-dependent binding of ortho-phenylphenol to protein but not DNA in the urinary bladder of male F344 rats.S. Murata M. Crit Rev Toxicol 2002. rat and man.43(7):14311437. The pharmacokinetics and metabolism of 14C/13C-labeled ortho-phenylphenol formation following dermal application to human volunteers. Zhao S. Fukushima S. EPA-560/5-89-003. Bromig KH. Stanley JS. van de Sandt JJ. Urinary physiologic and chemical metabolic effects on the urothelial cytotoxicity and potential DNA adducts of o-phenylphenol in male rats. J Agric Food Chem 2002. Christenson WR.20(5):851-857. Roy D. IARC Sci Publ 1984. Ito N. NTP Technical report on the toxicology and carcinogenesis studies of ortho-phenylphenol (CAS No. 4/9/09. Arch Toxicol 2000. Bomhard EM. Identification of SARA compounds in adipose tissue. Buchholz BA. Elliott GR. Hagiwara A.S. Arnold LL. The carcinogenicity of the biocide ortho-phenylphenol. Hum Exp Toxicol 1998. St John MK. Glas K. Relationship between metabolism and cytotoxicity of ortho-phenylphenol in isolated rat hepatocytes. food additives and natural products as promoters in rat urinary bladder carcinogenesis. Fourth National Report on Human Exposure to Environmental Chemicals 45 . Kwok ES. National Toxicology Program (NTP). Herbold BA. Analysis of genotoxicity and the carcinogenic mode of action for ortho-phenylphenol. 1989. 90-43-7) in Swiss CD-1 mice (dermal studies).epa. Meuling WJ.17(8):411-417. Environmental Protection Agency (U. Toxicol Appl Pharmacol 1998. Pathak DN. Christenson WR. J Chromatogr B Biomed Sci Appl 1997. et al. Mutat Res 1993. Reregistration Eligibility Decision (RED) for 2-phenylphenol and salts (Orthophenylphenol or OPP).S.703(12):97-104. EPA 739 R-06004. Narang A. Environ Mol Mutagen 2005. Timchalk C. Brzak KA. Imaida K.S. Food Chem Toxicol 1984. 2005. Determination and levels of the biocide ortho-phenylphenol in canned beers from different countries. Biochem Pharmacol 1992.gov/oppsrrd1/REDs/ phenylphenol_red. Carcinogenesis 1999. 4/13/09 Onstot JD. O-phenylphenol and its sodium and potassium salts: a toxicological assessment..22(10):809-814. Smith RA. Moore GA.pdf. EPA).150(2):402-413. July 28.28(6):579594. Bartels MJ. Centers for Disease Control and Prevention (CDC). Brusick D. Ito N.nih. Comparative in vitro-in vivo percutaneous penetration of the fungicide ortho-phenylphenol. Moriya K.45(5):460-481. Hirose M. Bartels MJ. Mendrala AL. Bartels MJ. Hagiwara A. J Agric Food Chem 2006.Fungicides References Appel KE. Environmental Protection Agency (U. Brendler-Schwaab SY.

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

EPA 2000. Urinary levels of acetochlor mercapturate were generally not detectable in the NHANES 2001-2002 subsample (CDC. U. including one that produces 2-methyl-6ethylaniline and its reactive metabolite.EPA considers acetochlor likely to be carcinogenic in humans. environmental levels) is available from U. which are often more prevalent in the environment. CAS No.. Urinary acetochlor mercapturate levels of 0. Feng and Wratten. 2000). 1998). but it has produced testicular atrophy. Additional information about external exposure (i. Acetochlor is moderately toxic to fish and honey bees. and it is unlikely to be genotoxic at relevant doses (Ashby et al. Acetochlor has not shown developmental or fetal toxicity in chronic animal studies.S. In animals. 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. Hladik et al. 2-hydroxyethyl-6-methylaniline.S. Acetochlor has low acute toxicity. However. 2006).gov/ pesticides/. animals have demonstrated tumors of the lung. People exposed to acetochlor will excrete acetochlor mercapturate in their urine. Acetochlor degrades in water to acetochlor sulfonic acid and acetochlor oxanilic acid.e. 2007). 2006). Finding measurable amounts of acetochlor mercapturate in the urine does not mean that the levels of acetochlor mercapturate cause an adverse health effect.S.EPA. Davison et al. Biomonitoring studies on levels of acetochlor mercapturate provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of acetochlor than are found in the general population.EPA. 2000. General population exposure to acetochlor may occur through diet or drinking water. 1994.5 to 449 μg/L were measured in commercial applicators within 24 hours following its application (Barr et al. mainly corn.S. 2006).. 2005.. and neurologic movement abnormalities (U.S.. Jefferies et al. 2000. and hydroxymethyl ethyl aniline (U. remains in soils for up to 3 months. 2006). and has been detected in watersheds of agricultural lands (Battaglin et al. 1989.S. 2005).0 μg/L (Curwin et al. in some species and at doses above maximum tolerated doses.. the latter which may account for some observed effects (Coleman et al. It is absorbed by plants and inhibits plant protein synthesis.epa. Human health effects from acetochlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown. and thyroid (U.. this metabolite is not a marker of exposure to most plant metabolites or environmental degradates.EPA. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. NTP and IARC do not have ratings regarding human carcinogenicity. nasal epithelia. Fourth National Report on Human Exposure to Environmental Chemicals 47 . Kolpin et al. 2005).Herbicides Acetochlor Biomonitoring Information Urinary levels of acetochlor mercapturate reflect recent exposure. however. renal injury. Acetochlor is microbiologically degraded. Acetochlor is not mutagenic. Estimated human intakes of acetochlor have been below recommended limits (U. EPA at: http://www. Plants can degrade acetochlor to 2-ethyl-6-methylaniline... 2000.. a major pathway for acetochlor metabolism involves mercapturate conjugation. but other pathways occur.. 1996). Acetochlor mercapturate was measured in the urine of farmers actively spraying the pesticide and the geometric mean was 8.

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

5/30/06. Feil VJ. EPA 738-R-00-009. Hsiao JJ. et al. J Expo Sci Environ Epidemiol 2007. Coleman S. Hodgson E. EPA). Hines CJ. acetochlor. 2000. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay.S. Wratten SJ. Larsen GL. and other herbicides in rivers. Fourth National Report on Human Exposure to Environmental Chemicals 49 . Roberts AL. Chem Res Toxicol 1998.17(6):559-566. Linderman R.EPA): http://pmep. Jefferies PR.S. Rose RL. Identification of human urinary metabolites of acetochlor in exposed herbicide applicators by high performance liquid chromatography-tandem mass spectrometry. Environmental Protection Agency (U. et al. Sci Total Environ 2000. Alavanja MC. Kier L.Herbicides References Ashby J. Striley CA. Wilson AG. Hladik ML. Deddens JA. sulfonamide. Curwin BD. Kinney PL.cornell. Barr JR. Atlanta (GA). Kolpin DW. Hum Exp Toxicol 1996.pdf. et al. March 2006. Bravo R. Lefevre PA.cce. EPA).S. Evaluation of the potential carcinogenicity and genetic toxicity to humans of the herbicide acetochlor. Third National Report on Human Exposure to Environmental Chemicals. 1998. U.24(10):1003-1012.gov/oppsrrd1/reregistration/REDs/acetochlor_tred. Reynolds SJ. Comparative metabolism and elimination of acetanilide compounds by rat.248(2-3):123-133. Casida JE. Barr DB. Linhart SM. Finding minimal herbicide concentrations in ground water? Try looking for their degradates. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. Feng PCC.248(2-3):115-122. 2005.39(17):6561-6574. Quistad GB. Comparative metabolism of chloroacetamide herbicides and selected metabolites in human and rat liver microsomes. Centers for Disease Control and Prevention (CDC).108(12):1151-1157.11(4):353359.S. Ward EM.edu/profiles/herbgrowthreg/24-d-butylate/acetochlor/acetochlor_pet_100.html. Battaglin WA. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. Barr DB. Davison KL. Environ Health Perspect 2003. Barr DB.S. Report of the Food Quality Protection Act (FQPA) Tolerance Reassessment Progress and Risk Management Decision (TRED) for Acetochlor. reservoirs and ground water in the Midwestern United States. Burkhardt MR. Furlong ET. imidazolinone. 5/30/06 U. Acetochlor (Harness) Pesticide Petition Filing 1/00. Heederik D.111(5):749-756. Hein MJ. J Expo Anal Environ Epidemiol 2005. Environ Health Perspect 2000. Number 15. Volume 65.15(9):702-735. Andrews HF. Available at URL(non U.37(4):10881093. Tinwell H. Federal Register: January 24. and metolachlor herbicides in rats. Dialkylquinonimines validated as in vivo metabolites of alachlor. Camann DE. Green T. pages 3682-3690. Occurrence of sulfonylurea. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. Available at URL: http://www. Environ Sci Technol 2005. Environmental Protection Agency (U. J Agri Food Chem 1989. Olsson AO.15(6):500-508. Sci Total Environ 2000. Xenobiotica 1994. epa. Sanderson WT. Whyatt RM. Peter CJ. Thurman EM.

. Alachlor is highly toxic to freshwater fish and slightly toxic to birds and some invertebrates. 1995.1 mg/L at various collection times (Sanderson et al. 50 Fourth National Report on Human Exposure to Environmental Chemicals .Herbicides Alachlor CAS No.. corn cropland was treated with alachlor. Feng and Wratten.6-diethylaniline and its reactive metabolite.S. 2003). 1999 and 2007. 1996. Because it can be absorbed through skin. 1998). the latter may account for some observed effects (Davison et al. peanuts and other crops. In chronic animal testing. but this metabolite is not a marker of exposure to most plant metabolites or environmental degradates which are often more prevalent in the environment. 1989. alachlor has demonstrated hepatotoxicity. and uveal degeneration. Additional information about is available from U. 2003). Human health effects from alachlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown. and thyroid only at either maximum tolerated doses or related to species-specific pathways (Heydens et al. Biomonitoring studies on levels of alachlor mercapturate provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of alachlor than are found in the general population.. 1997.EPA. Estimated human intakes have been below recommended limits (U.S. Hladik et al. Alachlor itself is not considered mutagenic. 2000. In a study of applicators and workers exposed to alachlor.epa. Finding measurable amounts of alachlor mercapturate in the urine does not mean that the levels of alachlor mercapturate cause an adverse health effect. Since the late 1980s alachlor use has been declining. U. Alachlor has a soil half-life of a few weeks.. EPA at: http://www. 2005. It is absorbed by plants and inhibits plant protein synthesis. alachlor is quickly absorbed after oral doses and mostly excreted as metabolites within a week (IPCS. General population exposure to alachlor may occur through consumption of contaminated food or drinking water. though positive genotoxic results are reported for several metabolites of alachlor (Brown et al. 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. In animal studies.S. 2003).EPA. U. U. Kolpin et al.S. but shows little bioaccumulation. 1998. U. as measured through conversion to deethylamine. 2003). Hines et al. 1998). WHO. 2000.gov/pesticides/. WHO. stomach. 1999. Jefferies et al. soybeans. 1996). 1998. Tessier and Clark. including corn.. but has not shown developmental or reproductive toxicity in mammalian systems (U. but another metabolic pathway can produce 2. mercapturate conjugates were predominant metabolites. USGS. 1995). 1998). 1996..EPA. 1988. 1998. hemosiderosis.. the dermal exposure route is potentially significant for applicators. In 1993-1995.EPA considers alachlor to be a probable human carcinogen at high doses. 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.S. (2003) showed that 2. whereas 60% of applicators had detectable amounts. NTP and IARC do not have ratings regarding human carcinogenicity. In animals.EPA.S. IPCS. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.. about 20-25% of the U. 2005). but not likely at low doses.EPA. and field workers. WHO. and on non-crop land for general weed control.1 to 1. It is both metabolized in plants and degraded microbiologically in agricultural soils into as many as 19 metabolites and degradates.S.2% of a reference population had detectable alachlor equivalents by immunoassay in their urine. People exposed to alachlor will excrete alachlor mercapturate in their urine (Driskell et al. 1994. ranged from 0. Urinary levels of alachlor mercapturate were generally not detectable in the NHANES 2001-2002 subsample (CDC.. WHO. Biomonitoring Information Urinary levels of alachlor mercapturate reflect recent exposure. formulators. Alachlor has low potential for acute toxicity. mean values of urinary concentrations of alachlor metabolites. Animal carcinogenicity studies have demonstrated tumors of the nasal turbinates. Hill et al..S.

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

No. An evaluation of the carcinogenic potential of the herbicide alachlor to man.S. Kolpin DW. Davison KL. Biological monitoring of commercial pesticide applicators for urine metabolites of the herbicide alachlor. Burkhardt MR. Lau H. 1999. acetochlor. 2/27/09 Jefferies PR. World Health Organization (WHO).43(25):2087-94. Driskell WJ. Hines CJ. March 2006.inchem. Thelin GP. Available at URL: http:// www.11(4):353359.org/documents/pds/pds/pest86_e. reservoirs and ground water in the Midwestern United States.56(6):853-859. Martens MA. Thake DC.php.395(2-3):159-171. The Quality of Our Nation’s Waters Pesticides in the Nation’s Streams and Ground Water. Quantitative assessment of the mutagenic potential of environmental degradative products of alachlor. Casida JE. Hull RD. 86. Mutat Res.18(6):363-391. Identification of a major human urinary metabolite of alachlor by LC-MS/MS. Striley CA. Erratum in: Life Sci 1989. International Programme on Chemical Safety (IPCS). U. Geological Survey (USGS). Shoemaker DA. Kolpin DW. Xenobiotica 1994. Camann DE. Alachlor in Drinking-water. et al. revised February 15. Barr DB. 1992-2001.usgs. Supplemental Technical Information (available on-line only).Herbicides References Battaglin WA. Biagini RE.24(10):1003-1012. EPA). Chem Res Toxicol 1998. Linhart SM. Whyatt RM. DNA adduct formation by alachlor metabolites. Sci Total Environ 2000. ALACHLOR.44(18):1325. Gilliom RJ). Bull Environ Contam Toxicol 1996. Quistad GB.epa. and metolachlor herbicides in rats. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. Larsen GL. Hill AB. California. Life Sci 1988. Third National Report on Human Exposure to Environmental Chemicals. Wilson AG. Available at URL: http://water. 1997. 1996.S. Reregistration Eligibility Decision (RED) Alachlor. Water-Resources Investigations Report: Distribution of Major Herbicides in Ground Water of the United States Water Resource Investigations Report No. and other herbicides in rivers. Ann Occup Hyg 2003. 2007. who. Tolos W. Furlong ET. Geological Survey (USGS).248(2-3):123-133.gov/oppsrrd1/ REDs/0063. 1998. WHO/ FAO Data Sheets on Pesticides. Dialkylquinonimines validated as in vivo metabolites of alachlor. Sacramento. December 1998. Hsiao JJ. Circular 1291. Feng PCC.111(5):749-756. Biagini R. Dialkylquinoneimine metabolites of chloroacetanilide herbicides induce sister chromatid exchanges in cultured human lymphocytes. 1999. Occurrence of sulfonylurea. Centers for Disease Control and Prevention (CDC). Heydens WF.43(9):2504-2512. sulfonamide. Available at URL: http://www. Henningsen G.htm.248(2-3):115-122. Sanderson WT. 2003. EPA 738R-98-020. Quistad GB. Comparative metabolism and elimination of acetanilide compounds by rat. Hum Exp Toxicol. J Ag Food Chem 1995. Kimmel EC. 98-4245 (by Barbash JE. Environ Health Perspect 2003.S. Geneva. Brown MA. Roberts AL. Shealy DB. et al. Deddens JA. Casida JE. Jefferies PR. Hladik ML. MacKenzie B. Peter CJ. 2/27/00 52 Fourth National Report on Human Exposure to Environmental Chemicals . 4/2/09 U.S. Environmental Protection Agency (U.int/water_sanitation_health/dwq/chemicals/en/alachlor. Thurman EM. Kinney PL.47(6):503-517. Andrews HF. J Agri Food Chem 1989. imidazolinone. World Health Organization. Feil VJ. Brown KK. Am Ind Hyg Assoc J 1995.pdf. Hines CJ. Available at URL: http://www. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns.gov/nawqa/pnsp/pubs/circ1291/ supporting_info. Tessier DM. Hill RH Jr. Clark JM.37(4):10881093. Sci Total Environ 2000. 2005.pdf. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. Environ Sci Technol 2005. Wratten SJ. 2/27/09 U. Barr JR. Atlanta (GA). Background document for development of WHO Guidelines for Drinking-water Quality.39(17):6561-6574. Kier LD. Finding minimal herbicide concentrations in ground water? Try looking for their degradates.56(9):883-889. Casida JE.

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

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

99(8):5476-5480. In a study of 60 farm worker children. Jones AD. Ann Occup Hyg 2003. Chen H. 82. Toxicological profile for atrazine.. Biological monitoring of human exposure to atrazine.115(8):1254-1260. Geneva. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample. et al.53(2):297-307. et al.2 μg/L in 15 farmers studied several days after spraying the pesticide (Curwin et al. Stoker TE. Collins A. Clayton CA. 2001). Blewett C. Gillis JH. et al. Goldman JM. Moseman RF. Environ Health Perspect 2001. Fleenor-Heyser DG. Lucas AD.109(6):583-590. Pesticide urinary metabolite levels of children in eastern North Carolina farmworker households. Breckenridge CB. Ferrell JM. Stevens JT. Cottica D. 2005). Freeman NC. Pfeifer KF. No. 3/11/09 Laws SC. Laws SC. Short-term effects of chlorotriazines on estrus in female Sprague-Dawley and Fischer 344 rats. Cooper RL.html. The mammary tumor response in triazine-treated female rats: a thresholdmediated interaction with strain and species-specific reproductive senescence. References Adgate JL. urinary concentrations ranged from 5-1756 μg/L (Lucas et al. Bersani M. A risk assessment of atrazine use in California: human health and ecological aspects.43(2):155-167. Simpkins JW. 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. Eldridge JC.Herbicides Biomonitoring Information Urinary levels of atrazine mercapturate reflect recent exposure. Atrazine disrupts the hypothalamic control of pituitary-ovarian function. Agency for Toxic Substances and Disease Registry (ATSDR).61(4):331-355. Lee M. Brown KK. Pest Manag Sci 2005. 3/11/09 Arcury TA. International Programme on Chemical Safety (IPCS).cdc. Aldous CN. Tapia J. Determination of atrazine metabolites in human urine: Fourth National Report on Human Exposure to Environmental Chemicals 55 .org/documents/pds/pds/pest82_e. Hayes TB. Cooper RL. Deddens JA. Through immunoassay atrazine equivalents (detected mostly as atrazine mercapturate). Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. J Expo Anal Environ Epidemiol 2005.15(6):500-508.64(9):672-678. The effects of atrazine on female wistar rats: an evaluation of the protocol for assessing pubertal development and thyroid function. levels of atrazine mercapturate were generally not detectable (CDC. Biagini RE.. Seiber JN. Gammon DW. Carr WC Jr. atrazine mercapturate was infrequently detected at the detection limit of < 1 μg/L. Sanborn JR.. Available at URL: http:// www. Goodrow MH. In a small number of field workers. Available at URL: http://www. 2001 [online]. Wetzel LT. et al. Extrom PC. J Agric Food Chem 1982. Gillis JH. 2007). Finding measurable amounts of atrazine mercapturate in urine does not mean that the levels of atrazine mercapturate cause an adverse health effect. 1993).43(2):155-167.58(2):366-376. Hein MJ. et al.76(1):190-200. Ferrell JM.inchem. Curwin BD. Quandt SA.. 2005). Pubertal development in female Wistar rats following exposure to propazine and atrazine biotransformation by-products. 2000). ATRAZINE. Mendoza M. Determination of urinary residue levels of the N-dealkyl metabolites of triazine herbicides. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. Perry et al. Striley CA. Maroni M. 2003. In the NHANES 2001-2002 subsample.atsdr. Barr DB. Cooper RL. Environ Health Perspect 2007. Tyrey L. Atlanta (GA). Stoker TE. 1999) and 83 Minnesota children with multiple urine collections during 1997 (Adgate et al. Toxicol Sci 2003. World Health Organization. Sanderson WT. Third National Report on Human Exposure to Environmental Chemicals. et al. Steroids 1999. Eberly LE. Catenacci G.. Saiz SG. Lioy PJ.gov/toxprofiles/tp153. J Toxicol Environ Health 1994. Vonk A. 1996.htm. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Heederik D. Hines CJ. atrazine was detected in only four children (Arcury et al. Barbieri F. Wetzel LT.69(2):217-222. Schmid J. Short-term effects of chlorotriazines on estrus in female Sprague-Dawley and Fischer 344 rats.47(6):503-517. Toxicol Sci 2000. Reynolds SJ. Stuart AA. 2005. Ferioli A. Grzywacz JG. Toxicol Lett 1993. McElroy WK. Bradway DE. Proc Natl Acad Sci USA 2002.30(2):244-247.. Stoker TE. Toxicol Sci 2000. J Toxicol Environ Health 1994. Eldridge JC. Barr DB. WHO/ FAO Data Sheets on Pesticides. The geometric mean of urinary atrazine mercapturate was 1.. the urinary geometric mean levels for herbicide applicators in Ohio and Wisconsin were about 6 μg/L (Hines et al. demasculinized frogs after exposure to the herbicide atrazine at low ecologically relevant doses. Centers for Disease Control and Prevention (CDC). Barr DB. Noriega N. Hermaphroditic. diamino-S-chlorotriazine and hydroxyatrazine. Shoemaker DA. In small studies of Maryland residents in 19951996 (MacIntosh et al.

Environmental Protection Agency (U.Herbicides development of a biomarker of exposure. Circular 1291. Pesticides in the Nation’s Streams and Ground Water.S. Lansbergen GW.epa. March 2006.182(1):44-54. revised February 15. The effects of atrazine metabolites on puberty and thyroid function in the male Wistar rat. EPA Office of Pesticide Programs. Toxicol Sci 2002.61(1):27-40. Determination of the effect of tridiphane on the pharmacokinetics of [14C]-atrazine following oral administration to male Fischer 344 rats. Toxicol Sci 2000. Chem Res Toxicol 1993. Tortorelli J.gov/oppsrrd1/REDs/ atrazine_ired. van den Berg M. Delzell E. EPA). Environmental Fate and Effects Division. Case No. 4/2/09 56 Fourth National Report on Human Exposure to Environmental Chemicals .S. 3/11/09 U. J Toxicol Environ Health A 1999. Office of Prevention. 2003b. Fenton SE. Exposure parameters necessary for delayed puberty and mammary gland development in LongEvans rats exposed in utero to atrazine. Ryan PB. Toxicol Appl Pharmacol 2004.67(2):198-206. 0062. J Expo Anal Environ Epidemiol 1999. Available at URL: http://www. Needham LL. Cooper RL. Laws SC. Wetzel L. Langvardt PW. Osborne DW.10(7):479.S.gov/scipoly/sap/meetings/2003/june/ finaljune2002telconfreport. The effect of atrazine on puberty in male Wistar rats: an evaluation in the protocol for the assessment of pubertal development and thyroid function. Sathiakumar N. A risk characterization for atrazine: oncogenicity profile. Timchalk C. Kastl PE.58(1):50-59. Supplemental Technical Information (available on-line only). Available at URL: http://water. 6/1/09 U. Stevens JT.pdf. MacIntosh DL. Guidici DL. Dryzga MD. Available at URL: http://www. Stoker TE. Toxicol Appl Pharmacol 2002. 1992-2001. Laws SC. White paper on potential developmental effects of atrazine on amphibians.195(1):23-34. Christiani D.gov/nawqa/pnsp/pubs/ circ1291/supporting_info. Boerma J. Dagenhart D.S. May 2003a. The Quality of Our Nation’s Waters. Stoker TE. Guidici DL. Rayner JL.php. Hammerstrom KA.epa. Urinary biomarkers of atrazine exposure among farm pesticide applicators. Wood C.usgs.9(5):494-501. Interim Reregistration Eligibility Decision For Atrazine.56(2):69-109. Sanderson JT. Pesticides and Toxic Substances. U. Singzoni B. EPA).6(1):107-116. Crit Rev Toxicol 1997.27(6):599612. A longitudinal investigation of selected pesticide metabolites in urine. Induction and inhibition of aromatase (CYP19) activity by various classes of pesticides in H295R human adrenocortical carcinoma cells. 2007. Toxicology 1990. Ann Epidemiol 2000. Cooper RL. Perry M. Breckenridge CB. Washington (DC).S. A review of epidemiologic studies of triazine herbicides and cancer.pdf. Environmental Protection Agency (U. Geological Survey (USGS).

S.EPA. renal and hepatic injury.30 (<LOD-2.260 (<LOD-.EPA.08) < LOD .22) < LOD . 4-D. Similar to other chlorophenoxy herbicides.4-D may occur during residential applications.4-Dichlorophenoxyacetic acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.230-. agricultural.4-D is eliminated mostly unchanged in the urine with an elimination half-life ranging from 10 to 33 hours (Arnold et al.70) 1.S.550-1.10 (<LOD-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.660) 1.4-D have been below recommended intake limits (U. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 1. It is rarely detected in ground waters (USGS. 2007).4-D is rapidly absorbed via oral and inhalation routes.05-2. hypotension.27 (1.540-.24 (.S.48) < LOD 1. Sauerhoff et al.420) < LOD . see Data Analysis section) for Survey years 99-00 and 01-02 are 0.80) 1.22) 962 1135 1015 1278 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .610-. and by consuming food or drinking water contaminated with 2.250 (<LOD-.690-1. and mecoprop). it acts as a plant growth hormone.420-.10 (<LOD-1.330 (.310) < LOD . headache.370-.02-1.490) < LOD < LOD < LOD .20 (.690 (.4-D at low environmental doses or at biomonitored levels from low environmental exposures are unknown.4-D were used in the U.21) 1.930 (. Intentional overdoses and unintentional high dose exposures to chlorophenoxy acid herbicides have resulted in weakness.4-Dichlorophenoxyacetic Acid CAS No. Fourth National Report on Human Exposure to Environmental Chemicals 57 . It was first registered with U.Herbicides 2. Kohli et al. and aquatic environments. As much as 62 million pounds of 2. 2004). 2.560-. dizziness.S.4-D can be applied either as an aqueous salt or as oil-soluble esters.32 (1. Survey Geometric mean (95% conf.680-1. MCPA.960-1.00-2.690 (.610 (..560-1.51 (1.890 (..4-D or exposed for prolonged periods.320) 90th . 94-75-7 General Information Widely used throughout the United States.350) < LOD < LOD < LOD . < LOD means less than the limit of detection. abdominal pain.10) < LOD 1. 1974. At low levels. General population exposure to 2.37) 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 . 2.07 (.49) 477 546 677 797 823 1070 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD .4-D) controls broadleaf weeds in residential. and delayed Urinary 2.27 (.20 (<LOD-1.16) < LOD . It is poorly bound in soils.40) 1.410) < LOD .490 (.55 (1. 1989.230 (<LOD-.210 (<LOD-.EPA in 1948. It is not well absorbed through the skin. 1977).910) < LOD .440-1.740 (. which may vary for some chemicals by year and by individual sample. Recent estimates of chronic intakes of 2. although dermal exposure may be significant for herbicide manufacturing plant workers exposed to high concentrations of 2.890) < LOD .310 (. myotonia. the chlorophenoxy herbicide 2. population from the National Health and Nutrition Examination Survey.66) < LOD 1.03) 695 659 520 668 589 892 Limit of detection (LOD.4-D has low acute toxicity.13) < LOD . and it is often mixed with other chlorophenoxy acid herbicides (such as dicamba. 2005).27-2. Acid and salt forms are much less toxic to fish and aquatic invertebrates than the ester forms. Once absorbed.400) < LOD .2.910) 1.690 (. these herbicides can enhance plant growth.930-1. 2. but at higher levels they are herbicidal.810-1. 2.910) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .670-1.4-dichlorophenoxyacetic acid (2.730 (.250 (<LOD-. nausea. Human health effects from 2.210-.952 and 0.43) 1. by direct contact with agricultural and residential areas after applications.60) 1. in 2001 (U.S.. with a half-life of several days to several weeks.760 (.

35) < LOD .4-D are eye irritants.780-1.670 (. IARC considers the chlorophenoxyacetic acids group of chemicals as possibly carcinogenic to humans..epa. 1996.380 (<LOD-. in small samples of children (Hill et al. Hill et al. with the exposure to chlorophenoxy herbicides as defoliants or contaminated herbicides..7.670 (. 2005).14 (.560-.56) .440 (.EPA. Kolmodin-Hedman and Erne. population from the National Health and Nutrition Examination Survey.. 2000).580-.790) < LOD .380 (<LOD-. 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.270 (<LOD-. myotonia. Survey Geometric mean (95% conf.S.24) 1.08 (.S. 2005.490 (. or teratogenic effects in chronic rodent studies (Charles et al.3. IPCS. and evidence of histological injury to the kidneys. 2.550-. U. thyroid.08 (.930-1. 1985. 1994). interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 1. The 95th percentiles of the NHANES 1999-2000 and 2001-2002 subsamples were roughly similar to the 95th percentile values reported in a nonrandom subsample from NHANES III (1988-1994) (CDC..4-D had urinary levels several hundred to several thousand times higher than the 95th percentiles of the NHANES subsamples (CDC.05) .. U. 2006. 2005).680) < LOD .390) < LOD < LOD < LOD .620-.330-.Herbicides neuropathy (Bradberry et al.590 (<LOD-1.340 (. 2005). U.740 (.610-.660 (. 2005).700 (..4-D was not found to be genotoxic or carcinogenic in animal studies (Garabrant and Philbert. other exposures.40) 695 659 520 667 589 892 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.480 (.8-tetrachlorodibenzo-pdioxin) (Garabrant and Philbert. 1995).850) < LOD .780 (. Frank et al.19) .13 (. urinary 2. Kutz et al. 1996.560-.890) < LOD 1. 2005. Knopp et al. 2003.590 (<LOD-1..EPA at: http://www.08 (.790) 1.410) 90th .73) .S.410) < LOD < LOD < LOD . 2001.39) < LOD 1.4-D does not have significant reproductive.820-1. eyes.4-D reflect recent exposure.16) 1. IPCS.32 (<LOD-2. 2002.4-D levels were detectable in less than a quarter of the individuals studied.610-. Biomonitoring Information Urinary levels of 2.570) < LOD .17 (.. or to contaminants in the herbicide formulations (specifically 2..990-1. such as soft tissue sarcoma and non-Hodgkin’s lymphoma.S. population (Hill et al. and of adults and children (Baker et al. 1992). 2004). IOM.340-.S. Acute high doses administered to laboratory animals produced ataxia. 1989).41 (1.29) 477 546 677 796 823 1070 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD . 1980. IPCS.670 (<LOD-1.380-. The acid and salt forms of 2.26) 962 1135 1015 1277 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .410) < LOD 1. CDC.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.270-.920) < LOD 1.980) < LOD 1. 2.380) < LOD . developmental.720 (.780) . Pearce and McLean. It is unclear whether these associations are related to the chlorophenoxy herbicides.810-1.470) < LOD .S.EPA 2005). 58 Fourth National Report on Human Exposure to Environmental Chemicals .. Post-application levels in farmers and home gardeners were dependent on Urinary 2.26) 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 .640 (.gov/pesticides/.780) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD . Epidemiological studies have reported associations of several types of cancer.410 (<LOD-. In previous samples of the U.810-1.EPA.4-Dichlorophenoxyacetic acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. 2005. 1996. 2002.S.890-1. 1995. liver.660) < LOD .27-1. 2005. adrenals and gonads (NTP.520-.EPA. Average post-application urinary levels of 2.13 (. Additional information is available from U. U.4-D production plant workers and a few forestry workers spraying 2.350 (<LOD-.

Holler JS. the amount of pesticide applied. Beasley VR. Reynolds SJ. Biomonitoring of herbicides in Ontario farm applicators. Sanderson WT. National Toxicology Program (NTP). 2005. Xenobiotica 1974. 2.S.Herbicides the time since application.60(1):121-131. Arnold EK.15(6):500-508.htm. Carter-Pokras OD. 2005). Mandel JS. J Environ Sci Health B 1992. Selected pesticide residues and metabolites in urine from a survey of the U. Cook BT. Available at URL: http:// www. Estimation of occupational exposure to phenoxy acids (2. Updated March 7. Assessment of exposure to 2. Bailey SL. 3/17/09 Institute of Medicine (IOM). Baker BA. J Toxicol Environ Health 1992.5-T).nih. Arch Environ Contam Toxicol 1985. Philbert MA. geometric mean urinary levels of 2. et al. Head SL. Hill RH Jr. In farm families.4-Dichlorophenoxyacetic Acid). et al. Brody D.4-dichlorophenoxyacetic acid and its forms.nap. Third National Report on Human Exposure to Environmental Chemicals. 2005. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 2005 Charles JM. 914. Kolmodin-Hedman B.4-D will result in an adverse health effect. Mandel et al. TOX-63 Peroxisone Project (2. Review of 2. 2006. Quantification of selected pesticide metabolites in human urine using isotope dilution high-performance liquid chromatography/ tandem mass spectrometry. Acquavella JF.4-.inchem. TOX-63: TOXICITY REPORT CURVES. Erne K. Solomon KR.4-D in urine does not mean that the level of the 2.edu/catalog.. Harris SA.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. Cole DC. J Expo Anal Environ Epidemiol 2000. Ripley BD.4-D were highest in the farmers who applied the 2.51(3):152-159. Dichlorophenoxyacetic acid. Shealy DB. Occup Environ Med 1994.4-D): exposure and urinary excretion. Murphy RS. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa.31 Suppl 1:90-97. Wilson RD.18(4):469-474.gov/index. van Ravenzwaay B. et al. the number of acres to which it was applied (Curwin et al. Hein MJ. Sircar KP. Chapman P. Honeycutt R. Harris et al.27(1):23-38.4:97-100. general population.4-dichlorophenoxyacetic acid (2. 1992). Driskell WJ. Needham LL. Biomonitoring for farm families in the farm family exposure study. Gupta BN. Forestry workers involved in aerial application of 2. 2003.31 Suppl 1:98-104. The pharmacokinetics of chlorinated phenoxy acid herbicides: a literature. Scand J Work Environ Health 2005. Arch Toxicol Suppl 1980. Baker SE. To T. Arch Environ Contam Toxicol 1989.org/documents/jmpr/jmpmono/v96pr04. Baker S. Dhar MM.10(6 Pt 2):789-798. Atlanta (GA). Crit Rev Toxicol 2002. Pesticide residues in urine of adults living in the United States: reference range concentrations. Barr DB.niehs. Heederik D. Sirons G J. and the use of protective clothing or equipment (Arbuckle et al. Frank R.31(2):121-125.. 3/17/09 Fourth National Report on Human Exposure to Environmental Chemicals 59 .4 dichlorophenoxyacetic acid (2. Tables.4-dichlorophenoxyacetic acid in the chemical industry: results of a five year biological monitoring study. Available at URL: http:// www.4-D).php?record_id=10603. Beeson MD. Survival and Growth Curves from NTP Toxicity Studies. Available at URL: http://ntp. cfm?objectid=06FF8DA6-E5A1-90CD-3F26562CEC5CDDE5. Vet Hum Toxicol 1989. Garabrant DH. Committee to Review the Health Effects in Vietnam Veterans of Exposure to Herbicides (Fourth Biennial Update. Kutz FW. Stephenson GR. Environ Res 1995.4:318-321. Exposure of homeowners and bystanders to 2.4-dichlorophenoxyacetic acid (2. Barr DB. Hill RH Jr. Tandon JS. Curwin BD. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children..37(2):277-291. J Expo Anal Environ Epidemiol 2005 Nov.4-D.4:427-435.4-D and 2. Scand J Work Environ Health 2005.4-D) epidemiology and toxicology. Gregg M. Hanley TR Jr. Biomonitoring studies of 2. Board on Health Promotion and Disease Prevention. Needham LL. Absorption and excretion of 2. Fast DM. Khanna RN. Washington (DC): National Academies Press. 3/17/09 Knopp D..32(4):233-257. Ritter L. Toxicol Sci 2001. 2005). Alexander BH. other family members had levels ranging only slightly higher than the 95th percentile levels in NHANES 1999-2000 and 2001-2002 subsamples (CDC. Kohli JD. Campbell RA. Centers for Disease Control and Prevention (CDC).4-D than levels found in the general population. Finding a measurable amount of 2. Veterans and Agent Orange: update 2002.4. Bus JS.4-dichlorophenoxyacetic acid in man. Pesticides residues in food: 1996 evaluations Part II Toxicology.71(2):99-108. Developmental toxicity studies in rats and rabbits on 2. References Arbuckle TE. Smith SJ. International Programme on Chemical Safety-INCHEM (IPCS).

Gehring PJ. Available at URL: http://www.S. Environmental Protection Agency (U. Supplemental Technical Information (available on-line only). 2007.usgs.pdf.8:3-1U.4-D RED Facts. Office of Prevention Pesticides and Toxic Substances. Washington (DC): U.epa. Toxicology 1977. 4/2/09 U.S.EPA).htm. revised February 15. March 2006. Pesticide industry sales and usage . Environmental Protection Agency (U. 2004. The fate of 2.epa. May. EPA 738 F-05-002. S. The Quality of Our Nation’s Waters. Circular 1291.gov/nawqa/pnsp/pubs/ circ1291/supporting_info. Pesticides in the Nation’s Streams and Ground Water. Blau GE. 60 Fourth National Report on Human Exposure to Environmental Chemicals .EPA. gov/oppbead1/pestsales/01pestsales/market_estimates2001. Available at URL: http://water.4-D) following oral administration to man.2000 and 2001 market estimates. Available at URL: http://www. June 2005.EPA).gov/oppsrrd1/ REDs/factsheets/24d_fs.S.php.S. Braun WH. 3/17/09.Herbicides Sauerhoff MW. Geological Survey (USGS).4-dichlorophenoxyacetic acid (2. 1992-2001. 3/17/09 U. 2.S.

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

see Data Analysis section) for Survey year 01-02 is 0. Survey Geometric mean (95% conf. population from the National Health and Nutrition Examination Survey.240) 679 701 957 Limit of detection (LOD. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.200 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.2.740) 679 700 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.Herbicides Urinary Metolachlor mercapturate Metabolite of Metolachlor Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.670 (<LOD-. 62 Fourth National Report on Human Exposure to Environmental Chemicals .S. population from the National Health and Nutrition Examination Survey. Urinary Metolachlor mercapturate (creatinine corrected) Metabolite of Metolachlor Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.440 (<LOD-. 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 . 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 .500) < LOD 1192 1345 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . Survey Geometric mean (95% conf. which may vary for some chemicals by year and by individual sample.S.220) < LOD 1192 1346 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .200 (<LOD-. < LOD means less than the limit of detection.

and other herbicides in rivers.S. Hodgson E. Roberts AL. streams and groundwater.php. imidazolinone. Kolpin DW.usgs.html. Available at URL: http://water. 2007. The Quality of Our Nation’s Waters Pesticides in the Nation’s Streams and Ground Water. March 2006. Quistad GB.248(2-3):115-122. Dialkylquinonimines validated as in vivo metabolites of alachlor.pdf 3/30/09 Hines CJ.usgs. Centers for Disease Control and Prevention (CDC). Circular 1291. Furlong ET. 6/1/09 Whyatt RM. Metolachlor in Drinkingwater. Environ Sci Technol 2007.41:3409-3414. acetochlor. Environmental Protection Agency (U. Available at URL: http://www. EPA).gov/nawqa/pnsp/pubs/circ1291/ supporting_info. Comparative metabolism and elimination of acetanilide compounds by rat. revised February 15. Available at URL: http://water.gov/oppsrrd1/ REDs/0001. U. Reregistration Eligibility Decision (RED) Metolachlor. Brown KK. April 1995. Feng PCC. Sci Total Environ 2000. R.37(4):10881093. Barr DB. Thelin GP. Background document for development of WHO Guidelines for Drinking-water Quality. Feil VJ. 4/2/09 U. Geological Survey (USGS).47(6):503-517. reservoirs and ground water in the Midwestern United States. 3/27/09 Fourth National Report on Human Exposure to Environmental Chemicals 63 . Curwin BD. Third National Report on Human Exposure to Environmental Chemicals. Davison KL. 2005. Heederik D. Jefferies PR. 3/26/09 U. Linderman R. California. et al. Ann Occup Hyg 2003. Xenobiotica 1994. Occurrence of sulfonylurea. Gillion. Environ Health Perspect 2003.ESTfeature_gilliom.S. Hsiao JJ. J Agri Food Chem 1989. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay.111(5):749-756. Water-Resources Investigations Report: Distribution of Major Herbicides in Ground Water of the United States Water Resource Investigations Report No.gov/nawqa/ pnsp/pubs/wrir984245/text. Finding minimal herbicide concentrations in ground water? Try looking for their degradates. sulfonamide. EPA 738R-95-006. Kinney PL. Supplemental Technical Information (available on-line only). Hein MJ.Herbicides References Battaglin WA. et al. Larsen GL. Barr JR. Geological Survey (USGS).pdf. Biagini RE. J Expo Anal Environ Epidemiol 2005. Thurman EM. 1998. Environ Sci Technol 2005.248(2-3):123-133. Reynolds SJ. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. Peter CJ.11(4):353359. Alavanja MC. Barr DB.S. Environ Health Perspect 2000. Gilliom RJ). Coleman S. Sci Total Environ 2000. usgs. Linhart SM. Ward EM.S. Atlanta (GA). Wratten SJ. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models.gov/nawqa/pnsp/pubs/files/051507.108(12):1151-1157.15(6):500-508. World Health Organization (WHO). Available at URL: http://www. Camann DE. Shoemaker DA. Kolpin DW. 2003. 1999. Hladik ML. Sacramento. Burkhardt MR. and metolachlor herbicides in rats. Sanderson WT.24(10):1003-1012. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor.epa. Comparative metabolism of chloroacetamide herbicides and selected metabolites in human and rat liver microsomes. Deddens JA. Casida JE. Available at URL: http://water.int/water_sanitation_health/dwq/chemicals/ metolachlor.39(17):6561-6574.pdf. Pesticides in U. 1992-2001.S. 98-4245 (by Barbash JE. Rose RL. Andrews HF. Striley CA. Chem Res Toxicol 1998.who.

it is not well absorbed through the skin. see Data Analysis section) for Survey years 99-00 and 01-02 are 1. 93-76-5 General Information 2. Mohammad and St. population from the National Health and Nutrition Examination Survey. with the exposure to chlorophenoxy herbicides as defoliants Urinary 2.5-T is eliminated mostly unchanged in the urine.4. 2004).4.S. Although 2. The half-life of 2. myotonia.4. with an elimination half-life of approximately 19 hours (Arnold et al.5-Trichlorophenoxyacetic acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. Survey Geometric mean (95% conf. abdominal pain.5-Trichlorophenoxyacetic Acid CAS No. Once absorbed into the body.. headache. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.3. 2.4. 2.4. 64 Fourth National Report on Human Exposure to Environmental Chemicals .4-D were used as defoliants in the Vietnam War (e.4.1. such as soft tissue sarcoma and non-Hodgkin’s lymphoma.5-T use as a herbicide in 1985. 1992).5-T (Holson et al..4. Teratogenic and developmental effects have been reported in studies of multiple rodent strains treated with high doses of technical grade 2.5-T at low environmental doses or at biomonitored levels from low environmental exposures are unknown.4. Human health effects from 2. < LOD means less than the limit of detection.4.4. Nelson et al. Omer.4. At low levels. hypotension. 2. dizziness. the general population is unlikely to be exposed to it..4. Intentional overdoses and unintentional high dose occupational exposures to chlorophenoxy acid herbicides have resulted in weakness.5-T in soil varies with conditions.Herbicides 2. renal and hepatic injury..4.4. 2007). Epidemiological studies have reported associations of several types of cancer. which may vary for some chemicals by year and by individual sample. 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. Given the commercial unavailability of 2.4. 1986. Kohli et al.5-T degrades to 2.5T is rapidly absorbed via oral and inhalation routes.. but higher levels are herbicidal.. Chlorophenoxy herbicides act as plant growth hormones. these herbicides can enhance plant growth.8-tetrachlorodibenzo-p-dioxin (TCDD) led to the discontinuation of 2. and delayed neuropathy (Bradberry et al. and concern about contamination with 2. 1989.5-T and 2. ranging from several weeks to many months.4.5-T.g. Ester forms of 2.5-trichlorophenol and other degradates. 1974).7.5-Trichlorophenoxyacetic acid (2. nausea. 1992.2 and 0. 2.5-T) is a chlorophenoxy acid herbicide that is no longer registered for use in the United States.5-T has been rarely detected in ground waters (USGS.5-T was once applied as either an aqueous salt or as an oil-soluble ester. Agent Orange).

5-T measured after a day of exposure in a few asymptomatic herbicide applicators were 35.5-Trichlorophenoxyacetic acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. 2003. Pearce and McLean.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. IOM.5-T also were below the limit of detection (Kutz et al.4. Finding a measurable amount of 2. In the NHANES 1999-2000 and 2001-2002 subsamples (CDC. or to contaminants in the herbicide formulations (specifically 2.8-tetrachlorodibenzop-dioxin) (Garabrant and Philbert. 2005. 2.4. 1980).4.gov/pesticides/. It is unclear whether these associations are related to the chlorophenoxy herbicides. Biomonitoring Information Urinary levels of 2.S.5-T were generally below the limit of detection.4. 2004). 1992).S. 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. similar to results of NHANES II (19761980). Biomonitoring studies on 2..4. Fourth National Report on Human Exposure to Environmental Chemicals 65 .4. population from the National Health and Nutrition Examination Survey.EPA at: http://www.5-T itself is not mutagenic. other exposures. 2002. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.5-T does not mean that the level will result in an adverse health effect.3. IARC considers the chlorophenoxyacetic acids group of chemicals as possibly carcinogenic to humans. 2005).000 times higher than the detection limit for the NHANES 2001-2002 data (Kolmodin-Hedman and Erne. Additional information is available from U. Survey Geometric mean (95% conf. U. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. urinary levels of 2.epa.4. Mean urinary levels of 2.5-T reflect recent exposure.4.S. Urinary 2. in which urinary levels of 2.4.5-T than levels found in the general population.EPA.7. 1996. IPCS.Herbicides or contaminated herbicides.

Washington (DC): National Academies Press.31 Suppl 1:1825. Garabrant DH.EPA. Board on Health Promotion and Disease Prevention.5-T).4.edu/catalog.S.S. Third National Report on Human Exposure to Environmental Chemicals.4-D and 2.htm.19(2):298-306.31(2):121-125. LaBorde JB.4-dichlorophenoxyacetic acid (2. Wolff GL. McCallum WF.4. Dichlorophenoxyacetic acid.23(2):65-73. Erne K.5-t mixture. 3/17/09 Institute of Medicine (IOM).Herbicides References Arnold EK. Neurobehav Toxicol Teratol 1986.4. Pesticide industry sales and usage . Absorption and excretion of 2.5-T). Veterans and Agent Orange: update 2002. Centers for Disease Control and Prevention (CDC). Multireplicated dose-response studies in four inbred strains and one outbred stock of mice. Agricultural exposures and non-Hodgkin’s lymphoma.5-trichlorophenoxyacetic acid (2.32(4):233-257.S.37(2):277-91.php?record_id=10603. Poisoning due to chlorophenoxy herbicides.4-D) epidemiology and toxicology. Developmental toxicity of 2. Available at URL: http://www. et al. McLean D. Available at URL: http:// www. Beasley VR. Philbert MA.5-trichlorophenoxy acetic acid in man.5-trichlorophenoxyacetic acid (2.pdf. Crit Rev Toxicol 2002. Gaines TB. Arch Toxicol Suppl 1980. Gaines TB. Atlanta (GA). Holson JF. I.8(5):551-60.4. Holson JF. 3/17/09 Kohli JD.2000 and 2001 market estimates. Fundam Appl Toxicol 1992. Arch Int Pharmacodyn Ther 1974. 2. LaBorde JB. Gupta BN. Washington (DC): U. Pearce N. U. Proudfoot AT. 914. 2005. Behavioral and developmental effects in rats following in utero exposure to 2.org/documents/jmpr/jmpmono/v96pr04. general population. Selected pesticide residues and metabolites in urine from a survey of the U. May.epa. Environmental Protection Agency (U. Murphy RS. Available at URL: http:// www.inchem. II. discussion 5-7. 3/17/09 66 Fourth National Report on Human Exposure to Environmental Chemicals .4:318-21. Pesticides residues in food: 1996 evaluations Part II Toxicology. Multireplicated dose-response studies with technical and analytical grades of 2.5-T in four-way outcross mice. Bradberry SM. et al. The pharmacokinetics of chlorinated phenoxy acid herbicides: a literature. Vale JA.4-. Carter-Pokras OD. 2004. Fundam Appl Toxicol 1992. Committee to Review the Health Effects in Vietnam Veterans of Exposure to Herbicides (Fourth Biennial Update. Khanna RN. Sheehan DM.nap. J Toxicol Environ Health 1992. Office of Prevention Pesticides and Toxic Substances. Estimation of occupational exposure to phenoxy acids (2.EPA). Mohammad FK. Sircar KP.4. Dhar MM. gov/oppbead1/pestsales/01pestsales/market_estimates2001. Nelson CJ. Kolmodin-Hedman B. Tandon JS.4. Toxicol Rev 2004.4.5-T). Brody D. 210:250-255. St Omer VE. Review of 2. Vet Hum Toxicol 1989.19(2):286-297. Kutz FW. International Programme on Chemical Safety-INCHEM (IPCS). Cook BT. Developmental toxicity of 2. 2003. Gaylor DW.4.4-D/2. S. Scand J Work Environ Health 2005. Nelson CJ.

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

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

In a study of pesticide applicators with occupational exposure to aldrin.atsdr.S. similar to results in a subsample of NHANES II (19761980) (Stehr-Green. 2005. Li et al. Biomonitoring Information In the NHANES 2001-2002 and 2003-2004 subsamples. and the FDA monitors foods for pesticide residues. Survey Geometric mean (95% conf. Levels of aldrin also were not detectable in 1996-1997 pooled samples from New Zealand adults (Bates et al. IARC has determined that aldrin and dieldrin are not classifiable with regard to human carcinogenicity. 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.. 2004). 2004)... 2005). vomiting.gov/toxpro2. Kanthasamy et al. dieldrin at higher doses caused irritability. 1995). OSHA has established workplace exposure standards for aldrin and dieldrin.6% of the subsample had dieldrin levels above the limit of detection (Stehr-Green 1989). population from the National Health and Nutrition Examination Survey. 78 Fourth National Report on Human Exposure to Environmental Chemicals . nausea.. 2000). seizures (Smith. the median serum dieldrin level was generally similar to the 90th percentile for females in this Report (Ward et al.. The U.html. 1991). 1989). 1998). tremors. 1998) and behavioral changes (Carlson and Rosellini. the offspring had altered CNS neurotransmitter levels (Sanchez-Ramos et al. The median level in pooled samples from New Zealand adults obtained in 1996-1997 was generally similar to the 90th percentile for adults in this Report (Bates et al. 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)..Organochlorine Pesticides twitching.S.e. Epidemiologic and animal studies have not conclusively associated dieldrin exposure with risk for developing Parkinson’s disease (Corrigan et al. 2000. EPA has established environmental standards for aldrin and dieldrin. environmental levels) and health effects is available from ATSDR at: http://www. Studies done in vitro showed that dieldrin binds to estrogen receptors (Soto et al. in which only 10.. Information about external exposure (i.. which may vary for some chemicals by year and by individual sample. 2000). 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. 1987). and occasionally.. serum aldrin levels were below the limit of detection. and seizures. 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. both aldrin and dieldrin caused liver enlargement and liver tumors... In samples obtained between 1973 and 1991 from Norwegian women.cdc. When dieldrin was fed to pregnant rodents. When fed to experimental animals. but no estrogenic effect was noted in a study that used cultured cells (Tully et al. * 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 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * * 50th < LOD < LOD 75th < LOD .0 (10.2) 15.1 (18.098 (.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.120-.8) 15.110 (.8-19.40-9.109-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.139 (.075) < LOD .060) .50 (8.100-.090-.4-18.8-17.1-18.069) < LOD < LOD .070 (<LOD-.140-.8-25.3 (18.7 (15.130) .1) 13.150 (.4) 95th 20.054-.190) .6) 16.4) 20.083-.8-17.6-33.80-10.055 (.140) .70 (7.4) 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 8.160 (.8) 14.30 (8.130 (.110-.130) .4-17.1-24.054-.080) .080 (.9 (12.150 (.077 (.090-.080-.048 (<LOD-.9 (13. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.0) < LOD 9.086-.4) 539 456 484 487 980 885 Limits of detection (LOD.242) .084-.110) .9-38.103 (.1-19.090-. which may vary for some chemicals by year and by individual sample.1) 20.089 (.2) 11.0-21.8 (9.3 (14.130-.5 and 7.100-.1) 15.30 (8.6-24.1) 15. population from the National Health and Nutrition Examination Survey.7) 716 587 1443 1365 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD 9.077-.058) < LOD .5) 21.190) .1-16.130-.5-15.4 (12.116) .8 (18.180) .063-.158) .8 (11.0) 19.10 (<LOD-16.056-.90) 90th 15.064 (. Fourth National Report on Human Exposure to Environmental Chemicals 79 .049-.138 (.147 (.6) 19.149) .103 (.130) .109-.7-22.40-10.9 (13.2) 12.2-15.1 (13.50) 15.4) 19.3 (13. Survey years 01-02 03-04 Geometric mean (95% conf.096-.090 (.1) < LOD 9.8-24.9-23.4) < LOD < LOD 16.093) .5 (<LOD-11.7 (<LOD-15.S.5 (16.064) 90th .7 (14.124) .110 (.9-22.108-.8) < LOD 8.9 (14.6 (14.113 (.2) Sample size 2159 1952 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD 10.1) 10.170) . 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 9.054-. 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.120) .112-.5-17.070) .062 (.80 (<LOD-10.80-9.S.4) 21.117) < LOD .160 (.100-.070-.120 (. which may vary for some chemicals by year and by individual sample.109 (.9 (12.112) 95th .110 (.0-25.090 (<LOD-.4) 14.8.182) 716 587 1443 1365 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD .00-14.7-19.073-.6) 9.6 (15.180) .0 (11.139 (.2) 14.053 (<LOD-.100) .3 (19.6 (15. see Data Analysis section) for survey years 01-02 and 03-04 are 10.5) 19.062 (.160) .177) Sample size 2159 1952 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD . < LOD means less than the limit of detection.110) .100) .7) 15.3 (18.0 (15.3-21.101) .062-.130-.1) 14.102 (.4 (12.088-.120 (.6-24.60-10.202) 539 456 484 487 980 885 < LOD means less than the limit of detection for the lipid adjusted serum level. Survey years 01-02 03-04 Geometric mean (95% conf.5) 15.059 (.0 (10.0) 21.140 (.138) . population from the National Health and Nutrition Examination Survey.120 (.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 .5-17.100 (.00 (8.

2 Classes of Pesticides. David VL.htm.org/documents/ehc/ ehc/ehc91. Garrett N. Shore RF. and lymphocyte sister chromatid exchange.Organochlorine Pesticides in the NHANES 2001-2002 and 2003-2004 subsamples (Edwards and Priestly 1994). Dieldrin-induced neurotoxicity: relevance to Parkinson’s disease pathogenesis.27:405-421. 1991. Buckland SJ.html. pp. The E-SCREEN assay as a tool to identify estrogens: an update on estrogenic environmental pollutants. Jorgensen T. Narahashi T. Andersen A. Sonnenschein C.fda. Lancet 1998.gov/toxprofiles/ tp1. New York. Aldrin and dieldrin: A review of research on their production environmental deposition and fate. 1989. Inc. Basit A.54:1431-1443.66(4):229-234.109(Supp1):113-139.150:263-271. August 2008. Stehr-Green. Olea N. Effect of occupational exposure to aldrin on urinary D-glucaric acid. Pesticides in the Nation’s Stream and Ground Water. Mann D. Exposure to low doses of the environmental chemical dieldrin causes behavioral deficits in animals prevented from coping with stress. Cancer Epidemiol Biomarkers Prev 2000. Schulte P. VT. Serrano FO. Priestly BG. Edwards JW. 731-915. Mink PJ. Kanthasamy A. Roy ML. Smith AG. Chapin RE. Environ Health Perspect 2001.html. Finley B. Li AA. Available at URL: http://www.14:95-102. J Toxicol Environ Health. 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. bioaccumulation. Ginsburg KS. 4/21/09 Bates MN. Rosellini RA. 2007 [online]. Kanthasamy AG. Int Arch Occup Environ Health 1994. Facca A. Song S. Available at URL: http://pubs. Environmental Health Criteria 91. Kitzazwa M. In Hayes WJ. Environ Health Perspect 1995. Toxicological profile for aldrin/dieldrin [online]. Carlson JN.cdc. 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. 6/1/09 Ward EM. Neurotoxicol 2005. September 2002. Chung KL. PA. Toxicity of dieldrin for dopaminergic neurons in mesencephalic cultures. toxicology. Patterson DG Jr. Evaluation of epidemiologic and animal data associating pesticides with Parkinson’s disease. Fernandez MG. Corrigan FM. No:429-436. 15. Demographic and seasonal influences on human serum pesticide residue levels.352:1816-1820.103(Suppl 7):113-122. Anantharam V. et al. Serum organochlorine levels and breast cancer: a nested case-control study of Norwegian women.64-65 Spec.59:229-234. Chemosphere 2004. Handbook of Pesticide Toxicology. Sodium and GABA-activated channels as the targets of pyrethroids and cyclodienes. International Programme on Chemical Safety (IPCS). Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. J Occup Environ Med 2005. Teta MJ. McIntosh LJ.47:1059-1087. Patterson DG Jr. Toxicol Lett 1992. plasma dieldrin. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. 4/21/09 Hoyer AP. either singly or in combination.gov/ circ/2005/1291/. 80 Fourth National Report on Human Exposure to Environmental Chemicals . Part A 2000.usgs. Hartvig HB. 1992-2001. Mumtaz MM. J Toxicol Environ Health 1989. Eds. et al. Food and Drug Administration (FDA). Wienburg CL. Needham LL.26:701-719. Reprod Toxicol 2000. Psychopharmacology (Berl) 1987. Grajewski B. Daniel SE. Soto AM. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Available at URL: http://www. Turner W. are nonestrogenic in transfected HeLa cells. Brock JW. Jr. and epidemiology in the United States. Organochlorine exposure and risk of breast cancer. Chlorinated Hydrocarbon Insecticides.9:1357-1367. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population.atsdr. Organochlorine insecticides in substantia nigra in Parkinson’s disease. Exp Neurol 1998.inchem. United States Geological Survey (USGS). Tully DB.cfsan. Jr and Laws ER. Available at URL: http://www. 4/21/09 Jorgenson JL. Aldrin and Dieldrin [online].91(1):122-126. Six high-priority organochlorine pesticides. Frey JM. Cox. Academic Press. Ellis H. Grandjean P.gov/~dms/ pesrpts. Revised Feb. Sanchez-Ramos J. References Agency for Toxic Substances and Disease Registry (ATSDR). Vol.

2) 22.4-40.8) 27. see Data Analysis section) for Survey years 99-00.9) 37.0) 21.7 (43.9 (17.69-10.9 (21.9) 11.5) 37.2 (39.9 (11.6) 8.3-24.7 (34.10-11.4 (22.8-61.4) 29.3-43.6-45.3 (20.5-65.9 (26.1 (17.0) 41.89-10. interval) Selected percentiles ( 95% confidence interval) Sample 95th 44.1 (<LOD-12.9) 23.1 (16. Chlordane is not currently produced or used in the U.2) 34.6-53.4) 37.9) 31.1) < LOD < LOD < LOD < LOD < LOD 8.7-14.7 (42.9) 47.8 (17.2) 46.1 (44.9) 11. and 7.0) 20.4) 12. buildings.6 (16. which may vary for some chemicals by year and by individual sample.2) * 12.8-23.7-12.Organochlorine Pesticides Chlordane CAS No.8) 53.8) 663 752 595 998 1497 1383 20 years and older Gender Males 99-00 01-02 03-04 * 11. 57-74-9 Heptachlor CAS No.2-56.7-56.5 (31.2-21.3) 18.9-21.2) < LOD 11.3-45.7 (10.0 (26.4) 18.3) 41.9 (11.7-39.S.1) * 11.74 (<LOD-10. population from the National Health and Nutrition Examination Survey.7) 42.8-20.6) 23.9-38. Heptachlor was used as a soil and seed treatment and for termite control in and around buildings until 1988.30-11. 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.9) 23.0 (16.5 (34.0 (<LOD-12.9 (18. As a result of the manufacturing process.8-33.9) 39.0-25.3 (27.5-13.5) 10.0-61.0-67.5-47.7) 19.3) 10.0-13.6) 9.1 (15.0-18.6) 36. 2007).1) 30.0-12.3 (25.7-25.9) 36.1-19.8-31.5) 628 557 462 350 501 493 559 1031 898 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.4 (10.20-10.9 (36. foods high in fat such as meat.1) * 11.9-21.1 (40.3 (<LOD-19. Heptachlor and chlordane are somewhat volatile and may be detected in the air and dust of buildings long after treatment for termite or insect control (Whitemore et al.5) < LOD < LOD 9.4 (30.1) 30.90 (8.36-11.9 (26.4-21. Heptachlor and chlordane and their metabolites bioaccumulate in fatty animal tissues.5) 44.1) 22.8) 18.0) 27.6 (9.8-33.2-26.7) 19.3-45. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.20-11. Technical grade chlordane had contained 7% trans-nonachlor.2 (9.6) 39.. 1994).10 (8.4) < LOD < LOD < LOD 23. 10.1 (<LOD-12.5-41.2 (28.7 (<LOD-32.3 (11.1 (20.8) 52.1-15. chlordane was used to kill termites and other insects on agricultural crops.2) < LOD 11.4 (35.5) 38.7) 9.9-40. 1994.4 (<LOD-12.8-32.6-24.3) 10.2 (37.9 (29.6) 48.2) 33.1-65.8) size 1661 2249 1978 Total years 99-00 01-02 03-04 50th < LOD 11.70 (<LOD-10.1 (11. the technical grade product of each chemical contains 10%-20% of the other chemical.3 (9.6 (9.9 (31.4-45.1-50.63 (8. Both of these chemicals and their metabolites can cross the placenta and are excreted into breast milk.8-42.4 (31.3 (26.4) < LOD 11.6-18.1 (27.1-25.8 (18.S.5-42.6 (25.9 (15.8. 76-44-8 General Information Chlordane and heptachlor are structurally related organochlorine pesticides and were used in the U.7 (19. Until 1988.5-43.S.5.2 (36.0) 75th 20. Since 1992. 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.3) 18.4-14.1-25.8-73.8 (10.7-70. and in soil.2-49. Survey Geometric mean (95% conf.5-38. heptachlor use has been limited to treatment of fire ants near power transformers.7 (17.5) 56.3 (28.0 (20.37 (8.1) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * 12.3 (21. 01-02.8 (40.6) 48. Fourth National Report on Human Exposure to Environmental Chemicals 81 .5) 9. in addition to trace amounts of numerous other related compounds (ATSDR.8 (17.3-32.8 (42.6) < LOD 11.8) 52.8-43.1 (25.5-40.5.5-32.6) 20.9) 17.1) 90th 34.0-33.5 (8.3) 37.9-42.1 (<LOD-12.7 (<LOD-13. lawns.0 (37. Consequently. and 03-04 are 14.2 (41.6) 11.2 (21.1) 16.82-11.4) 39.1-51.6-24.9) 13.5 (33.6) 9.7) 28.9 (15.6) 49. fish.2) 36. < LOD means less than the limit of detection. and dairy products are the usual sources of exposure to these chemicals in the general population.3-49.7) 31.9) 10. respectively.4-51.5-44.5) 21.5 (41.7 (34.5) 793 1049 963 868 1200 1015 Females 99-00 01-02 03-04 Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * 11.8 (10.8) 44.4 (30.4) 22.5) < LOD < LOD < LOD < LOD 13. from the early 1950’s until the mid-1980’s.7) 35. 2007).7 (32.0 (32.0) 31.20 (<LOD-11.2-49.2) 37.2-28.2 (10.10-18.6-12.0) 37.5 (<LOD-12.6 (43.

OSHA has established occupational exposure criteria.370 (. The major metabolite of heptachlor is heptachlor epoxide.076) < LOD .270 (.330 (.077) .070-.300-.056 (.240 (.053-.160) .287) .310-. 1977a.070) .230) .106-.064) < LOD . interval) Selected percentiles ( 95% confidence interval) Sample 95th .291) size 1661 2249 1978 Total years 99-00 01-02 03-04 50th < LOD .140 (.140-.560) .100 (.110 (<LOD-.260 (.230 (.210 (.091) .120 (. and NIOSH and ACGIH have recommended workplace exposure levels for each pesticide.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.240) .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 * * * * .220-.092) .290) .071 (.070 (<LOD-. dermal.050-.090-. IARC considers chlordane and heptachlor as possibly carcinogenic to humans.130-.115 (. No clear evidence of excessive cancer rates was demonstrated in human epidemiologic studies (ATSDR. 2006). Smith.300) .069 (<LOD-.148) .370 (.100-. Chlordane is metabolized primarily to oxychlordane and to a lesser extent.430) .270 (.189 (.350 (.087-.149 (.070 (<LOD-. and breast milk is a major excretion route in lactating women.400) .310) .207 (.066 (<LOD-.190-.128 (.060 (<LOD-. Le Marchand et al. 1991. which is also persistent in the body (ATSDR.170) .350) .079) < LOD < LOD < LOD .225 (.073) < LOD < LOD < LOD < LOD .213) * .258-.180-.130 (.119 (.140 (.066 (.170) .083) .210 (. and inhalation exposure.227) < LOD .063) .065-. Chlordane and heptachlor are absorbed after oral.083 (.066-.063 (.160 (.310) .Organochlorine Pesticides (Dallaire et al.077) .230-.280-.180) .410) .062) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * . neonatal mortality.290) .302) .063 (. characterized by seizures and paralysis.170-. 1981). which may vary for some chemicals by year and by individual sample.290 (.130-.063 (.115-. high doses of either chlordane or heptachlor block inhibitory neurotransmitters and result in central nervous system toxicity. EPA has established environmental criteria for chlordane and heptachlor.348) .253-..320 (. chronic doses of heptachlor have produced liver enlargement and injury.130) .061-. 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.053-.048-.320) .280-. population from the National Health and Nutrition Examination Survey.S.246-.270 (.180) .110-.130 (.070) < LOD < LOD < LOD < LOD < LOD .258 (.290-.200-.100 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.150 (.200-.300) .300) .300 (.057) * .320) .165-.062) < LOD .150 (.070-. Takahashi et al.286 (. 2007.203-.104-.108-.136) .120-.320 (.077) .340) .080 (.440) .130) .310 (.271 (..340) .280 (. Survey Geometric mean (95% conf.230 (.120-.370 (. Shindell and Ulrich. 2001.070 (<LOD-.315 (.080) . to heptachlor.140) . and heptachlor epoxide in foods and bottled water.063 (..204 (.080 (.140-.049 (<LOD-.350 (. 1991).080) .231) .280 (.150-.260-.130-.180-. The U.220 (.320) 663 752 595 998 1497 1383 20 years and older Gender Males 99-00 01-02 03-04 * .066-. Elimination of all these chemicals from the body occurs over months to years.250 (.400) .100-.090) .250-.112 (.286 (.240-.320 (.073 (.130-.310) .160) .216-.057 (.450) . 2002.200 (. 1977b.260 (. both chlordane and heptachlor induced hepatic cytochrome P450 enzymes and increased the incidence of liver tumors (NTP. In laboratory animal studies. and the U.170) .058 (.208 (.075 (.430) .320 (.140 (.220-.240-.055-.200-.290-.130-.120-.070 (.450) .S.130 (.230-.070 (<LOD-.057-..290-.080) . Acute.207) .063-.280) .280-.082 (.074-.058-.104) .199-.190-.063) * .047 (<LOD-. Rogan.360) .269 (.058-.242-. heptachlor. Human health effects from either chlordane or heptachlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown.148-.168-.170) .245-.068) .146) < LOD < LOD .090) . 1996.126 (.300) .133) 90th .050 (<LOD-.230-.068-.146) .189-. Chronic feeding studies with either chlordane or heptachlor have demonstrated reduced fertility.223) .070-. 1986).S.170) .079) . FDA established allowable residues of chlordane.380) .068) 75th . 2007).150) .140 (.150 (.067 (.510) .160) .190-.210-. 82 Fourth National Report on Human Exposure to Environmental Chemicals . IARC. 1986).250 (.126) .373) .077) .260 (. Subtle neurodevelopmental effects have been observed rodents after prenatal exposure to heptachlor (IPCS. and alterations in immune function of offspring.

2002). respectively.gov/toxpro2. transnonachlor. respectively.cdc.html. or heptachlor epoxide in serum does not mean that the level of oxychlordane. 1993). Biomonitoring Information Serum oxychlordane and trans-nonachlor levels in NHANES 1999-2000. resulting in human exposure to heptachlor epoxide that was excreted into the milk. than the 90th percentile values of NHANES 1999-2000 (Baker.. Biomonitoring data can also help Fourth National Report on Human Exposure to Environmental Chemicals 83 .atsdr. environmental levels) and scientists plan and conduct research on exposure and health health effects of chlordane and heptachlor is available effects. than the 90th percentile values of NHANES 1999-2000 (Stehr-Green et al. Two episodes (one each in Arkansas and Hawaii) of inadvertent heptachlor contamination of dairy cattle feed occurred in the early-to-mid 1980’s. from ATSDR at: http://www.htm#ref. Finding a measurable amount of oxychlordane. mean serum heptachlor epoxide and oxychlordane levels were about sevenfold and threefold higher. In the Hawaii episode. trans-nonachlor.Organochlorine Pesticides about external exposure (i. 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.. Biomonitoring studies on levels of oxychlordane. In serum samples obtained in between 1994 and1997 from Inuit women in different Arctic countries. 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. 2000).. the mean serum heptachlor epoxide and oxychlordane levels were more than twice as high.. For the exposed persons drinking milk in the Arkansas episode..org/documents/cicads/cicads/cicad70. A recent assessment of heptachlor is available at: http://www. 1988). 2001-2002. and 2003-2004 subsamples were comparable to levels measured in Swedish women from 1996-1997 (Glynn et al. Levels of heptachlor epoxide among females in this Report were approximately one tenth of the corresponding 90th percentile for a cohort of pregnant women in California studied from 1963 to 1967 (James et al. 2003).e. transnonachlor. Serum transnonachlor levels among females in the NHANES 19992001 subsample were about one half the levels obtained between 1994 and 1996 from women in New York (Wolff et al. 2006).. 2004). inchem. 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 causes an adverse health effect..

8) 14.6-17.1) 23.1) 13.8-24.5) 19.5) 598 553 460 336 503 490 539 1041 888 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. 10.0 (15. Survey Geometric mean (95% conf.6 (13.6 (<LOD-27. see Data Analysis section) for Survey years 99-00.8) 13.3) 18.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. < LOD means less than the limit of detection.1 (19.9-23.7-19.S.3) 23.8-23.4 (11.0) 13.7-25.5 (<LOD-21.9 (15.8 (18.2) 13.2-16.5 (18.5 (11.0 (11.6-21.5 (11.3) 10.9-29.6 (14.0) size 1589 2259 1963 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th 90th 15.8 (18. which may vary for some chemicals by year and by individual sample.7 (13.2 (18.0-19.20 (<LOD-9.5 (<LOD-32.2-27.3) 16.0-17.7-18.2 (<LOD-25.6 (16.9) * * * Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 8.6) 14.5) < LOD 14.6 (16.6) < LOD < LOD < LOD 27.9 (12.6. population from the National Health and Nutrition Examination Survey.8) 21.4) 21. respectively. interval) Selected percentiles ( 95% confidence interval) Sample 95th 24.8) 19.0-54. and 7.6 (11.5.9) 15.4 (<LOD-54.4 (15.8. and 03-04 are 14.5) 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 7.2-27.1-38.1-16.6 (12.90 (<LOD-9.3) 27.5 (10.1) 20.8-24.8) 16.8 (13.6) 22.1-15.2) 20.3 (<LOD-25.1-29.2) 15.8) 14.4) 18.3 (13.8-46.2-17.8) 19.8 (13. 84 Fourth National Report on Human Exposure to Environmental Chemicals .0-16.8 (15.3-18.4 (11.50) < LOD < LOD < LOD 17.7 (10.10-13.8-24.4 (<LOD-19.9-29.2 (<LOD-62.6 (8. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.7 (16.8) 15. 01-02.2) 26.8 (<LOD-23.6) 13.3) 22.3) 18.40) 15.9-25.0-17.0) 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 13.3) 18.2 (<LOD-16.8) 13.9-16.8) 20.1 (16.

108-.106-.090-.200) .090-.170 (.120-.180 (.170) .057 (<LOD-.111-.110 (.074-.090 (<LOD-.150 (.116) < LOD < LOD < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.097) < LOD .110 (.200) .130) .190 (.053-.220) .100 (<LOD-.S.130) .110 (<LOD-.110) .149) .087 (.170 (.180) .180) .126 (.090-.120 (.130-.070-.310) .069 (.067-.101 (.120) .190) .130-.111) .170) .063) < LOD < LOD < LOD .173) 638 741 592 951 1518 1371 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .120 (<LOD-.110-.055 (<LOD-.104) .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.090 (.100 (.180 (<LOD-.120) .150 (.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.157) .170) .180) .110 (<LOD-.077-.170 (.110-.130 (.110) .380) .140-. which may vary for some chemicals by year and by individual sample.071-.108) .310) .077-.270) .150 (<LOD-.113-.100 (.108) * * * Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .135 (.135 (.133 (. Fourth National Report on Human Exposure to Environmental Chemicals 85 .096 (.090-.094 (.100 (.130 (<LOD-.180) .140) . interval) Selected percentiles ( 95% confidence interval) Sample 95th .063) .161) size 1589 2259 1963 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th 90th .190) .098 (.107-.140) . Survey Geometric mean (95% conf.240) .130-.094 (.120 (<LOD-.076-.100-.100 (.130-.100-.117) .200 (.128 (.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 .170 (<LOD-.082-.190) . population from the National Health and Nutrition Examination Survey.101 (.113) .090-.090-.

1) 62.0-20.6 (<LOD-14.3-50.3) 16.3) 25.2 (26.8-19.1) 18.3 (58.4 (67.1) 17.9) < LOD < LOD < LOD 20.5) 48.8 (13.9-40.8) 80.6) 84.3) 15.9) 14.5-36.3) 30.1) 17.1) 17.1) 31.0 (19.4) 59.6 (57.6) 56.0 (16.6 (12.2) 39.2 (64.4-67. see Data Analysis section) for Survey years 99-00.6 (16.7) 78.9 (51. 86 Fourth National Report on Human Exposure to Environmental Chemicals .7 (28.7-35.1-20.3 (17.1) 17.0-123) 74.1 (22.0 (13.0) 49.8 (30.3 (49.6 (52.8 (71.5-20.3-86.2 (15.2 (14.4-36.1) 17.5-69.8-41.4) 19.7-113) 68.S.6) 54.2 (36.0) 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. < LOD means less than the limit of detection.5-111) 68.3) 36.0 (42.4) 107 (84.3-32.3) 18.0-113) 68.2-18.5 (13.8 (28.9 (66.1-34.2 (25.4 (28.1) 17.7) 73.2 (60.1-16.8 (42.2-37.3 (14.8-79.9-65. interval) 18.7-22.3-58.1) 17.0-143) 112 (68.4) 55.9) 14.1 (41.4-35.0 (42.4) 20.9) 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) 13.6-22.0-23.1-34.0-24.5) 22.9-65.4 (30.0) Selected percentiles ( 95% confidence interval) Sample 95th 79.3) 18.3 (56.0 (29.6) 56.86-13.2 (19.8-16.8 (15.8 (17.0) 18.5-17.5) 35.4-62.7-160) 86.7) 17.8) 51.5) 14.1 (65.5-95.5) 9.6) 82.9 (<LOD-14.0-93.1) 16.0 (15.5) 14.4-22.7) 14.8 (26.1 (47.2) 34.8 (11.6 (32.70 (<LOD-12.5-87.6) 25.9-89.8 (49.1) 14.3) size 1933 2286 1955 Total years 99-00 01-02 03-04 50th 17.0-23.9 (15.Organochlorine Pesticides Serum trans-Nonachlor (lipid adjusted) Metabolite of Chlordane Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U.7 (30.7-32.9-20.5) 78.7-77.7 (59. respectively.0 (13.3-39.3) 32.2-18.4-52.10 (<LOD-11.6-20.5) 30.3-57.2-23.2) 19.4) 16.7) 35.7) 59.1 (17.0 (60.4 (45.8 (19.8-67.3-74.2 (59.9-35.7) 28.8 (45.6) 34.5-19.0) 19.7-18.0) 40.8-77.4-23.6-66.2-16. and 03-04 are 14.6-19.3-30.0-59. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.2-17.1) 78.5) 20.9-22.7 (59.2 (7.2 (14.1-55.1-18.0-68. Survey Geometric mean (95% conf.0-22.7) 15.6-88.8 (28.3 (16.3 (45.5 (15.6 (50.6 (56.7-17.8-21.9-58.0 (14.7 (18.5.7-20.7) 78.8.0 (48.0 (62.2) 20.9 (29.6) 60.9) 51.9-69.8 (13.8 (26.6) 10.8 (<LOD-20.8 (12.2-21.0) 75th 31.4) 48.9-36.1) 18.0) 33.8-129) 74.2) 17.7-21.3) 32.2-88.6 (56.5) 36.1) 30.1) 32.4-18.7 (35.9 (47.8-19.5) 19.8 (16.5) 26.2 (27.9) 51.8 (26.1-22.8 (28.7) 52.5 (15.8-16.1-51.0-93.8-90.4 (16.1 (10.2) 30.1-126) 67.0 (16.5.9 (16.2) < LOD 10.7-38.7 (16.7-23.5 (44.8-90.8-110) 59. 10.7 (74.1 (48. and 7.3) 19.7-29.5) 90th 55.8) 19.9 (28. 01-02.4 (11.6-82.0) 13.0-37.4 (12.7 (13.3) 30.5 (45.9-64.9 (19.2) 59.3 (14.7-34.6 (15.3-21.9 (51.8) 47.3) 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.0) < LOD < LOD 8. which may vary for some chemicals by year and by individual sample.5) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * 20.1-28.0 (15.0-38.7 (11.9 (36.5 (25.1) 78. population from the National Health and Nutrition Examination Survey.9-45.5) 77.6-54.1-16.7) 56.9 (15.

242) .129) .081-.161-.091-.440) .600 (.080-.630) .590 (.180-.100-.350-.108 (.116 (.330 (.079-.111-.096-.135 (.640 (.220 (.055 (<LOD-.100 (.360-.125) .060 (<LOD-.390) .080-.090 (.103 (.090-.350 (.160 (.108) .240 (.290-.400) .205 (.237) .100-.684) .400-.190-.840) .510-.071 (<LOD-.095-.110 (.630) .125 (.440-.122) .113) .127) < LOD < LOD .330-.110-.141) .080-.186-.119) < LOD < LOD < LOD .510 (.630) .540) .270-.565) .300) .417 (.134) .460) .130 (.288 (.250) .068-.130) .430-.062 (.080) .099-.190-.230 (.310-.580 (.340-.110 (.120-.S.130) .130 (.232) .320-.480) .100) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * .130) .310-.390-.240) .285-.680) .490 (.090-.130) .080-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.108) 75th .098 (.110 (.580 (.380 (.830) .272-.114) .122) . population from the National Health and Nutrition Examination Survey.220 (.234) .126) .470 (.098-.120-.590) .330-.047-.559) .210 (.173-.150) .089 (.110 (.116) .310-.120) .20) .120) .651) .150) .160-.090-.240) .930) .210-.400 (.590 (.190-.092 (.580 (.558) size 1933 2286 1955 Total years 99-00 01-02 03-04 50th .220 (.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.099-.100 (.360-.260) .041 (<LOD-.085-.371) .093-.301-.090-.112 (.367) .327 (.106 (.120 (.211) 90th .100-.120 (.080 (.060-.461 (.220 (.310-.117) .100-.300-.093-.186 (.210 (.960) .130) .409-.120) . Survey Geometric mean (95% conf.279-.180-.158-.343 (.690) .090-.161) .470-.310) .800) .210 (.395-.240) .145-.124) .317 (.120) .070 (.110 (.096-.130) .106 (.069) .594) .220 (.430-.340-.286-.600) .220) .060) .096) .110) . Fourth National Report on Human Exposure to Environmental Chemicals 87 .260) .098 (.490 (. which may vary for some chemicals by year and by individual sample.104 (.410-1.183 (.119) Selected percentiles ( 95% confidence interval) Sample 95th .340) .288-.690) .460) .320-.078-.130) .414 (.079-.420 (.400-.109 (.140) .520 (.240-.355 (.237) .430-.190-.210) .120 (.120-.105 (.078 (.090) .497-.220 (.106 (.081 (.310 (.520) .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 .113) < LOD . interval) .111 (.097) .250) .830) .520 (.103 (.177-.131) .470 (.210) .397-.390 (.390 (.210) .370 (.054-.110 (.390 (.180-.091) .405) .128 (.390 (.190-.061-.191 (.490-.390) .324 (.680 (.069-.084-.220 (.470-.082) .573 (.220 (.190-.760 (.093) .565) 922 1062 955 1011 1224 1000 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 * .470 (.116-.090-.400 (.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.085-.410-.104-.092 (.170 (.280) .460-.171-.085-.202 (.458 (.112 (.141) .093-.490) .420) .087 (.450) .210-.094 (.098) .109 (.550 (.500) .370 (.090 (<LOD-.250) .395) .

niehs. An evaluation of serum pesticide residue levels and liver function in persons exposed to dairy products contaminated with heptachlor. Inc. Toxicological profile for chlordane [online]. National Toxicology Program (NTP). 2001. Head SL. Arch Environ Health.nih. Loo S. J Occup Med 1986. Organochlorine exposures and breast cancer risk in New York City women.atsdr. Bjerselius R. Muckle G. New York. Aune M. Chashchin V. Handbook of Pesticide Toxicology. Hertz-Picciotto I. Distribution of polychlorinated biphenyls.330:55-70.84:151-161. Lawrence River (Quebec. A Report to the Hawaii Heptachlor Research and Education Foundation.28:497501. August 2007. Willman E. Available at URL: http://www. Kolonel LN.htm. Available at URL: http://www. Hansen JC.cdc. Stehr-Green P. Hawaii Med J 1991.cdc.inchem.gov/ntp/ htdocs/LT_rpts/tr008. 6/1/09 National Toxicology Program (NTP).50(3):108-118.gov/toxprofiles/tp31. Wolff MS. et al. Sci Tot Environ 2006. Keller JA. Dendle WH. 1963-1967. Dewailly E. Available at URL: http://www.htm. May 1994. Organochlorines in Swedish women: determinants of serum concentrations. Covaci A. Jr and Laws ER.org/ documents/cicads/cicads/cicad70. 1991 pp. Darnerud PO. Environ Res 2000.org/documents/iarc/ vol79/79-12.150:981-990. Available at URL: http://www. Chlorinated Hydrocarbon Insecticides. Lulek J.niehs. Voorspoels S. Takahashi W. Canada). Ayotte P. Evaluation of human exposure to the heptachlor epoxide contamination of milk in Hawaii. Academic Press. Wohlleb JC. Berkowitz GS. Environ Health Perspect 2002. Temporal trends of organochlorine concentrations in umbilical cord blood of newborns from the lower north shore of the St. Wong L. Siegel BZ. 79.372:20-31. Sci Total Environ 2004. Available at URL: http://www. Laliberte C. Concise International Chemical Assessment Document 70 Heptachlor [online].heptachlor. KalubaSkotarczak A. Organochloride pesticide residues in human milk in Hawaii. In Hayes WJ.8:1-123. Chlordane and heptachlor [online].9:1-109. Estimation of Human Exposure to Heptachlor Epoxide and Related Pesticides in Hawaii. 4/21/09 Baker DB. Bleiweiss IJ. Jaraczewska K. Granath F.Summaries & Evaluations. Bioassay of heptachlor for possible carcinogenicity. maternal serum and milk from Wielkopolska region.111:349355. Barker J.atsdr. Smith AG. 88 Fourth National Report on Human Exposure to Environmental Chemicals . Baker DB. Charles MJ.html. Pollutants in breast milk. 1994-1997 organochlorine compounds. Odland JO.pdf.110:617-624. 1993. 731-915. Natl Cancer Inst Carcinog Tech Rep Ser 1977a.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Takei G. et al.html. Trends in birth defects for a Hawaiian population exposed to heptachlor and for the United States.inchem.41:145–148. Glynn AW. gov/toxprofiles/tp12. Brower S. 6/1/09 Rogan WJ. 4/21/09 Dallaire F.110(8):835-838. Jr. Senie R. Environ Health Perspect 2002. Tartter P. Bull Environ Contam Toxicol 1981:27:506-511. 2006. organochlorine pesticides and polybrominated diphenyl ethers in human umbilical cord serum. 1979-1980. Atuma S. Toxicological profile for heptachlor and heptachlor epoxide [online]. Vol. 1986. Shindell S and Ulrich S. Vol.html. 9/25/07 International Programme in Chemical Safety (IPCS). et al. International Agency for Research on Cancer (IARC).259(3):374-377. Available at URL: http://ntp. Environ Health Perspect 2003. Mortality of workers employed in the manufacture of chlordane: an update.org/site/foundation/ research/projects2. 4/21/09 James RA. Dewailly E. Van Oostdam JC. International Agency for Research on Cancer (IARC) . Saidein D. JAMA 1988. Determinants of serum polychlorinated biphenyls and organochlorine pesticides measured in women from the child health and development study cohort. Available at URL: http://ntp. Circumpolar maternal blood contaminant survey.gov/ntp/ htdocs/LT_rpts/tr009. Eds. Poland. Drews K. 4/21/09 Agency for Toxic Substances and Disease Registry (ATSDR). Gilman A. Bioassay of chlordane for possible carcinogenicity. et al.pdf.nih. 2 Classes of Pesticides. Natl Cancer Inst Carcinog Tech Rep Ser 1977b. LeMarchand L. Arch Pediatr Adolesc Med 1996. Royce W.

8) 36. These chemicals are highly persistent in soil.0 (18. Food imported from countries that still use DDT may contain the chemical or its residues.6 (9.p’-DDD (4% or less).S.6 (<LOD-25. particularly meat.9) < LOD < LOD 9.9 (10. inhalation.7-16.1-71.p’-DDT (65%-80%). interval) Selected percentiles ( 95% confidence interval) Sample 95th 28. The biodegradation half-life of DDT in soil varies from 2 to 15 years.9 (<LOD-20.3) 28.90 (<LOD-12.0) 19. DDT usually refers to the technical product. Smith. 01-02.5) 23. Gunderson. although DDT and DDE intakes have decreased over time (FDA.9 (21. DDT can be absorbed after ingestion. and trace amounts of several related compounds.8. DDT and DDE are distributed to all body tissues with the highest concentrations found in adipose tissues (ATSDR.2) 155 (59.0-37.0-15. Survey Geometric mean (95% conf.2-bis(p-chlorophenyl) ethane (DDD).0) 40.p’-DDT (15%-21%).9) 17.1) 31.p'-Dichlorodiphenyltrichloroethane (DDT) (lipid adjusted) Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U.6-33.1’-dichloro-(2.5 (23.5-36. population from the National Health and Nutrition Examination Survey. including 1.7 (15. fish.3 (<LOD-31.S.0 (10.5) size 1679 2305 1965 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * * 11. as well as in plant and animal tissues. 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. and 7.8) 30.5 (23. Both Serum p. It is still used in some countries.6 (31.0 (18. DDT is converted in the environment to other more stable chemical forms.3-590) 293 (104-541) 48. 1988). In the general U.2 (<LOD-40.1 (23.3 (<LOD-21. population.2-95.S. DDT and DDE can cross the placenta. In the body. 2002. DDT was used at one time as a treatment for head and body lice.9 (10.4) < LOD < LOD < LOD 61.8-17.4) < LOD 17.2) < LOD < LOD 9.6 (22. It was produced and used in the U. o. resulting in fetal exposure.2) 30.1 (33.9-28.2-65.1 (<LOD-39.2 (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 8.7) 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 10.0-53.6) 635 566 461 356 514 490 564 1061 890 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. food.3) 22. sediments.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. respectively. or dermal exposure. p. Fourth National Report on Human Exposure to Environmental Chemicals 89 .4 (23.Organochlorine Pesticides Dichlorodiphenyltrichloroethane (DDT) CAS No.0-27.3-16. Only a small proportion of DDT is metabolized and excreted (Smith.9) 29.7 (19.8-23.3) 21. air. and dairy products.8) 15.0) 20.0 (21.5) < LOD < LOD 9.9-34. continues to be the primary source of DDT exposure. when virtually all use of it was banned. particularly for endemic vector and malaria control.0-155) 83.8-26.4.7) 12.5 (14.9 (10.10-13. 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.7) < LOD 18. DDT is converted to DDE and several other metabolites.7.2-dichloroethenylidene)-bis[4-chlorobenzene] (DDE) and 1.3 (27.0-35. see Data Analysis section) for Survey years 99-00.8-39.3) 21.5) 25. 1991).1-27.0) 26.10 (<LOD-12. depending on conditions.3-236) 24.6 (25. and 03-04 are 20.70 (8.9) 14. < LOD means less than the limit of detection. after World War II until 1972.5 (15. 17. which is a mixture containing p. and water. 1991). 2008.5-54.00 (<LOD-10.1’-(2.50-11.

180 (. Gray et al.120-. Gladen and Rogan.160-.150-. overt signs of acute human toxicity include vomiting.343) < LOD . premature delivery...098-. 2001).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. Studies of DDT exposure and pancreatic cancer. 2002.190 (. 2006).g.p’-DDE can produce anti-androgenic effects (Gray et al.150 (<LOD-. Jusko et al.143) < LOD < LOD . fertility.140-.084 (. although the risk for preterm delivery may be related to maternal DDE levels (Longnecker et al. 1996). 2006).170) .150-. and seizures.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 .079) < LOD < LOD .530 (.26) 1.570-4..140) ..Organochlorine Pesticides chemicals are excreted in breast milk.420) . dioxins and furans). Animal studies reported reduced fertility.130 (<LOD-.105-.054-.p’-DDD and p. tremor.00) .078 (. In high dose.203) . In laboratory animals.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 .180) . 90 Fourth National Report on Human Exposure to Environmental Chemicals .00 (.106) < LOD < LOD .061) < LOD < LOD < LOD .400 (. and duration of lactation.400) .207) 799 1073 959 880 1232 1006 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .048 (<LOD-. Longnecker et al..071-. 2006). Experimental human dosing studies conducted over an 18 month period and during which doses well above environmental levels were given did not demonstrate overt clinical abnormalities (ATSDR.075) 1. 1997). Calle et al.230) .220) .130 (<LOD-. 2004. reproductive organ abnormalities. 2006.107) 635 566 461 356 514 490 564 1061 890 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the lipid adjusted serum level.130 (<LOD-. and leukemia have also been inconclusive (ADSDR.. Mariussen and Fonnum.189-.078-.128 (..069) .180 (.180-.086 (.074-. 2001).220) .150 (<LOD-.230) .112 (. resulting in exposure to nursing infants (Rogan. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 1995.200 (. which may vary for some chemicals by year and by individual sample.290) .. 2002. 2006.530) . Survey Geometric mean (95% conf.190-1.250 (.064 (.167) size 1679 2305 1965 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * * .095) < LOD .146 (. Snedeker.130-.106) . 2000.146 (. Beard. A workplace standard for DDT has been established by Serum p. 1998).150) . have not been consistently demonstrated (Beard. DDT may bind to estrogen receptors (Chen et al.080-.132-.627) . 2002.068-.330-4.142 (.260) .. and altered behavior after neonatal exposure (Eriksson and Talts. 2001). both DDT and DDE may induce specific cytochrome P450 isozymes (Nims et al. polychlorinated biphenyls.180) .S.120 (<LOD-. Jusko et al.065-.106-..01) . 2001).108 (.063 (<LOD-. interval) Selected percentiles ( 95% confidence interval) Sample 95th . Human health effects from DDT at low environmental doses or at biomonitored levels from low environmental exposures are unknown.114-.190 (.34) . other organochlorines. Hayes et al.240) .240 (.051 (<LOD-.170 (.071 (. 2006.313 (. Several reviews of cancer epidemiologic studies have concluded that a link between DDT and breast cancer is inconclusive (Beard. 1956). and o. lung cancer.62 (. 2002. Reproductive effects in humans affecting birth weight.250-1.201 (. population from the National Health and Nutrition Examination Survey.170-. accidental exposures..059-. It is difficult to attribute outcomes in human studies solely to DDT because of potential co-exposure to other persistent organohalogen chemicals (e.087 (. Epidemiologic studies of children with environmental exposure to DDT and DDE have not demonstrated neurologic or developmental abnormalities (Gladen et al..

3.7-119) 113 (100-140) 93. and 7. population from the National Health and Nutrition Examination Survey.8. environmental levels) and health effects is available from the U. 2002. 2002.. Compared to females in the NHANES 1999-2000 subsample. Smith. 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. 1998.Organochlorine Pesticides OSHA and a guidance established by ACGIH. 1991).. mean serum levels of DDT and DDE in the U.p’-DDT) as a possible human carcinogen. so serum DDE levels may be an indicator of historic exposure and may be higher than DDT levels in the same person.html. Biomonitoring Information DDE persists in the body longer than DDT. the lipid-adjusted geometric mean levels of DDT and DDE were each fivefold to tenfold higher than the 95th percentile and geometric mean levels. EPA at: http://www.e. population declined by about fivefold to tenfold. IARC classifies DDT (p. Fourth National Report on Human Exposure to Environmental Chemicals 91 ..6 (81. 2004).S. respectively. 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. 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.atsdr. In general. and the most recent median levels for German adults and children are similar to levels in this Report (Becker et al. Survey Geometric mean (95% conf.S. 2004). Declining DDE levels over time have also been observed in the German population. Since the 1970’s. More information about external exposure (i.. respectively. for males and females in the NHANES 19992000 subsample (Pavuk et al.gov/ toxpro2. 2005). In a population-based sample of men and women from eastern Slovakia.. levels of DDT and DDE increase as a person ages as a result of cumulative exposure (ATSDR..cdc.6.0-114) 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. 1989). compared to levels observed in this Report (Anderson et al.gov/ pestcides/ and from ATSDR at: http://www. mean DDE levels were about fivefold higher among women of southern Spain exposed by virtue of Serum p. see Data Analysis section) for Survey years 99-00. NTP considers DDT as being reasonably anticipated to be a human carcinogen. 2003. 8.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... and 03-04 are 18. Link et al. Heudorf et al. Stehr-Green.S. 01-02.epa.7-129) 297 (256-344) 338 (303-376) 268 (217-332) 108 (97. 2003).

11 (2.59 (1.7) 13.29 (1.93 (7.32 (1.77 (1.51-49.17 (3.71 (5.7) 16.1 (9.21) 3.06) 1.07) 1.80) 1.97-4.85-10.18-1.57 (3.91 (6. 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.59 (4. 2005).80 (2.69 (.37 (1.69 (1.4) 13.820-1.66) 1..4) 14.76-3.63 (6.31 (1.85 (1.994-2.91) 3.0) 657 566 457 416 515 487 732 1053 888 Non-Hispanic blacks 99-00 01-02 03-04 99-00 01-02 03-04 Non-Hispanic whites 92 Fourth National Report on Human Exposure to Environmental Chemicals .963-1.25 (.14 (1.10-5. In the NHANES 1999-2000.34-11.34-3.52 (1.965-1.70-3.69) 8.p’-DDT.76) 1.66) 3.09-1. In a subsample of NHANES II (19761980) participants.8 (13.52 (3.32-1. High mean levels of whole blood DDT (about 3.37-16.03-4.3 (8.1) 7.15-4.3) 13.49 (1.26-10.0) 2. 1989).84-3.12-1.7 (8.90-8. or p.71 (6.07) 1.726) .43-8.59 (1.72) 1. o.870 (.22 (7. 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.78 (4.46 (1.90) 22.611-1.19-14.36 (3.77 (1.63 (1.55 (2.62-6.2 (6.53) 1.40-4.590 (.64-2.10-1.5) 5.51-8.26) 3.81) 11.623 (.25) 1.36) 3.43-4. 2004).S.9 (26.3) 10.01) 1.88 (2.52-6.16-1.p’-DDT.14-1.24-17.54-7.32-1.2) 19.53-15.6 (7.69 (2.68) 2.48-4.9) 5.31-12.6 (9.561 (.500-.3) 937 1069 955 1027 1229 1001 Females 99-00 01-02 03-04 Race/ethnicity Mexican Americans 99-00 01-02 03-04 3.01-11.66) 1. serum levels of o.91-3.34 (7.75 (8.02-8.860 ng/L) and DDE (about 14.60-13.46 (1.05 (3.9-38.24) 1.87 (5.32-9.600) . Survey Geometric mean (95% conf.13) 4.2 (9.53) 7.43-4.456 (.76 (2.96) 1..10) 2.557) 1.48 (6.79) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 .56-6.30-1.p’-DDT (Stehr-Green.7-20.51) 3.63 (1.p’-DDE in serum does not mean that the level of the chemical causes an adverse health effect.61-2.71) 12.430-.88-35.520 (.2 (9. 2001-2002 and 2003-2004 subsamples.8) 686 758 588 1278 1540 1368 20 years and older Gender Males 99-00 01-02 03-04 1.6) 12.7-48.79) 4.30 (1.36-1.5) 22.2-32.99) 1.50 (2.2) 26.18-1.25) 8.87-16.56-3.56-2.18 (6.82 (1. population from the National Health and Nutrition Examination Survey.14-9.8-90.730) .01) 1.02 (2.14) 2.51-15.81-5.25-14.6) 13.81-18.44) 1.18-3.13-2.31-2.49 (6.10) .34) 2.490 ng/L) were found many years ago in a study of pesticide workers in Argentina (Radomski et al.07 (5. Workers involved in production or application of DDT developed neurologic abnormalities associated with blood levels around 100-300 mg/L.01-11. which is similar to the overall geometric mean of 260 ng/g lipid in the NHANES 1999-2000 subsample (Bloom et al.534-.9 (15.7-19. 2004).28) 1.72) 1.40 (3.18) 1.37-4.33-1.22-1.39-2.59) 3.01-15.516 (..51) 1.00) 7.419-.04-1.66-4.75 (4.37-1.63-15.6) 11.6 (8.41-12..9-17.4-19.32 (1.32) 1.61 (1.05) 1.57 (1.71) 32.7) 9.5) 16.6) 9.65 (1.80) 3.23 (7.26-2.43 (5. 1971).1 (8.47 (1.75) 1.75) 6.27) 3.9) 7.53 (2.8 (9.00-1.8 (13.4 (12.57-2.39) 1.30-1.66-2.796 (.25-16.1) 40.01-1.85-4.58) 75th 3.45 (1.39 (3. Finding a measurable amount of p.p'-Dichlorodiphenyldichloroethene (DDE) (whole weight) Metabolite of Dichlorodiphenyltrichloroethane Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U.3 (9.8 (14.2 (19.82) 1.35) 1.80) 1.6) 9.488-.1) 12.0) size 1964 2298 1956 Total years 99-00 01-02 03-04 50th 1.04 (6.38 (1.24 (1.5) 7.11-1.12 (.36-2.46-2.57 (1.25 (1. 309 versus 268 ng/g lipid.646) .41 (1.34) 6.76) 1.84 (3.p’-DDT were below the limits of detection.03-1.83 (1.54) 8.385-.06) 3.57-13.890-1.49) 8. interval) 1.01-1.57-3.66) 4.92 (3.30 (1.01-5.3) 16.97 (3.66-17.96) .45 (1.68-4.59) 6.91-2.12 (6.8) 15.57) 2.02) 1.81 (1.13 (1.69) 4. 1991).20 (.17-3.58) 1.26 (1.16 (2.4 (8.55-9.39-1.92 (3.65) 1.64) 3.56) 2.47) 3.0 (9. Consumers of Great Lakes sport fish had mean serum DDE levels that were only slightly higher than nonconsumers.50-17.00 (. considerably higher than levels in this Report (Smith.18-4.49 (1.5) 10.58) 1.37-10.79) Selected percentiles ( 95% confidence interval) Sample 95th 11.27-1.3-43.680-1.6) 8.21) 90th 7. Serum p.70) 1.6) 9.4) 9.6) 9.54 (1.81 (7.6 (17.36-11.40-8. less than one percent had detectable serum levels of o.0 (12.14) 2.Organochlorine Pesticides nearby agriculture (Botella et al.635) 1.22) .38 (1.51 (1. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.19) 4.68 (2.75) 2.00 (6.40-4.92) 1.

S. and 03-04 are 20.Organochlorine Pesticides Serum o. population from the National Health and Nutrition Examination Survey. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD < LOD size 1669 2279 1946 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD < LOD 90th * * * Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 667 756 588 1002 1523 1358 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 796 1059 949 873 1220 997 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 632 565 458 354 507 486 560 1045 880 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. respectively. and 7. Fourth National Report on Human Exposure to Environmental Chemicals 93 . 01-02.8. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.7.4. 17.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. < LOD means less than the limit of detection. Survey Geometric mean (95% conf. see Data Analysis section) for Survey years 99-00. which may vary for some chemicals by year and by individual sample.

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

HCH.7(3):248-264. Barr DB. Environ Res 2004. Bjerselius R. Thun MJ. Longnecker MP.58:1185-1201. Willman EJ. Neonatal exposure to neurotoxic pesticides increases adult susceptibility: a review of current findings. Environ Health Perspect 1998. Maternal DDT exposures in relation to fetal and 5-year growth. Becker K. et al. April 1982 to 1984. Effects of environmental antiandrogens on reproductive development in experimental animals. hypospadias. Biomonitoring of persistent organochlorine pesticides. Prenatal DDT exposure in relation to anthropometric and pubertal measures in adolescent males. DDE and shortened duration of lactation in a northern Mexican town.72:261265. Jr. Needham LL. Current internal exposure to pesticides in children and adolescents in Germany: blood plasma levels of pentachlorophenol (PCP). Piechotowski I. Greenfield TA. et al. Angerer J. Jr.gov/~dms/ pesrpts.gov/ toxprofiles/tp35. Gabrio T. Rivas A. Bates MN. Buckland SJ. hexachlorobenzene. DDE. Hediger ML. Ostby J.206:485-491. Bull Environ Contam Toxicol 2004. Vorojeikina DP. Henley SJ. Rogan WJ. Charles MJ. Saiyed HN.358:110-114. Am J Epidemiol 2002. Maternal serum level of 1. Int J Hyg Environ Health 2003.21(1-2)37-48. Levels of DDT. Swanson MK. Paepke O. Profiles of ortho-polychlorinated biphenyl congeners. et al. Hurd C.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Jusko TA. Ellis H. Chemosphere 2004. Gray LE Jr. et al. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. DDT and human health. Krause C. Patterson DG Jr. et al.cdc. Longnecker MP. and polythelia among male offspring. Environ Health Perspect 2003. Olson J. Zoellner I.355:7889. Atuma S.96:34-40.cfsan. Falk C. Frumkin H. FDA total diet study. Neurotoxicol 2000. Katz SH. Gray KA.html. Needham LL.. and Mirex among male Lake Ontario sportfish consumers: the New York State Angler cohort study. J Assoc Off Anal Chem 1988. Organochlorines in Swedish women: determinants of serum concentrations.111:349355.162:890-897. and other chemicals. Zaidi SS. Darnerud PO. Am J Public Health 1995. Fourth National Report on Human Exposure to Environmental Chemicals 95 . Bhatnagar VK. Arnold SF.17(6):692-700. Beard J. Kulkarni PK. Needham LL. Toxicological profile for DDT. Koepsell TD. Zhou H. Available at URL: http://www. Davis MD. August 2008. Seiwert M. Lancet 2001. Klebanoff MA. Aune M. Hum Reprod Updat 2001. Cerrillo I. Sci Tot Environ 2006. Epidemiology 2006. selected elements. Hayes WJ. Kashyap R. et al. and HCB residues in human blood in Ahmedabad. Parks L.html. Schulz C. Calle EE. Klebanoff MA. Int J Hyg Environ Health 2002. Botella B. JAMA 1956. Gladen BC. et al.54:1431-1443. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods.atsdr.2-bi(p-chlorophenyl)ethylene and risk of cryptorchidism. Heudorf U. Burse VW. Gunderson EL. Transcriptional activation of the human estrogen receptor by DDT isomers and metabolites in yeast and MCF-7 cells. Drexler H. September 2002. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Durham WF. Olea-Serrano MF. Organochlorines and breast cancer risk. Kaus S. dichlorodiphenyldichloroethylene.205:297-308. Chemosphere 2005. Olson JR. Bloom MS.1-dichloro2. Brock JW. Granath F. Klebanoff MA. and DDD [online]. Lepom P. Exposure of women to organochlorine pesticides in Southern Spain. Biochem Pharmacol 1997. Cueto C. Glynn AW. Vena JE. Crespo J.52:301-309. The Great Lakes Consortium.97(2):178192. Chen CW. Brock JW. Eriksson P.112(17):1761-1767. Environ Res 2005. Olea N.53(8):1161-1172. Garrett N.155(4):313-322.fda. 4/21/09 Gladen BC. and dichloro(diphenyl)ethylene (DDE). Zhou H. Available at URL: http://www. lindane (g-HCH). a biostable metabolite of dichloro(diphenyl)trichloroethane (DDT). The effect of known repeated oral doses of chlorophenothane (DDT) in man. Food and Drug Administration (FDA). Environ Health Perspect 2004. Association between maternal serum concentration of the DDT metabolite DDE and preterm and small-for-gestational-age babies at birth. Furr J. Savitz DA. Talts U. 4/21/09 Anderson HA. Notides AC. Herrman T. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. Wolf CJ. Moysich KB. Lambright C. dietary intakes of pesticides. et al. Hanrahan L. CA Cancer J Clin 2002.85:504508. et al. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. Link B.71(6):1200-1209.106(5):279-289. Baker RJ. India.

Inc. et al. 96 Fourth National Report on Human Exposure to Environmental Chemicals .53:455-477. Demographic and seasonal influences on human serum pesticide residue levels. Nims R. Smith AG. DDE.27:405-421. Crit Rev Toxicol 2006. Thomas PE. Rogan WJ. Snedeker SM. Fonnum F. Deichmann WB. Jones CR. Pollutants in breast milk. and DDD in male rat liver and cultured rat hepatocytes.54:1509-520. Jr. and dieldrin. J Toxicol Environ Health 1989. et al. Lubet R. Lynch CF. Blood levels of organochlorine pesticides in Argentina: occupationally and nonoccupationally exposed adults. Chemosphere 2004. Academic Press. Petrik J.109:35-47. Chlorinated Hydrocarbon Insecticides. children and newborn infants. Environ Health Perspect 2001. 731-915. Neurochemical targets and behavioral effects of organohalogen compounds: an update. New York. DDE. 2 Classes of Pesticides. Environmental exposure to PCBs and cancer incidence in eastern Slovakia. Radomski JL. Pesticides and breast cancer risk: a review of DDT. Toxicol Appl Pharmacol 1971. Pavuk M. Stehr-Green. Comparative pharmacodynamics of CYP2B induction by DDT. Vol. PA. Reddy AB. Schecter A.Organochlorine Pesticides Mariussen E. Cerhan JR.20(2):186-193. Astolfi E. Chovancova J. In Hayes WJ. Arch Pediatr Adolesc Med 1996. Eds.36:253-589. 1991 pp.150:981-990. Handbook of Pesticide Toxicology. Fox S. J Toxicol Environ Health Part A 1998. Jr and Laws ER. Rey AA.

unless the dose is high and the exposure is very recent. Smith. largely the result of historical agricultural application or run off from contaminated soils (ATSDR.S. Endrin is absorbed rapidly after ingestion.10 (<LOD-5.60 (5. or from contact with contaminated soils and sediments in areas where endrin was applied. 72-20-8 General Information Endrin. endrin blocks inhibitory neurotransmitters in the central nervous system resulting in excitation and seizures (Narahashi et al. endrin usually is not detected in serum of exposed individuals. 2008). is no longer manufactured in the U. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Endrin was used as an insecticide. interval) Selected percentiles ( 95% confidence interval) Sample 95th 5..40-5.S. 1992). see Data Analysis section) for Survey years 01-02 and 03-04 are 5. All uses of the pesticide in the U. characterized by generalized seizures in previously healthy persons occurred in Pakistan when sugar contaminated with endrin was ingested (Rowley et al. endrin has been detected with declining frequency in U. endrin can persist for years. 1996. Endrin was not widely used as a termiticide. In the body. 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. fatty infiltration. have been cancelled by the U.40) < LOD 547 433 487 446 1000 831 Limit of detection (LOD. Kavlock et al.. Endrin does not accumulate in body tissues (IPCS. 1991). a stereoisomer of dieldrin. rodenticide and avicide.50) < LOD 5. An epidemic of acute endrin poisoning. Survey Geometric mean (95% conf. manufactured.Organochlorine Pesticides Endrin CAS No. IPCS. General population exposure can occur after ingestion of endrin residues on food items imported from countries where endrin is still used. Skeletal abnormalities and cleft palate in the offspring were associated with endrin when it was fed to pregnant laboratory rodents (Chernoff et al. 1992).. 1992).30 (<LOD-6.50) < LOD < LOD < LOD 5. 1987). Further conversion occurs to 12-ketoendrin and various conjugated metabolites which are excreted in urine and feces.8. Endrin has been detected in soils. inhalation or dermal exposure routes.S.S. Over time. High doses produced renal tubular necrosis and diffuse kidney degeneration in animals. and occasionally at low levels in sediment and surface waters. endrin is converted rapidly to its major metabolite. Human health effects from endrin at low environmental doses or at biomonitored levels from low environmental exposures are unknown. Hepatic effects of endrin exposure have included necrosis.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. which may vary for some chemicals by year and by individual sample. population from the National Health and Nutrition Examination Survey. Because it is metabolized so rapidly. 1979. total diet surveys (FDA. or discarded. Fourth National Report on Human Exposure to Environmental Chemicals 97 . and inflammation (Smith.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. Ketoendrin is a major photodegradation product (IPCS. 1992.40) < 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. Depending on soil conditions. anti-12hydroxyendrin.20 (<LOD-5. EPA.20 (<LOD-5. 1981).S.. 1991).09 and 7. < LOD means less than the limit of detection.30) < LOD 5.40 (<LOD-6. At high doses.10 (<LOD-5. unlike aldrin and dieldrin.

2000). 2004. Ward et al. which may vary for some chemicals by year and by individual sample. and the FDA monitors foods for pesticide residues. Information about external exposure (i. environmental levels) and health effects of endrin is available from ATSDR at: http://www. IARC has determined that endrin is not classifiable with regard to human carcinogenicity.gov/toxpro2.020-.020 (<LOD-. Workplace exposure standards for endrin have been established by OSHA.S. This finding is consistent with other general population studies (Bates et al. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. EPA has established environmental standards for endrin. 98 Fourth National Report on Human Exposure to Environmental Chemicals .020 (<LOD-.S.24 ng/mL (about 6.020 (<LOD-. with the highest value 6.. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 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. serum levels of endrin were below the limit of detection.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 .html.. 2004)..020) < LOD 547 433 487 446 1000 831 < LOD means less than the limit of detection for the lipid adjusted serum level. interval) Selected percentiles ( 95% confidence interval) Sample 95th . Biomonitoring Information In the NHANES 2001-2002 and 2003-2004 subsamples.020 (<LOD-.24 ng/g of serum) (Botella et al.020 (<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-.020) < LOD . population from the National Health and Nutrition Examination Survey.Organochlorine Pesticides The U. endrin was detected in 9% of serum samples.020) < LOD . Finding a measurable amount of endrin in serum does not mean that the level of endrin causes an adverse health effect..cdc.e.020) < LOD < LOD < LOD .atsdr.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 < LOD < LOD 1022 885 1165 940 01-02 03-04 01-02 03-04 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .020 (. In a small study of Spanish women hospitalized for elective surgery. Survey Geometric mean (95% conf.

Rogers E. Roy ML.96:34-40. Available at URL: http://www. Inc. 4/21/09 Kavlock RJ. Ellis H. Exposure of women to organochlorine pesticides in Southern Spain. In Hayes WJ. New York. Pediatrics 1987.html. Ginsburg KS. Cancer Epidemiol Biomarkers Prev 2000. Grajewski B.gov/toxprofiles/tp89. Garrett N. Jr and Laws ER. Perinatal toxicity of endrin in rodents. Olea-Serrano MF. Rivas A. Needham LL. No:429-436. et al. Kavlock RJ. Environ Res 2004. Vol. Olea N. et al.21:141-150. Available at URL: http://www. Fetotoxic effects of prenatal exposure in hamsters. Sodium and GABA-activated channels as the targets of pyrethroids and cyclodienes.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Saleem M.gov/~dms/ pesrpts. Ward EM. et al. Environmental Health Criteria 130. Rowley DL. Cerrillo I. Whitehouse DA. Andersen A. 4/21/09 Bates MN. 1992.9:1357-136.cfsan. Convulsions caused by endrin poisoning in Pakistan. Liddle J. Toxicol Lett 1992. Food and Drug Administration (FDA).fda.html.79(6):928-934. Jr. Eds. II.cdc.64-65 Spec. Serum organochlorine levels and breast cancer: a nested case-control study of Norwegian women. Academic Press. Fourth National Report on Human Exposure to Environmental Chemicals 99 . pp. Buckland SJ. Hardjotanojo W. Perinatal toxicity of endrin in rodents. Narahashi T. 4/21/09 International Programme on Chemical Safety (IPCS).org/documents/ehc/ehc/ ehc130. Smith AG.13:155-165. Hanisch RC. Turner W. Gray LE. I.atsdr. Chemosphere 2004. Chernoff N. 2 Classes of Pesticides. Gray LE. Fetotoxic effects of prenatal exposure in rats and mice. August 2008. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. August 1996. Patterson DG Jr. Endrin [online]. Gray J. Frey JM. Toxicology 1979.inchem. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. Toxicology 1981. Gray JA. Crespo J. Chlorinated Hydrocarbon Insecticides. Hanisch RC. Handbook of Pesticide Toxicology. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Rab MA. Botella B. Burse VW. 1991. Available at URL: http://www. Sokal D. Chernoff H. Schulte P. Toxicological profile for endrin [online].54:1431-1443.htm. 731-915. Patterson DG Jr. et al.

1997).8 (26.2-15.7 (27.5 (13.5) < LOD < LOD 18.7-16.0) < LOD < LOD 15. see Data Analysis section) for Survey years 99-00.9-32.9) < LOD < LOD 16. air. and sediment (Barber et al.S.. HCB may be created as either a byproduct or an impurity in the manufacturing process for certain chemicals and pesticides.4) < LOD < LOD 14.9) < LOD < LOD 19. respectively. 01-02.8 (15.6-19.9-15.7 (15. 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.6) < LOD < LOD 26.4. 2.2 (17. HCB is well absorbed after oral administration.3 (14.6-33. EPA cancelled its use in 1984.7) * * 14.4 (18.7-15. HCB has been detected in fewer foods since the 1980s (FDA. The general population may be exposed to HCB through diet.4. which may vary for some chemicals by year and by individual sample. 1976).5-15.9) < LOD < LOD 20.0 (18.8) < LOD < LOD 27.1 (14.8) size 1702 2277 1961 Total years 99-00 01-02 03-04 50th < LOD < LOD 14.4 (22. HCB is slowly metabolized.1 (13. and 03-04 are 118.0-19.9-17.6) < LOD < LOD 25. particularly by consuming fish. 31.9 (25.4.4) < LOD < LOD 33.8) 583 554 460 350 511 488 636 1052 888 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.2) < LOD < LOD 29.8 (22.0-25.2 (24.9 (25. wildfowl.3-26.7 (19.4) < LOD < LOD 22.2-15. breast milk is an additional route of elimination in nursing women.6) < LOD < LOD 26. 2002).2 (14.7-29.4) < LOD < LOD 19. 100 Fourth National Report on Human Exposure to Environmental Chemicals . distributes widely throughout the body.. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.7) 807 1058 957 895 1219 1004 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * 16.4) < LOD < LOD 23.8.8-15.1-20.S. 2008.7 (15.7-30. It is a persistent chemical and bioaccumulates in both aquatic and terrestrial food chains (ATSDR.Organochlorine Pesticides Hexachlorobenzene CAS No.0) < LOD < LOD 15. Workers in chemical manufacturing industries may be exposed to HCB via inhalation or dermal pathways.6 (21..4.9) < LOD < LOD 15. and elimination occurs by renal and fecal routes.4) < LOD < LOD 18.3 (16.4 (11.1 (14.5-18. Urinary metabolites include pentachlorophenol (PCP). and 7.9) < LOD < LOD 20.1 (17.3-22.S.2 (13.5-TCP) and 2. 2005).9) 19.6) < LOD < LOD 24.S.6) < LOD < LOD 14.6 (23.2 (14.6-trichlorophenol (2.1) < LOD < LOD 15.9-20.4 (18.3 (22.0-28.6) 591 747 588 1111 1530 1373 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * 14.1-16.3 (20.9-24. 1988).3 (12.9) < LOD < LOD 28.7) < LOD < LOD 24. water. and accumulates in fatty tissues where it persists for years. 118-74-1 General Information Hexachlorobenzene (HCB) was used from the 1930’s to the 1970’s in the U.5-14.7-21.7) < LOD < LOD 75th < LOD < LOD 90th * * 15..5-trichlorophenol (2.6-26.7-26. primarily as a fungicide and seed treatment until the U. Although it is not manufactured as an end-product in the U. and has been detected in soil. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD 28.9 (23.4-16.6 (24.0 (25.4. or game taken from areas with HCB contamination. population from the National Health and Nutrition Examination Survey.3) < LOD < LOD 29.0-16.0 (14.3 (22.4-15.7-16.5 (13.0 (18.3) * * 15.7-22. Hexachlorobenzene has entered the environment as a result of industrial activities and pesticide applications.9-30.6-44.1) * * 15.5-14.6-TCP) (To-Figueras et al.0. Therefore.5-33. < LOD means less than the limit of detection.3) 24.3-20. The FDA dietary surveys have shown that over time.0) < LOD < LOD 24. Survey Geometric mean (95% conf. Gunderson.6-32.4) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * 13.0) * * 15.5-15. and foods with a high fat content.2) < LOD < LOD 13.5 (14. these metabolites can also be produced after exposure to other chlorinated compounds (Kohli et al.2-31.3) < LOD < LOD 20.9 (14.

092-.081 (.069) * * .085) * * . EPA has established a drinking water standard.086-. which may vary for some chemicals by year and by individual sample.212) size 1702 2277 1961 Total years 99-00 01-02 03-04 50th < LOD < LOD . Schmid.102 (. Fourth National Report on Human Exposure to Environmental Chemicals 101 .cdc.069) < LOD < LOD .163) < LOD < LOD .179 (.125 (.097 (.145-. which is manifested by increased deltaaminolevulinic acid synthase activity and decreased uroporphyrinogen decarboxylase activity.099) < LOD < LOD . EPA at: http://www.113-.111) < LOD < LOD . and the FDA has established a bottled water standard for HCB.109) * * . 2002).094) < LOD < LOD .gov/pesticides/ and from ATSDR at: http://www.127-.095 (. Survey Geometric mean (95% conf. population from the National Health and Nutrition Examination Survey.097) < LOD < LOD .094 (. 1960).163-.123 (.073-.169-.182 (.092 (. thyromegaly.102) < LOD < LOD .081-.155) < LOD < LOD .141) < LOD < LOD ...072-.120 (.132) < LOD < LOD .157-.064 (. HCB interferes with normal heme synthesis.090 (.epa.088-.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.107-.156 (.190 (.143-.Organochlorine Pesticides chemical.118) < LOD < LOD .062-.157 (.089-.191 (.203) < LOD < LOD .099) < LOD < LOD . With chronic exposure. This condition.077-.095) < LOD < LOD 75th < LOD < LOD 90th * * .091-.088-.152) < LOD < LOD .088-.147 (.123 (. and weakness. Biomonitoring Information Serum concentrations reflect the body burden of HCB.140 (.S. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.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 * * .html.gov/toxpro2. IARC classifies hexachlorobenzene as possibly carcinogenic to humans.095) * * .065 (.163 (.130) < LOD < LOD . ACGIH has developed workplace exposure limits for HCB.226) 807 1058 957 895 1219 1004 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * .225 (.135-.115 (.090 (.090 (.060-.145-.203) < LOD < LOD .171 (. and many died before 2 years of age (Peters et al.111-.atsdr. as well as hypertrichosis. very high.e. Infants were exposed transplacentally and through breast milk.176-. acute doses produce central nervous system depression and seizures.092 (.174-.176) < LOD < LOD .090-.173) < LOD < LOD .092 (. anorexia.098 (. arthritis.082-.126) .186 (.107) < LOD < LOD .086-.079 (. and NTP classifies hexachlorobenzene as reasonably anticipated to be a human carcinogen. immunologic abnormalities.129) < LOD < LOD .114-. 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.147-. a consequence of these heme abnormalities is a condition known as acquired porphyria cutanea tarda.167) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * . In humans.178-.089-.095 (.123 (.175) < LOD < LOD .100) < LOD < LOD .121 (.087 (.S.148-. More information about external exposure (i.159-.S. reproductive and developmental toxicities.167 (.095-.085-.104 (. The U. Human health effects from HCB at low environmental doses or at biomonitored levels from low environmental exposures are unknown.196) < LOD < LOD . Chronic feeding studies in animals have demonstrated kidney injury. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD .160 (.099) < LOD < LOD . and liver and thyroid cancers (ATSDR. 1982.114-.078 (.118-. environmental levels) and health effects is available from the U.122) < LOD < LOD .083) < LOD < LOD . were seen in an epidemic of poisoning in Turkey that occurred from 1955 to 1959 when HCB-treated seed grain was diverted for bread production.118-.097) .258) < LOD < LOD .086) < LOD < LOD .

Canada). Biol Neonate 2002. 1999)..17:388–399. Herrman T. Jones KC. Epidemiology of hexachlorobenzene-induced porphyria in Turkey: clinical and laboratory follow-up after 25 years. Link et al. Gunderson EL. Dallaire F. et al. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. 2002. Cripps DJ. Kohli J. Muckle G. Krause C. 102 Fourth National Report on Human Exposure to Environmental Chemicals . Barr DB. Temporal trends of organochlorine concentrations in umbilical cord blood of newborns from the lower north shore of the St. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003.54(3):203-208. selected elements. Chemosphere 2005. 2005).gov/~dms/ pesrpts.349:144.. distribution.fda. In Spain. 1989). Kaus S. Ayotte P. Darnerud PO. In a representative sample of the 1998 German adult population. factory workers chronically exposed to HCB and residents near the factory had serum HCB levels that were 150 to 50 times higher. Environ Health Perspect 2003.Organochlorine Pesticides in the NHANES 1999-2000 and 2001-2002 subsamples. Food and Drug Administration (FDA). Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.111:349355. Reference values updated. Int J Hyg Environ Health 2002.gov/ toxprofiles/tp90. declines in background HCB levels ranging from around 50%90% have been documented in studies using cord blood (Dallaire et al. 2003). Sci Tot Environ 2005. Otero R. Lackmann GM. 2006). Arch Neurol 1982. and the geometric mean concentration of HCB in whole blood was 0. Glynn et al.. Safe A. Kemper FH. Lawrence River (Quebec. As a result of the lower limit of detection in NHANES 2003-2004. Seiwert M.. HCB levels were directly related to age. Hexachlorobenzene in the global environment: emissions.cfsan.110(8):835-838.. 2002).. Granath F.9% of participants had quantifiable levels (Stehr-Green. Polychlorinated biphenyls and hexachlorobenzene in full-term neonates. Hexachlorobenzene content in human whole blood and adipose tissue: experiences in environmental specimen banking. Bradman A. April 1982 to 1984. et al. References Agency for Toxic Substances and Disease Registry (ATSDR).. Peters HA. Herrero C. Factors predicting organochlorine pesticide levels in pregnant Latina women living in a United States agricultural area.81(2):82-85. Aune M. than the limits of detection (on a whole weight basis) in NHANES 19992000 and 2001-2002 (Herrero et al. Zoellner I. van Wijk D. 2002. Laliberte C. 4/21/09 Barber JL. et al.71(6):1200-1209. September 2002. Can J Biochem 1976. Over the past two decades.77:173182. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. and other chemicals. levels.39(12):744-749. Muller C. August 2008. Lepom P. Available at URL: http://www. Ozalla D. 4/21/09 Glynn AW. dietary intakes of pesticides. Bradman et al. Toxicological profile for hexachlorobenzene update [online]. Sweetman AJ.44 mg/L. Lackman. Finding a measurable amount of hexachlorobenzene in serum does not mean that the level of the hexachlorobenzene causes an adverse health effect. The metabolism of higher chlorinated benzene isomers. Piechotowski I. Gocmen A. Agerelated increases of HCB in body fat and serum have been consistently noted in general population studies (Becker et al. IARC Sci Publ 1986. however. 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. Environ Health Perspect 2002. Holland NT.. Bjerselius R.. Schulz C.html. Jones D. but approximately five times higher than the overall geometric mean level in 2003-2004 (Becker et al. Residency near industrial or agricultural areas has been associated with higher serum HCB levels (Barber et al.html. respectively.. FDA total diet study. et al. Bryan GT. 2005. J Assoc Off Anal Chem 1988. Paepke O. but overall. Arch Dermatol 1999. Atuma S. more HCB levels were quantified. Biomonitoring of persistent organochlorine pesticides. only 4. In the 1976-1980 NHANES subsample. Bertram et al. Becker K. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. HCB detection in serum also was proportional to age. 2002. Bertram HP. lower than the limit of detection (on a lipid adjusted basis) in NHANES 1999-2000 and 20012002.205:297-308.58:1185-1201.atsdr. Gabrio T. 2002) and among children (Link et al. Available at URL: http://www. Lackmann. Fenster L. 1986.cdc. 2005).. 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. Urinary porphyrin excretion in a human population highly exposed to hexachlorobenzene. Dogramaci I. Organochlorines in Swedish women: determinants of serum concentrations. Schwartz JM. 2002. Santiago-Silva M. J Exp Sci Environ Epidemiol 2007. trends and processes.135(4):400404. Sala M. Dewailly E. Link B. Lecha M. Eskenazi B.

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

1-27.2-17.36.7) 73.0 (<LOD-12.0) 8.4) < LOD < LOD < LOD 46.4) 21.Organochlorine Pesticides Hexachlorocyclohexane CAS No. The gamma isomer.1-32.4-50.5 (16.9-14.6) 36.1 (16.0 (19.1 (27. and 7.7-69. 608-73-1 beta-Hexachlorocyclohexane CAS No.4-45.7 (35.1) 71.2-20.4 (12. 01-02. As pesticide applications of HCH were increasingly restricted or eliminated. each result has been multiplied by 1.5) 14.1) 13.8 (10.0) 17.2) 9.8) 7. Lindane has a half-life of about two weeks in soils and water. In 2006. 58-89-9 General Information Hexachlorocyclohexane (HCH). which may vary for some chemicals by year and by individual sample. the U.9) 17.7) 10.4) 10.8 (17.8) 12. However.6 (17.80 (<LOD-14. HCH isomers are lipophilic.7) 23.8-68.9 (26. It is no longer produced or sold in the U.9-21.8) 95th 68.5 (14.6 (33. formerly referred to as benzene hexachloride.6 (10.1) 12.0) 35.0-70.3) 25.7-26.1 (18.S.04-10.30-11.3 (42.46-11.0 (14.3) 14.7) 32.S.5) 29.7-69.4-73.09) < LOD Gender Males 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD 14.S.45) < LOD Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 99-00 01-02** 03-04 16.4 (16.5 (43.0 (35.8) < LOD 10.7 (<LOD-16. exists in several isomeric forms.5-29.70-19.8 (23.9 (30.7) 97.5) 11.4) 44.6 (22.0-111) 70.4) 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. and have been used either as fungicides or to synthesize other chemicals.0) 41. respectively.60-13.4-111) 84.5 (37.6) 47.80 (6.0) 71.0 (8.1-37.0-34.4) 27. Technical grade HCH is a mixture of all four isomers.7-96. and 03-04 are 9.50) 8. and sediment as a result of historic production and use.5) 16. 2005).1-15.2-98.9 (9.0-70.2 (31.4 (8.2-42.3 (26.4) 901 1067 952 992 1224 1007 Females 11. interval) 9.1 (21.3-38.8 (21. **In survey period 2001-2002.90-8.9-81.2) 13.61-12.6-18.0 (37.6-135) 69.2 (34. and delta.5) 90th 42. 6.2 (48.3) 34.7 (29.9 (32.76.6-89.9 (11.5 (8.5) 22.7 (30. commonly known as lindane.8) * * * * * * 15.68 (<LOD-10. see Data Analysis section) for survey years 99-00.9-24.6) 653 758 589 1240 1533 1370 20 years and older 10.70 (8.89 (<LOD-9. 104 Fourth National Report on Human Exposure to Environmental Chemicals .8-19.8 (33. beta.3) 37.7) 27.3) 51.90-8. can be used as an insecticide and has been used to kill soil-dwelling and plant-eating insects.0-23.5) 40.8) 39.8 (32.6) 35.70-12.9-178) 48.7 (13.4 (11.8) 27. soil.3 (42. Survey years 99-00 01-02** 03-04 Geometric mean (95% conf.2-22. particularly alpha and gamma have been detected widely in air.9-56.9-51.6-37.1 (9.1) 31.9 (62. HCH isomers.3 (13.7 (25.5-123) 49.5 (24.6-14.6) 50. so they can accumulate in fatty tissues of animals. Lindane (1%) lotion and shampoo are available by prescription for singleuse application to treat human scabies and head lice. including alpha.7-20.4) 11.6) 16. population from the National Health and Nutrition Examination Survey.1 (11.5) 632 563 460 403 513 487 702 1051 887 Non-Hispanic blacks Non-Hispanic whites Limits of detection (LOD.7 (53.5528.4 (52.7 (62. The other isomers can be formed during the synthesis of lindane. 2005).66-12.6-47.8 (9.2-87.3-85.5) 67.6-20.2 (18.1-32.8.4 (50.3 (62.2-46.9) 81.5 (11.7-96. EPA cancelled agricultural uses of lindane (ATSDR.8 (64.8-54. 319-85-7 gamma-Hexachlorocyclohexane CAS No.6-62.1-16.0 (33.2-67.2) 142 (99. environmental levels declined.1-49.8-87.1 (9.8) 52.2) 62.3-56.43 (<LOD-9. gamma.6) 18.2-55.2 (29.0) 7.0-20.7) < LOD < LOD < LOD < LOD < LOD < LOD 37.20-16.9) Selected percentiles ( 95% confidence interval) Total * * 50th < LOD < LOD < LOD 75th 19.70 (6.2 (9. 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.56-12. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.6 (40.9 (40.8-199) 134 (85.87 (9. See the section “What’s New” at the beginning of this Report for details.1 (12.8-16. containing about 64% alpha and 10%-15% gamma isomers.6-42.9) 45.1) 12.7) 56.0-21. < LOD means less than the limit of detection.9 (50.4) < LOD 9.7) 18.7-166) 70.1 (30. HCH does not bioaccumulate to an appreciable extent in plants (ATSDR.4) 51.2) 36.9) 15.1-36. water.90) 7.6 (16.7) 10.2-52.2 (50.

HCH crosses the placenta and is also excreted in breast milk (Radomski et al.080 (.580 (.330-.250 (.131-.222 (.048 (<LOD-.287 (.360-.140) .103) 90th .191-.. Saxena et al.220-.190) .01 (.160) .173-.244-.S.05) .310) . for lindane.120 (.070-.297-.090-.067 (.065 (.100-.460 (.150) .290 (.270 (.100-.410) .370-.840) .587) 653 758 589 1240 1533 1370 20 years and older ..210-.056-.216 (.069) .281 (.290) .070 (.050 (.080-.220 (.330 (.058 (<LOD-.410 (.098 (.560) . When animals were chronically fed lindane at high doses.200-.070) .144 (.110) .090 (.254) 95th . Workers who directly handled HCH have complained of headache.600) . 1983).064) .150 (.125) < LOD < LOD < LOD . HCH isomers are absorbed after inhalation. 2008.700) .062 (.400) .308-. Distribution is mainly to fatty tissues.100) . enlarged livers.091) .103 (. EPA has established a drinking water standard.382-.380 (.090 (.501) . ataxia.081-.050 (<LOD-.404) .250-. tremors.160-.290 (.310) .120-.690) .160 (.290) . 2002). and memory loss (Nigam et al.250 (. and seizures. The beta isomer accumulates in fatty tissues and is metabolized more slowly. hepatic enzyme induction.050 (.319) .620-1.240-..057) < LOD Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 99-00 01-02** 03-04 .210 (.210) .050-. Pesticide applicators or agricultural workers could be exposed to HCH by inhalation and dermal pathways.130) .073-.360 (.250-.100) . from 6% of samples in 1982-1984 to 2% in 1994 (FDA.240 (.214) .059-.470 (.390-. 1986).064 (.450 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.100 (.305) . population from the National Health and Nutrition Examination Survey.521 (.080 (.083 (.120-. or dermal exposure. Human health effects from HCH isomers at low environmental doses or at biomonitored levels from low environmental exposures are unknown.120-.910 (.051-.089-.077) < LOD . See the section “What’s New” at the beginning of this Report for details. interval) .420-.580-1.092 (.057 (<LOD-.050-. the serum half-life was about 20 hours among children (Ginsburg et al.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 .450) .140) .260-.470) .221-.190-1.372 (.620) . 1971.068-. paresthesias.062 (.210 (.080) * * * * * * .680) .167 (.661) 901 1067 952 992 1224 1007 Females .146-.310 (. and FDA has established a bottled water standard and food residue tolerances for lindane.175 (.077) < LOD .250) .050-.390 (.220) .190) .480) .412 (. probably by blocking inhibitory neurotransmitters in the central nervous system. which may vary for some chemicals by year and by individual sample.191-.S.083) .150-.050-. U. Fourth National Report on Human Exposure to Environmental Chemicals 105 .360) .320 (.480 (. and nephropathy developed (IPCS.331 (.100 (.080-.560 (.260) .139 (.170-.057-. 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.119) . Acute high doses of lindane after ingestion or excessive skin application of the 1% lotion have produced seizures in humans.180-.070-.280-.130 (.056-.710) .080) .120 (. Gunderson 1988).065 (.078 (.086) < LOD < LOD < LOD < LOD < LOD < LOD .Organochlorine Pesticides exposure to HCH is through the diet.442 (.140) .300-. resulting in a half-life of about seven years.067) .480 (.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.294-.280-.110) .32) .250 (. FDA pesticide monitoring program has shown a temporal decline in the detection of lindane.089) .140 (.072 (.340-. OSHA and ACGIH have established workplace standards and guidelines.170-.090 (.37) 1.050) .150) . each result has been multiplied by 1.350) .050 (<LOD-. 1981).460) . Acute high dose toxicity in rodents affects the central nervous system producing decreased activity.190-.120) .070 (.100-.340) .066) Selected percentiles ( 95% confidence interval) Total * * 50th < LOD < LOD < LOD 75th .051 (<LOD-.120 (.350 (. HCH isomers are metabolized to chlorophenol metabolites that are excreted in the urine (Angerer et al.410-.5528.290 (.096) .040-. The U.234 (. ingestion.120) .174) ..124-.118 (.220-.S.200 (.260) .450-. Rogan.047-. respectively.130-.400) .110-.110) .080-.230-.058) < LOD Gender Males 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD .200-.070-.057-. Survey years 99-00 01-02** 03-04 Geometric mean (95% conf.410) .570 (.118-. 1977).. After dermal application of lindane 1% lotion. **In survey period 2001-2002.510) .814) .103-.060) . 1996.

.cdc. More information about external exposure (i. 1989. 2004. 1971.5.S. the maximum and 95th percentile beta-HCH values. In NHANES 1999-2000. and 7. 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. 1998). respectively. 1989). Sturgeon et al. Survey Geometric mean (95% conf.atsdr. Kutz et al. and a diet that includes meat (Becker et al..epa. 1991. and 03-04 are 14. 10.S. Stehr-Green. population from the National Health and Nutrition Examination Survey. serum levels of lindane were generally below the limits of detection. < LOD means less than the limit of detection. Link et al.5.Organochlorine Pesticides hexachlorocyclohexane isomers as possibly carcinogenic to humans.. 1998... In populationbased studies of New Zealand adults and German adults and children..e. 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. Bates et al. Kutz et al. Stehr-Green. 1991. which may vary for some chemicals by year and by individual sample. older age. Biomonitoring Information Because of its longer half-life. In an earlier (1996-1997) sample of German children. were similar to the 95th percentiles in this Report. studies in populations with environmental exposure have reported lindane levels below the limit of detection in most persons (Anderson et al. respectively. 2004). EPA at: http://www. and NTP classifies hexachlorocyclohexane isomers as reasonably anticipated to be human carcinogens. Studies of general populations have shown declining beta-HCH levels since the 1970s (ATSDR.gov/pesticides/ and from ATSDR at: http:// www. 01-02. In recent years. 2001-2002. 2005. 2004) and India (Bhatnagar et al. which were considerably lower (as much as twentyfold) than mean levels reported in small studies of adults in Spain (Botella et al. beta-HCH may be detected in a higher percentage of the general population than are the other HCH isomers. and 2003-2004.8. 2002)... 2005. Becker et al.. Radomski et al.gov/toxpro2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. male sex. 106 Fourth National Report on Human Exposure to Environmental Chemicals .html. environmental levels) and health effects is available from the U.. aged 9-11 years. 2002. see Data Analysis section) for Survey years 99-00.. Additional factors associated with higher beta-HCH levels include rural residence..

Finding a measurable amount of HCH isomers in serum does not mean that the level of HCH isomers causes an adverse health effect. Survey Geometric mean (95% conf. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 1986. Serum gamma-Hexachlorocyclohexane (Lindane) (whole weight) Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U. the median beta-HCH levels were similar or slightly higher than the 95th percentile in this Report (Anderson et al. Radomski et al. in this Report (Nigam et al. 1998).. Fourth National Report on Human Exposure to Environmental Chemicals 107 . respectively.. 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. 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).S. 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. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD < LOD size 1799 2280 1960 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD < LOD 90th * * * Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 660 758 593 1139 1522 1367 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 863 1060 952 936 1220 1008 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 631 563 461 380 509 490 646 1045 884 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the lipid adjusted serum level. In a small study of adults who consumed sport fish from the Great Lakes.. 1971).. 2003)..Organochlorine Pesticides 2001-2002 survey period (Link et al. 2005). Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. which may vary for some chemicals by year and by individual sample. population from the National Health and Nutrition Examination Survey.

Schulz C. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Placental transfer of pesticides in humans. dietary intakes of pesticides.106(5):279-289.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Toxicological profile for hexachlorocyclohexanes update [online]. Cancer Causes and Control 1998.htm.111:349355.27:405-421. Arch Toxicol 1981. Zoellner I. Angerer J. Needham LL. Bjerselius R. 4/21/09 Kutz FW. Bhargava AK. Rey AA. Stehr-Green. Reisch JS. Cerrillo I. Toxicol Appl Pharmacol 1971.71(6):1200-1209. J Toxicol Environ Health 1989.48:127-134. Bull Environ Contam Toxicol 2004. Link B. children and newborn infants. Available at URL: http://www. et al.inchem. Available at URL: http://www. selected elements. Krishna Murti CR. Organochlorines in Swedish women: determinants of serum concentrations. Bates MN. et al. Maass R. 108 Fourth National Report on Human Exposure to Environmental Chemicals . 2002. Siddiqui MKJ. Pollutants in breast milk. Darnerud PO. Brinton LA.205:297-308. Burse VW. HCH. India.96:34-4Food and Drug Administration (FDA). Buckland SJ. Olson J. available at URL: http://www. et al.cdc.54:1431-1443.150:981-990. Occupational exposure to hexachlorocyclohexane. Saiyed HN. Hanrahan L. gov/toxprofiles/tp43. Environ Health Perspect 2003. Sturgeon SR. Lepom P. Levels of DDT. FDA total diet study. Int J Hyg Environ Health 2002. Garrett N. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. Int Arch Occup Environ Health 1986. Chemosphere 2005. Needham LL. International Programme on Chemical Safety (IPCS). Wood PH. August 2008. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Demographic and seasonal influences on human serum pesticide residue levels. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. The Great Lakes Consortium. Glynn AW. Biomonitoring of persistent organochlorine pesticides.html.58:1185-1201. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. Heinrich R. Deichmann WB. Metabolism of gammahexachlorocyclohexane in man. Lindane. Kashyap R. Patterson DG Jr. Radomski JL.72:261265.html. Atuma S. PA. Nigam SK.20(2):186-193. Needham LL. Karnik AB. Visweswariah K. Kaus S. Brock JW. and other chemicals. Krause C. Olea N. Aune M. Serum hexachlorocyclohexane residues in workers engaged at a HCH manufacturing plant. VI. Astolfi E.cfsan. Bai KM.9(4):417-424. and HCB residues in human blood in Ahmedabad. Falk C. Rev Environ Contam Toxicol 1991. Bottimore DP.52(1):59-67. Absorption of lindane (g benzene hexachloride) in infants and children. Zaidi SS. Chemosphere 2004. Pesticide residues in food-2002-Joint FAO/WHO meeting on pesticide residues.gov/~dms/pesrpts. Piechotowski I. J Assoc Off Anal Chem 1988. Potischman N. Seiwert M. J Pediatr 1977. et al. Becker K. August 2005. Rivas A. April 1982 to 1984. Herrman T. Rothman N.120:1-82. Exposure of women to organochlorine pesticides in Southern Spain. Organochlorine pesticides and polychlorinated biphenyls in human adipose tissue. Botella B. Paepke O. Lowry W. Int Arch Occup Environ Health 1983. Saxena MC. Crespo J. Kulkarni PK. Environ Res 2004.57(4):315-320.fda. Serum concentrations of organochlorine compounds and endometrial cancer risk (United States). et al. org/documents/jmpr/jmpmono/2002pr08. Rogan WJ. Olea-Serrano MF. Gabrio T. Raju GS. et al. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. Majumder SK. Kutty D. Arch Pediatr Adolesc Med 1996. Gunderson EL. Granath F. Bhatnagar VK. Environ Health Perspect 1998. Blood levels of organochlorine pesticides in Argentina: occupationally and nonoccupationally exposed adults.atsdr. 4/21/09 Anderson HA. Ellis H. 4/21/09 Ginsburg CM. et al.91:998-1000.

2 (7.90-29.0 (<LOD-108) < LOD < LOD 50. population from the National Health and Nutrition Examination Survey.6) < LOD < LOD < LOD < LOD 71.0 (14.6) 9. 1995). 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.3) < LOD < LOD < LOD < LOD < LOD < LOD < LOD 15. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.5-291) 11. and 03-04 are 14. 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.5 (9.. Mirex is absorbed through the skin and from the gastrointestinal tract.70-24.7) < LOD 66.40 (<LOD-13. which may vary for some chemicals by year and by individual sample. mirex was detected in human adipose samples.S.4 (8.3 (15..0-374) 11.7) 8. 01-02. In studies conducted in the 1970’s and 1980’s. it is a highly persistent chemical in the environment. 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 (<LOD-65. Some states and the U.1 (8. animals.0 (12.10 (<LOD-15. soil. aquatic organisms. 1985.6-305) 15. disposal.4) < LOD 63.4) < LOD 15.5 (<LOD-42.5-425) 40.5 (<LOD-115) 153 (30.1 (13. or pesticide application. resulting in exposure to newborns and nursing infants.4) 617 548 459 398 500 484 688 1049 884 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. EPA have issued public health advisories or warnings that fish from contaminated lakes and rivers may contain mirex.6 (<LOD-23.70-40. 10.7 (12.10-37.3-225) 15.8) < LOD 15.8 (12. see Data Analysis section) for Survey years 99-00.8.5. and 7. Mirex can cross the placenta and be excreted in breast milk. Ingested mirex that is not absorbed is eliminated in the feces within about 48 hours. Occupational exposure is limited to workers at sites where mirex contamination is present. where it has a half-life of 12 years. and foods. water. since 1977. after which it is widely distributed in the body and stored in fat.4-230) 18.0) * * * Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 19.6) size 1853 2257 1951 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th 15. Formerly. Fourth National Report on Human Exposure to Environmental Chemicals 109 .2) 51.1) 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 16.7 (<LOD-47. 1991).S. 2385-85-5 General Information Mirex has not been produced or used in the U. Mirex has been detected in air.2-230) 13. sediments. (Kutz et al. especially those from persons living in the southeastern U. where it was applied directly to soil and by aerial spraying. respectively. Mirex binds strongly to soil.1 (<LOD-104) < LOD < LOD < LOD < LOD 39.8 (<LOD-73.6 (<LOD-31. < LOD means less than the limit of detection.6 (<LOD-108) 9.3 (15. Mirex contamination of Lake Ontario and adjacent waterways has been well documented (ATSDR.S.S.S.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 13.70 (<LOD-15. Mirex is not metabolized in the body.6.Organochlorine Pesticides Mirex CAS No. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 57. Survey Geometric mean (95% conf.5-82.

2001-2002.062-..cdc.090 (<LOD-.220) .268) < LOD .gov/toxpro2.102) < LOD < LOD < LOD < LOD . 2004).100 (<LOD-.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 .470) .41) .090 (<LOD-.73) . Laboratory animals fed high doses developed liver enlargement and liver tumors.215) 659 728 592 1194 1529 1359 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .450) 1. and the FDA monitors foods for pesticide residue and has established an action level for mirex in fish tissue. environmental levels) and health effects is available from the ATSDR at: http://www.090 (<LOD-. 1995.170) < LOD . 7. 110 Fourth National Report on Human Exposure to Environmental Chemicals .450 (.html.170-3.370 (.256 (.e. serum mirex levels were generally below the limits of detection (Stehr-Green. reproductive toxicity included decreased fertility and testicular damage.080-1.110 (<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.310 (.S.140 (<LOD-.053-.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 .070-1.79) . The geometric mean mirex levels of the Inuit mothers were 8.112 (. IARC classifies mirex as possibly carcinogenic to humans. 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.410 (.100 (<LOD-.8.470 (. Survey Geometric mean (95% conf.170) size 1853 2257 1951 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .090-1.atsdr.054 (<LOD-.690) .08 (.090-1.089-..079 (<LOD-. EPA has established environmental standards for mirex. which may vary for some chemicals by year and by individual sample.510) < LOD < LOD . Inuit mothers from three Arctic areas had geometric mean serum mirex levels that were threefold to sevenfold higher than nonInuit mother from other Arctic regions. as well as in a subsample of NHANES II (1976-1980) participants. 1989). In addition. and 2003-2004 subsamples.055-.37) . 1991).470) .79) .220 (<LOD-.090-1.02) .052-. Fishermen in New York who consumed Great Lakes sport fish had median levels of lipid-adjusted serum mirex that were lower than the 95th percentile value among males the NHANES 2001-2002 subsample (Bloom et al.92) .064 (<LOD-. and 4.Organochlorine Pesticides exposures are unknown.240) < LOD < LOD < LOD < LOD < LOD < LOD < LOD .106) < LOD ..S. population from the National Health and Nutrition Examination Survey.080-1.7 ng/g of lipid. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD . In samples obtained between 1994 and 1997. and NTP classifies mirex as reasonably anticipated to be a human carcinogen. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Smith. The U.430 (. developmental abnormalities including cataracts and edema in the offspring have been reported (ATSDR.106 (.059 (<LOD-.093 (.108 (.610) < LOD < LOD < LOD < LOD . 2005).077 (<LOD-. 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. More information about external exposure (i.635) < LOD . Biomonitoring Information In the NHANES 1999-2000.

Rev Environ Contam Toxicol 1991. Carra JS. References Agency for Toxic Substances and Disease Registry (ATSDR).97(2):178192.120:1-82. Hansen JC.html. Gilman A. Fourth National Report on Human Exposure to Environmental Chemicals 111 . Dewailly E. Circumpolar maternal blood contaminant survey. J Toxicol Environ Health 1989. 4/21/09 Bloom MS. Bottimore DP. August 1995. Van Oostdam JC. Organochlorine pesticides and polychlorinated biphenyls in human adipose tissue. Stroup CR. 731-915. Watts DL. 1991 pp. Toxicological profile for mirex and chlordecone [online]. Profiles of ortho-polychlorinated biphenyl congeners. J Toxicol Environ Health 1985. New York. Strassman SC. 1994-1997 organochlorine compounds. Stehr-Green.cdc. Eds.gov/toxprofiles/ tp66. Wood PH. et al. hexachlorobenzene.330:55-70. Demographic and seasonal influences on human serum pesticide residue levels. Smith AG. Vol. dichlorodiphenyldichloroethylene. Chashchin V. Odland JO. Jr. Kutz FW. Moysich KB. Kutz FW. et al. and Mirex among male Lake Ontario sportfish consumers: the New York State Angler cohort study. 2 Classes of Pesticides. Environ Res 2005.atsdr. Olson JR. Leininger CC. In Hayes WJ. Chlorinated Hydrocarbon Insecticides. Swanson MK. Jr and Laws ER. Handbook of Pesticide Toxicology.27:405-421. Sci Total Environ 2004. Vena JE. Academic Press. Inc.15:385-394. PA. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.Organochlorine Pesticides effect. Available at URL: http://www. 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. The human body burden of mirex in the southeastern United States.

00-3. Trichlorophenols have been detected in fish taken from waters near waste water treatment and industrial discharges (ATSDR.40 (.0) 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. < LOD means less than the limit of detection. 2.S. interval) Selected percentiles ( 95% confidence interval) Sample 95th 16.4.71 (<LOD-8. Both chemicals have been detected in air. and sediments.6-TCP).30-44. Trichlorophenols are no longer manufactured commercially.60 (2.50-25.4.0) < LOD 973 1178 1021 1319 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .7) 24.9 and 0.50 (.71 (<LOD-8.0) < LOD 21.40 (.6-TCP in any of the samples (U.4.20) < LOD 5.80 (1.40 (1.0 (5.Organochlorine Pesticides 2. other organochlorines. surface water.40 (2. including hexachlorobenzene and hexachlorocyclohexanes.0) 2.940-3.0) < LOD 5.40 (2.4.980-3.40) < LOD 6.40) < LOD 4.0) 2. 2006).30 (.4. 1999). and polychlorinated benzenes (Kohil et al.0 (4.00-8.30-40. 2. General population exposure may occur by ingesting contaminated food or water and by inhaling contaminated air. may occur by inhalation or dermal routes.S.0) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 1.72) < LOD 1.19 (<LOD-6.00 (3. usually at herbicide production or waste incineration facilities.7.0 (3.50) < LOD 1. hexachlorobenzene.6-TCP were used as intermediates in the production of certain pesticides.920-3.5TCP and 2.40-18. 112 Fourth National Report on Human Exposure to Environmental Chemicals .30) < LOD 4.6-Trichlorophenol CAS No.30) < LOD < LOD < LOD < LOD < LOD 1.40-11. which may vary for some chemicals by year and by individual sample.0) 2. soils.4.4.30-11.0 (4.0) 2.10-3. Environmental sources of these compounds include industrial discharges or run off from pesticide facilities or disposal sites.60) < LOD 8. 2.4. EPA.20) < LOD 90th 5.5-trichlorophenol (2.80-41.0 (3..4.6-TCP was also used as a wood preservative and may still be used in production of some fungicides (ATSDR.80) < LOD 1.30-27.5-TCP) and 2.8) 21.4.8-tetrachlorodibenzo-p-dioxin occurs during the synthesis of 2.0) < LOD 5.S.50-63.0) < LOD 11. however.80 (2. Occupational exposures. Such workers would probably Urinary 2.0) < LOD 5.90-33.42 (<LOD-12.4. 1976).900-2.20) < LOD 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 1.20 (4. 95-95-4 2.50 (2. Exposure to trichlorophenols also may result from metabolism of lindane.00 (2.60-18.27) 696 661 521 696 603 939 Limit of detection (LOD.0) < LOD 11. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.63) 18. Historically. are metabolites of several organochlorine chemicals.31 (<LOD-9. public drinking water systems did not detect 2.40 (1.40 (2. population from the National Health and Nutrition Examination Survey.950 (<LOD-1.30-3.30-27. 1999).42 (<LOD-8.00-3.0) 5.60-8.27) 482 570 681 815 831 1112 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD 1.980-3.0 (4. Survey Geometric mean (95% conf.20-36. but they may be produced as by-products during manufacturing of other chlorinated aromatic compounds. recent sampling of U.40 (2.9 (<LOD-121) 9.40) < LOD 1.50 (1.5-trichlorophenol.60 (4.57 (<LOD-15.60 (.6-trichlorophenol (2.20-71.0 (8.30-27.4.50-16. 88-06-2 Metabolites of Organochlorine Pesticides and Other Environmental Chemicals General Information The chlorophenols.0) 14.0) 2.3.5-Trichlorophenol Metabolite of Several Organochlorine Insecticides 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.03) 9.9. Formation of 2.5-Trichlorophenol CAS No.

05-8. recent small studies have not demonstrated increased exposure to trichlorophenols in workers who dredged contaminated soils or incinerated waste materials (Agramunt et al.cdc..3 mg/L reported in German adults aged 18-69 years (Becker et al.78 (3.1 (<LOD-58.86 (3.S.4) 5..atsdr.6) 4.5) < LOD 12. At lower doses. In the same 2-6 year old children.0 mg/L. 1989).68-4.html.16) < LOD 90th 5.57 (<LOD-7.3 mg/L in a nonrandom subsample from NHANES III (Hill et al.4.64 (4.13-13. 1989).6) 4. furans.36 (1. Survey Geometric mean (95% conf.37) 16.15) < LOD 2. Biomonitoring Information In the NHANES 1999-2000 and 2001-2002 subsamples.4. Urinary 2.e.16 (.93-11.24) < LOD 1.4.02-3.43 (2.69 (2.4.53-3. Radon et al.82 (<LOD-32.32) < LOD 4. environmental levels) and health effects is available from ATSDR at: http://www.5-TCP or 2.2 (2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. the 95th percentile urinary 2.6-TCP as reasonably anticipated to be a human carcinogen.78) < LOD 1. More information about external exposure (i. leukemias.95 (3. Neither 2.2) < LOD 5.24-11.37) 696 661 521 695 603 939 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.7 (4.4.55 (4. interval) Selected percentiles ( 95% confidence interval) Sample 95th 11. which includes trichlorophenols..980 (<LOD-1.62-20.33) < LOD < LOD < LOD < LOD < LOD 2. 1995) were similar. 2003).50) < LOD 2. Laboratory animals chronically fed high doses of 2.8 (5.4.4.47-8.05-17.4. 2004).78-19..28-25.24) < LOD 5.5-TCP and limited for 2.69-18.88-16.gov/toxpro2.4) < LOD 3.19-4.00-19.4. in addition to dioxins.0) 7.60-3.6) 4. as being possibly carcinogenic to humans.4.00-29.68 (<LOD-8. but almost twenty times higher than 95th percentile values reported in German adults aged 18-69 years (Becker et al.4.9) 12. the 95th percentile urinary 2.5-TCP.4.67 (1.19-12.37-11.46 (1.24) < LOD 6.920-2. Human health effects from 2..67 (1.Organochlorine Pesticides be exposed to mixtures of chlorophenols.820-2.3 (5. However.5-TCP nor 2.57 (<LOD-7.5-Trichlorophenol (creatinine corrected) Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.5-TCP among adults in this Report and in a nonrandom subsample from NHANES III (Hill et al.20-6..4.5) 11.6-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.6-TCP.4 (6. and lymphomas.24 (3.80 (1. 2003). population from the National Health and Nutrition Examination Survey.81 (<LOD-9..02) < LOD 7.73 (<LOD-8.6-TCP levels at the 95th percentile were up to eight times higher than 3.29 (1.90 (4.6-TCP were developmental or reproductive toxicants in animals (ATSDR 1999). The 95th percentiles for 2. animals showed hepatocellular abnormalities.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..57 (3. 1995) and up to 19 times higher than the 95th percentile value of 1.53-3..31) < LOD 2.6-TCP at low environmental doses or at biomonitored levels from low environmental exposures are unknown.8) < LOD 9.6-TCP had increased rates of hepatic tumors.27-17.75 (3.44 (.74) 11.4) < LOD 3.8) 4. IARC classifies combined exposures to polychlorophenols.1) 2.2) 2. 2003.49 (1. IARC considers the experimental evidence for animal carcinogenicity inadequate for 2. 7. Fourth National Report on Human Exposure to Environmental Chemicals 113 .17) 9. Among 6-11 year old children in NHANES 1999-2000.00) < LOD 4.83-12.79-4.43) < LOD 12.2) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 2.3) < LOD 973 1178 1021 1318 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * . was similar to the corresponding percentile for 6-11 year olds in NHANES 1999-2000 (Hill et al.75 (<LOD-6. and other chlorinated compounds.9 (5.11) 482 570 681 814 831 1112 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD 1.44 (1. NTP classifies 2. urinary 2.

32) * 3.85 (2.5-TCP level of 0.80-25.8-24.40-32.59) 4.26 (2.0 (14.10-3.80-7.60-3.0-38.0 (15.53) 2.73-9.30-2.0) 9. 1998).12) 2.6 (11.90 (4.0 (6.5-TCP or 2. 2004). 0.6-TCP exposure and health effects.4.0 (4.4.8) 18.10) 2.98-11.30-11.40-2.00-4.28) * 2.78 (2.72-10.78 (2.45 (2. Biomonitoring data will also help scientists plan and conduct research about 2.3) 37.5-TCP and 2. Urinary 2.4.6-TCP levels that were as much as 450 times higher than the median level among adults in the NHANES 1999-2000 subsample (Pekari et al.0 (20.6TCP causes an adverse health effect.0 (7.S.6-19.70-3.0) 19. which may vary for some chemicals by year and by individual sample.60 (2.4. Biomonitoring studies on levels of 2.7) 33.76) 3.4. population from the National Health and Nutrition Examination Survey. 1991).90) 2.36 (1.0 (16. Urinary 2.6 mg/g creatinine) and 2.4 (17.0-68.56 (3.25-11.0-54.0) 14.70) 3.4.18) Selected percentiles ( 95% confidence interval) Sample 95th 25.28) 24.51-12.3.0) 10. < LOD means less than the limit of detection.9) 13.6) 26.0) 6.4. In harbor workers exposed to chlorophenol-contaminated river silt.45-9.7) 21.3) 20.4.70 (2.69 (3.0) 13.90 (3.46-3.0) 13. the median urinary 2.0) 7.4.09-7.53) 4.89 (3. respectively.1) 16.35-3.4.40-4.4.32) 3.33-4.60-21.23) 3.58 (1.6-TCP level.2 (14.60) 6.90-8.4.0) 14.74 (2.52-3.0-50.9) 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 2.0) 19.18-3.8-13.40-2.6-TCP than are found in the general population.4 (9.3 (11.4 (8.2) 12.40) 2.45) < LOD 11.57 (<LOD-2.95-6.98-7.30) 4.0 (12.80-6.01-6.8) 32.95) 3.2) 481 574 678 820 830 1109 99-00 01-02 99-00 01-02 2.0) 7.0 (6.3-26.0) 10.7 (9.6-TCP in urine does not mean that the level of 2.04) 2.06) * 2.65) 15.6-Trichlorophenol Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.65 (5.5-TCP and to the median 2.0) 12.48-26.70) 5.80 (2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.00-21.66 (8.91-4.59-6.68 (<LOD-2.Organochlorine Pesticides A small study of adults who ate Great Lakes sport fish reported a mean urine 2.6) 970 1178 1019 1325 99-00 01-02 99-00 01-02 99-00 01-02 2.7) * 99-00 01-02 99-00 01-02 99-00 01-02 4.67-12.31) * 2.20 (3.0 and 1.0) 13.63) 90th 15.9 (11.00 (2.00 (4.14 (2.10-2.20 (3.9 (13.0-38.5 mg/g creatinine) were similar to the limit of detection for 2.5-TCP or 2.4.54) 6.99) 6. for males in NHANES 19992002 (Agramunt et al.0 (11.07 (<LOD-3.40 (2.60) < LOD 5.0-44.7 (13.23) 2.8 (9.0) 17.0-37.80 (2.55-3.0-43. interval) 2.08 (2.60 (3.70-6.7-3. Sawmill workers exposed to chlorophenol wood preservatives had urinary 2.4 (10.4.6-TCP (0..4.6-TCP were monitored in a group of hazardous waste incinerator workers from 19992002.5-TCP or 2.8-15.4.30-2.0) 9.50 (2.67) 4.36-5.2) 25.6) 21.4.74-3.87-14.49 (6.3-17.6-22.80 (3.4.70) 5.47 (3..0-18.45 (5.6 (12. see Data Analysis section) for Survey years 99-00 and 01-02 are 1.0) 15.23-2.52 (2.7 mg/L.4.6-17. was about six times lower than the median urinary levels for males in this Report (Radon et al.44) 75th 4.58-3.5-46.0) 13.3) 23.40) 4.0 (14.50-5.0 (6.31 (3.40-14.40) 3.0 (14.1 (8.75 (8.80) 1.0 (13.95 (4.0) 11.70-6.4-17.36 mg/g creatinine.70 (2.20-3.6TCP values. Mean values of 2..60 (3..3 (11.84) 2.0 (20.30-33.32-4. similar to the limit of detection for this Report (Anderson et al.10 (5.5-TCP (0.24 (2.0 (9.00 (1.10-3.40-7.6-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. 2003).0 (8.89-6.20) 4.0-41.09) 15. 114 Fourth National Report on Human Exposure to Environmental Chemicals . Finding a measurable amount of 2.79 (5.60-37.2-0.20-23.02) 2.70) 1.0) 17.85) * 3.10) 6.1-25.92 (2.40 (2.7-16.9) 694 677 519 696 602 931 Limit of detection (LOD.80-20.5-TCP and 2.40) 2. Survey Geometric mean (95% conf.0 (15.0) 11.1 (10.5-TCP or 2.4.0 (8.20-6.

38 (4.53 (3.51) 18.10) 4.9 (9.16-10.00) 4.83 (3.44 (3.4.82) 2.60 (4.98) 10.32-19.40 (7.Organochlorine Pesticides Urinary 2.5) 9.8) 21.7-36.8) 19.63-15.95-2.33) * 2.4) 8.9) 8.78) 2.2 (12.87 (3.9-32.46-14.26) * 99-00 01-02 99-00 01-02 99-00 01-02 4.9-29.00 (3.5) 11.82 (8.67-17.29-4.76) 2.88) 5.00) 4.10-9.2 (7.0 (11.17) 13.2 (13.22 (1.9-64.6 (22.76) 1.09-3.65) 18.1 (13.15 (1.81) Selected percentiles ( 95% confidence interval) Sample 95th 21.02 (1.00 (2.8) 11.1-21.87-6.82 (3.6 (9.11) 10.65-21.4 (12.49) 4.5-28.04-16.6) 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 2.52 (5.33 (7.23 (1.88-7.0 (6.77-4.78 (2.06) 4.54 (2.99-2.3) 8.7 (14.38-5.51-21.70-9.6) 12.82-2.87-7.72) 32.1) 14.41-6.87) * 2.55-2.89) 10. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.56-5.23) 4.79-17.4) 9.24 (1.81-9.56 (7.91 (7.8) 12.5) 12.13 (1.71 (3.6) 13.92) 4.75) 75th 4.6 (5.1) 11.60-2.3-23.47-5.68) 2.6 (6.62-15.9-34.17) 2.18-2.1) 694 677 519 695 602 931 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.59 (2.56) < LOD 11.38) 22.53) 4.5 (10.7) 25.10 (6.63-13.87) 2.52) 2.01 (3.2 (8.42) 2.30-2.88) 4.17-4.90 (1.0 (9.98 (1.43 (2.13-6.94-13.14-13.63 (2.6) 8.88 (2.26-13.14-2.22-9.52) 2.05 (6.50 (2.88) 1.33-2.6 (9.32 (2.90) 2.7) 6.1-32.29-4.5) 11.83-6.2) 19.35 (3.S.50-8.25-15.83-5.25-17.18-4.73-22.83-6.26 (6.9) 481 574 678 819 830 1109 99-00 01-02 99-00 01-02 2.58 (4.8 (7.5) 8.19-5.43-7.1 (8.76) 4. interval) 2.73) 5.25 (3.33 (1.4) 4.9 (9.52 (3.9) 19.81) 2.96) < LOD 4.02) 3.63) * 4.41 (3.68) 2.0) 8.91 (3.63) 4. population from the National Health and Nutrition Examination Survey.9) 7.88) 4.9) 8.78) 90th 12.25 (3.0) 10.53-11.6 (10.65-2.4 (11.40 (2.6-31.3-37. Fourth National Report on Human Exposure to Environmental Chemicals 115 .29 (6.25-2.88) * 2.8 (8.6) 970 1178 1019 1324 99-00 01-02 99-00 01-02 99-00 01-02 2.38 (2.63 (<LOD-2.22 (3.48-2.6-Trichlorophenol (creatinine corrected) Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. Survey Geometric mean (95% conf.04-2.51 (2.42 (2.72-16.53) * 2.28-4.6 (12.06-2.22 (<LOD-2.43 (<LOD-2.22-2.20-2.65) 2.15 (6.49-3.27-9.5 (7.91-2.76-8.77) 2.08-2.3 (9.06) 11.89-2.21-11.5 (8.05 (3.66-4.

Falk C.cdc. Chlorophenol exposure in harbor workers exposed to river silt aerosols.epa. Luotamo M. et al. Pesticide residues in urine of adults living in the United States: reference range concentrations. July 1999. Seiwert M. The Great Lakes Consortium. Kaus S.71:99108. Domingo JL. Int J Hyg Environ Health 2003. Hill RH Jr. Schulz C. Hill RH Jr. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children. Pekari K.gov/safewater/ccl/pdfs/reg_determine2/report_ ccl2-reg2_ucmr1_occurrencereport. Aitio A. Toxicological profile for chlorophenols [online]. Hanrahan L. 206:15-24.S. Lindroos L. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR).63:57-62. U. html. Safe A. Olson J. Domingo A.EPA). Jarvisalo J. Gregg M. Heinrich-Ramm R. Needham LL.18(4):469-474. Kohli J. December 2006 Draft. Anderson HA. Becker K. 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]. Available at URL: http://www. Am J Ind Med 2004.45:440-445. Int Arch Occup Environ Health 1991. Available at URL: http://www. et al. Szadkowski D. Fast DM.atsdr. To T. Toxicol Lett 2003. Baur X.pdf. Bailey SL. 4/21/09 Agramunt MC.gov/toxprofiles/tp107. Head SL. Needham LL. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Arch Environ Contam Toxicol 1989. S. Shealy DB.106(5):279-289. Can J Biochem 1976. Monitoring internal exposure to metals and organic substances in workers at a hazardous waste incinerator after 3 years of operation. 5/19/09 116 Fourth National Report on Human Exposure to Environmental Chemicals . Corbella J. Jones D.54(3):203-208. The metabolism of higher chlorinated benzene isomers. et al. Radon K. Seifert B. Urinary excretion of chlorinated phenols in saw-mill workers. Environmental Protection Agency (U.146:83-91. Environ Health Perspect 1998. Baker S. Holler JS. Environ Res 1995. Smith SJ. Poschadel B. Burse VW. Wegner R.

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

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

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

00-27.10 (.530 (<LOD-2.10 (.2) 672 678 473 509 696 578 595 948 752 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.80 (2.50-5.4) 17.810-1.56 (1.60) .2) 16.70 (4.S.4) 20.740-2.47) 5.70-14.33-18.00) 3.80) 4.46) 10.0) 9.27-15.8 (12.10 (2.70) < LOD < LOD 75th 3.80-4.8) 19.60-18.29) * * 1.00 (1.80) .58) Selected percentiles ( 95% confidence interval) Total * * 50th 1.54 (3.82) 10. respectively.98-5. 01-02.8) 7.52) 6.89) 9.00 (5.8 (9.35-12.7 (14.33 (5.38-5.0) 6.58 (3.12) 4. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.50) 2.17-3.70) < LOD < LOD 1.04) < LOD 1.91) 4.981 (.7) 11.0 (12.4 (7.52-11.290 (<LOD-.19) 9.0 (8.0 (8.20-30.82-12.15-12.5 (8.10 (2.0) 7. and 03-04 are 0.0 (6.35-16.58 (5.6) 7.15) 14.954 (.0) 11.34-7.56-13.20 (.26-6.16) 4.40-16.2 (9.02) 4.80) 2.21 (.45 (2.780) < LOD 3.2.8 (8.90) 2.670-1.0) 5.36-4.26 (5.79-7.8-32.70-23.39 (3.97) 90th 7.81) 1.5) 20.71 (2.758-1.80-22. interval) 1.08 (<LOD-2.61 (3.47) * * 1.13 (2.21) 9.13-2.4 (7.56 (4.60-25.2) 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 1.70 (2.620-1.2 (9.0) 10.20-4.60 (5.93-24.0) 15.42) .42-3.74 (8.90-4.1 (9.00-12.20 (2.00 (4.30 (2.579-1.60) < LOD < LOD 4.0 (7.9) 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 1.40-5.0) 11.8) 7.0) 5.0) 5.55-6.80) 3.73) * * .0) 6. 120 Fourth National Report on Human Exposure to Environmental Chemicals .5) 15.600 (<LOD-1.0 (4.750-1.30 (2.890 (<LOD-2.40-11.623-1.5-16. < LOD means less than the limit of detection.860-2. population from the National Health and Nutrition Examination Survey.599-1.39 (8.16 (2.67) 3.80) .0 (9.68-7.14) * * .40 (.9-18.3) 17.490-2.0) 6.2 (14.48-7.00-7.5 (11.9) 14.66) * * 1.30-6.11 (.3) 14.08-2.7 (12.43-12.6) 18.10-7.0 (9.00-27.0) 11.44 (2.700-1.0 (7.13 (2.4) 18.2 (7.12-19.1) 13.0) 20.70-11.60 (1.63) 1.40-19.5-17.52) * * 1.00) 3.0 (8.0) 10.81) 11.2-20.0 (7.08-15.71-9.98-12.20 (.90-5.96-3.70-19.2 (11.4 (9. see Data Analysis section) for Survey years 99-00.8) 11.0) 10.0 (6.07-10.94) * * .28) 1.97) 8.2) 14.93 (4.2 (7.00-12.2) 16.44-38.80) 2.0) 11.81) 11. and 0.34-3.56 (6.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.20 (.53) 4.0-27.2.0 (5.61) 4. 0.35-11.80) 11.0 (7.3) 16.0) 10.9) 8.1.2 (7.99 (5.2) 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 1.85 (3.32 (.0-28.02-5.50 (.26-8.74 (8.9 (8.50 (2.10) < LOD < LOD 4.76 (2.86-15.80 (4.840-1.90 (1.50 (4.1) 10.72) 5.00-19.51) 2. which may vary for some chemicals by year and by individual sample.55-8.40-1.757-2.27-3.58 (2.23-5.90) 3.30-4.40-14.830 (<LOD-3.37 (3.970-2.57-7.1 (10.1-23.01) * * 1.290 (<LOD-1.86 (1.20-7.30 (4.60-11.0) 10.8 (14.44-3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.83 (5.70) .1) 95th 13.79 (5.4 (9.50-36.1-17.22 (.95) 5.05-7.10) < LOD .717-1.80) 2.20 (.0) 12.2 (14.32) 1.94) 3.3-15.955 (.80-24.03 (.

40-14.36) * * 1.5) 7.02 (2.51-5.23) 4.68) < LOD < LOD 3.533-1.55-20.25) < LOD .10-13.855 (.29) * * .05) .67-19.77 (6.87 (3.11-6.29 (2.79-3.7 (10.574-1.30) 2.4) 4.6) 13.00) 8.40-5.870-2.60) 2.56) 7.5 (4.7) 5.5) 11.94 (2.7 (8.2 (10.2 (8.7) 18.540-1.75) 2.40-3.2) 5.94 (4.38) .1 (8.40-12.40) 4.2) 9.8) 16.620-1.37-5.78 (2.05 (.1 (6.8) 6.80 (7.3) 16.60-9.3) 12.94-23.6) 9.88) 2.98) 9.19 (4.28 (2.98) .47) * * .6 (10.67) 1.58) * * 1.13) 4.6) 11.860 (.83 (7.500-1.9) 11.9 (5.74) 4.61-13.900 (.39 (2.47 (3.5-32.82-14.88 (5.42 (3.81 (1.71) 10.54-11.9 (9. interval) .76-4.62-5.45-5.98-5.67) 4.47) 2.98 (3.790 (.46-5.93) 9.35 (1.69) 4.57 (4.4) 13.92-5.61-29.75) 14.66-15.54-2.430-1.31-14.57) 4.06-2.820 (.61 (1.8 (10.3) 5.2) 7.69-10.07 (.82-14.27) < LOD 2.2) 13.41) .95 (3.53) 9.43 (.30 (1.883 (.87-5.43 (3.56) .94-10.20-8.88-15.9-28.88-10.710 (<LOD-1.40) < LOD < LOD 75th 2.09-11.28) 10.780 (<LOD-1.28-9.2) 95th 12.90-5.7 (9.1 (9.34) * * .15-10.93-9.920 (.66 (1.34) < LOD < LOD .9) 12.26) * * .41-12.05 (1.04-6.68-4. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.633-1.52) 4.84) 7.32-12.549-1.2) 5.94-22.1 (11.94-9.5) 7.7) 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 .66 (5.00 (4. Fourth National Report on Human Exposure to Environmental Chemicals 121 .87 (1.81-5.3) 952 1187 927 997 1332 1001 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.00 (4.608-1.44 (2.54-15.62) .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.8) 7.1 (7.1) 4.35) < LOD < LOD 3.54-4.03 (7.01-2.560-1.924 (.98) .1-15.0) 7.10 (3.996 (.47 (3.80 (2.09) 2.53 (6.82-26.03 (2.75 (3.00-19.3) 15.2 (6.95) 2.53-11.72) 11.40-28.1 (10.00-13.02 (7.45-11.85) 2.4 (4.03) 2.960 (<LOD-2.34 (6.79-9.570-1.75 (7.83) 8.02-2.76) < LOD .890 (<LOD-1.45-5.0 (8.37) 9.510-1.890 (<LOD-1.84 (5.818 (.14 (3.28 (5.1) Sample size 1949 2519 1928 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.03-6.773-1.37 (5.S.66-34.830-1.69) 2.80) 9.5-16.42) 12.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.21-23.8) 8.57 (6. population from the National Health and Nutrition Examination Survey.60) * * .40 (3.00-17.64-5.89) * * 1.1) 4.4) 4.440 (<LOD-2.02-14.71-2.932 (.66 (2.98-22.41) Selected percentiles ( 95% confidence interval) Total * * 50th .37 (4.85 (6.47 (1.90-8.566-1.80 (6.03) 2.18 (.82-6.50) 7.38 (1.4 (9.8) 12.28 (4.69 (4.46) 2.750 (<LOD-1.56) 4.650-1.92-2.7) 12.5) 8.25) 6.0) 6.5-20.57-10.54) .5-13.2) 8.74) 90th 7.960 (.04 (1.6) 8.93-5.89-3.9) 16.34 (6.9 (9.61 (1.24-3.75-7.6 (9.09 (.5) 12.56-13.37-3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.31 (3.23 (4.43) 2.73 (1.

5.42 (1.52 (6.3) 8.670 (<LOD-1.67-10.80 (5.3) 10.3) 22. and 03-04 are 0.8-20.22) 8.27) 4.30) 8.0) 11.92-17.6 (10.06 (2.95 (2.72) 2.80) .7) 16.50) .1 (10.90) 8.0-24.50) 5.5-26.5 (8.39-13.0 (10.70) 2.9-17.90 (5.37 (3.46-28.00) < LOD .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 1.7-21.00-16.0) 7.90-15.0 (5.61 (3.50-4.60) < LOD < LOD 2.27) 9.740 (<LOD-1.80 (2.33-11.90) 4.53 (3.0 (10.10-15.81-6.95 (5.4) 7.40) < LOD < LOD 75th 2.9-15.95-9.0-29.17 (7.16-1.7-19.35) 4.66-13.4) 672 678 498 509 695 579 595 948 757 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.9 (12.27) .90 (6.22-12.50) 3.0) 18.0) 23.86-10.24 (2.77-3.60 (2.64) 10.34-3. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th .80) 5.90 (2.8-21.10-4.4 (10.90-9. 01-02.0) 12.4) 11.24-5.90 (6.31-12.0) 13.7) 15.58.9) 16.7) 22.670 (<LOD-1.80 (2.74) * * * * * 1.20) 3.6) 14.6) 14.20) 3.88) 10.25 (2.98-9.6-41.67) 3.S.9-14.18) * * * * * * * * 1.30) < LOD < LOD 4.6 (10.6-19.1) 11.62-17.67) 4.0 (8.10 (.70-9.80-12.9) 95th 14.31) 1. and 0.2 (7.5) 471 576 310 664 822 717 814 1121 938 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * .7) 14.50-5.29-4.90 (6.78) 5.4 (10.70-9.10) 6.80-3.15-2.61-32.8) 8.6) 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 * * * 1.8 (12.40 (2.90 (6.9 (7.2 (9.3 (9.70 (1.0 (13.0) 9.0) 6.650-1.7 (10.80-6.0) 19.89 (2.60 (6.20 (<LOD-2.00) 3.9) 9.28 (7.680 (<LOD-1.8) 9.0 (9.6) 18.6) 11.80-8.97-4.90 (1.80) .59-3. see Data Analysis section) for Survey years 99-00. < LOD means less than the limit of detection.96) 90th 7.7 (11.0 (9.0) 11.30) 3.580-2.00-4.8 (12.51) < LOD 1.0 (15.00) 8.0) 14.90-15.58 (1.670 (<LOD-1.3) 20.18 (3.0-24. respectively.0-33.30) 3.41) 3.70-8.34-10.89) 2.14 (6.7) 10.39 (5.84-4.0) 14.0) 12.0-19.70-5.790 (<LOD-1.88) 3.35 (6.5.5 (9.0) 9.00-18.5) 21.82) 8.80-21.49-4.3 (9.4-17.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. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.70 (8. 0.90-31.4 (14.66) 4.75 (2.22 (6.5 (8.3 (6.0) 12.96) 3.15-6.1-23.90 (2.8-17.970 (<LOD-2.04 (3.34-5.46-4.9) 10.45 (3.20) .01 (2.20-8. 122 Fourth National Report on Human Exposure to Environmental Chemicals .73) 7.29) < LOD < LOD < LOD < LOD 3.00-9.11-6.00 (.99 (3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.3) 14.41-5.92) 9.10 (<LOD-1.37) 2.3 (11.2) 14.80-4.47-6.8-20.00-18.670 (<LOD-1.60 (5.0) 13.3 (7. which may vary for some chemicals by year and by individual sample.0 (14.910 (<LOD-2.90 (2.20-4. population from the National Health and Nutrition Examination Survey.10-10.63-14.77-14.27 (7.1 (10.20-18.3 (12.35-3.40 (2.75 (3.22 (6.27 (3.34 (6.80-14.0 (7.31-7.30) < LOD < LOD .12 (4.00) 7.00) 3.00-4.

1 (8.77 (2.77) 3.1) 10.86) 9.973 (.89-3.2 (9.4) 16.00 (3.16-14.7) 15.79-9.5 (9.3) 6.4) 9.85-8.3) 12.44-6.67 (7.11 (5.50 (6.0-21.3-15.620 (<LOD-.4-15.9-17.55) .54) 9.2) 10.30) 2.07-3.38 (2.2) 16.29 (5.96-11.0 (8.28 (1.01-5.27-13.2) 12.99) 2.89) 5.7 (10.42-19.69-11.68-4.97-4.32-8.940) < LOD < LOD 1.30) 7.810 (<LOD-1.63 (6.92) 3.80) 3.9 (9.03) 3.89-10.38-13.5 (8.2) 12.3-17.4-16.52-3.75-3.91-9.81 (7.51-7.27) 5.5 (15.4) 7.06 (<LOD-1.68-19.4-18.2) 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.95) 90th 8.00 (5.00) 8.99 (4.03 (6.2) 15.15 (1.95 (2.15) < LOD < LOD 75th 2.20-3.6) 12.7) 14.43 (2.85-17.30) 8.63 (2.0 (10.7 (8.45) 3.05-3.4-16.74-19.6 (12.0) 14.6 (11.71 (1.690 (.6 (10.6) 6.7-19.12) < LOD < LOD 4.78-10.6) 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 1.94-14.88 (1.71) < LOD < LOD 2.36 (2.5) 8.14 (2.94 (5.32) 2.12 (7.4) 7.4) 6.89 (3.27) * * * * * * * * 1.03 (2.38 (.2) 19.3) 9.S.07) 2.70-2.38) 1.6) 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 * * * * * * .53-8.8) 16.91) 3.00 (<LOD-1.97) < LOD .890-2.0 (11.6) 952 1187 945 997 1331 1017 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * .5 (11.02-4.07) 2.88-7.55 (2.25 (4.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.93 (6.74-4.47-9.3 (7.1 (19.93 (2.4) 7.34) < LOD < LOD < LOD < LOD 3.6) 13.68-10.3-21.54 (7.86-3.8 (8.0-19.00) 2.06) .78) 4.30-5.27) 1.33-10.6 (13.8) 14.8 (10.7 (10.2-15.86 (3.96-10.77 (2.2 (9.29) 3.0 (13.920 (<LOD-1.2) 8.87 (3.3-17.92 (5.37) 3.6 (11.21) * * * * * 1.9 (9.89-3.2) 12.00 (<LOD-1.9) 16.42) 7.3-34.54-5.64-11.09-11.07 (5.83 (6.950) .9-25.25-9.29 (2.70-35.72-4.48 (2.1) 20.68) . population from the National Health and Nutrition Examination Survey. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th .5) 22.2-30.41 (7.21-21. Fourth National Report on Human Exposure to Environmental Chemicals 123 .23-3.3) 8.530-1.27) < LOD .75-3.9) 19.45) 6.590 (<LOD-.37-5.7) 9. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.28) 6.7) 14.95) 3.61 (2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.89 (2.29-2.780-1.78 (6.42) 8.79-6.4 (11.7 (11.67 (1.59-3.5) 10.82-11.6 (13.1) 13.33) 3.55) 16.00 (7.83 (7.28-12.09-11.34-18.04) 9.6) 7.910 (<LOD-1.93 (<LOD-2.760 (<LOD-1.58 (4.6-19.7) 12.7-23.11-3.8) 11.78 (4.5 (10.5) 13.38 (1.51-10.89-13.6) 95th 16.82-8.72) 4.39-17.93-10.4) 15.850 (<LOD-1.00 (2.5-17.18) 2.6) 14.1 (13.9 (9.19) 3.16 (3.73 (5.50-17.

780) .910) 1.303-.46) 1.730) . and 03-04 are 0.382-.80) 2.17) 1.380-.31-3. which may vary for some chemicals by year and by individual sample.740-1.83 (2.570-1.58 (1.60) 2.960) .20-1.32 (1.549 (.550 (.80) 5.01-3.20 (1.510 (<LOD-.05-2.75-2.18 (1.780 (.96-3.18 (.540 (.22-3.90) 2.750) 1.30-3. 0. 01-02.90) 2.970) 1.940) < LOD .50-2.34) 2.336-.990-1.78) 952 1187 907 997 1332 998 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * .22 (1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.10) 1.680-1.60 (2.31-3.95) 2.860) < LOD < LOD .930 (.50 (1.96-5.54) .26) .03) 1.580-.87-3.910 (.710 (.425 (.390-. population from the National Health and Nutrition Examination Survey.57 (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.585) * * .10) 3.09.449 (.73-5.597) * .61 (1.949) . respectively.65 (2.930-1.80) 3.10) 1.60) 3.950) 90th 1.91) 2.74-5.10-1.78) .69-4.20-2.14-1. 124 Fourth National Report on Human Exposure to Environmental Chemicals .160 (<LOD-.570 (<LOD-.80 (2.50 (1.57 (2.690 (.00-2.80 (1.14 (1.700) .20-3.77 (1.440-.359-.41-5.22-3.70 (1.27 (2.48 (1.94) .459 (.29-2.46 (2.740 (.75 (2.39) 2.89) 672 678 478 509 695 553 595 948 745 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.32-1.650-.1.S.20) 2.560-.30) 4.960) .90 (1. interval) Selected percentiles ( 95% confidence interval) Total * .20) 1.11-3.59-2.83) 1.500 (<LOD-.15) 2.930) < LOD .600-1.38) 1.380-.390-.820 (.48 (2.240 (<LOD-.759) * .70 (1.30) 1.343 (.16) 1.710) .45 (1.50 (1.880 (.980) 1.880) < LOD 75th .33-2.54 (2.340-.55 (3.98-3.16-3.01-1.09 (.30) 4.30) 2.749 (.740-.10) 1.20) 2.22-2.21) 3.800 (.94 (3.455 (.380) .30 (.260 (<LOD-.80) 3.27 (3.690-1.350-.970) .510 (.70 (1.25-1.76 (1.16) 2.10-1.30 (.820 (.350-.46 (1.740 (.88) 1.00) 2.37-2.584) .20 (1.587) * * .17-4.570 (.13) .960-1.657) * * .50-2.388-. and 0.15) 2.31) 2.40 (1.95 (2.98) .20) 1.590-.80) 2.17) 1.50) 1.20) 3.11-3.505 (.690) .47) 2.600-.36-4.400) .570 (<LOD-.76-6.49) .42-2.98 (2.80) 3.74) 3.710 (.01) .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 * .40 (1.00) 1.592-.810) .32) 3.04) 1.22-8.680-1.398-.59-6.30 (.45 (2.570 (.83 (2.30-3.46-3.880) < LOD .79) .2.30 (1.50 (1.94 (2.720 (.31) 95th 2.780 (.930) 1.19-1.83) 2.68-5.86) 3.600 (<LOD-.760 (.41 (2.45 (1.20 (1.592) * .13) 2.201-.64 (1.86 (1.34) 2.570) * .592) * 50th . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.20 (2.280-.49) 2.210 (<LOD-.45-4. see Data Analysis section) for Survey years 99-00.70-2.20) 3.700) . < LOD means less than the limit of detection.750-1.08 (2.720-1.54-2.467 (.70-7.08 (2.78) Sample size 1949 2519 1905 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * .95-5.00 (1.453 (.63 (1.83) .618) * .910-1.47 (1.620-1.960 (.97 (2.850) < LOD .550 (.20-2.720-1.89-6.830 (.23-3.89) .35) 1.26 (2.73 (2.60-4.690-.490 (<LOD-.30-1.580-1.450 (<LOD-.77-2.00-4.04) .790 (.90-4.89) 1.670) .05-3.90) 3.960) 1.460-.840 (.457 (.353-.50 (1.73 (1.29) 1.79) .

71 (1.38 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.08-2.700 (.22-3.33) .25-3.460 (.453 (.790) .36) 3.510-.04-1.72 (2.348-.38 (2.05-4.32) 5.688) * . Fourth National Report on Human Exposure to Environmental Chemicals 125 .02-3.840) 1.485) * * .39 (1.39) 2.640 (.05) < LOD .62 (1.22-2.640 (.58) 3.180 (<LOD-.98) 1.645) .750 (.16-2.700 (.330 (<LOD-.390-1.870 (.99) 2.18-2.24) 4.23) 3.79) 1.43) 1.91 (1.77 (3.840) .310 (<LOD-.32) 1.480) .72 (1.08-2.630) * .02-6.05 (1.320-.58-6.640 (.79 (1.05) 1.42-6.22 (2.350) .444-.08-3.590 (.136-.70 (3.88) .08 (2.320-.82) 2.830) 90th 1.42-8.57-4.270-.08 (.980-1.32) 2.69 (3.372 (.550-.55 (1.460) .710 (.90) 2.62 (2.71) .07) 1.380) .89 (1. interval) Selected percentiles ( 95% confidence interval) Total * .920) .412-.80) 2.590-1.47 (1.92 (1.58 (1.850) 1.14 (2.97) 1.08-2.830 (.60) .23) 2.77-4.44-2.72) 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 * .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.540-.22) .07-3.448 (.75 (2.08-3.580 (.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 * .19 (1.330-.11 (.800-1.680 (.840) 1.310 (<LOD-.92-8.49-4.310-.900) 1.49 (1.470 (<LOD-.S.370-.31-1.30) 3.38-3.742) * * .67) .57 (1.28 (1.34 (1.710 (.390) .800) < LOD .94) .22) 1.22-3.67) 1.730) .253-.710 (.02-3.06) 4.10) 2.70 (2.67-3.990-1.270-.08-3.380-.740) < LOD 1.305 (.97) 2.00-3.44) 2.11) 1.280 (<LOD-.510 (.65) 2.368) * .393 (.97 (1.500-.42) .64 (2.95) 1.73-3.71) 2.75 (1.820) 1.690) < LOD < LOD .23) 2.520-.61-3.300-.11-2.16) 1.13 (1.76) 1.550-.400) .470) .515) * * .760) < LOD 75th .52) 3.230 (<LOD-.32-1.740) .57 (3.234 (.00 (3.318-.72-4.61) 2.400-1.66) .560 (.590) * 50th .75) 6.535 (.880) 1.41 (.720-1.81) 2. population from the National Health and Nutrition Examination Survey.597) * .250 (<LOD-.55-3.23) 1.43 (1.22) 4.660-.870) .53) .30-2.03-1.07) 1.03-2.42 (.520 (.940-1.447 (.760) .66 (2.552 (.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.591 (.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 * .72) 1.403) .20) 1.07) 5.07) 1.510 (.45 (1.750 (.84-6.60 (1.29-4.720 (.47-4.73 (2.07-2.930-1.00-1.09) .92) 3.67 (1.69 (1.47 (1.790 (.61-3.67 (1.17) 2.471-.20-7.460-1.17-2.52 (1.88 (1.670 (.20-2.580) .43) 2.530 (.550) .04) 95th 2.08) 2.910) < LOD .07 (.700 (.50 (1.509 (.580-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.23 (.16-1.84 (2.87 (2.377-.32 (.33 (1.440-1.335-.270 (<LOD-.300 (<LOD-.560-.78) 3.250 (<LOD-.60) 1.08-3.17) 2.950-2.75-3.490 (.61 (3.04-5.820) .99) 1.480-1.45 (2.89-3.82 (2.64 (2.97 (1.08) 1.43) 2.06-2.560-.63 (1.285-.05-2.60 (2.57-2.550-1.77-3.739) * .380-1.50) 1.

13 (1.9 (19.36-2.90-8.41) 1.6-54.10 (1.70 (1.690-3.57-2.1) 95th 48.35-6.44-7.0) 4.26 (.3 (12.0 (8.18) 6.3 (24.3) 28.0 (13.0) 3.49-2.5-40.0) 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 2.96) 5.0) 5.30) 11.29-9.8) 32.6-45.32 (2.1-25.04) 3.79 (1.70-6.1 (10.92-5.9) 48.81-3.1 (25.54 (3.69) 2.4-22.0) 6.77) 38.05) 1.98) * 2.9 (27.07-5.8) 41.00-24.2-47.70-17.44) 3.80) 1.64-8.18) 14.33 (5. and 0.1 (26.8) 671 678 498 509 695 579 595 947 757 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.S.0-110) 34.8-21.0-58.0) 45.0 (40.6 (26.77 (1.83 (1.0) 33.0 (25.2) 31.70 (1.57-2.50-20. 0.0) 32.0-49.4) 38.0-260) 34.0 (38.0) 28.79-2.25-3.0-50.8 (12.3 (23.0) 17. population from the National Health and Nutrition Examination Survey.0) 15.65 (4.0 (17.45) 2.53) 40.0) 3.70 (.0-230) 35.0) 15.1) 38.5-74.59 (1.54 (1.530-4.5-27.05) * 2.80) < LOD 1.83 (3.40) 50th 2.2 (19.80-18.9 (19.19) 2.0) 19.1) 38.0 (38.10) .86-3.30 (.99 (2.8-24.0) 4.0) 17.90 (1.41 (1.2-27.80-2.7 (12.83-2.13 (1.0) 20.4.44) 2.0 (6.59 (1.1) 18.1) 140 (46.0) 16.0 (38.3 (14.60 (2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.5 (24.0-39.7) 47.75-14. < LOD means less than the limit of detection.41) 5.1 (25.74-2.0 (26.04-8.8) 62.0 (7.18) 20.0) 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 2.2-39.48) 5.3) 31.7 (12.0-110) 42.02 (2.76 (2.0) 8.23-2.95 (5.78) 9.0 (20.0 (20.53 (1.14) 5.7-22.0 (33.2-26.0) 28.52 (4.1-47.1-40.06) * 2.92) * 2.600-2.53) 1.29) 2.41) 1.0-52.50 (2.79 (2.13) 12.0 (38.0 (21.46-6.0) 30.20 (2.0-62.40) < LOD 2.40) < LOD 1.2-33.16) 2.50-2.5.2-27.81-2.7-41.20) 1.6 (9.0) 4.9 (23.71-2.0 (38.0-39.0) 42.5-45.0-41.50-17.12 (3.58) 16.0) 3.70) 1. interval) 1.8 (12.10 (1.830-4.91 (4.5-20.0-47.23) 9.0) 31.4-76.0 (19.21 (3.3) 38.30) 4.18.98 (1.7 (28.0 (32.05-3.9) 18.86 (1.9 (10.94 (1.3 (12.30-14.0-41.21 (4.11) 2.26) 75th 11.76 (2.1 (22.0) 13.6 (15.21 (1.97) 6.3) 33.82 (1.60) < LOD 1.470 (<LOD-1.42) 1.43-7.41-4.04 (<LOD-2. 126 Fourth National Report on Human Exposure to Environmental Chemicals .0-31.0 (38.0) 20.3 (10.9) 17.0 (8.70 (7.83-2.46 (.0-29.10 (1.830-3.8) 39.0-43.11 (4.4 (15.44) Selected percentiles ( 95% confidence interval) Total * 2.70) 5.80) .46-2.10-13.50-7.19-2.9-21.1-46.8) 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 1.12) 1.06 (1.0 (11.0-92.16) * 1.45) 2.00 (.3) 26. respectively.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.0-69.09 (4.29-4.71 (4.0-41.2-80.9) 38.90) 11.63-6.67 (1. see Data Analysis section) for Survey years 99-00.0 (24.6-27.17-2.8 (26.660-2.88) 1.78 (1.48-2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.0 (38.4) 19.23-2. 01-02.1-19.72 (1.40-16.0) 16.20-4. which may vary for some chemicals by year and by individual sample.0) 18.61-2.0) 3.0-58.10 (7.4 (10.50-5.66-5.93-3.8 (22.27-6.1-20.0-62.10-4.71) 5.85) * 2.6 (11.70) 1.48-2.61 (1.80) 90th 38.2) 16. and 03-04 are 0.31-6.5) 69.4 (19.10) 39.85 (1.0 (37.0-53.6-22.10 (1.6) 52.2 (12.00 (.5) 30.90 (1.610 (<LOD-1.9-51.58-2.64-3.87-7.0 (8.88) 3.53) * 2.40-4.0-53.2-62.1 (11.7) 20.

5 (41.7 (11.97 (1.5 (17.7) 26.50 (2.5 (13.19-14.899-2.9-37.61-22.3) 13.6) 23.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.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 1.75 (1.69-5.32-3.09 (5.38 (3.00 (4.9 (26.95 (2.6-49.6) 3.8 (7.94) 19.0 (23.99-4.83) .08 (1.71-2.2-34.9 (10.2-47.06) 1.0) 48.1) 36.0 (39.3 (8.870-3.95) 90th 32.06-1.53) 1.19) 5.7-37.68) 47.59-15.12) 3.860 (<LOD-1.47 (1.8-43.94) 1.7) 61.20-5.24 (1.94-20.36-13.96-16.9-36.9) 3.6 (7.3 (10.20) Selected percentiles ( 95% confidence interval) Total * 1.9) 54.19) 5.46-6. interval) 1.2) 33.91 (6.47-17.64 (1.1) 52.50-5.80-8.7) 34.60) 4.43) * 2.07-2.96) 2.27) 50th 2.9 (39.43-12.38) 5.76-2.3-19.71) 8. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.0 (19.79-17.7) 95th 51.07-2.22 (2.2 (22.16 (1.57 (6.0-70.88 (1.5 (34.58-17.17-3.9 (19.0 (32.7-38.1 (25.17) 2.82) 1.870-3.3 (10.35) 1.35) .0-118) 29.7 (24.1) 15.61-2.2) 36.2 (9.27-3.86) * 3.4 (5.54-15.2) 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 1.1 (12.4) 14.7-43.6-51.5 (15.930 (<LOD-1.23-1.870-3.88 (4.66 (1.45 (1.66 (1.91-2.3-27.0 (17.5 (15.8) 23.0-71.75-6.0-40.8) 3.1-22.95-16.70-4.4 (11.67-3.62) 4.75) * 1.4-21.6) 112 (40.7 (10.3 (9.0) 47.4) 12.3-22.32 (3.3 (20.59-2.1 (39.48) 1.0) 30.37 (1.88 (1.1) 27. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.71 (1.18) * 2.1 (34.1 (33.680-4.2) 41.25-3.62 (2.670-1.60 (.6-32.890-4.2 (15.22-3.1) 27.16 (1.26-2.11) < LOD 1.7 (18.9) 24.46) 1.8) 15.0) 3.8) 31.03-2.4 (9.27) 10.0 (23.23) 37.1) 13.33-5.7) 30.48 (4.00-16.888-1.56 (2.44) 9.2-28.67-16.54-2.9 (13.03) 1.28) 1.4 (19.58-2.3-42.6 (24.2-70.8-45.28 (1.55 (2.5) 70.2 (21.22-2.79 (2.5-190) 30.1-60.35 (2.11-2.7 (18.67 (1.5-43.00) 6.38-1.4 (21.66) 8.9) 3.3) 28.01 (.9-95.46-5.15 (.75 (1.43-2.4-71.750 (<LOD-1.19-6.59-2.2-38.82 (2.0 (6.6) 7.19 (1.14-8.40 (2.52-4.00) 1.07) 9.6 (11.4 (25.0) 10.08) 1.9-41.23) < LOD 2.2 (8.9-18.5) 27.52 (1.18-1.9) 24.51) < LOD 1.36 (4.56) 1.0) 25.4) 12.02) 1.18) 3.21 (4.30) 28.26-4.22 (.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 2.9 (7.02) * 1.7-19.02 (.8-26.0) 13.7) 23.63-5.2) 4.7-47.7) 15.5-36.8-37.06) 75th 9.2) 13.41 (2.6 (27.45-1.7-109) 22.34) * 1.37-2.7-20.84-13.33) 1.51) .2 (16.1) 25.16-2. Fourth National Report on Human Exposure to Environmental Chemicals 127 .36) 10.67 (1.31) 2.39 (1.5 (8.6) 19.70 (1.40-7.33) 2.90 (.40-4.69-18.06) 1.8) 11.4 (25.2) 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.0 (14.88 (4.9-52.5 (6.4-34.1) 13.1) 25.S.0 (25.80 (1.4 (12.8) 32.1-63.27 (6.4) 3. population from the National Health and Nutrition Examination Survey.38-5.12 (1.16 (1.61 (1.47 (3.86) * 2.4-67.9) 12.93) 5.6-38.6) 3.68 (1.1) 17.4-39.29-5.8-34.6) 11.83 (.46-22.40 (5.2) 13.72) 2.7) 66.5-97.33) < LOD 1.57) 4.1 (50.14 (.95-16.

540 (<LOD-.380-.30) .540) 672 678 498 509 694 579 595 947 757 Non-Hispanic blacks .090 (<LOD-.830) .1.610-1.580) 471 576 310 664 822 717 814 1118 938 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * .990 (.42) .42) .290 (<LOD-.870 (.720 (.10) .350) .120 (<LOD-.090 (<LOD-.560 (.380-.690-1.700-1.850) < LOD .720-1.780) < LOD 1.290) < LOD < LOD < LOD < LOD .870 (.310) < LOD < LOD < LOD < LOD .640-1.330-.630 (. < LOD means less than the limit of detection.390) < LOD < LOD .130-.830 (.840) .100 (.760) < LOD .140-.510-1.300-.170-.410-.36) .110-.090 (<LOD-. respectively.310 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.360-.360-.380-.280) < LOD < LOD < LOD < LOD .410) < LOD < LOD < LOD < LOD .860-1.730-.540) .740) < LOD .120-. population from the National Health and Nutrition Examination Survey.230-. see Data Analysis section) for Survey years 99-00.300-1.58) .870 (.117 (.130 (.470 (.00) .700-1.099-.190 (.130-.S.120-.290) < LOD < LOD < LOD < LOD 90th .610 (.370-.32) . and 0. 01-02.150) .630 (.650) .150 (<LOD-.260 (.200) < LOD < LOD .570) .130) .190 (.10) .610-.290) < LOD < LOD < LOD < LOD Non-Hispanic whites Limit of detection (LOD.210 (.084-.090 (<LOD-.530-.130-.870 (.650) .680) .10 (.162) * * * * * .940 (.220 (<LOD-.1.30) .310) < LOD < LOD < LOD < LOD . 0.450 (.820 (.160) .550) .620 (.220 (.600 (.770) < LOD 95th .830 (.240 (<LOD-.12 (.840) .680-1.410-. and 03-04 are 0.560 (.320-.090 (<LOD-.430-.05.450 (.700-1.090 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.210 (.730) . which may vary for some chemicals by year and by individual sample.650 (.130) .15) .140) .190 (.400-.430 (.450 (.140-.10) .420-.410-1.770 (.540) .080 (<LOD-.490 (.350) < LOD < LOD < LOD < LOD .830) < LOD .930 (.30) .680 (.080 (<LOD-.650-1.180) .60) 1.850 (.440-1. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th 75th .20) .850 (.700-1.640) .680-1.820 (.310-.720) .270 (.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.650-1.900 (.990) .870) < LOD .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 * * * * * * * * * .050-.460-.13) .460 (.640 (.610 (.390 (.230) .140-.860) .171) * * .160) .640) .160-.370-.310 (.660 (.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 .870 (.40) .990) .320 (.470-1. 128 Fourth National Report on Human Exposure to Environmental Chemicals .03) .

730) .580) .03 (.310) < LOD < LOD < LOD < LOD Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.78) .36 (1.140-.520-.720 (.230) < LOD < LOD < LOD < LOD .500 (<LOD-.410 (.750) < LOD 95th .110) .290) < LOD < LOD < LOD < LOD 90th .230-.260) .090 (<LOD-.580 (.890 (.280) < LOD < LOD < LOD < LOD .860 (.110) .67) .650-1.260-.560 (.540) 471 576 310 664 821 715 814 1118 937 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * .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.62) 1.510) Sample size 1949 2515 1962 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * .190-.03 (.080 (.380-.390-.450 (.670 (.540) .440-1.080 (<LOD-.300-.700-1.650) < LOD .670 (.01 (.700 (.570-1.210 (.570-.43) .390-.800-1.200 (.860 (.24) .880-1.580) < LOD .400 (<LOD-.500) .150-.360 (.550 (.700) .700 (.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 .270) < LOD < LOD < LOD < LOD .110) .20) 1.00) < LOD .03) .740) < LOD 1.170 (.470 (<LOD-.140-.330-. Fourth National Report on Human Exposure to Environmental Chemicals 129 .02) .200 (. population from the National Health and Nutrition Examination Survey.100 (<LOD-.02-1.670-1.270 (.080) .500-1.730) .66) 1.370 (<LOD-.58) 1.330-.490-1.580 (.540 (.940) .440 (.110-.100-.070 (<LOD-.400) .410-.057-.310) < LOD < LOD < LOD < LOD .170 (.880 (.140-.520) 672 678 497 509 693 578 595 947 756 Non-Hispanic blacks .460 (.410) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.960) .060-.220) < LOD < LOD < LOD < LOD .710-1.084-.410-.570 (.730) .116 (.330-.070 (<LOD-.450) .360) < LOD < LOD < LOD < LOD .380-.380 (.070 (<LOD-.300 (.220 (.180-.340-.940) .330 (.090 (.12) < LOD .19 (.600) .380-1.190 (.09) .140) .161) * * .870) .140-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.780 (.S.410) < LOD < LOD .29 (.540 (.660-1.780) < LOD 1.360-.360-.170) < LOD < LOD .86) .580-1.070 (<LOD-.140-.600-1.760) .120) .60) .410 (.300-.860-2.990) .120) .990) .810 (.14) 1.640-1.850 (.740 (.050 (<LOD-.110) .970) .03 (.610-1.38) 1.86) .320 (<LOD-.330 (.730 (.510-.24 (.230 (<LOD-.250-.550 (.720 (. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th 75th .240-.380-.190 (.111) * * * * * .

00-17. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th 2.0) 2.830 (.16) Sample size 1949 2518 1930 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .30-3.66) 4.590 (.20 (1.83) 2.0) 4.31-10.14) 2.80 (4.0-40.60) 1.0-40.65) 1.0-38.42) 2.770 (<LOD-1.10 (3.0 (5.00) 1.14) .83-3.90-28.0 (4.480-.110 (<LOD-.18) 1.70) 2.80) < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 4.0 (5.51-8.350-.70-50.99) 19. respectively.28-9.70-30.510-.910) 2.14-5.30 (1.30 (. see Data Analysis section) for Survey years 99-00.10-3.0 (17.28) 1.0-39.425-1.10-3.0 (17.88-3.38-3.62-8.94-8.0 (7.30-6.0 (3.20-4.12-1.39 (2.40-4. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.85-3.080-1.07-3.48) 13.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. 130 Fourth National Report on Human Exposure to Environmental Chemicals .63 (3.360-1.50) 2.60) .40 (1.55-4.0) 2.850) 16.30 (1.36-3.53-7.0) 5.620-1.76 (1.07) 1.08.53 (2.05-3.380-.61 (1.21) 3.0) 5.23-6.840-3. which may vary for some chemicals by year and by individual sample.0) 7.750-1.0 (17.30) .600 (.87) 5.21-3.49 (1.40) 2.0) 2.0 (4.0-38.07-3.90 (1.90-20.900 (.0) 2.0) 2.45 (2.26 (2.20) < LOD < LOD < LOD < LOD < LOD 1.70-3. and 0.03 (. and 03-04 are 0.86) 4.42) .840 (.05 (3.51 (2.05 (2.00) .750-2.720) 2.S. population from the National Health and Nutrition Examination Survey.0) 4.87) 12. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.960 (<LOD-1.52 (1.770) 2.40-8.6) 672 678 498 509 695 552 595 947 752 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.68) 2.74) 5.70-7.46 (1.730 (.0 (13.0) 2.260-.610) < LOD < LOD < LOD < LOD < LOD 2.840 (<LOD-1.30-7.691 (.90) .70-17.62) 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 * * * * * * .29-10.67 (1.52) 5.49 (1.190-1.1.870) < LOD < LOD .90-9.800) 90th 13.0-38.67 (2.800-4.350-.94-3.610 (.43-4.82-4.740 (.50) .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 * * * * * * * * * .11) 13.370-.35-10.90-37.210-1.74 (3.00 (.32-9.0) 4.170-1.00 (1.0 (16.800) 17.90 (2.40-7.24-7.0) 5.640 (.6) 5.0 (6.40-20.0) 5.97) 20.880) 5.580 (.11) .30) 95th 19.35) 11.35) 5.0 (17.99 (1. 01-02.960 (.0) 3.15) 14.30 (2.01) 5.0) 4.96 (1.59-5.15) 19.63) 32.20-4.10 (.07 (3.52 (1.10 (3.20 (1.1.890 (.40) 1.20-17.330 (<LOD-1.0 (17.11 (1. 0.0-44. < LOD means less than the limit of detection.83-3.55-8.48 (2.00-17.07 (3.30 (1.0 (5.90) .53) 20.49) 17.94 (1.0 (5.640 (.99) 11.32 (1.37) .0 (5.39) .250 (<LOD-.31) .12) * * * * * * * * .33 (4.28) .13 (3.690 (.97) 20.47 (3.00) .40 (1.400-1.90) .07 (1.36-3.10-9.0) 2.67) .

5) 2.15) 9.32-6.09-3.86 (3.8 (20.320-1.474-1.12 (4.53) .55) 21.6) 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 * * * * * * * * * .10 (2.88 (2.430) 1.79 (.04 (1.630-1.07-21.57-40.31-7.1 (7.73 (4.64) 30.56) .64-4.33-3.44-11.22) 2.790 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.3) 3.91) 2.35 (.22-27.5-40.39) 20.28-6.57) 8.830 (.470 (.7 (12.700) < LOD < LOD < LOD < LOD < LOD 1.30 (4.84) 9.55 (3.690-5.370 (.31-18.71 (2.4) 2.88-3.540 (.98 (4.32) 9.41) 18.4-34.00) .820) .92 (2.8) 4.850-3.8-33.370-1.24) 3.62 (1.81-17.800-2.18) * * * * * * * * .67) 1.56 (1.33 (1.8) 7.430 (<LOD-.33 (3.83 (4.83-11.31) .340-.7) 6.960 (.5) 7.55) 21.02 (.780-4.51-44.600 (<LOD-1.970-3.370) < LOD < LOD < LOD < LOD < LOD 1.33-4. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.67-6.190-1.450 (.13 (2.90-6.82-11.2 (8.150 (<LOD-.44) .8) 7.9) 6.748 (.0 (9.1) 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.620-3.4 (4.670 (.250 (<LOD-.50 (2.7) 3.47) .7 (6.25-9.8) 1.21-3.89 (2.66-47.1 (5.01 (1.74 (2.61) 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 .43) .580 (.88) 17.0) 4.340-.29-4.3) 2.03) 16.330-1.65 (2.650) 90th 10.48 (4.67) 2.11-5.40-2.710 (<LOD-1. population from the National Health and Nutrition Examination Survey.40-12.50 (4.53) 27.37) 4.57 (.890 (.5 (8.71 (.02) .50) .75) 5.97) .96) 2.02 (1.07 (2.48-7.7) 5.59 (1.36 (. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th 1.60 (1.52 (.8) 2.310-.27 (2.47-10.56) 2.00-19.80) 3.1) 2.25-38.860-2.47-10.240-.11) .840-3.0 (4.14 (1.85 (1.96-8.1) 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 * * * * * * .7) 4.10-3.730-3.41 (4.08) .47) 5.29 (4.50) 11.2-38.40 (.340 (.260-.85-3.660) < LOD < LOD .700) 6.930) .5 (9.05) .60) < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 4.590) 2.33-5. Fourth National Report on Human Exposure to Environmental Chemicals 131 .9 (11.270 (<LOD-.02-4.14-6.96-25.17) 5.45 (1.9) 5.62-17.49-2.88 (.57) 1.500 (.23-7.38 (2.86) .69) 2.580-1.940-4.69-7.580) 16.25 (1.390-.48-42.18) 1.580) 1.5 (11.10) 2.67 (2.270-.80 (.770) .03) 2.17 (1.12-4.830-3.260-.51-4.40) 1.8) 2.820 (.91-4.18) 95th 21.560 (.650 (.740-1.340-.77 (.S.04-16.790) 11.360 (.540-1.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.5) 2.06 (.31) .

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et al. Am J Ind Med 1987. Occup Environ Med 1995. National Research Council (NRC). Irish RM. Nell V. Eskenazi B.113(4):504-508. Twenty-four-hour urinary excretion of ten pesticide metabolites in healthy adults in two different areas of Italy (Florence and Ragusa). Effects of long-term organophosphate exposures on neurological symptoms. Seiber J. Keefe TJ. Sci Total Environ 2004. Weisskopf C. 1/12/09 Peiris-John RJ.30(2):98-103. Bradman A. Hore P. Arch Environ Health 1988. Available at URL: http://books. S. Keifer M. McCauley L.44(4):352-357. National Academy of Sciences. et al. Wickremasinghe AR. McConnell R. Chronic central nervous system effects of acute organophosphate pesticide intoxication. Rodnitzky RL.43(1):38-45. Washington (DC). 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. Am J Public Health 1994. 4/7/09 Young JG. Jenkins B. Buccafusco JJ. J Toxicol Environ Health A 2005. Robson MG. EPA.26(2):199-209.38(4):546-563. Pedersen L. Jamal GA. The Pesticide Health Effects Study Group.epa. Prendergast MA. van der Hoek W.2000 and 2001 market estimates. Rothlein J. Salvini S. Burcar PJ. Heaton RK. Available at URL: http://www.12(2):134-141. Bull Environ Contam Toxicol 1994. Pesticide industry sales and usage . Visuthismajarn P. Washington (DC): U.332(1-3):71-80. Effects of chronic. Russo J. Variation in organophosphate pesticide metabolites in urine of children living in agricultural communities. et al.84(5):731-736. Int J Occup Environ Health 2006. Occupational exposure to organophosphate pesticides: a neurobehavioral study. A behavioral evaluation of pest control workers with short-term. Saieva C. Stokes L. Monitoring of urinary alkyl phosphates in pestcontrol operators exposed to various organophosphorus insecticides. Tumino R. Neurotoxicol Teratol 1998.20(2):115-22. Arch Environ Contam Toxicol 2000. Claypoole K. Hansen S. 2004. Spurgeon A. Vitayavirasak B.edu/ openbook.php?record_id=2126&page=1. Fourth National Report on Human Exposure to Environmental Chemicals 133 . Daniell WE. U. Thompson ML. metabolite clearance. vibration sense and tremor among South African farm workers. EPA). Lancet 1995. Biological monitoring of organophosphate pesticides in preschool children in an agricultural community in Thailand. Neurotoxicology 2005. Caltabiano LM. Association between in utero organophosphate pesticide exposure and abnormal reflexes in neonates.pdf. Environ Health Perspect 2005. Rohlman D. Smit LA. 1991. Gillham R. Office of Prevention Pesticides and Toxic Substances. Schenker M. Weerasekera G. Samuels S. Aprea C. gov/oppbead1/pestsales/01pestsales/market_estimates2001. May. Barr DB. Scand J Work Environ Health 1998. Ames RG. Lewis JA.68(3):209-227 Maizlish N. Bravo R. London L. Levy LS. Petchuay C.52(2):190-195. Neuropsychological effects of long-term exposure to organophosphates in sheep dip.nap. Johnson C. Calvert IA. Effects of occupational exposure to organophosphate pesticides on nerve and neuromuscular function. Lancet. Chronic neurological sequelae to organophosphate pesticide poisoning. Stark A. Organophosphate pesticide exposure and neurobehavioral performance in agricultural and non-agricultural Hispanic workers. and spatial learning in monkeys and rats.345(8958):11351139. Kidd M. Chronic neurological sequelae of acute organophosphate pesticide poisoning. Mounce LM. Lambert WE. Pesticides in the Diets of Infants and Children. Myers JE. Narang A. Santana J.338(8761):223-227. Marshall E. Environ Health Perspect 2006. Terry AV Jr. Frasca G. Steenland K. Rothlein J. Arch Environ Health 1975. The presence of dialkylphosphates in fresh fruit juices: implication for organophosphorus pesticide exposure and risk assessments.12(2):153-172.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Krieger RI. Neurotoxicity among pesticide applicators exposed to organophosphates. Environmental Protection Agency (U. Occup Environ Med 2001. low-level exposure to the organophosphate diazinon. low-level organophosphate exposure on delayed recall. et al. Stephens R.24(1):18-29. 1993 [online]. Chrislip D. Lasarev M.114(5):691-696. Gladstone EA. Phillips J. J Occup Environ Med 2002. discrimination. Pilkington A. Dinoff TM. Malathion deposition. Ruberu DK.52(10):648-653. Lu C.S. Takamiya K. Savage EP. Masala G. Beach J. O’Malley M. and cholinesterase status of date dusters and harvesters in California. Rosenstock L. Scherer J.S. et al. Muniz J. Lasarev M. Muniz J.58(11):702710. Berry H. Buchanan D.

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 . the level may reflect exposure to the environmental degradation products of these pesticides.5. The table below shows the parent organophosphorus insecticides and their metabolites measured in this Report. For general information about the organophosphorus class of insecticides. malathion is metabolized to malathion dicarboxylic acid. In addition to reflecting exposure to the parent insecticide. For example.” 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. see the section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites. 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.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.

63 (8.36 (4.60-4. For instance. 2002).55-5.30 (4.9) 11.17 (1.67 (1.70-5.50-4.8) 9.2) 972 1183 1022 1326 99-00 01-02 99-00 01-02 99-00 01-02 1. dermal.50 (1.50-4. and on plants for days to several weeks.39) 4.Organophosphorus Insecticides: Specific Metabolites Chlorpyrifos CAS No.68 (7.6-Trichloro-2-pyridinol Metabolite of Chlorpyrifos and Chlorpyrifos-methyl Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. Chlorpyrifos is very toxic to fish and aquatic invertebrates and shows modest degrees of bioconcentration.30-5.90 (1.28) 2.0) 11.0) 10. 2007). and inhalation routes.5.30 (2.45 (1.00) 1.89-2.20-14.10) 2.0) 12.66-4.72-4.10 (1.0 (7.22) 2.59-2. Chlorpyrifos is Urinary 3.90 (3.70-15.70-16.52-2. 5598-13-0 General Information The chemical 3.80) 2.7-23.0) 12.80 (1.1-16.44-5.19-3.60-3.61 (1.13-3. applied to structures to kill termites.80) 4.99-4.98-15.70-11.0) 18. 2002).4 (8.20 (2.29) 90th 7.80-10.9 (7.4 and 0.6) 7.64) 3.66-15.35) 1.7) 8.47-9.40-13.61) 75th 3.31-2.00) 3.0) 7.0-28.67 (2.10 (3.00) 2. Chlorpyrifos is not well absorbed through the skin but dermal exposure can be significant when other routes of exposure are low.20-2.3) size 1994 2509 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th 1.57 (2. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.43-2.8-15.09 (3.7) 9.90) 7. and is infrequently detected in ground water (IPCS.30-2.31-2.47-13.04-10.16) 2.60) 5.20 (4.20-16.90 (1.S.30-1.29-1.50 (2.76 (1.4 (10.10) 6.50-5.02 (7.20) 10.90 (6. staying bound to soil particles.76 (1.0) 10.70) 1.32-1.10 (5.03) 99-00 01-02 99-00 01-02 99-00 01-02 2.63 (2.88 (1. It also has been applied directly on animals to kill mites.40-26.97-7.1) 5. Chlorpyrifos is degraded in agricultural soils with a half-life of several months.30 (2.50-2.37 (4.0) 15.87-6.0) 12.10-17.0) 12.47 (4.0 (7.90-4.40) 9.37) 5.20-3.5-24. pre.20) 4.0 (7. Chlorpyrifos is a broad spectrum organophosphorus insecticide that has been widely used to control insects on food crops such as corn.97) 2.S.S.9 (10.8) 10.72) 2.15 (1.60-3.67 (2.70 (1. and dust.02 (1.40 (5.27 (7. population from the National Health and Nutrition Examination Survey.70 (1.81-2.4 (9.70-17. Inhalational and dermal routes of exposure are important in pesticide formulators and applicators.74 (1. air.50-8.80) 12. but can be detected in streams receiving runoff from application sites.44 (3. Approximately 21-24 million pounds per year were used domestically from 1987-1998.91) 16.80) 1.000 pounds are used per year.60 (5. 2921-88-2 Chlorpyrifos-methyl CAS No.21) 3.0) 10. and sprayed to kill mosquitoes.47-11.71 (1.80 (7.90 (2.40 (5.62-2.30-11.71 (6.09 (2.3) 8.19 (1.90-8.22 (1.84) 1. in 142 urban homes and preschools in North Carolina.0) 8. Approximately 80.5.68-2.78 (7.20) 2.51 (1. Survey Geometric mean (95% conf.50 (2.2 (10.83) 1.60 (2.4) 481 573 681 823 832 1113 99-00 01-02 99-00 01-02 1.77-15.90) 3.77) 1.13 (1.79-2. 1999.20-11.40-2.30-9.01) 1.50-14.51-2.4-15.10 (4.0) 6.0) 12.97) 7.and post-construction structural applications for termite control were to be phased out by 2005 (U.5 (8. Exposure can also result from contact with contaminated surfaces.24-3.03) 1.60-2.9 (9.25) 1.05-5. 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.26) 7.34) 1. The general population may be exposed to chlorpyrifos via oral.95 (4.28-3.89 (2.90-7.95) 7.9-18.43-2.3 (11.52-12. chlorpyrifos and TCPy were detected in all indoor air and dust samples (Morgan et al. 2005). Fourth National Report on Human Exposure to Environmental Chemicals 135 .63 (1.40 (6.39-2.46-2.94 (4.7) 13.77-6.32) 2..0) 14.0 (7. After 2001.0 (7.6-trichloro-2-pyridinol (TCPy) is a metabolite of chlorpyrifos and chlorpyrifos-methyl.47) 1.20) 2.04-10.14) Selected percentiles ( 95% confidence interval) Sample 95th 10.0 (13.00-24.91 (1.02) 1.60 (4.5) 7.97) 2.00-8.4.35) 2.86) 4.3 (10.50 (2. interval) 1. Chlorpyrifos-methyl is an organophosphorus insecticide also used in agriculture and not registered for residential use.05) 1.40-10.80-8.30-12.25) 3.3 (8.92 (1.50 (1.30) 4.0 (10. Estimated intakes from diet and water have not exceeded recommended intake limits.50-2.59) 2.30) 4.0 (9.71 (2.40) 2.0) 8.96) 3. USGS. It has low leachability.24-1.0) 9.74-9.90-2. chlorpyrifos was no longer registered for indoor residential uses in the United States.77 (1.EPA.97) 4.38 (3.53 (1.30) 5.37 (1.9) 697 660 521 701 602 947 Limit of detection (LOD.61-7.51) 1.EPA.20-4.44-2.

92) 3.27-7.98 (6. Overt cholinergic toxicity from chlorpyrifos has been described following suicidal ingestion and unintentional high level occupational exposure.49 (1.83-11.94-14.56) 5.59) 3.49-2. In pesticide applicators.91) 10..08) 6.3) 8.93) 5.19-2.49-2.85 (2.60 (1.940-1.47 (1.92 (1.05-8.33-7.23-1.85) Selected percentiles ( 95% confidence interval) Sample 95th 8.49-2.8) 9.97) 3.01) 3.65-15.85) 4.46 (2.5) 5.86 (3.09-2.6-Trichloro-2-pyridinol (creatinine corrected) Metabolite of Chlorpyrifos and Chlorpyrifos-methyl Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. chronic exposure to chlorpyrifos may be associated with slight alterations in some components of neurophysiologic testing (Steenland et al. 2006b).97) 3.41 (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 1.20 (2.85) 1.24-4. cholinergic effects.76 (2.0) 12.88 (1.70-4.56) 2. the detection of TCPy in a person’s urine may reflect exposure to the environmental degradates.01) 1.56-2.09-3. vomiting.24-24.75 (1. phosphorothioates such as chlorpyrifos are metabolically activated to the “oxon” form which has greater toxicity than the parent insecticide.25-11.19) 6.. population from the National Health and Nutrition Examination Survey.53 (2.22) 1. 2006.14) 1. Urinary 3. and behavior may occur at systemically nontoxic doses or at doses of chlorpyrifos that do not result in cholinergic signs (Aldridge et al.37 (1.46 (1.07) 5.S.88-8.81 (3.80) 3. These organophosphorus insecticides share a mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system.93) 2.12) 1.17-4.63 (4.57) 9..24) 75th 2.24) 5.54 (2.25-1. 2005.88-10. Human health effects from chlorpyrifos or chlorpyrifosmethyl at low environmental doses or at biomonitored levels from low environmental exposures are unknown. Based on animal data and human cholinesterase monitoring during occupational exposure.66 (1.88-9. Roy et al.85 (3.48 (1.47 (5.54) 5. 2000).17-4..91) 1.26-14... and other metabolites.9 (12. Survey Geometric mean (95% conf.33 (. and seizures. and producing acute symptoms such as nausea.24 (1.22 (4.02) 7.33 (1.5 (6.35) 1.3) 9.82 (3.99-8.55 (4.91) 1.EPA.1-21.4) 4.16) 6. 2005.00 (7.25-12.72) 2.03) 1.39 (4.36) 1.2 (7.90-9.11 (2.6) 9.09-1.58-5. resulting in excess acetylcholine at nerve terminals.16 (4.60-3.43 (4.55) 1.33) 2.11 (2.91) 2.57-2.44 (5.82 (2.78 (1.64 (1.88-8.05-1.30-4. interval) 1.86 (1..71 (1.64-2.96) 3.38) 3.44 (1.35) 2. 2006a.65-11.31-4.00) 1.48 (2.42 (6.20-1.11-9. Ricceri et al.33 (5.3) 8.52 (5.56 (1.82) 8.79-13.91 (4.45 (1. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”).00-8. Recent in vitro and in vivo animal studies suggest that effects on neuronal morphogenesis.39) 6.06 (5.05) 3.51 (1.8) 972 1183 1022 1325 99-00 01-02 99-00 01-02 99-00 01-02 1. 2005.05-4.97 (2. Chlorpyrifos is eliminated from the body primarily in the urine with a half-life of approximately 27 hours (Nolan et al.81) 2.91-4.01) 99-00 01-02 99-00 01-02 99-00 01-02 3. neurotransmission.42 (5.93 (1.95 (3.85-4.1-38.82-4.11) 7. Howard et al.44 (1.97 (3.62) 1.80-6.7) 7.19-1. Slotkin et al. ubiquitous lowlevel environmental exposures in humans would not be expected to result in inhibition of cholinesterase activity.64-7.80-4.99) 1.19) 3.63-2.89) 4. 1984).62-7.83-2. Chlorpyrifos and chlorpyrifos-methyl both demonstrate moderate acute toxicity in animal studies.Organophosphorus Insecticides: Specific Metabolites rapidly absorbed following ingestion.47-2.55 (1.14-8.0) 10.92-2.12-1.68) 6.58) 5.87-3. 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.72) 1.00-13. 2002).44 (6..23) 14.57-2.94-12.59-2.1 (7.0) 16.47 (1.05-3.88) 6.73 (1.02 (5.58 (1.21-1.77) 1.45-1.39 (2.57) 2. Metabolic hydrolysis leads to the formation of TCPy.58 (1.66) 1.2) 6.24-5.58) 1.28) 2.3 (7.30-1.42-2.27-1.09 (1.56 (4.22 (6.68) 1.12-3.83) 1.66-11.93 (4. TCPy can also occur in the environment from the breakdown of the parent compounds.74) 1.5.95 (1.07) 1.43-10.39-1.91-13.44 (5.S.34-1.53-5.35-1.80-11.06 (1.75) 6.98 (7.28) 2.24-1.40) 1. Thus..58 (4.01) 3.97-3.31) 1. The metabolite TCPy does not inhibit acetylcholinesterase enzymes.88 (1.0) 481 573 681 822 832 1113 99-00 01-02 99-00 01-02 1.44-6.50 (4. paralysis.0) 6.71) 3. Once absorbed.15 (4. Betancourt et al.91 (3.32) 1. In addition to being a metabolite of chlorpyrifos and chlorpyrifos-methyl in the body.7) 697 660 521 700 602 947 136 Fourth National Report on Human Exposure to Environmental Chemicals .69 (1. TCPy is more persistent in the environment than chlorpyrifos itself (U.63 (5.84-6.93 (2.62) 90th 5.21-6.76 (3.1 (10.29 (3.22-6.86 (1. weakness.6) 10.06-4. 2006.72-2.31-1.

Lioy PJ. but not chlorpyrifos. Biomonitoring Information Urinary TCPy levels reflect recent exposure.. 2003. Aldridge JE. 2000). median urinary levels on the conventional diet were several fold higher than those in the NHANES 1999-2000 subsample (Lu et al..S. 76% had detectable levels of TCPy and levels were similar to those reported for NHANES 1999-2000 (Eskenazi et al. Chlorpyrifos exposure and biological monitoring among manufacturing workers. Other small studies of environmentally-exposed persons have shown a high frequency of detecting low levels of TCPy. urinary TCPy levels in children were reported not to have increased (Hore et al.S.html and from U. et al. Betta A. but levels were roughly four to six times higher than the geometric means in the U..cdc. Burgess SC. representative subsample of NHANES 19992000 (CDC. 2005). Freeman NC. Albers JW.. Perera et al. 2005. suggesting changing low-level exposure and variance in collection timing with respect to exposure (Meeker et al. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample. 2002). Fourth National Report on Human Exposure to Environmental Chemicals 137 . 2006) and episodically many times higher for pesticide applicators than median levels from NHANES 1999-2000 (CDC.. Levels of TCPy in the U..gov/pesticides/. et al. subsamples of NHANES 1999-2000 and 2001-2002 (CDC.atsdr. 2004). 2001) than the corresponding values reported for the group aged 6-11 years from the NHANES 1999-2000 subsample (CDC.109(6):583-590. et al. 2005) appear roughly similar to values reported for a nonrandom subsample of NHANES III (1988-1994) participants (Hill et al. Berent S. Estimation of dose or intake based on the urinary excretion of TCPy indicates that environmental doses are generally below recommended limits (Hore et al. U. Lotti A. 2001). Following crack-and-crevice application of chlorpyrifos in their homes.S. the weighted population mean of TCPy measurements was approximately three times higher (Adgate. Carr RL. Curwin et al. 1995) and were similar to levels reported in studies of healthy adults in Germany (Koch et al. 1992. Replacing conventional diets with organic diets in 23 children led to about a fourfold decrease in urinary levels of chlorpyrifos. 2005). Meyer A.. Toxicol Sci 2006.e. Eberly LE. Barr DB. 2005.epa. Measurements of urinary TCPy in single spot urine collections show variability over time in environmentally exposed individuals and are poorly correlated between collections. urinary TCPy levels averaged about sixfold higher than those in the NHANES 1999-2000 subsample (Mandel et al.EPA. In Iowa farm families using several different pesticides... Clayton CA. Garabrant D. 2005). In Minnesota and South Carolina farmers who used chlorpyrifos. environmental levels) and health effects is available from ATSDR at: http://www. (1999) reported mean urinary TCPy levels in a sample of Maryland adults that were about three times higher than adults in the U. Occup Environ Med 2006.Organophosphorus Insecticides: Specific Metabolites 2004..S. Whyatt et al. 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. 2004).82(2):305-312. Betancourt AM. EPA at: http://www. Environ Health Perspect 2005. J AOAC Int 1999. 2005). References Adgate JL. 1999). Additional information about external exposure (i.. In a probability-based sample of 102 Minnesota children aged 3-13 years. Finding a measurable amount of TCPy in urine does not mean that the level will result in an adverse health effect.. CDC. Chlorpyrifos levels in house dust and hand rinses did not correlate with levels of TCPy in urine (Lioy et al.. 2006).gov/toxpro2. Slotkin TA. Koch et al.63(3):218220.92(2):500-506. 2001) and Italy (Aprea et al.. the geometric mean urinary TCPy levels were similar in parents and children. Chlorpyrifos is not considered to be mutagenic or carcinogenic (NTP. 2005). Haidar S.Reference values of urinary 3.. 2005. Of 482 pregnant women living in an agricultural community. 2007). Seidler FJ.5. MacIntosh et al. Urinary levels of TCPy have been found to be hundredsfold higher for chlorpyrifos manufacturing workers (Burns et al. Environ Health Perspect 2001. Alterations in central nervous system serotonergic and dopaminergic synaptic activity in adulthood after prenatal or neonatal chlorpyrifos exposure. population (CDC.. Aprea C. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Some reproductive and teratogenic effects in animal testing were only observed at high doses of chlorpyrifos that caused overt maternal toxicity.S. Burns CJ. Barisano A.6-trichloro-2-pyridinol in the Italian population—validation of analytical method and preliminary results (multicentric study). Effect of developmental exposure to chlorpyrifos on the expression of neurotrophin growth factors and cell-specific markers in neonatal rat brain.113(8):1027-1031. Catenacci G. Magnaghi S. Giordani B. 2005).

114(5):746-751. Biological monitoring of exposure of the general population to the organophosphorus pesticides chlorpyrifos and chlorpyrifos-methyl by determination of their specific metabolite 3. Chrislip DW.nih. Curwin BD. Barr DB. Freeman N. Hein MJ. mothers and fathers living in farm and non-farm households in Iowa. Environ Health Perspect 2005. Urinary pesticide concentrations among children.6-trichloro 2-pyridinol in their everyday environments.niehs. Roy TS. Gregg M. Morgan MK. Available at URL: http://ntp.10(4):327-340. A longitudinal investigation of selected pesticide metabolites in urine. Freeman N. Harley K. Interim registration eligibility decision for chlorpyrifos. Toepel K. et al. 2005. Camann D.204(2-3):175-180. Hill RH Jr. Ricceri L. Ryde IT. Effects of transplacental exposure to environmental pollution on birth outcomes in a multiethnic population. J Expo Anal Environ Epidemiol 2005. chlorpyrifos. Jones PA. Fenske RA. Shealy DB. Wartenberg D. Jett DA.108(4):293-300.93(1):105-113. Environ Health Perspect 2003.114(2):260-263. gov/ntpweb/index. Toxicol Sci 2006. Weltzien E. Barr D. Levin ED. MacIntosh DL. Howard AS. Toxicol Appl Pharmacol 1984. Robson M. EPA). Gurunathan S.112(10):1116-1124. Tsai WY. 4/7/09 Perera FP. Seidler FJ.S. Seidler FJ. J Expo Anal Environ Epidemiol 2000. Herrick RF. Croghan CW. Howell RJ. Ryan L. Capone F. Brain Res Dev Brain Res 2005. Quantitative morphological assessment reveals neuronal and glial deficits in hippocampus after a brief subtoxic exposure to chlorpyrifos in neonatal rats. House dust levels of selected insecticides and a herbicide measured by the EL and LWW samplers and comparisons to hand rinses and urine metabolites. Nolan RJ. Saunders JH. Bravo R.inchem. Slotkin TA. Ozkaynak H. Lorenzini P. Environ Res 1995.113(2):211-219. Slotkin TA. Environ Health Perspect 2006a. National Toxicology Program (NTP). Meeker JD.S. et al. Developmental neurotoxicity of organophosphorous pesticides: fetal and neonatal exposure to chlorpyrifos alters sex specific behaviors at adulthood in mice. Bucelli R. Needham LL. Pesticide residues in urine of adults living in the United States: reference range concentrations. Int J Hyg Environ Health 2001. Kromhout H. Hines CJ. Baker BA. EPA 738-R- 138 Fourth National Report on Human Exposure to Environmental Chemicals . Adgate JL. 1999. Mandel JS. et al. Hore P. 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. Barr DB. Seidler FJ. Environmental Health Criteria 198. Environ Health Perspect 2000.htm. Pellizzari E. Edwards RD. Ann Occup Hyg 2007. Chlorpyrifos. Lioy PJ. Rauh V. Yang D.114(10):1542-1546. Barr DB. Eskenazi B. Chuang JC. Sheldon LS. Hardt J. Biomonitoring for farm families in the farm family exposure study. Zhang J. Jewell NP. Baker S.73:8-15. Sharma V. 4/7/09 Koch HM. Exposures of preschool children to chlorpyrifos and its degradation product 3. Angerer J. Toxicol Appl Pharmacol 2005. Chlorpyrifos: pharmacokinetics in human volunteers. Alexander BH. Temporal variability of urinary levels of nonpersistent insecticides in adult men. Cometa MF.207(2):112-124. February 5. Bravo R. Fortuna S. Available at URL: http://www. J Expo Anal Environ Epidemiol 1999. Robertson GL. Levin ED. Chlorpyrifos accumulation patterns for child-accessible surfaces and objects and urinary metabolite excretion by children for 2 weeks after crack-and-crevice application. Environmental Protection Agency (U.51(1):53-65.71:99108. Kinney P. Steenland K. Lu C. Honeycutt R. Dick RB.Organophosphorus Insecticides: Specific Metabolites Centers for Disease Control and Prevention (CDC). Neurologic function among termiticide applicators exposed to chlorpyrifos. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population. Striley C. Environ Health Perspect 2006.155(1):71-80. et al. Executive summary of safety and toxicity information. Third National Report on Human Exposure to Environmental Chemicals. Sanderson WT. Bennett DH. Rick DL. International Programme on Chemical Safety-INCHEM (IPCS). Atlanta (GA). Lein PJ.31 Suppl 1:98-104. Venerosi A. et al. Ryan PB.5. Acquavella JF.org/documents/jmpr/jmpmono/ v99pr03. Reid TM. 2921-882. Tate CA. et al. Bailey SL. Environ Health Perspect 2004.15(3):271-281. Chapman P. Freshour NL.15(4):297-309. et al. Hammerstrom KA.6-trichloro-2-pyridinol. Bruun D. U.cfm?objectid=6F5E95EB-F1F6-975E7C20F4211536F46F. J Expo Anal Environ Epidemiol 2005. Environ Health Perspect 2006b.111(2):201-205. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. Slotkin TA. Irish R. 1992. et al. Heederik D. Bradman A. Head SL. Chlorpyrifos exerts opposing effects on axonal and dendritic growth in primary neuronal cultures. et al.9(5):494-501. Comparative developmental neurotoxicity of organophosphate insecticides: effects on brain development are separable from systemic toxicity.5. et al. Scand J Work Environ Health 2005.

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

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

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. population from the National Health and Nutrition Examination Survey. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2481 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .200 (<LOD-. Survey Geometric mean (95% conf.670 (<LOD-1.S. < 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. Survey Geometric mean (95% conf.560) < LOD 659 700 920 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.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 . Fourth National Report on Human Exposure to Environmental Chemicals 141 . 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. population from the National Health and Nutrition Examination Survey.380 (<LOD-.200 (<LOD-.27) < LOD < LOD 567 814 1099 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1169 1311 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . 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. see Data Analysis section) for Survey year 01-02 is 0.S.270) < LOD 659 701 920 Limit of detection (LOD. which may vary for some chemicals by year and by individual sample.

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

2004). diazinon was widely used in residential and garden application. since 2004.11) < 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. about 13 million pounds of diazinon were used annually on agricultural sites in the United States. 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. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Metabolic hydrolysis leads to the formation of 2-isopropyl4-methyl-6-hydroxypyrimidine.EPA. Prior to 2000. which may vary for some chemicals by year and by individual sample. 2007).05) < LOD < LOD 644 678 484 700 554 956 Limit of detection (LOD. 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. Most granular formulations. It has been infrequently detected in general groundwater sampling but has been detected in streams receiving runoff from application sites (IPCS. USGS. diazinon produced wild bird kills before use restrictions were in place. 333-41-5 General Information The chemical 2-isopropyl-4-methyl-6-hydroxypyrimidine is a metabolite of diazinon. It is also used for cattle ear tag applications to control flies and ticks and. Inhalational and dermal routes of exposure can be significant for pesticide applicators. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”). and particularly when it was ingested in granular form.Organophosphorus Insecticides: Specific Metabolites Diazinon CAS No.EPA. It is toxic to birds. in the past. aerial. Once absorbed.S. Experimental diazinon exposure in people has demonstrated its rapid elimination into urine. 1998). and other metabolites. but these uses have been phased out. Diazinon is biologically and chemically degraded in soils with a half-life of about a few weeks. Diazinon is not well-absorbed through the skin. and forage crops.49 (<LOD-2. 1998. seed and foliar applications are planned to be phased out (U. Before these restrictions. but is rapidly absorbed orally (IPCS. Fish and aquatic invertebrates show modest degrees of bioconcentration and are very sensitive to toxic effects.7. phosphorothioates such as diazinon are metabolically activated to the “oxon” form which has greater toxicity. population from the National Health and Nutrition Examination Survey. see Data Analysis section) for Survey years 99-00 and 01-02 are 7. in some pest strips. an organophosphorus insecticide that is used to control insects on nuts. Survey Geometric mean (95% conf. Fourth National Report on Human Exposure to Environmental Chemicals 143 .2 and 0. Estimated intakes from diet and water do not exceed recommended intake limits (U. < LOD means less than the limit of detection.45 (<LOD-3.S. 2004). diazinon cannot be sold for residential use. vegetable.S. 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. fruits.

. 2000. Survey Geometric mean (95% conf. subsamples of NHANES 1999-2000 and 20012002. EPA at: http://www. Human health effects from diazinon at low environmental doses or at biomonitored levels from low environmental exposures are unknown.S. weakness. 1992). and seizures. although the 95th percentiles for children 6-11 years old and for non-Hispanic blacks were 1.76 (<LOD-3. in the 2001-2002 subsample (CDC. 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. Additional information about external exposure (i.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. and producing acute symptoms such as nausea. 1986.49 μg/L.html and from U. Biomonitoring Information Urinary levels of 2-isopropyl-4-methyl-6hydroxypyrimidine reflect recent exposure. Olsson et al. vomiting. diazinon and other organophosphorus insecticides share a mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system. teratogen. In animals. respectively. 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. In two nonrandom samples of United States adults and children.S. In the U.S. In addition to being a human metabolite of diazinon. 144 Fourth National Report on Human Exposure to Environmental Chemicals . Thus.. most of the measurements of 2-isopropyl-4-methyl6-hydroxypyrimidine in urine were below the limit of detection. 2003).cdc. 2-isopropyl-4-methyl-6-hydroxypyrimidine can also occur in the environment from the breakdown of the parent compound. the detection of 2-isopropyl4-methyl-6-hydroxypyrimidine in a person’s urine may reflect exposure to the environmental degradate.Organophosphorus Insecticides: Specific Metabolites from dialkyl phosphate metabolite excretion (Garfitt et al. 1998). Diazinon is not considered to be a mutagen.gov/pesticides/. respectively (Baker et al.. population from the National Health and Nutrition Examination Survey.45 and 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. or reproductive toxicant (IPCS.atsdr.gov/toxpro2.S. There has been only limited study of diazinon at systemically non-toxic doses that do not result in cholinergic signs (Anthony et al. 1998). 1986 Rajendra et al. resulting in excess acetylcholine at nerve terminals. Seifert and Pewnim.. agricultural. At high doses. environmental levels) and health effects is available from ATSDR at: http://www. Diazinon has moderate acute toxicity in animal studies. diazinon does not accumulate in tissues (IPCS. Intoxications in humans from intentional overdose.. paralysis.48) < LOD < LOD 644 678 484 699 554 956 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.72 (<LOD-4. cholinergic effects.epa.e.. The U. 2-isopropyl-4-methyl-6-hydroxypyrimidine was detectable in 57% and 43% of the 130 and 140 participants.EPA considers diazinon unlikely to be carcinogenic in humans. and indoor applications have been documented. 2002). animal carcinogen.

EPA 738-R-04-006. Banister EW. Carrier G. Available at URL: http://www.376(6):808-815.usgs. 1998. Oloffs PC. Kruse RL. Environ Health Perspect 2006. Quantification of selected pesticide metabolites in human urine using isotope dilution high-performance liquid chromatography/ tandem mass spectrometry. Needham LL. Study for Future Families Research Group. International Programme on Chemical Safety-INCHEM (IPCS). urinary 2-isopropyl-4-methyl-6hydroxypyrimidine was detected in less than 14% of multiple samples collected during varied diets (Lu et al.gov/circ/2005/1291/. U. Brunet RC. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. Nguyen JV. Rajendra W. May 2004. Pesticides in the Nation’s Streams and Ground Water. Bull Environ Contam Toxicol 1986.htm. Olsson AO. Atlanta (GA). Baker SE. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Barr DB. Liu F. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine. Environmental Health Criteria 198. 2006). Interim reregistration eligibility decision (IRED.10(6 Pt 2):789-798. Environ Health Perspect 2003. Fenske RA. J Expo Anal Environ Epidemiol 2000. Jones K. Geological Survey (USGS). Available at URL: http://www. Environmental Protection Agency (U. Oloffs PC. Diazinon. Dumas P. Sadowski MA.org/documents/ehc/ehc/ehc198. Ann Occup Hyg 2006.Organophosphorus Insecticides: Specific Metabolites 2005).epa. Garfitt SJ.44(11):2243-2250. Irish R. Banister E.S. Driskell WJ. Semen quality in relation to biomarkers of pesticide exposure. Anal Bioanal Chem 2003. Effect of sublethal levels of diazinon: histopathology of liver. Third National Report on Human Exposure to Environmental Chemicals. Barr DB. Exposure to the organophosphate diazinon: data from a human volunteer study with oral and dermal doses. Biochem Pharmacol 1992. 1992-2001.S. Drug Chem Toxicol 1986. Centers for Disease Control and Prevention (CDC). Barr DB.. Alteration of mice L-tryptophan metabolism by the organophosphorous acid triester diazinon. Seifert J. Bravo R. Cocker J. 1/14/09 U. Barr DB. Effects of chronic intake of diazinon on blood and brain monoamines and amino acids.9(2):117-131.inchem.. Pewnim T. et al.S. 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. 6/1/09 Fourth National Report on Human Exposure to Environmental Chemicals 145 .gov/ oppsrrd1/REDs/diazinon_ired. Bouchard M. References Anthony J. March 2006. 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. Redmon JB. revised February 15. 2006). EPA). Noisel N. (2003) found that 2-isopropyl4-methyl-6-hydroxypyrimidine was detectable in 96% and 58% of the subjects. urinary 2-isopropyl-4-methyl-6-hydroxypyrimidine levels were below the limit of detection (Bouchard et al. In 54 Canadian greenhouse workers. 2007 [online]. Diazinon. Biological monitoring of exposure to organophosphorus insecticides in a group of horticultural greenhouse workers. In a small number of men visiting fertility clinics in Missouri and Minnesota.111(12):1478-1484.50(5):505-515. 4/7/09 Lu C. Swan SH. Toxicol Lett 2002. Mason HJ. Beeson MD. Toepel K.37(4):501-507. The Quality of Our Nation’s Waters. Swan et al. 2005.134(1-3):105-113. Available at URL: http://pubs.pdf.114(2):260-263. In 23 children. Drobnis EZ.

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

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

74(2):following table of contents. Neutra R.pdf.Organophosphorus Insecticides: Specific Metabolites References Adgate JL. revised February 15. Flessel P. Available at URL: http://pubs. Szyfter K.38(4):546-553.S. Barr DB. Ryan PB. Available at URL: http://www. 2007 [online].gov/oppsrrd1/REDs/ malathion_red. Toxicol Sci 2003 May. Jaloszynski P. 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. Prasad SB. Environmental Protection Agency (U. Jewell NP. A longitudinal investigation of selected pesticide metabolites in urine.514(1-2):223231. Kedan G. Erratum in: Toxicol Sci 2003 Aug. Sharma GD. Albertini RJ.epa. EPA). Mutat Res 1999. Gosselin NH. Curl CL. Genotoxic effects of malathion: an organophosphorus insecticide using three mammalian bioassays in vivo. Atlanta (GA). et al. Lu C. J Expo Anal Environ Epidemiol 1999. Harris JA.109(6):583-590. 2005.inchem. O’Neill JP. and cholinesterase status of date dusters and harvesters in California. metabolite clearance. Pesticides in the Nation’s Streams and Ground Water. Mutat Res 2002. Pesticides residues in food: 2003 FAO/WHO Meeting on Pesticide Residues. Grether JK. Am J Public Health 1987. Krieger RI. The Quality of Our Nation’s Waters. Environ Health Perspect 2004. Dumoulin MJ. Barr DB. Environ Mol Mutagen 1993. Comparison of organophosphorus pesticide metabolite levels in single and multiple daily urine samples collected from preschool children in Washington State.gov/circ/2005/1291/. Samuel O. Toepel K. 1992-2001. Quintana PJ. 6/1/09 148 Fourth National Report on Human Exposure to Environmental Chemicals . Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population. Trzeciak A. March 2006. Barr DB. Nicklas JA.usgs. Environ Health Perspect 2001. Cancer Res 1996. Hooper K.56(10):2393-2399. Reregistration eligibility decision (RED) Malathion. Available at URL: http://www.S. Am J Epidemiol 1990. Needham LL. Harley K. Irish R. Petitti D.22(1):7-17.112(10):1116-1124. Eberly LE. Fenske RA. Weltzien E. Eskenazi B. Kizer KW: Exposure to aerial malathion application and the occurrence of congenital anomalies and low birthweight. EPA 738-R06-030. July 2006. Malathion deposition. Swan SH. J Expo Anal Environ Epidemiol 2005. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. Giri A. Geological Survey (USGS).15(2):164-171. Bravo R. MacIntosh DL. Bradman A. 4/7/09 Kissel JC. Goldhaber M.73(1):182-94. et al. Giri S.114(2):260-263.org/documents/jmpr/jmpmono/v2003pr06. Dinoff TM. Carrier G.9(5):494-501. Hammerstrom KA.445(2):275-283. Third National Report on Human Exposure to Environmental Chemicals. htm. Blasiak J. Environ Health Perspect 2006. Genetic toxicity of malathion: a review. 6/1/09 U. Bouchard M. Reproductive outcome in women exposed to malathion. Brunet RC. Hertz-Picciotto I. Freeman NC. Pluth JM. et al. Clayton CA. Malathion (addendum). Arch Environ Contam Toxicol 2000. Barr DB. International Programme on Chemical Safety-INCHEM (IPCS). Rappaport E.77:1009-1010. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample. Lioy PJ. Lu C. In vitro studies on the genotoxicity of the organophosphorus insecticide malathion and its two analogues.S. Thomas D. Centers for Disease Control and Prevention (CDC).132(4):794-795. Griffith W. U.

12) < LOD < LOD 1.30 (1.50-14.0) 3. on cereal grains. Methyl Parathion.0) 3.60 (4. In the 1990s. 2007).770 (.90 (1.67) < LOD 1.300-.37-4. phosphorothioates such as methyl and ethyl parathion are metabolically activated to the “oxon” forms which have greater toxicity than the parent insecticides.70-6.80 (1.01-4.Organophosphorus Insecticides: Specific Metabolites Methyl Parathion CAS No. In animal studies. Ethyl and methyl parathion are infrequently detected in groundwater sampling (USGS. and of the chemical nitrobenzene. binds tightly to soils resulting in low leachability.15-3. ethyl parathion.37-2.10 (3. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Urinary para-Nitrophenol Metabolite of Ethyl Parathion.700 (<LOD-.28 (1.32 (1. more slowly absorbed through the skin.910) < LOD . methyl parathion was rapidly absorbed after ingestion.10 (<LOD-6. and has a short half-life in soils and on plants. Methyl parathion is not registered for residential use in the United States.10) 4.33 (1. the potential for human exposure to either ethyl or methyl parathion through the diet or drinking water is low. and to a lesser extent. and eliminated rapidly from the body after absorption (Kramer et al.79) 4.02-6. Estimated intakes from diet and drinking water have been below recommended limits.S.71 (2. Fourth National Report on Human Exposure to Environmental Chemicals 149 .90-9.33) 2. and oral routes can occur in pesticide and agricultural workers (Muttray et al. pulmonary.70 (<LOD-3..70-6.40-3.92) 5.28-4.EPA.60) 1.940 (<LOD-2.20-5.01) 695 660 518 679 603 941 Limit of detection (LOD.70-6.70 (2. and aquatic invertebrates.850) < LOD .50 (2.21-1..860 (<LOD-1.89 (2.45 (1.26 (1.16) < LOD 1.40) 4. Increased risk of exposure via dermal.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 1.74) 5.20 (2.24) 479 565 680 813 830 1099 99-00 01-02 99-00 01-02 * * * * < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.0) 3.60-24.27) 2. fish.45) 5.01) 4.09-1.90-11. peak domestic use was as high as 5-6 million pounds per year.92-2.37-4.71 (3. 2006). Ethyl parathion.50 (1.20 (<LOD-2.62 (1.EPA. Methyl parathion use is highly restricted.85 (2. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.30 (2.298-00-0 Ethyl Parathion CAS No.66 (2.61) < LOD 1. Metabolism of ethyl or methyl parathion leads to the formation of paranitrophenol. was once a restricted-use insecticide with limited applications on certain agricultural crops.00) 3. Many previous registered agricultural uses of methyl parathion have been cancelled (U. 2003). first registered in 1948.0 (3.37) 2.70 (2.0) 3.58) 3. 2000).61) < LOD 1.70) 2.41-4.69 (2.0) 4.50) 3.70 (2.40) 2.40 (1. and Nitrobenzene Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.50 (1.80 (2.80) 2.32-3.11) 2. Both are toxic to birds.1.50 (1.0) 2.0) 3.80 (2. It had been applied to cotton. 1977).10 (3.00 (2.30-16. 2002.50 (1.20) 5. with limited applications in agriculture.70) 2.19 (.57) 1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 5.21 (2.67 (1.11-4.70 (3. which may vary for some chemicals by year and by individual sample. 56-38-2 General Information Para-nitrophenol is a metabolite of the insecticides methyl parathion.60-5. population from the National Health and Nutrition Examination Survey.50 (2.910) < LOD < LOD .05) 4.34 (3.44) 2.18-3.60-19.32-1.28 (1. all registered uses were voluntarily cancelled (U.00 (2. Given its limited use.50) 2.70) 2.10-11.10-1.990-1. < LOD means less than the limit of detection.S.91-3.71) 971 1164 1018 1313 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD . Once absorbed.8 and 0.50-9.48) 90th 2.50) 1.30-3.32-1..730 (<LOD-.70-3.36-1.13-1.72 (3. but by 2003.S.40) 1. Morgan et al.57-4. Survey Geometric mean (95% conf.30-5.790 (<LOD-.60-36.46 (3.47) 2. O-ethyl-O-(4-nitrophenyl) phenylphosphonothioate.910) < LOD < LOD < LOD 1.22-3.10) 22.40-4. Methyl parathion has low water solubility.70-3.49 (1.02) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .69) 4.50) 3.40-4.

870) < LOD .01 (2. 1991).61) 4.71) 1.45) 695 660 518 678 603 941 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. Thus.720-1.44-3. accidental exposure.31) < LOD .35-3.540) < LOD .43) 4.73 (1. Parathion and methyl parathion have high acute toxicity in animal testing.78-2.38-3.Organophosphorus Insecticides: Specific Metabolites Metabolites”).35-3.. and Nitrobenzene Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. Overt cholinergic toxicity and death from methyl and ethyl parathion have been described following suicidal ingestion.00 (1.17-4.25 (2.55) 2.850-1.21) 1.33-6.33-3.e.690-1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 4.77-7.84) 3..48-4.33-3.530) < LOD < LOD < LOD .07) 2.13) 4. but lists ethyl parathion as a possible human carcinogen.90 (1.57) 6.310-.730-1. does not inhibit acetylcholinesterase enzymes.20 (3.00 (1. and other metabolites.04 (2. Methyl parathion is not considered genotoxic.89 (2.82) < LOD .70) 3. ethyl parathion. Methyl Parathion.01-3.430 (.78 (2. environmental levels) and health effects is available from ATSDR at: http://www.9) 1. 1995. vomiting.55 (<LOD-3.980 (.60-2.31-3.56-2. WHO.970 (.930 (.00) 2.7) 3.97-10. IARC does not consider ethyl parathion and methyl parathion classifiable as human carcinogens. 2004). cholinergic effects.94-47.4 (3. At high animal doses of methyl parathion.21-21.EPA considers methyl parathion unlikely to be carcinogenic to humans.80 (1..940 (<LOD-1.720 (<LOD-.3) 2.37-1.17) .29) 1..83 (1. and seizures.08-3.2) 2.88) 1. The metabolite.29 (2.93 (2.26) 17.79 (1.830-1. and unintentional acute or chronic high-level occupational exposure (Hill et al. 2004).06) 971 1164 1018 1312 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .. gov/toxpro2.33) 479 565 680 812 830 1099 99-00 01-02 99-00 01-02 * * * * < LOD . methyl parathion..08) < LOD .2) 2. weakness. teratogenic. Urinary para-Nitrophenol (creatinine corrected) Metabolite of Ethyl Parathion.79) 1.440 (<LOD-.23) size 1989 2476 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD 75th .98-7. Slotkin et al.11-4.07 (1.680 (<LOD-1.20) 3.epa.97 (2. 150 Fourth National Report on Human Exposure to Environmental Chemicals .S.400 (<LOD-.78-2.640) < LOD < LOD 1.29) 2.25) 1.57-7.14-3.04) 1. 1978.82 (2.78) 2. or generally to have reproductive toxicity at doses below those causing acetylcholinesterase inhibition in most animal studies (IPCS. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Additional information about external exposure (i.13-12.30-1. Jaga and Dharmani. the detection of para-nitrophenol in a person’s urine may also reflect exposure to the environmental degradate. Survey Geometric mean (95% conf. U. 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. Orsorio et al.03) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .800-1.15) 3. para-nitrophenol can also occur in the environment from the breakdown of the parent these organophosphorus pesticides and from nitrobenzene. resulting in excess acetylcholine at nerve terminals. 2006. and producing acute symptoms such as nausea.10 (1.10) 90th 2.370 (<LOD-.S.cdc. paranitrophenol.30) 3.16-4.60 (1.500) < LOD < LOD .67-2.15-10.950) < LOD .97 (<LOD-4.S.09) 2. 1995).80 (1.20) .930 (.05) 4.790-. 1990. population from the National Health and Nutrition Examination Survey.95) 1.23) 1.11) 1. Karanth and Pope et al.91) 1.96 (1.790-1. and other organophosphorus insecticides share a common mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system.92 (2.1) 2. Lores et al.72-2.60) 2. In large doses.970 (.39) 1.08 (1.44-3.41-2.. EPA at: http://www.atsdr. retinal atrophy and sciatic nerve degeneration have also been observed (IPCS.840 (.67 (3. Human health effects from parathion or ethyl parathion at low environmental doses or at biomonitored levels from low environmental exposures are unknown. In addition to being a metabolite of methyl and ethyl parathion.94-4.89 (2.91 (1.86 (2.01 (.. 2005.87 (1.88 (1. 2003.59 (1. 2006.html and from U. paralysis.26 (1.57-2. gov/pesticides/. Zurich et al.880 (.96 (1.39 (1.76-14.71 (1.

Barr DB. Karanth S.Organophosphorus Insecticides: Specific Metabolites Biomonitoring Information Urinary levels of para-nitrophenol reflect recent exposure.110 Suppl 6:1075-1078.6(2-3):159-173. Kissel JC. Cline RE. 2005. Pesticide residues in urine of adults living in the United States: reference range concentrations. Barr DB. International Programme on Chemical Safety-INCHEM (IPCS). Hryhorczuk DO..56(7):449553. Barr JR. Lewalter J. Dharmani C. McCann KG. 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. et al. Lu C.5 mg (500 µg)/g creatinine for workers at the end of shift.110 Suppl 6:1085-1091. Measurement of p-nitrophenol in the urine of residents whose homes were contaminated with methyl parathion. Giordano G. Needham LL. 4/7/09 Jaga K. Slach EF. In a study of workers who handle parathion. Morgan DP. McClure PC. Rubin et al. Turner WE. and levels were similar or slightly lower that those in a small convenience sample of the U. Bradway DE. Centers for Disease Control and Prevention (CDC).14(4):213-216. Runkle KD. 2002). Rockhold RW. Baker RC.25(5):599-606. J Expo Anal Environ Epidemiol 2005. Lin LI. Hetzler HL. Parathion-Methyl (addendum). et al. Effect of organophosphorus insecticides and their metabolites on astroglial cell proliferation. Environ Health Perspect 2004. J Biomed Sci 2002. 2005). Alley CC.htm.. population (Olsson et al. Baker SE. end-of-shift urinary para-nitrophenol levels ranged from 190 to 410 µg/ gram of creatinine (Leng and Lewalter. Comparison of organophosphorus pesticide metabolite levels in single and multiple daily urine samples collected from preschool children in Washington State. Arch Environ Contam Toxicol 1977. Pesticide workers may have much higher levels following pesticide applications. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population.9:311-320. Head SL. Griffith W. Wellman SE. Occup Environ Med 1999. References Barr DB. Eskenazi B. 2002. Leng G. Baker S. Environ Health Perspect 2002. J Anal Toxicol 1990. Kedan G. Chicago area methyl parathion response. 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. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. ACGIH recommends a BEI of 0. Pharmacokinetics of methyl parathion: a comparison following single intravenous. Methyl parathion: an organophosphate insecticide not quite forgotten. Harley K. 2005. general population (CDC. et al. 1999). Moseman RF.S. Neurotoxicol Teratol 2003.33(5):270-276. Bradman A. Pathak S. Gregg M. a range of values several hundred times higher than levels found in the U. Guizzetti M. Hill et al. Third National Report on Human Exposure to Environmental Chemicals. Curl CL. Costa LG. Urinary excretion of paranitrophenol and alkyl phosphates following ingestion of methyl or ethyl parathion by human subjects..15(2):164-171. Lores EM. 2005). Laboratory investigation of a poisoning epidemic in Sierra Leone..71:99108.. Bailey SL. Arch Environ Health 1978. McCann et al. and many residents were symptomatic (Barr et al. Shealy DB.. 1995. Rev Environ Health 2006. et al. Atlanta (GA). Environ Health Perspect 2002. Moomey CM. oral or dermal administration. Finding a measurable amount of para-nitrophenol in urine does not mean that the level will result in an adverse health effect. 2005. DiPietro E.S. 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. Pope C.112(10):1116-1124. Toxicology 2005.org/documents/jmpr/jmpmono/v95pr14. Available at URL: http:// www. 2003) and in 482 pregnant females from an agricultural region of California (Eskenazi et al. Role of individual susceptibility in risk assessment of pesticides.21(1):5767.inchem.215(3):182-190. CDC. Organophosphorus pesticide poisonings in humans: determination of residues and metabolites in tissues and urine. Hill RH Jr. Clark JM. Fourth National Report on Human Exposure to Environmental Chemicals 151 . Age-related effects of chlorpyrifos and parathion on acetylcholine synthesis in rat striatum. 2004). 1995). 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. Kramer RE. Ashley DL. Hill RH Jr. Jewell NP. Environ Res 1995.. Barr DB. Weltzien E. Head SL. et al. 2002.

Levin ED. EPA-738-FOO-009.pdf. 0153. 1995-1996. Ethyl parathion. Available at URL: http://www. Schilter B.E. Am J Ind Med 1991. Involvement of glial cells in the neurotoxicity of parathion and chlorpyrifos.201(2):97-104. 2004. May 2003. 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. Monnet-Tschudi F. Pesticides in the Nation’s Streams and Ground Water. Available at URL: http://pubs. Investigation of a fatality among parathion applicators in California. Barr DB. R. Available at URL: http://www. September 2000.epa.epa. Rosenberg J. U. WHO/SDE/WSH/03. EPA). Ames RG. Slotkin TA.110 Suppl 6:1047-1051. Dunlop B. pdf. Olsson AO. Ryde IT.D. Anal Bioanal Chem 2003.pdf. Hill RH Jr. Rubin C. Geological Survey (USGS). Toxicol Lett 2006.S. Environmental Protection Agency (U.gov/circ/2005/1291/.Organophosphorus Insecticides: Specific Metabolites Muttray A. 1992-2001.376(6):808-815. 1/12/07 U. Assessment of human exposure and human health effects after indoor application of methyl parathion in Lorain County.114(10):1542-1546.S. Esteban E. The Quality of Our Nation’s Waters. External and internal exposure of wine growers spraying methyl parathion.int/water_sanitation_health/dwq/chemicals/ methylparathion. et al. Sadowski MA. Environ Health Perspect 2002.20(4):533-546. Environ Health Perspect 2006. 1/14/09 U.162(2-3):219-224. Mengle DC. Interim reregistration eligibility decision (IRED) for Methyl Parathion. Letzel S. Costa LG. Yacovac R. Seidler FJ.usgs. Nguyen JV. Tate CA.S. Environmental Protection Agency (U. 2007 [online]. Hill G. Osorio AM. revised February 15. 152 Fourth National Report on Human Exposure to Environmental Chemicals . Backer G. Case No. Toxicol Appl Pharmacol 2004. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine.who. 6/1/09 World Health Organization (WHO). EPA). Ohio. gov/oppsrrd1/REDs/methylparathion_ired.04/106.gov/oppsrrd1/REDs/factsheets/0155fct. 5/19/09 Zurich MG. Kieszak S. Facts. Jung D. Available at URL: http://www. Methyl parathion in drinking water. March 2006.S. Honegger P.S.

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

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 .780 (. Survey Geometric mean (95% conf.64) .470 (.850 (. 154 Fourth National Report on Human Exposure to Environmental Chemicals . population from the National Health and Nutrition Examination Survey.410 (<LOD-1.210-1.880) 567 810 1104 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD .08) 1165 1316 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .27) .760 (<LOD-.2.55) .500 (. population from the National Health and Nutrition Examination Survey.610 (<LOD-1.740-1. which may vary for some chemicals by year and by individual sample.680 (<LOD-.210 (<LOD-.780 (<LOD-1.250 (<LOD-.S.820) < LOD < LOD .840) 669 687 929 Limit of detection (LOD. Urinary 2-(Diethylamino)-6-methylpyrimidin-4-ol/one (creatinine corrected) Metabolite of Pirimiphos-methyl Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. see Data Analysis section) for Survey year 01-02 is 0.930) 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 .580-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.740 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th .840 (.Organophosphorus Insecticides: Specific Metabolites Urinary 2-(Diethylamino)-6-methylpyrimidin-4-ol/one Metabolite of Pirimiphos-methyl Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.17 (.07) .700-1. interval) Selected percentiles ( 95% confidence interval) Sample 95th .670) 567 810 1104 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD .31) .430 (<LOD-.210-.780 (. < LOD means less than the limit of detection.94) .00) 669 687 929 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.670 (<LOD-1.15) < LOD .300-1.780 (<LOD-1.21) < LOD .200-.700-.950) < LOD < LOD 1.460) 1165 1316 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.S. Survey Geometric mean (95% conf.

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

1997. but pyrethroids are highly toxic to fish and some aquatic invertebrates. and deltamethrin have been used frequently on cotton. The general population may be exposed to pyrethroid insecticides primarily from the ingestion of food or from residential use. solvent oils. Pyrethroid insecticides are the most common active ingredient in commercially available insect sprays and are also used as structural termiticides.2-Dichlorovinyl)-2. 2005. which are natural chemicals found in chrysanthemum flowers. WHO... such as piperonyl butoxide.2-Dibromovinyl)-2. by either ester hydrolysis or hydroxylation. This class of pesticides has low toxicity in birds and mammals. 2006b). EPA. animal facilities. Pyrethroids are not well absorbed through the skin (ATSDR. After absorption from inhalation or ingestion... Soderlund et al. 1992). cyfluthrin. About two million pounds of permethrin and one million pounds of cypermethrin have been applied annually (U.. deltamethrin has been used for indoor protection against mosquitoes that carry malaria. 2002).. Woollen et al. they are not persistent in the environment due to their rapid degradation within days to several months. They are ranked as having moderate acute oral toxicity. Woollen et al. 2003. Compared with other classes of insecticides such as organochlorines. 2003. 2005). followed by conjugation. Pyrethroid pesticides are generally formulated as complex mixtures of different chemical isomers. 2002.2-dimethylcyclopropane carboxylic acid (55701-05-8 ) trans-3-(2. pyrethroids are rapidly metabolized. Estimated intakes from diet and drinking water are below recommended limits. Pesticide applicators can be exposed to pyrethroid pesticides via dermal and inhalation routes from powders and liquid formulations.2-dimethylcyclopropane carboxylic acid 3-Phenoxybenzoic acid (3739-38-6) 156 Fourth National Report on Human Exposure to Environmental Chemicals .EPA. The table shows the urinary pyrethroid metabolites measured in this Report.Pyrethroid Pesticides Pyrethroid Pesticides General Information Pyrethroid pesticides are synthetic analogues of pyrethrins. organophosphorus. Pyrethroid pesticides have low volatility. Dermal exposure with the potential for inadvertent ingestion may occur when lotions or shampoos are applied to treat lice or scabies. bind to soils.S. Generally. They are also applied on livestock to control insects. Adverse effects from large doses are related to the action of pyrethroids on the nervous system. and synergists. but may be poorly transferred across the placenta (ATSDR. Outside the U. and greenhouses.2-Dichlorovinyl)-2. Leng et al. and are rarely detected in ground waters (USGS. pyrethroid pesticides have less acute toxicity in animals and people. Human health effects from pyrethroid pesticides at low environmental doses or at biomonitored levels from low environmental exposures are unknown. Unmetabolized pyrethroids have been measured in breast milk.S. resmethrin. in some situations replacing the use of DDT... Certain pyrethroid insecticides (such as permethrin. 1999. 2007). and sumithrin) are also registered for use in mosquito-control programs in the United States. Possible other additional actions on neuroreceptors Pyrethroid Insecticides Metabolites in this Report Pyrethroid (CAS number) Cyfluthrin (68359-37-5) Cypermethrin (52315-07-8) Cyfluthrin (68359-37-5) and Permethrin (52645-53-1) Deltamethrin (52918-63-5) Cyhalothrin (68359-37-5) Cypermethrin (52315-07-8) Deltamethrin (52918-63-5) Fenpropathrin (39515-41-8) Permethrin (52645-53-1) Tralomethrin (66841-25-6) Urinary metabolite (CAS number) 4-Fluoro-3-phenoxybenzoic acid (77279-89-1) cis-3-(2. Soderlund et al. 1992).2-dimethylcyclopropane carboxylic acid (55701-03-6) cis-3-(2. 2006a. where these chemicals prolong sodium channel opening when a nerve cell is depolarized (Shafer et al.S. cypermethrin. or carbamate pesticides. Permethrin is also used in skin lotions and shampoos as medical treatments for lice and scabies. Pyrethroid pesticides are used to control a wide range of insects in public and commercial buildings. 2002). so usage is restricted near water (U. warehouses. agricultural fields. and then eliminated over several days in urine and bile (Kuhn et al. In agriculture. There are about 30 different pyrethroid pesticides in use.

2000. Shafer. et al. Levsen K. Leng G. Kang IH. bioallethrin and deltamethrin. Wolff MS. though a few pyrethroid pesticides and some metabolites have shown weak or inconsistent estrogenic effects on standardized assays (ATSDR. Environ Health Perspect 1999. Toxicokinetics of pyrethroids in humans: consequences for biological monitoring.atsdr.. Lack of (anti-) androgenic or estrogenic effects of three pyrethroids (esfenvalerate.27(4):609-614. Richardson JR. Kunimatsu T. 2005). Varoli FM. Neurosci Lett 2001. epa. et al. Toxicol Appl Pharmacol 2006. 2002). Ranft U. McCarthy AR.50(2):245-255. 1999. Kuhn K. Neurodevelopmental consequences of gestational exposure (GD14-GD20) to low dose deltamethrin in rats. Abell AD. References Agency for Toxic Substances and Disease Registry (ATSDR). Garey J. 2001. fenvalerate. Garey and Wolff. EPA at: http://www. 2003. 2003..35(2 Pt 1):227-237. Kim et al. and catecholaminergic pathways and behavioral changes have been demonstrated at subacute and subchronic doses for some pyrethroid pesticides (Aziz et al. September 2003.. Kim IY. motor activity. Seth PK.cdc.251(3):855-859. Garey J. Xenobiotica 1997.62:101-108. Kim TS. Transient dermal paresthesias have been reported among pesticide applicators after direct contact with certain types of pyrethroid pesticides. Caudle WM. Okuno Y. Yang J. WHO. J Environ Monit 2006. [Effects of fenvalerate on reproductive and endocrine systems of male rats] Zhonghua Nan Ke Xue 2002. 2006). and seizures (ATSDR. neurochemical changes in cholinergic. Florio JC.108(1):78-85. Generally.gov/toxprofiles/ tp155. Spinosa HS. cyfluthrin was the most frequent pyrethroid associated with symptomatic effects (irritant respiratory and dermal effects.. In California. Sugiri D.. Cruz-Casallas PE. Shukla Y. 1991. Lazarini et al.211(3):188-197.107(3):173-177. McCarthy et al.. Bull Environ Contam Toxicol 1999. Pogo BG. Miller GW. Estrogenic and antiprogestagenic activities of pyrethroid insecticides. Eriksson and Fredriksson. 2003. Human doseexcretion studies with the pyrethroid insecticide cyfluthrin: urinary metabolite profile following inhalation.. Fredriksson A. Go V. Kuhn KH. Idel H. Adhami VM. Zhao RC. In developing rodents.205(6):459-472. 2005). Neurotoxicol Teratol 2005. Salzgeber SA. 2005). dopaminergic. Ray et al. 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.. 2006. Effects of prenatal exposure to deltamethrin on forced swimming behavior. and striatal dopamine levels in male and female rats. paresthesias) reported in agricultural workers from 1996 to 2002 (Spencer and O’Malley. Moniz AC. Neurotoxicol Teratol 2001. Leng G. Hu JY. Chen JH. 2003. Neurotoxic effects of two different pyrethroids. Elwan MA. 2005). Concomitant exposure to organophosphorus insecticides may increase pyrethroid toxicity by slowing metabolic clearance of the pyrethroid. Toxicol Appl Pharmacol 1991. Toxicological profile for pyrethrins and pyrethroids. Elwan et al. Biochem Biophys Res Commun 1998.8(1):197-202. Pauluhn J. 2002).. Idel H. Estrogenicity of pyrethroid insecticide metabolites. Berger-Preiss E. Behavioral and endocrine changes induced by perinatal fenvalerate exposure in female rats. Lee SJ.gov/pesticides/ and from ATSDR at: http://www. Lazarini CA. Kamita Y. Human cases of systemic poisoning are rare and usually result from accidental exposure or intentional ingestion of pyrethroid insecticides. the pyrethroids are not considered genotoxic in in vitro testing or carcinogenic in animal testing (WHO. Soderlund et al. Kunimatsu et al. Thomson BM. Leng G. et al. Available from URL: http://www. tremor. Yamada T..Pyrethroid Pesticides and other ion channels may also explain some pyrethroid effects.gov/toxpro2.1/15/09 Aziz MH.8(1):18-21. Agrawal AK. et al.. 2002. Sunami O. hypersensitivity. Bernardi MM. Pyrethroid pesticide-induced alterations in dopamine transporter function. Hu et al. Leng A. salivation. Estrogenic potential of certain pyrethroid compounds in the MCF-7 human breast carcinoma cell line. Assessing estrogenic activity of pyrethroid insecticides using in vitro combination assays. Go et al. Ose K. Int J Hyg Environ Health 2002. Bernardi MM. J Reprod Dev 2004. Shin JH. 2006.300(3):161-165. Wieseler B. cdc. 2001. Kim HS. Lemonica IP. Song L.html. 2004.. Fourth National Report on Human Exposure to Environmental Chemicals 157 . Wang SL. Moniz et al. Signs and symptoms of acute pyrethroid poisoning after massive ingestions include agitation.27(12):1273-1283. choreoathetosis. 1998. Additional information about pesticides is available from U. IARC considers deltamethrin and permethrin as not classifiable as to their human carcinogenicity. Guillot TS.atsdr.S. Shaw IC. The pyrethroids in general use are not considered teratogenic or to have significant reproductive toxicity (ATSDR.. Regul Toxicol Pharmacol 2002.html. Indoor pyrethroid exposure in homes with woollen textile floor coverings.23(6):665-673. Eriksson P. on immature and adult mice: changes in behavioral and muscarinic receptor variables. and permethrin) in the Hershberger and uterotrophic assays. Lewalter J. Wolff MS.

Permethrin. Pesticide and Evaluation Scheme. March 2006. Rev Environ Contam Toxicol 2006.usgs. Reregistration Eligibility Decision for Cypermethrin. The metabolism of cypermethrin in man: differences in urinary metabolite profiles following oral and dermal administration. EPA). sumithrin synthetic pyrethroids for mosquito control.gov/oppsrrd1/REDs/ factsheets/permethrin_fs. EPA).epa. Sheets LP. Clark JM. 19962002. June 2006a. Available at URL: http://www.S. Pyrethroid insecticides: poisoning syndromes.171:3-59.S. synergies.gov/oppsrrd1/REDs/cypermethrin_red. U. Laird WJ.epa. Shafer TJ. Available at URL: http://www. Soderlund DM. 5/26/09 158 Fourth National Report on Human Exposure to Environmental Chemicals .Pyrethroid Pesticides Ray DE. Lesser JE. pdf. 5/26/09 U.38:95-101. Revised February 25. 2007. April 2002. June 2006b. Toxicology 2002. Mullin LS.who.htm. Environmental Protection Agency (U.S. Geological Survey (USGS). J Toxicol Clin Toxicol 2000.22(8):983-991. Environmental Protection Agency (U. Pesticides in the Nation’s Streams and Ground Water.pdf.htm. 5/26/09 U. Piccirillo VJ.int/hq/2005/WHO_ CDS_WHOPES_GCDPP_2005. EPA). Available at URL: http://www.S. and therapy.epa. 2005. Mechanisms of pyrethroid neurotoxicity: implications for cumulative risk assessment. Available at URL: http://pubs. resmethrin. Sargent D. Crofton KM. Permethrin Facts (Reregistration Eligibility Decision Fact Sheet). Environ Health Perspect 2005. Meyer DA.113(2):123-136. O’Malley M.186:57-72.S. Safety of pyrethroids for public health use. et al.gov/pesticides/ health/mosquitoes/pyrethroids4mosquitoes. Developmental neurotoxicity of pyrethroid insecticides: critical review and future research needs. World Health Organization (WHO). 1992–2001. Environmental Protection Agency (U. 5/26/09 Woollen BH. 5/26/09 U. Spencer J. Marsh JR. Available at URL: http://whqlibdoc. Pyrethroid illnesses in California.gov/ circ/2005/1291/.10.S.S. Xenobiotica 1992. Forshaw PJ.

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

< LOD means less than the limit of detection.2.2 and 0. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.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. population from the National Health and Nutrition Examination Survey. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1949 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. which may vary for some chemicals by year and by individual sample. 160 Fourth National Report on Human Exposure to Environmental Chemicals .S. Survey Geometric mean (95% conf.

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 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. Fourth National Report on Human Exposure to Environmental Chemicals 161 .S.Pyrethroid Pesticides Urinary 4-Fluoro-3-phenoxybenzoic acid (creatinine corrected) Metabolite of Cyfluthrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.

Angerer J.46(3):281-288.209(3):221-233. Hadnagy W. Butte W. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides. Isotope dilution highperformance liquid chromatography-tandem mass spectrometry method for quantifying urinary metabolites of synthetic pyrethroid insecticides. Hoppe HW. Atlanta (GA). Ranft U. Human exposure to indoor residential cyfluthrin residues during a structured activity program.Pyrethroid Pesticides References Baker SE.186:57-72. Bernard CE.77(1):67-72. Arch Environ Contam Toxicol 2004.109(3):213-217. Angerer J. Schulz C. Krieger RI. 162 Fourth National Report on Human Exposure to Environmental Chemicals . Kolossa-Gehring M. Angerer J.206(2):85-92. Pyrethroid illnesses in California. Environ Health Perspect 2001. Int J Hyg Environ Health 2006. Williams RL. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Berger-Preiss E. Leng G. J Expo Anal Environ Epidemiol 2003.209(3):293-299. Idel H. Becker K. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. Heudorf U. Heudorf U. Drexler H. Int Arch Occup Environ Health 2004. Ball M. Int J Hyg Environ Health 2003. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation.13(2):112-119. Sugiri D. Angerer J. Heudorf U. Seiwert M. 19962002. Third National Report on Human Exposure to Environmental Chemicals. O’Malley M. Barr DB. Centers for Disease Control and Prevention (CDC). et al. Rev Environ Contam Toxicol 2006. Spencer J. Olsson AO. 2005. Int J Hyg Environ Health 2006.

370 (.08) 947 1193 1004 1346 99-00 01-02 99-00 01-02 99-00 01-02 * * .670 (.12 (.890 (.670-1. 1999). ciscypermethrin and cis-cyfluthrin.210) .2-dichlorovinyl)-2. trans-permethrin.790-1.2dimethylcyclopropane carboxylic acid in urine not only reflects the metabolic transformation of any of the three pesticides.77 (.250 (.790) .28) 671 680 518 701 591 957 Limit of detection (LOD.2dichlorovinyl)-2.140 (<LOD-.15) .200) < LOD < LOD < LOD .870) 1.690) .220-. and ciscyfluthrin.440 (.202 (.S. < LOD means less than the limit of detection.250-.490-1.780) . The presence of cis-3-(2.370-.730 (. 1985.140 (.700) .350) .630) .420-.or trans-3-(2. Generally.920) 1.580) 1.650-1.200-. cis-cypermethrin.280-.68 (.43) .900 (.510 (.2-dimethylcyclopropane carboxylic acid that is formed in the environment from the degradation of these pesticides (George.550) .510 (.490-. transcypermethrin and trans-cyfluthrin. but can also reflect exposure to trans-3(2.28) 468 580 667 831 816 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .120-.2-dichlorovinyl)2.430-.68) .2-Dichlorovinyl)-2.200) . and cis-Cypermethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.120-. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.270 (.300-.44 (.580-1.200) .500 (. Similarly.Pyrethroid Pesticides Cyfluthrin the cis-metabolite is found in the urine.380-. more of the trans-metabolite than Urinary cis-3-(2.470 (.630) .180 (.80) .21) .610) .35) .2-dimethylcyclopropane carboxylic acid Metabolite of cis-Permethrin.110-.2-dimethylcyclopropane carboxylic acid formed in the environment from the degradation of these pesticides (George.270 (.740 (.670-1.510 (.500 (.240) .300-.730 (.570-.68359-37-5 Cypermethrin Permethrin CAS No. Kuhn et al.790 (.47 (.380-. trans-cypermethrin.710) .300 (. Cyfluthrin.680-3..530 (. and trans-cyfluthrin.1 and 0.570 (.770-1.160 (<LOD-.710-1.490-.150 (.160 (. 1999). cis-permethrin.730 (.740) 1.770) .600 (. cis-3-(2. 1985. population from the National Health and Nutrition Examination Survey.2-dimethylcyclopropane carboxylic acid in urine not only reflects the metabolic transformation of any of the three pesticides. Biomonitoring Information Urinary levels of cis.52645-53-1 General Information Several pyrethroid pesticides are formulated as a mixture of cis. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.120-.950-2.280 (.460-.670-2. the presence of trans-3-(2.50) .460 (.160 (.680 (.32) .260 (.220-.200-.890 (.180) . but it can also reflect exposure to cis-3-(2.340) .680) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .220) .08) .340-.110-.380 (.630 (.850 (. Survey Geometric mean (95% conf.270 (.410) .960 (.240) .200 (.210) 90th .600) .600-1.460-1.2-dimethylcyclopropane carboxylic acid is a metabolite formed from trans-permethrin.and trans-isomers. The chemical trans-3(2.410) .310) .640 (.110-.2-dichlorovinyl)-2.230) .13 (.155-..300 (.740-1. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.210-.880 (.610) .220-.790-1. Fourth National Report on Human Exposure to Environmental Chemicals 163 .1.820 (.220-.630-.35) 1.270-.120-.24) 1.340) . Kuhn et al.330) .470-1.10) 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 . which may vary for some chemicals by year and by individual sample.740-2.910-5. In the body.380) .380-.330 (.2dichlorovinyl)-2.2-dichlorovinyl)- CAS No. 52315-07-8 CAS No. The cis-isomer of permethrin has more potent insecticidal activity than transpermethrin.53) .2-dichlorovinyl)-2.54) .200-.68) .110 (<LOD-.07 (.520) .400-.490-1.170 (.11) .2-dimethylcyclopropane carboxylic acid is a metabolite formed from cis-permethrin.262) * * * < LOD < LOD .

.S.67 (.890 (.560) 1.680-1.29 (.11 (..340-.710-3..450-.08) 468 580 667 830 816 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .260 (. 2006.170 (.250-.2dimethylcyclopropane carboxylic acids at the 95th percentile that were similar or slightly less than the 95th percentiles in the U.200) . These studies indicated that intake is mainly from the diet and that dermal absorption contributes little to intake (Heudorf et al. Studies in Germany of 396 children and adolescents (Becker et al. 2006) and 1177 urban adults and children (Heudorf et al.260-.33) .290 (.2-dichlorovinyl)-2.840 (. urinary trans-3-(2.11) 1.560) .2-dichlorovinyl)-2. urinary levels of cis-3-(2.. 2005).540) .440 (. 2003).640 (.550) .03) 1.550 (.880) .640) 1.220 (.240 (<LOD-.Pyrethroid Pesticides 2. 2006).160 (<LOD-.380) .2-Dichlorovinyl)-2.2dichlorovinyl)-2. post- Urinary cis-3-(2.540 (.138 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.680-1.380 (.2-dimethylcyclopropane carboxylic acid levels at the 95th percentile were about one-third of the 95th percentile in the NHANES 20012002 subsample (CDC.33 (.390-.2-dimethylcyclopropane carboxylic acid did not increase at 24-72 hours after exposure to nearby pest control operations (Leng et al. In a study of volunteers.2dichlorovinyl)-2.340) . Schettgen et al.640-.430-1.580) .890) .550) .830) .260 (.230-.520) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .49) .920 (.360-1.200-.11) . In the same residents.12 (.220) .280-. representative NHANES 2001-2002 subsample (CDC.810 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.182) * * * < LOD < LOD .2-dichlorovinyl)-2.190) .290) .270 (.320-.150-.11) .200 (.700-2. 2005).250) 90th .440-.280 (.300) .700) .37) . 2004).150-.59 (1.2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of cis-Permethrin. 2006.140-.and trans-3(2.390-.320) .21) .420 (. 2001) showed urinary levels of cis.120 (.290-. the levels at 24-72 hours were slightly less than the 95th percentile in the NHANES 2001-2002 subsample (CDC.430-.130-.780) 1.340) .350) .210-. 2001.440-.270) .2dimethylcyclopropane carboxylic acid at the 95th percentile were about half the 95th percentile in the NHANES 20012002 subsample (CDC.750-1..570) .400 (.250) .440 (.170) < LOD < LOD < LOD .12-2.S..230-..390 (.190) .530 (.2-dimethylcyclopropane carboxylic acids in children were related to residential pesticide use and house dust levels (Becker et al.780 (. Urinary levels of the two chemicals in adults were similar to those in children in these studies (Heudorf et al.24) .2-dimethylcyclopropane carboxylic acid reflect recent exposure to either their parent pyrethroid pesticides or their environmental degradates.170 (. Cyfluthrin.550-1.580-1..590 (.530 (.80) .500 (.104-..31) .590) .270-.680 (.180-. and cis-Cypermethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.370-.59) .840 (. population from the National Health and Nutrition Examination Survey.180 (.350 (.470-1. 2002).67) . 2005) In a small group of indoor pest-control operators.370-.450-1.250 (<LOD-. the median and 95th percentile of urinary levels of cis-3-(2..14) 671 680 518 700 591 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.640-1.600 (. 2005).540 (. 2006).2-dichlorovinyl)-2.260 (.11) 947 1193 1004 1345 99-00 01-02 99-00 01-02 99-00 01-02 * * .080-.430 (. Survey Geometric mean (95% conf.450 (.640-1..260) .750 (.300 (.300 (. median urinary levels of trans-3-(2.230 (. 2005).200-.690-1.370-. Other studies have provided evidence that urinary levels of cis.510-1.900 (. 2004. Lu et al.700) . In a study of urban residents in Germany (Berger-Preiss et al.59) . 164 Fourth National Report on Human Exposure to Environmental Chemicals .230-.250-.380-. In these volunteers.270) . 2002).710 (.410) .300) .150-.550-1. Estimated daily pyrethroid intakes based on urinary levels in the German children were below the acceptable daily tolerances (Heudorf et al.250-.220 (.290) . though the 95th percentile levels increased several fold after exposure to nearby pest control operations (Leng et al. the levels at 24-72 hours were slightly less than the 95th percentile in the NHANES 2001-2002 subsample (CDC.2-dimethylcyclopropane carboxylic acid did not increase.400-1.and trans-3-(2.03) 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 .190 (. 2003).300-.800 (.250) .

01 (1. < LOD means less than the limit of detection.570) 90th 1.22 (1.09 (.11-2.42) 1.58) 961 1184 1015 1341 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .910-1.17 (.850-1.19 (2. however.55-3.910-1.68) 1.03-1.4 and 0.560 (.800-1.560 (.500 (.42 (2.10) 2. 2005).54 (1.40 (1.69 (1.660) 1. 2003) were similar to the 95th percentiles for adults in the NHANES 2001-2002 subsample (CDC.4. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Finding a measurable amount of cis.68) 1.530) .410-.470 (.580 (.07-3.63) 1.66) .480-.77) 2.620) < LOD 2.2-dichlorovinyl)-2. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.17-1.54) 4.11-1.60) 1.970 (.28 (1.520-.91 (1.59 (1.17 (.56) 2.750) .08-6.95) 3.76-3.68-3.490 (<LOD-.490-1.85) 4.55-4.62 (1.780 (.95) 2. trans-Cypermethrin.860) .550 (.68) 2.07 (1.77 (1.400-.56) 2.19 (3.670) .14) 1.16) 1.760) .940 (.14-6.43) 2.7) 2.440 (<LOD-.500-.840-1.87 (1.2-dimethylcyclopropane carboxylic acid (Hardt and Angerer.810-1.2-dichlorovinyl)-2.2dichlorovinyl)-2.730) . which may vary for some chemicals by year and by individual sample.68-2.520) .460-.2-dimethylcyclopropane carboxylic acid in urine does not mean that the level causes an adverse health effect.41 (1.5) 2.and trans-3-(2.60-4. 2005). Survey Geometric mean (95% conf.35) 1. Fourth National Report on Human Exposure to Environmental Chemicals 165 .64-4.25-3.56 (1.69) 1.39 (1.560 (.49-3.70) 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 .27 (1.420 (<LOD-.400 (<LOD-.20 (. Urinary trans-3-(2.460-. population from the National Health and Nutrition Examination Survey.66) 691 680 518 690 595 954 Limit of detection (LOD.20 (.01) 4.76-4.03-1.670) .23 (.56 (1.49-3.60) .500) .84 (1.77) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .81) 2.410 (<LOD-. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.89 (2.08-4.700) .66) 478 576 675 826 823 1123 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD . interval) Selected percentiles ( 95% confidence interval) Sample 95th 3.19) 1.55-5. The maximum post-application urinary levels.12-6.410-.S.13) . Biomonitoring studies on urinary levels of cisor trans-3-(2. and trans-Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.23) 2.50 (1.08) 1.90) 1.710 (.2-Dichlorovinyl)-2.14-2.920-1.410 (<LOD-.48) 4.830-1.94 (1. were up to 27 times higher than the 95th percentile for adults in the NHANES 2001-2002 subsample (CDC.63) 1.680-1.77) 1.Pyrethroid Pesticides application median urinary levels of summed cis.700-1.20 (.28 (2.2-dimethylcyclopropane carboxylic acid provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of pyrethroid pesticides than are found in the general population.610) 1.97-11.25 (1.39-5.or trans-3-(2.37 (1.2-dimethylcyclopropane carboxylic acid Metabolite of Cyfluthrin.26 (.470 (<LOD-.49-5.41-14.820) .

45 (1.930-1.750) .470 (.64 (1.28) 2.540) .22-1.75 (1.700 (.850-3.41) 1.35) 1.68) 3.19) 961 1184 1015 1340 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .29) 1.91-11.48-2.27-2.850) .70 (.07) 2.580) .520 (<LOD-.26 (1.19 (1.42 (.Pyrethroid Pesticides Urinary trans-3-(2.00 (1.500-.44) 2.74) .87-8.20-2.610-.47 (1.530 (.00-5.39) 1.3) 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.27-2.570-.36) 2.440-.880 (.780) 90th 1.08 (.60 (1.36 (1.91 (1.570 (.00) 1.570 (<LOD-.15-3. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.880-1.42) 1.11) .760 (.88) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 1.22-2. and trans-Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.56-5.640) .33 (1.47-2.11) 478 576 675 825 823 1123 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .87 (1.07-1.16 (1.87-3.560 (. trans-Cypermethrin.39 (1.61) 1.00) 1.48 (1.30-6.13) .900 (<LOD-1.780 (<LOD-.S.12-1.60) 2.55 (2.56 (1.10) size 1976 2524 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD 75th .530 (<LOD-.2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of Cyfluthrin.89) 2.580 (.65) 1.45-2.780) . 166 Fourth National Report on Human Exposure to Environmental Chemicals .15-3.31) 1.57 (1.57) 3.700 (.65 (2.13) 1.47-2.470-.80) 1.660) .15 (1.800-1.31 (.86 (2.30-3.34-3.40-2.11) 691 680 518 689 595 954 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.22) 1.12 (.07-3.670) .820-2.91) 1.33-1.34-4.880 (<LOD-1.2-Dichlorovinyl)-2.700-.98 (1. population from the National Health and Nutrition Examination Survey.800-1.74) 2.67 (2.740) .15-3.02-1.15) 3.19) .720 (<LOD-.480-.56-2.81 (2.20 (1.00) 5.07) 2.35 (1.60) 2.87) 1.08 (.730) . Survey Geometric mean (95% conf.07-2.770) < LOD 2.33-2.850) 1.87) 1.31 (2.970 (.55 (2.720-1.410-.55 (2.37 (1.720-1.15) 2.

Kuhn K. et al. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. Fourth National Report on Human Exposure to Environmental Chemicals 167 . A longitudinal approach to assessing urban and suburban children’s exposure to pyrethroid pesticides. 2005. Leng G. Ball M. Angerer J. Heudorf U. Barr DB. Heudorf U. Angerer J. Heudorf U. Berger-Preiss E. Idel H.209(3):293-299. Bravo R. Seiwert M. Pearson M. Int Arch Occup Environ Health 2004. Sugiri D. Schettgen T. Environ Health Perspect 2006. Toxicokinetics of pyrethroids in humans: consequences for biological monitoring. Idel H. Butte W. Angerer J. Int J Hyg Environ Health 2006. Leng G. Int J Hyg Environ Health 2002. Centers for Disease Control and Prevention (CDC). Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine. Schulz C. Bull Environ Contam Toxicol 1999. Bartell S. Pyrethroid exposure of the general population-is this due to diet? Toxicol Lett 2002. Leng G. Wieseler B. Idel H. J AOAC 1985. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Int J Hyg Environ Health 2003. Drexler H.76(7):492-498.68(6):1160-1163. Angerer J.114(9):14191423. Int J Hyg Environ Health 2006. Levsen K.209(3):221-233. Hardt J. Sugiri D. Hadnagy W. Environ Health Perspect 2001. Ranft U. Atlanta (GA). Ranft U.206(2):85-92. Angerer J. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides. Berger-Preiss E.109(3):213-217. Hoppe HW. George DA. Drexler H. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. Indoor pyrethroid exposure in homes with woollen textile floor coverings. Angerer J.205(6):459-472. Lu C. Kolossa-Gehring M.77(1):67-72. Heudorf U.134(1-3):141-145. Biological monitoring of workers after the application of insecticidal pyrethroids. Third National Report on Human Exposure to Environmental Chemicals. Permethrin and its two metabolite residues in seven agricultural crops.Pyrethroid Pesticides References Becker K. Int Arch Occup Environ Health 2003.62:101-108.

S.2-dibromovinyl)-2.2-dibromovinyl)-2.2-dimethylcyclopropane carboxylic acid were below the limit of detection (CDC.2-dibromovinyl)2.2-dibromovinyl)-2.. 2005).39 µg/L. Outside the U.3-0. 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 of 0.2-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. Deltamethrin can degrade to cis-3(2. in some situations replacing the use of DDT. Baker et al. 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. in detection of cis-3-(2. 168 Fourth National Report on Human Exposure to Environmental Chemicals . Studies in Germany of 396 children and adolescents (Becker et al. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 2005). mean peak urinary levels of cis-3-(2.. The peak mean levels in these children were more than 800-fold higher than the detection limit in the 2001-2002 NHANES subsample.Pyrethroid Pesticides Deltamethrin CAS No.2-dibromovinyl)-2.2-dibromovinyl)-2. 52918-63-5 General Information Cis-3-(2. Following residential spraying with deltamethrin for malaria protection in Mexico.1 μg/L) for the NHANES 2001-2002 subsample (CDC.2-dimethylcyclopropane carboxylic acid is a metabolite of the pyrethroid insecticide deltamethrin. In the NHANES 2001-2002 subsample. 2005).2dimethylcyclopropane carboxylic acid formed in the environment..2-dimethylcyclopropane carboxylic acid in the environment (IPCS. deltamethrin has been used against mosquitoes that carry malaria. urinary levels of cis-3-(2. 2001.2-dimethylcyclopropane carboxylic acid in urine does not mean that the level will result in an adverse health effect.2-dibromovinyl)-2. In an analysis of 217 urine specimens from a nonrandom sample of United States residents. 1990).2dimethylcyclopropane carboxylic acid reflect recent exposure to deltamethrin or its environmental degradate.. (2004) reported a geometric mean concentration of cis-3(2.5 μg/L) than the detection limit (0. 2004).. 2006) and 1177 urban adults and children (Heudorf et al.2-dimethylcyclopropane carboxylic acid in the urine may reflect exposure to deltamethrin or to cis-3-(2. Thus.2-dibromovinyl)-2.2-dimethylcyclopropane carboxylic acid at the 95th percentile ranged slightly higher (0. Biomonitoring Information Urinary levels of cis-3-(2. Urinary levels for adults and children in these studies were similar (Heudorf et al. 2001) showed that urinary levels of cis-3-(2. Finding a measurable amount of cis-3-(2.

< LOD means less than the limit of detection. Survey Geometric mean (95% conf.Pyrethroid Pesticides Urinary cis-3-(2.2-Dibromovinyl)-2. population from the National Health and Nutrition Examination Survey. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.1 and 0. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.1. which may vary for some chemicals by year and by individual sample. Fourth National Report on Human Exposure to Environmental Chemicals 169 .S. 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-dimethylcyclopropane carboxylic acid Metabolite of Deltamethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.

170 Fourth National Report on Human Exposure to Environmental Chemicals . population from the National Health and Nutrition Examination Survey. Survey Geometric mean (95% conf.2-Dibromovinyl)-2.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.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.Pyrethroid Pesticides Urinary cis-3-(2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.

Heudorf U.htm. et al. Heudorf U. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine. Atlanta (GA). Heudorf U.113(6):782-786. Environ Health Perspect 2005. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides. Environmental Health Criteria 97. Fourth National Report on Human Exposure to Environmental Chemicals 171 . Angerer J. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. Environmental health assessment of deltamethrin in a malarious area of Mexico: environmental persistence. Third National Report on Human Exposure to Environmental Chemicals.209(3):221-233. Angerer J. Lopez-Guzman OD. et al. Deltamethrin. Centers for Disease Control and Prevention (CDC). 5/26/09 Ortiz-Perez MD. Kolossa-Gehring M. Int J Hyg Environ Health 2006.inchem. Int Arch Occup Environ Health 2004. Available at URL: http://www.org/documents/ehc/ehc/ ehc97. 2005. and genotoxicity in exposed children. Schulz C. Grimaldo M. Angerer J.209(3):293-299. [online] 1990.77(1):67-72. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Hoppe HW. Ball M. Environ Health Perspect 2001. Torres-Dosal A.109(3):213-217. Carranza C. Angerer J. International Programme On Chemical Safety (IPCS). Int J Hyg Environ Health 2006. Seiwert M.Pyrethroid Pesticides References Becker K. Batres LE. Butte W. Drexler H. toxicokinetics.

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

710 (.406) .300 (.560-.295) .05) .510-.26) 2.560-.38 (2.200-.53) 1.700-1.78) 1.352-.13) .780) 4.13 (.760 (.18 (2.28) 1.800) 1.72 (1.30 (.90) 1.26-2.750) .230-.190-.292 (.33) .41-2.700 (.73) 1.83-11.25 (2.810) 1.50 (2.S.78) 6.33 (1.52-5.276-.590 (.990) .850) .30) 3.750-1.570-.230 (.314) .210-.36) 1.362) .277-.01 (1.550-.680 (.16) 974 1193 1024 1346 99-00 01-02 99-00 01-02 99-00 01-02 .820) .233-.570-1.27-2.640 (.12) .730 (. Deltamethrin.190-.Pyrethroid Pesticides Urinary 3-Phenoxybenzoic acid Metabolite of Cypermethrin.320) .29-1.530-.350-.38 (2.370) .12 (.280 (.820) . see Data Analysis section) for Survey years 99-00 and 01-02 are 0.02-6.530-.210-.18 (1.360) .800 (.345) Selected percentiles ( 95% confidence interval) Sample 95th 4.600 (.54) 1.300 (.34) 8.670 (.250-.71 (1.48-2.870 (.630) .86 (1.49 (1.240 (.64) 697 680 524 701 603 957 Limit of detection (LOD.62-8.51-3.8) 3.740 (.384) .230 (.05) 1.250 (.220-.69) 3.260-.35 (2.55 (1.33 (2.320) .315 (.340) 1.81 (1.266-. Survey Geometric mean (95% conf.14-6.41 (1.328 (.49-2.298 (.76 (1.92-3.560-1.34 (2.320) .52-4.53-3.840-1.710 (.230-.374) 99-00 01-02 99-00 01-02 99-00 01-02 .63 (3.230-.390) .25 (2.75 (1.300) .227-.369) .78 (1.12) 4.46) 2.610) .62-6.373) .830-2.78) 1.27-11.69 (1.93 (1.434) .340) .850) .30 (1.247-.39) 2.190-.25-4.21 (2.79) 3.430-.43) 3.320) .267 (.417 (.320 (.35) 2.200-.16-1.32 (2.470-.440) .60) .490) .750) .428-.48-2.25) 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 .740 (.42-2.34-6.1) 3.1 and 0.16) 483 580 682 831 833 1128 99-00 01-02 99-00 01-02 .260 (.586) .420) .595) .04-5.27-2.180-.45 (2.41) 3.364) .35) 2.960 (.253-.160-.32 (1.454 (.04) .200-.160-.273 (.03 (3.44) 5.56-5.240 (.940) 1.520 (.49 (1.353 (.226-.25-1.65-2.590-.238-.830) 90th 1.265-.330) .290 (.23 (2.65 (1.25-7.63-3.260 (.62) 5.321 (.297 (.330) .1) 3.190-.270 (. and Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.246-.35) 1.601) .311 (. interval) .450 (.49-2.314 (. population from the National Health and Nutrition Examination Survey.325 (.46) . Fourth National Report on Human Exposure to Environmental Chemicals 173 .35 (1.300 (.32-21.250 (.288 (.387) .507 (.292-.270) .41-3.1) 3.490-.16) 1.620-1.510-.1.89-71.51-6.336 (.288-.26) 2.427) .260 (.45-5.271-.430-.355) .250 (.340) 75th .650 (.

73) 1.640 (.238-.00) 5.64-5.03-1.490-.320) .02 (2.270) .480 (.290) .220 (.41-4.74) 3.370-.55 (1.15-2.19) 974 1193 1024 1345 99-00 01-02 99-00 01-02 99-00 01-02 .63) 1.230) .49 (1.63-3.61-2.83 (1.160-.44 (1.25-2.35-3.840-1.390-.378 (.270 (.49) 3.480-.48 (1.630) .83) 1.670) .21-4.590-1.35 (1.540 (.200-.860 (.210 (.860-1.250 (.300-.13 (.60) 1.16-4.91) 9.17-1.55) 3.270 (.640 (.670) 3.19) 2.173-.700-1.00) 1.94 (1.13-1.810) 1.275 (.274 (.11 (.32 (2.240 (.550 (.740) .09-2.730-1.490 (.21 (1.52 (1.02-1.590) .590) .550 (.00) 1.09-2.278) .54 (1.150-.410-.450 (.225-.510 (.323 (.250 (. Survey Geometric mean (95% conf.39) 1.350 (.43-64.730) .290) .91) .86 (1.590) .271-.230-.357) .220-.329) .35) 1.274-.280 (.253) .49) 1.401) .19 (2.53 (1. Deltamethrin.309 (.329) .06-3.500) .261-.05-3.304) Selected percentiles ( 95% confidence interval) Sample 95th 3.88-5.530-.280 (.380-.400-.460-.92) 483 580 682 830 833 1128 99-00 01-02 99-00 01-02 .96 (1.370 (.36 (1.272 (.350) .240-.311 (.440-.720) 90th 1.80) 4.400) .330) .570) .91 (2.437) .210 (.272) .240 (.Pyrethroid Pesticides Urinary 3-Phenoxybenzoic acid (creatinine corrected) Metabolite of Cypermethrin.27) 1.43) 1.200-.226-.280) .560 (.230-.410) .750-1.178-.510 (.380 (.37) 1.440-.62) .216-.44) 2.446) .299-.240-.11 (.650) .62) 1.60-4.210-.37 (1.52) 2. and Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.10 (2.372) .309) .335-.440-.312 (.03 (.91-4.760) .224-.35) .362 (.190-.04 (3.250) .240 (.43 (1.330 (.25-5.720 (.17 (.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 .07-5.234 (.09 (.490 (.227 (.22 (1.25) 2.190-.321-.270-.860-1.677) .387) .610 (.43 (2.0) 3.420-.580) .67 (1.19-6.40) 2.330) 1.04 (.67) 1.200-.730) .190 (.202-.460-.07) 2.930) 1.330) .264 (.75-8. population from the National Health and Nutrition Examination Survey.36-6.530-.S.280 (.550 (.261 (.84 (1.09) 3.534) .310) .423 (.246 (.330) 75th .328) .580 (.41) 1.229-.95) 1.72 (1.300-.49-2.51-7.510 (. interval) .48) 697 680 524 700 603 957 174 Fourth National Report on Human Exposure to Environmental Chemicals .316 (.270) .400-.200-.73-4.67 (1.13-1.240 (.240-.81 (1.280-.960-1.40 (1.90) 3.240-.930) .365) 99-00 01-02 99-00 01-02 99-00 01-02 .280) .290-.

113(6):782-786. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Barr DB. Batres LE. Environmental health assessment of deltamethrin in a malarious area of Mexico: environmental persistence.111(1):79-84. Deych E. Olsson AO. Sugiri D. Ortiz-Perez MD. Environ Health Perspect 2005. toxicokinetics. Int J Hyg Environ Health 2002. Arch Environ Contam Toxicol 2004. Berger-Preiss E. Levsen K. Liu Z. Indoor pyrethroid exposure in homes with woollen textile floor coverings. Idel H. Isotope dilution highperformance liquid chromatography-tandem mass spectrometry method for quantifying urinary metabolites of synthetic pyrethroid insecticides. A longitudinal approach to assessing urban and suburban children’s exposure to pyrethroid pesticides. Int J Hyg Environ Health 2003. urban cohort. Leng G.206(2):85-92. Becker K. Berger-Preiss E. Environ Health Perspect 2003. 2005. Biological monitoring of workers after the application of insecticidal pyrethroids.209(3):221-233. et al. Bravo R. Exposure to indoor pesticides during pregnancy in a multiethnic.76(7):492-498. Barr DB. Int J Hyg Environ Health 2006. Ranft U. Centers for Disease Control and Prevention (CDC). Lu C. Bartell S. Hardt J. Idel H. Hadnagy W. Fourth National Report on Human Exposure to Environmental Chemicals 175 . Grimaldo M.46(3):281-288. Godbold J. Angerer J. Pearson M. et al. Berkowitz GS. et al. Sugiri D. Environ Health Perspect 2006.Pyrethroid Pesticides References Baker SE. Hoppe HW. Carranza C. Ball M. Third National Report on Human Exposure to Environmental Chemicals. Atlanta (GA). Int Arch Occup Environ Health 2003. Kolossa-Gehring M. Lapinski R.205(6):459-472. Leng G. and genotoxicity in exposed children.114(9):14191423. Ranft U. Torres-Dosal A. Lopez-Guzman OD. Obel J. Angerer J. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. Seiwert M.

108 (.190-.115-.270-.160 (.160) .250-.200 (. 0.350-.350 (.360 (.330 (.150 (.170-.070-.400) . Two antimony compounds (sodium stibogluconate and antimony potassium tartrate) have been used as antiparasitic medications.280-.190-.130 (.220-.160) .210) .260) .250-.090-.150-.260) .122 (.120) .220) .360) .133) * .108-.300 (.109-.137) . It is also used in paints.260) .04. Stibine is a metal hydride form of antimony used in the semiconductor industry.110-.160-.117-.130) .190-. and glass.350) .158 (. fireworks.120-.280 (.400) .134-. 01-02.180-.090 (<LOD-.440) .120 (.390) .120 (.130) . metal bearings.130) < LOD .190) .320-. water.210) .170 (. It is used in metal alloys.280-. sheet and pipe metal.146 (.135) * . and excretion of antimony vary depending on its oxidation state.470) .117-.190 (.120) .130 (.310) .088-.130 (. and 0.300) .300-.143 (.240 (.390) .490) .160-.360) .140) .220 (.240 (.178) .440) .510) .270 (.150) .250 (.110-.150) 90th .220-.330) .290 (.240) .126-.570) .390) .340) .310 (.410) .350-.180 (.430 (.270) .128 (.240 (.390-.230-. storage batteries.180 (.280-.098-.160) .460) .210) .207) .130-.140) .07.280) .230) .330-.200-.350 (.150-.350 (.390 (.112-.099 (.200) .190 (.095 (.350 (.200-.156-.140) .200-.136-.500) .320) 787 683 618 554 667 723 768 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.04.320 (.150) .310 (.180 (.260 (.350) .150) .230 (.134 (.440 (.160-. or other substances containing antimony is another means of exposure.340 (.200) .132 (.070 (<LOD-.710) . enamels. The absorption.120) .119-. ammunition. < LOD means less than the limit of detection. +3.330) 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 .130 (.240-.470 (.310-.320) Total .125 (.330) .270 (.140-.280 (.290-.130 (.330) .320) .130) .180) .190) .430 (.190 (.170-.130-.120-.190-.120-.370-.093 (.490 (.260 (.S.080 (<LOD-.100-. 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. which may vary for some chemicals by year and by individual sample.080-.150-.390) .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 .270 (.400) .250-.080) .120 (. Antimony can exist in one of four valences in its various chemical and physical forms: -3.140 (.220) .176 (.114) .123 (.154) .180) .130-.260 (.190 (.184) .141-.150-. ceramics.200 (.120) .170 (.160-. to a lesser extent.360-.200) .160) .079-.400-.070 (<LOD-.161) .220) .230) . from air and drinking water. Workplace exposures can occur at smelters.320-.120 (.280-.130-.180-.200 (.142 (.430 (.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 . and as a fire-retardant in textiles and plastics.137) .410-.400 (.350 (.130-.190) . People are exposed to antimony primarily through food and.200 (. interval) .157) . Dermal contact with soil.140) .200 (.230 (.300-.180 (.250-.300) .120-.270) . Antimony enters the environment from natural sources and from its use in industry.280-.360 (.131-. 0.560) .180 (.220-.330) .160 (.310 (.145) Selected percentiles ( 95% confidence interval) 50th . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.280) . see Data Analysis section) for Survey years 99-00.140) .140) .110-.460 (.090-.370) .200) . population from the National Health and Nutrition Examination Survey.240-.130-.120-.144) .330 (.120 (.210-.350-.095-.190) .230-.180-.160) .140 (.160 (.240 (. coal-fired plants.310-.390-.210 (.460 (.220-.270 (.136) * .250 (.390-.600) .110-.350) . respectively.210-.120-.420) .115) .320-. and +5.180 (.087-.145 (.100 (.119) .150 (. castings.100 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.130-.180-.220-.310) .320-. and pewter.240 (.170) .Metals Antimony CAS No.280) .110 (.230 (.190) .410) .150 (.090) 75th . 7440-36-0 General Information Antimony is found in ores or other minerals.310 (.120-.130 (.400 (.470) .200-. distribution.350) .103) .500) .128 (.090 (.250) .170-. solder.220-.110) .300-.164-. 176 Fourth National Report on Human Exposure to Environmental Chemicals .200 (.130 (.140 (.100) .230-.190-.105 (.180-.120-. and 03-04 are 0.080) .260-.300) .340 (.190 (.320 (.530) .230) .280) .126 (.210 (.300 (.210) .220) 95th .169 (.230-.100-.132 (.140 (.230-.250 (.220 (.130 (.170-.170-.290-. often combined with oxygen to form antimony trioxide or with sulfur to form stibnite.154) .400 (.330-.330 (.148-.120-.160) .175 (.260-.197) . and refuse incinerators that process or release antimony.460 (.210) .154-.150-.

222 (.167 (. and route of exposure (Elinder and Friberg.115 (. 1944).077) .137 (.148-.267) .113) .120 (.134) .193) .333 (.112 (.071-.186) .214) .235-.135 (.226 (.111 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.277 (. Ming-Hsin et al.425) . myocardium.200-.228 (.154-.126-.114 (.135) . and kidney have been demonstrated in high dose animal studies depending on the dose.227-.500) .138-.429) .156-.178-.160 (.102-.176 (.338 (.108-.257) .139 (.200-.245) .229-.119-.250 (.228 (.164 (.081) .182 (.207) .129 (.213 (.321) .230-.338) .364 (.108 (. 1988.200-.333) .120 (.295 (.209-.371 (.140) < LOD . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.352 (.162-.103-.181) . and ulcers (Werrin.119-.192 (.. diarrhea.203) .139 (.276 (.286 (.220) .250-.250 (. An elimination half-life of approximately 95 hours has been estimated after occupational exposures (Kentner et al.127) . Pulmonary edema may occur in severe cases of inhalation exposure (Cordasco et al.099-.092-.250-.146-.255-.225) .114 (.107-.125-.193 (.115-.170 (.224 (.185-.225 (. resulting in hemolysis with abdominal and back pain (Dernehl et al.315) .255) .313-.236 (.143) 90th .164) .385 (.082) .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 . Acute inhalation of antimony has been associated with irritation of the respiratory tract and impaired pulmonary function (Renes.300) .239-.191 (.074 (.164-.098-.149) .211) .068 (.241-.250-.167 (.230) 95th .248-.421) .280-.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 .209) .106-.156 (.111-.117-.121) .116 (.123) . 1986). abdominal pain.146) .278 (.265 (.173) .199-.082 (<LOD-.247) .320 (.444) .250-.167-.106-.144-.138) * .116-.333-.109 (.269 (.265-.143) Selected percentiles ( 95% confidence interval) 50th .120 (.485) .310) .195-. The toxicity of stibine after acute inhalational exposure is similar to that of arsine.113-.122 (.118 (.147) .146-.145) .364 (.414) ..198) .447 (.317) .086) 75th .115 (.310) .209) .176 (.192) . Histopathologic inflammatory and degenerative changes in the lung.163 (.195 (.082) .176-.317) .405) .261) .444) .103-.129 (.104-.104-.267-.132) .115-.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.238) .161) .253-. population from the National Health and Nutrition Examination Survey.138 (.200) .. interval) .149-.143) .112 (.129) * .338 (.127) .122 (.173 (.181) .373) .204-.117-.333-.308-..194-.189 (.300) .159-.092) .121 (.080 (<LOD-. 1954).089) .268) .107-.151) .087) .741 (.175 (.233 (.119 (.098) .320 (.109 (.159-.124-.123 (.135 (.308) .317) .078 (.079 (<LOD-.318-.126) .080 (.318-.075 (.228-.150-.081 (<LOD-.143) .109-.244-.333 (.208 (. liver.263-.241-.310 (.288 (. Dysrhythmias and T-wave changes on electrocardiogram have also been noted after both therapeutic (Berman.480) .085) .30) .069-.130) .320-.124-.127) .233) .096-.126 (. 1953).135) .238 (.352) .380 (.417) .124) .333 (.153-.124 (.173-.173 (.333-1.129) .099-.256 (.130) .163 (.253 (.217 (.115) .114 (.320-.147-.272) . skin.161) .188-.131-.206-.183) . Fourth National Report on Human Exposure to Environmental Chemicals 177 .130 (.208-.S.471 (.320) .400 (.068-.117-.131 (.187) .115 (.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 .171) .205-.357-.112-. species.188) .143 (.391) .153 (.248) .266 (.132 (.152) .098-.148) * . 1962).278) .203) .233-.108-.430) .061-.429 (.150-. Human health effects from antimony at low environmental doses or at biomonitored levels from low environmental exposures are unknown.152) .438) .076-.159-.271-.131) . 1958) and occupational exposures (Briegner et al. Inorganic antimony salts irritate the mucous membranes.105-.095-.209 (.076-.118 (.298 (. 1995).108-.113-.136) .727) .178 (.471) .095-.097-.086 (.195-.391) .192-.333-..102-.259 (.185 (. and eyes.238) . 1986).250) .280 (.125 (.343 (.179-.300 (.069-.267 (.185 (.075 (.121 (.148-.263 (.127) .130) . Acute antimony poisoning may cause a metallic taste.084) .357) .196 (. and gastrointestinal symptoms such as vomiting.146-.Metals than for trivalent compounds (Elinder and Friberg.281-.172-.181) .128-.294) Total .140) .135) .127 (.167 (.107-. 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.138-.100 (.242-.741) .133) . 1973).120 (.417) .

Centers for Disease Control and Prevention (CDC). and a drinking water standard has been established by the U. Buchet JP. References Berman JD. Luedersdorf R. Element reference values in tissues from inhabitants of the European community. Pulmonary edema of environmental origin. J Occup Environ Med 2004. Piatnek DA. Pilgrim L. Industrial Medicine 1944.e. 20012002. Costeloe K... Stasney J. 1997). J Trace Elem Med Biol 2002. Mahieu P. Third National Report on Human Exposure to Environmental Chemicals. Carelli G. Yang C-Y. 1986. Levels of urinary antimony in infants appeared to be similar to those reported by CDC (2005) for young children (Cullen et al.. Apostoli P. Gebel TW. or exposure differences.59:469-474. Iavicoli I.106:33-39. 2002. Biomonitoring Information Levels of urinary antimony reflect recent exposure.48:93-97. Experimental and human studies on antimony metabolism: their relevance for the biological monitoring of workers exposed to inorganic antimony. arsenic. Kiberd B. plasma and urine and a critical evaluation of reference values for the United Kingdom population. EPA. Sabbioni E. Lauwerys R. Paschal et al.S. Sci Total Environ 1994. Dezateux C. et al.. Chemotherapy for leishmaniasis: Biochemical mechanisms.10(3):560-586. Schacke G. clinical efficacy. 1998) or compiled reference ranges (Hamilton et al. HH. Mayer P.. 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.. Gallorini M. New York: Elsevier. Delves HT. Stead FM. 1998). Antimony. Petrucci F. Lenert G. gallium. Wu M-T.. Pietra R. Bailly R.64(2):182-185.67:119-123. and antimony in optoelectronic industry workers. and hydrogen sulfide. Earlier measurements in general populations (Minoia et al. Ludersdorf et al.46:931-936. Caroli S. VI.16: 33-39. 1990. Sabbioni E.cdc. and 2003-2004. gov/toxpro2. 1995. Arch Dis Child 1997. Int Arch Occup Environ Health 1987. Liao Y-H et al.76:432436. J Clin Pathol 1998. environmental levels) and health effects is available from ATSDR at: http://www. Biological assessment of exposure to antimony and lead in the glass-producing industry. Cullen A. Wade A. Environ Health Perspect 1998. Human biomonitoring of arsenic and antimony in case of an elevated geogenic exposure.)1954. Vouk VB. In: Friberg L. Schaller KH. et al. Dunkelberg. Int Arch Occup Environ Health 1995. Antimony trioxide is rated by IARC as a possible human carcinogen. Dernehl CU. 1994) have reported values slightly higher than those in this Report.. Stone FD. Kentner et al. Delves HT. Industrial Medicine and Surgery (Dec. Minoia C. Br J Ind Med 1991. population. 1987). Mechanism and treatment of cardiac arrhythmias in tartar emetic intoxication. Arsine. Nau CA.76(2):103-115. Trace element reference values in tissues from inhabitants of the European community I. Briegner H. Urinary antimony in infancy. Shao-Chi C. Cheng-Wei L.. stibine. 1991. Iavicoli et al.. Industrial antimony poisoning. Antimony in blood and urine of infants. Yu H-S. respectively. indium. and future strategies. Roland H. 2nd ed. Dezateux et al. Chin Med J 1958. Leinemann M. Biological monitoring of exposures to aluminum. 2004. Elinder CG. Kuo-Juie Y. Cordasco EM.atsdr. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Review of elements in blood.521-523. Alimonti A.html. 26-42.. Bolten C.158:165-190. Rev Infect Dis 1988. Semisch CW. Nordberg GF. pp. A study of 46 elements 178 Fourth National Report on Human Exposure to Environmental Chemicals . Kentner M. Atlanta (GA). Hamilton EI. Konings J. Friberg L. Chia-Yu H. et al. Weltle D. Biomonitoring of a worker population exposed to low antimony trioxide levels. Chest 1973. Skulsukai G. Pozzoli L. Liao Y-H..51:238-240. 1998. Fuchs A. Matthews T. Van der Venne MT. Information about external exposure (i. eds. Stocks J. Suchenwirth R.Metals to antimony have been established by OSHA and ACGIH. Chen J-R. Several investigations of airborne antimony exposures in workers have found urinary levels that are many times higher than those seen in NHANES 1999-2000. Urinary antimony was not associated with locally elevated soil levels in a study of more than 200 German residents (Gebel et al. which may be due to methodologic. Mayne P. 2005. Handbook on the toxicology of metals. Ho C-K. Finding a measurable amount of antimony in urine does not mean that the level of antimony causes an adverse health effect.13:361-362. even when exposure levels were below workplace air standards (Bailly et al. Ju-Sun P. Ming-Hsin H. O’Regan M. External and internal antimony exposure in starter battery production.

Sampson EJ.Metals in urine. Morrow JC. Fourth National Report on Human Exposure to Environmental Chemicals 179 . Industrial Hygiene and Occupational Medicine 1953. blood. Sci Total Environ 1990. Environ Res 1998. Quarterly Bulletin of the Association of Food and Drug Officials 1962. and serum of Italian subjects. Trace metals in urine of United States residents: reference range concentrations. Chemical food poisoning. Paschal DC. Renes LE.95:89-105. Antimony poisoning in industry. et al. Werrin M. 27:38-45.76(1):53-59. Pirkle JL. Jackson RJ.99-108. Ting BG.

55 (7.8) 34. Arsenic trioxide (As2O3.12-10.8) 17.9 (8.3) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites Sample size 2557 03-04 03-04 03-04 7.9) 68. psoriasis. though in some locations arsenite may be prevalent (WHO.80 (5.7 (11. were used as treatments for syphilis. lead.5 (34.6-43. and foods. +3 and +5).8) 7.70) 8. The United States no longer produces arsenic from mining but imports about 22.5) 95th 65. a trivalent compound known as white arsenic) is a common natural and commercial form that can be released into the air during volcanic action.9-62. Groundwater Urinary Total Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.5 (36.08 (5.70 (6.90 (5.5 (40.4 (26.S.4) 40.7) 65.7) 24. and produce. Arsenic and its compounds have had many uses in the past and present as medicines. 2001).2 (51. alloys.2 (41. solders. In the last century. see Data Analysis section) for Survey year 03-04 is 0. trimethylarsine oxide.2 (13. 2005). cancers. and arsenosugars.5-19.80) 6.9 (17.29 (8.8) 7.00-9.25-9.000 metric tons annually. 7440-38-2 General Information Arsenic is an element that is widely distributed in the earth’s surface in small amounts.30 (7.12 (6. General population exposure to inorganic arsenic can occur through consumption of drinking water and.5) 66.1 (32.90) 16.4 (48.19-9.4) 13.50 (8. and indium arsenides are used in the semiconductor industry.8-77.10-10.6 (13. Various arsenic compounds were used in paint pigments and for tanning animal hides. Arsenic trioxide is approved to treat acute promyelocytic leukemia. Arsenic is measurable in most soils. Since the 1940s. Gallium.2-61.41 (7. cacodylic acid.6-35.6 (15. Arsenic can also combine with organic substances in nature to form such organic arsenic compounds as arsenobetaine. as alloy in metal bearings. and monosodium methyl arsenate were used as pesticides but contemporary uses are restricted. arsenic compounds.1-40. and as a cosmetic to lighten complexion. Water sources contain mostly inorganic arsenate.2 (12.8 (48. aluminum. or rarely as elemental metalloids (yellow. interval) 8. to a lesser extent. and arsenates (oxidation states of -3. and other metals.6 (9. Roxarsone and other organic arsenicals are anticoccidial agents added to poultry feed. Survey years 03-04 Geometric mean (95% conf. and gray forms).90-14. particularly arsenic trioxide.2) 46.0-60. Arsenic can combine with such non-carbon chemicals as sulfur and oxygen to form arsenides. and.90) 75th 16. gaseous hydride manufactured in small quantities for use in the semiconductor industry.66-8.8) 30. grain.3-15.8) 33.1) 1281 1276 03-04 03-04 03-04 9.6) 618 722 1074 Limit of detection (LOD.57) Selected percentiles ( 95% confidence interval) 50th 7.6-141) 53.97) 8. 180 Fourth National Report on Human Exposure to Environmental Chemicals . it is found in over 200 crystalline or mineral forms.10 (6. to a lesser extent.5) 41.0 (11.5 (23.90-8.1) 290 725 1542 03-04 03-04 9. and in lead-acid storage battery grids.5-178) 46. mental disorders.84) 8.90-8.3-111) 78.10-7. from coal burning. and play sets.84) 8.9-46.0 (15.4 (31.20 (8.90 (7.1) 7. such as arsenopyrite (FeAsS) and realgar (As4S4). ocean and fresh waters.2-20. and as homicidal poisons. arsenites. sodium arsenite. mostly for use in wood preservation (ATSDR.90-7.1) 15.4 (7.70-9.74.7-83.6) 11.5-41. Various forms of inorganic arsenic can occur in groundwater from natural sources or as a result of soil application or industrial waste. pesticides.13-8.5-52.90-11.0 (14. population from the National Health and Nutrition Examination Survey.0-19. chromated copper arsenate (CCA) has been used to treat outdoor timbers and pressure-treated woods to prevent wood rot. Although it is still widely used in the United States.34-9.5 (14.90 (7.80-9.1 (38.02-8. semiconductors.00 (6. In nature.30 (6.50-14. lead hydrogen arsenate.0 (43. copper arsenates.1-18. arsenocholine.34-10.4 (24. retaining walls.0 (22.2-17.Metals Arsenic CAS No. referred to as inorganic arsenic compounds.8) 29.4) 60.77) 6.27) 9.6 (32.40) 7.4-65. black. Arsine (AsH3) is a reactive.7) 90th 37.5) 43.3-19. meats. Before the 20th century.30) 17.9-34.8-61. Also. arsenic as elemental metalloids may be used in some ammunition.7-95.2) 15. the smelting of copper.3) 10. CCA-treated wood has been restricted since 2003 and no longer can be used in residential applications such as decks.10) 10.2-93.9) 21.

Extremely high groundwater arsenic levels.0-69.7) 28.88) 7.3-41.8 (11.3 (24.3 (27.4 (12. Arsenate is reduced in the body to arsenite (oxidation state +3).75) 13.25-9.5-120) 40. selenium. These organic forms of arsenic from seafood are absorbed and quickly excreted in the urine (WHO.31 (6.47-6.2-46.3) 6.45) 5.5 (9..2) 15.9-56.. trimethylarsine oxide (TMAO).76 (6.2 (12. The semiconductor dopants.59) Selected percentiles ( 95% confidence interval) 50th 7.4) 32.06 (4.6) 45.g.28-7.4 (42. shellfish. 2001).47 (7. 2007.S. 2001).7-35.1) 6. Tseng.0) 42.44-11.1-36. though some reduction may occur in the gut prior to absorption. age.1) 8.Metals sources of drinking water often have measurable arsenic and several regions of the United States have naturally higher arsenic levels than the U.7) 95th 50. are used in enclosed ultraclean operations within the semiconductor industry. Inorganic forms of arsenic demonstrate high acute toxicity.7-18.4-64.24 (7.41) 6. 2006. and some other seafood can contain organic forms of arsenic including arsenobetaine. 1988).0) 33.8) 27.4 (26.13) 8..04 (5. 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.8-32.1) 58.S.0-18.38-10. gallium arsenide and indium arsenide. arsenocholine.1) 7.2) 90th 30.18 (5.9) 13. and contact with CCA-preserved wood structures. 2001).07-9..1 (11. but is poorly absorbed dermally (WHO.93-9. Inorganic arsenic and its metabolites have elimination half-lives of approximately 2–4 days (Lauwerys and Hoet.01) 7.0) 1281 1276 03-04 03-04 03-04 8.30-9.4 (11.9 (45. WHO. Though modest bioconcentration occurs in some aquatic life.7 (11.9) 53. Gamble et al.7-188) 27. cacodylic acid and monosodium methyl arsenate.6 (17.66 (7. 2003.7 (25. Chowdhury et al..4 (24. Smoking tobacco is also a source of inorganic arsenic.8 (20.64 (7.1) 24.5) 17.33-10.3-64.11 (5. so exposure to the general population is extremely limited.04) 7. In aquatic organisms.0) 26.75 (5.99-9.4) 54.23-7.44) 6.6-17.0) 12.0) 14.S.0-38. After absorption. arsenocholine is converted to arsenobetaine and also to small amounts of TMAO (Christakopoulos et al.4 (40. arsenic does not show biomagnification in the food chain (WHO. Inorganic arsenic is well absorbed from the gastrointestinal tract and absorbed to a lesser degree through inhalation.20-9..7-34. interval) 8. 2001). and arsenosugars.35) 7.81-9.7-17.9) 618 722 1074 Fourth National Report on Human Exposure to Environmental Chemicals 181 . Smelter workers can have significant inhalational exposures to airborne arsenic trioxide for which air standards have been established.32 (5. WHO. 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.3) 9.8) 22.10-16. TMAO is also formed in the environment from microbiological action and is a metabolite of arsenic in certain mammals. 2001). mine tailings).3-62.0 (17. 2007. 2001.61 (7.50 (6. EPA’s maximum contaminant level (Hughes. EPA. population from the National Health and Nutrition Examination Survey.10-8.0 (31.1 (14.6 (35.5) 290 725 1542 03-04 03-04 8. dust. with trivalent inorganic arsenic (arsenite) being more toxic than pentavalent inorganic arsenic (arsenate) (NRC.33 (6. Direct exposure to DMA and MMA may result from use of the two pesticides.66-8. Ingestion of arsenosugars in kelp and algae can also lead to the excretion of DMA. 2007.3-53.96) 12. kelp.2-15.88 (5. have caused clinical arsenic poisoning. Arsenite is then oxidatively methylated to the monomethylarsonic acid (MMA) and dimethylarsinic acid (DMA) with subsequent excretion primarily in the urine (NRC.7 (9. inorganic arsenic is widely distributed within the body.12-10.25 (6.86-17. 2001).66-8.6 (10.8-75.93-8. Fish. Survey years 03-04 Geometric mean (95% conf.0-26. U.5-17. In aquatic sediments.00 (6. 2006.8 (27.5) 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. 2001). NRC.58-10.47 (6. organic arsenic can be converted back to methylated and inorganic arsenic. 2001). dose level. as observed in Bangladesh where millions of people have been exposed.8 (12. Steinmaus et al.01) 11.8-62.2) 40.51) 75th 14. 2001.40) 8.8 (21. Children may have additional exposures from ingestion of contaminated soils (e. and folate status (Chen et al.

apoptosis. and peripheral neuropathy may also occur with large doses or after surviving an acute overdose. increased oxidative stress. 2001. Laboratory studies using inorganic arsenic have shown chromosomal aberrations. Bredfeldt et al. and it also will inhibit succinate dehydrogenase. 2001). and altered gene expression. Acutely. arsenic trioxide) includes hemorrhagic gastritis with nausea.. WHO. Chronic elevated arsenic intakes have been associated with diabetes. 2001).20 (<LOD-1.. which may vary for some chemicals by year and by individual sample. Such actions may lead to decreased energy production. and by uncoupling oxidative phosphorylation (NRC.. The risk of lung cancer appears more pronounced when large environmental exposures start in childhood (Smith et al. drinking water have not been associated with increased cancer rates (Schoen et al. and endothelial injury (Kumagai and Sumi. and childhood neurodevelopmental effects in observational human studies. Raml et al.. Studies of arsenic at levels typical of U. 2006.. 2004. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. and production of glutathione may be affected as well. OSHA and ACGIH have established workplace standards and guidelines for arsenic exposure and monitoring. Acute toxicity resulting from the ingestion of large amounts of trivalent arsenic (e. < LOD means less than the limit of detection. and DNA repair inhibition (Cohen et al. some of these effects may take years to develop. 2007).. Cohen et al. NRC. interference in signal transduction pathways.. 2004). hyperkeratosis. respectively. gluconeogenesis. With chronic exposure. 2007. and bladder cancer (IARC. noncirrhotic portal hypertension.10 (<LOD-1. 2006.. peripheral vascular disease. Chronic human intake of arsenic at less than acutely toxic doses. leading to a decrease in adenosine triphosphate energy production. Cardiac arrhythmias. WHO..20 (<LOD-1.. 2001). lung.S.30) 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1.S. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th < LOD 90th < LOD Sample size 1. including inhibition of numerous enzymes. Taiwan. 182 Fourth National Report on Human Exposure to Environmental Chemicals . hematocytopenias. cell transformations. 2006) and newly discovered thioarsenic metabolites may also be as toxic (Naranmandura et al. see Data Analysis section) for Survey year 03-04 is 1.g.S.0. 2001). 2001. NRC. it may have its own separate toxic action by substituting for phosphate in glycolysis and other pathways. U. food residue. renal failure. Arsenic has many actions demonstrated in cellular studies. hepatotoxicity. 2001). The organic forms of arsenic occurring in seafood have little known toxicity. Survey years 03-04 Geometric mean (95% conf. WHO.Metals +3) shows greater toxicity than arsenite itself (Aposhian et al.20 (<LOD-1. 1998.10 (<LOD-1. and diarrhea. Acute unintentional inhalation of arsine gas can produce hemolysis of red blood cells. but additional or confirmatory research is needed (Kapaj et al..80) 1. The U.60) 1. Bangladesh.EPA. Chile). including drinking water sources with elevated arsenic levels (e. and hyperpigmentation of the skin (NRC.50) 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD 1.10 (<LOD-1. vomiting. hypertension.S. population from the National Health and Nutrition Examination Survey.g.50) 1. can cause peripheral sensorimotor neuropathies.. 2000.50) 2568 95th 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1.50) 621 725 1078 Limit of detection (LOD. WHO. Although arsenate is reduced in the body to arsenite.30) 1.EPA has established drinking water. fatty acid oxidation.60) 1.10 (<LOD-1. which can lead to dehydration and shock. 2001).20 (<LOD-1. 2007. 2004). cytotoxicity. 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. arsenite will inhibit cellular pyruvate dehydrogenase by binding to the sulfhydryl groups of dihydrolipoamide. substitution in phosphate metabolism. Cellular glucose uptake.10 (<LOD-1. Chronic arsenic exposure in humans is considered to be a cause of skin. 2006) or when exposure occurs in smokers (Chen et al. 2006.

and were about two-fold lower than those for the U.. though air levels of arsenic fume and dust are correlated with urinary arsenic levels at higher occupational inhalational exposures (Jakubowski et al.00) 1.S. 2006).18 (<LOD-3.. 2006.. Vahter et al. Additional information about external exposure (i. Levels of total urinary arsenic in the U. IARC and NTP recognize inorganic arsenic and arsenic compounds as human carcinogens. higher mean or median total urinary arsenic levels have been reported among people living in specific western areas of North America (Calderon et al. 2005) and Urinary Arsenic (V) Acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. 2008).S. Meza et al. DMA produced bladder cancer in some chronic rat studies (Cohen et al.89) 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2.. environmental levels) and health effects is available from ATSDR at: http://www. median urinary total arsenic levels in 4052 adults varied with seafood intake.. WHO... 1999.. In the German Environmental Survey III of 1998.. 2001). 2007. Caldwell et al. 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. Caldwell et al. 2004. Shalat et al. 1986). Though CCA-treated wood contains several thousand times more arsenic than untreated wood. 2003. the median total urinary arsenic in about 200 people was approximately four times higher than that of the U. population (Rubin et al. In animal studies.html. population in NHANES 2003–2004 (Schulz et al. 2001).. 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. Consequently. 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.33 (<LOD-3.75 (<LOD-2. 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.61 (<LOD-3. Compared with this Report. Offergelt et al.Metals compounds. 2006.. arsenic has been fetotoxic and teratogenic. 2000. 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. 1999). although urinary arsenic levels were not associated with CCA contact (Shalat et al.. Pellizzari and Clayton. 2004.33 (<LOD-3. 1999. 2008.atsdr.cdc.e. In a Nevada town where groundwater levels were naturally elevated..80 (<LOD-4. Shalat et al.70) 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD 2. but generally only at maternally toxic doses (WHO. urinary arsenic levels have been accepted as a good biomarker of dose (WHO. Daily variation in creatinine-corrected urinary arsenic is relatively small when intake is constant (Calderon et al. 2001)..18) 3. 2006).S.41) 3. Josyula et al.95) 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. Valenzuela et al.75 (<LOD-2. and the FDA has established a bottled drinking water standard.S. population from the National Health and Nutrition Examination Survey....50) 1.. 2006). Fourth National Report on Human Exposure to Environmental Chemicals 183 .. 2006). gov/toxpro2. Survey years 03-04 Geometric mean (95% conf. had decreased since the prior 1990– 1992 survey. 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.. 2006. 2008). 2007. Pellizzari and Clayton. 2000).19) 3.69 (<LOD-3.50) 2568 95th 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2.. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.. 1992. Pellizzari and Clayton 2006). 1998.04 (<LOD-3.

Metals other areas of the world (Ahsan et al. In the late 1980s.9 (6. Valenzuela et al.80) 1.93) 1.2 (6.S. and duration of exposure are also considered important. which may vary for some chemicals by year and by individual sample. Caceres et al.40-7.4-35. When seafood intake is avoided.5 (14.19 (.40) 5.5) 29. and peripheral neuropathy) have been associated with urinary levels as low as 50–100 μg/L in chronically exposed populations (ACGIH.. 1996..6 (25. in NHEXAS 1995–1996.900-1. 2000.800 (. Caldwell et al.8-40. Chowdhury et al. interval) 1.1-25. Great Lakes region residents had median urinary DMA levels that were slightly less than median levels in NHANES 2003-2004 (Caldwell et al. arsenocholine.. The higher percentiles of total urinary arsenic levels in the U.00-12.. These associations are stronger at higher urinary levels.S. population showed a higher contribution of arsenobetaine (Caldwell et al. population from the National Health and Nutrition Examination Survey.8. population (Ahsan et al. DMA has been the predominant metabolite composing the majority of measurable inorganic-related arsenic in the urine (i.800 (. 2005.83) Selected percentiles ( 95% confidence interval) 50th 1.90-7.20) 3. 2000.7) 13.S.6.10) 4.0 (26. 2008.30) 2.3) 1284 1284 03-04 03-04 03-04 1. 1990.30 (1. a control population of 696 Tacoma residents had median urinary DMA levels similar to those for NHANES 2003–2004 (Kalman et al. Also. 2008). and two methylated metabolic products.871-1. Urinary Arsenobetaine Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.05) < LOD . and arsenobetaine being the main contributors to the total urinary arsenic levels (Caldwell et al.20 (2.0) 29. 2008). 2008).80 (4.7 (21. arsenite.10 (4.g.7-22. 4. arsenite.. 2008).50) 90th 16. dermal keratosis.50) . 2003). In the residents of a Chilean town who consumed water with high levels of arsenic. Caldwell et al.50-6. Total arsenic measured in the urine includes all species of inorganic and organic arsenic.. arsenobetaine.20-25.1) 45.3 (9.3) 95th 35.70 (3.. 2007).55 (1.30 (2.800-1.7) 15.1-94.80-5.2-35. Pellizzari and Clayton.4) 23. and urinary DMA represented about 67% of the total urinary arsenic (Hopenhayn-Rich et al. < LOD means less than the limit of detection. methylation capacity.11-1. population in the NHANES 2003–2004 subsample.62) 2.5 (26. For residents of Inner Mongolia.3-39.6) 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 * * 1.6 (11.6 (13.80 (. DMA and MMA.600 (.8) 35.30) 10.3 (21.8-50. geometric mean levels were about 70-fold higher than for the U.3) 35.43-1.0-23.17-1.60-3. 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.9) 13.800-4. Measurable organic arsenic species in this Report are three biologically generated environmental forms.9-23.70) 6.1-51.e.00) 3..74 (1.. 2007) with higher levels of arsenic in the drinking water.20 (1.. Aposhian et al..900 (. 2008.66 (1.S. MMA.7 (13.4) 31. arsenocholine.00 (.70-21. 1985. and TMAO were detected in only 7.20 (4.9 (7..5) 32. Caldwell et al.37 (1.20 (. WHO. Detectable levels of MMA reported in NHANES 2003–2004 were found only at the upper percentiles and.00-1..0) 4.28) 1. and TMAO.45 (1.. 2006). Arsenate. respectively. arsenobetaine and arsenocholine will greatly increase the level of total urinary arsenic and comprise the highest percentage of the total urinary arsenic level.40) 75th 5.20-190) 31.20-3. 2000.31-1.3% of a representative sample of the U.40-6. 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.5) 292 728 1548 03-04 03-04 1.. China.0 (27.8 (12. median levels of urinary DMA were about 40-fold higher than the adult median reported in NHANES 2003– 2004. 1.. 2005.60) 1.4.800) 1. 2005.70-21. when seafood organic arsenic is subtracted). with DMA.10) 8.2-38. population (Sun et al.700-1.500-1.00-4.50) . and other factors such as nutrition. 184 Fourth National Report on Human Exposure to Environmental Chemicals .20) 7.6-44.. Some noncancer effects of arsenic (e.68) .48-2.400-.. Tseng et al. vasospasm. After recent seafood ingestion.S. In most human studies.8 (17.700-1. 2001). and 0.70 (5. Individually measurable species resulting from inorganic arsenic exposure are arsenate.1) 18.. 2001.00 (1. Blom et al.5) 621 725 1078 Limit of detection (LOD. DMA and MMA compose most (about 75%) of the total arsenic species measured in urine. as evidenced by trace or nondetectable levels of arsenobetaine and arsenocholine in the urine.6. Levels of DMA and MMA increase in approximate proportion to the intake of inorganic arsenic.20) 18.90-29.00-6. see Data Analysis section) for Survey year 03-04 is 0. Sun et al.29 (1.80 (3..4 (16.

28) 1.877 (. 2006..5) 26.32-7.3-24.0) 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. 2001).4 (24.47 (1.. 1998..6 (9.4-21.638) 1. Finding a measurable amount of arsenic in urine does not mean that the level of arsenic causes an adverse health effect.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 * * 1.53 (.5 (18.58 (3. Biomonitoring studies of urinary arsenic can provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of arsenic than are found in the general population. 2007).51) 5.2 (12. which is below the ACGIH BEI (Caldwell et al.43) 14. Vahter et al.50-15. Information about the biological exposure indices is provided here for comparison.6-32.3) 95th 29.80-153) 17. not to imply a safety level for general population exposure.13-39.12) < LOD .4-28.6-46.43) 75th 5.29 (4.9 μg/L.8) 29.67) 1.91) 90th 16.39-3.959-1.4) 292 728 1548 03-04 03-04 1.14 (1.1-18.19-2.5-20.909-1.30-1.67) 4.531 (.76-27.65 (1.S.93 (1.4-82.6-29.40) 1. these levels were much lower than those found in other studies where environmental exposures were highly elevated (Chowdhury et al.11 (.3 (10.1 (26.82) Selected percentiles ( 95% confidence interval) 50th 1.40 (1.78-5.6 (6.64-29.786-1.45) 1.9-18. population from the National Health and Nutrition Examination Survey.47 (2. interval) 1.00 (1.79 (1.55) 1.05 (.Metals as with DMA.50-7.51-2.83) 2.72) 12..7) 9.80) .29-14. Sun et al.2 (12. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. In recent years.9) 32.1) 26.37-2.2 (4.400-.78 (3..18-1.05) 1. The American Conference of Governmental Industrial Hygienists (ACGIH) provides an occupational biologic effect index (BEI) for urinary inorganic arsenic plus metabolites equal to 35 μg/L (ACGIH. 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.3) 1284 1284 03-04 03-04 03-04 1.10 (. 1992.91 (4.5 (18. WHO. 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.81 (4.901-2.7) 17. Fourth National Report on Human Exposure to Environmental Chemicals 185 .15-1.938-1. Survey years 03-04 Geometric mean (95% conf. 2001).15-4.25-7. Caldwell et al.3 (10. 2003.73-6.30) 1.36) 2.2 (13.0-36.16 (. Offergelt et al.15-1.7) 30.612-1.88) 2.88 (5.0 (9.62-6..4) 32.44 (1.70) 5.82) 4. occupational monitoring and research studies have focused on the sum of inorganic-related species (arsenate + arsenite + DMA + MMA) as a measure of inorganic arsenic intake.1-36. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.00 (3.21) 5.5) 17.4) 13.833-1. 2008).6) 19.25 (. population for the sum of inorganic related species was 18. 1986.68 (1. Urinary Arsenobetaine (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. 2008)..61-6.54 (1.83) 8.9 (13.S.. The 95th percentile of the U.4 (11.9) 14.9 (25.

< LOD means less than the limit of detection. 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. 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. Survey years 03-04 Geometric mean (95% conf. 186 Fourth National Report on Human Exposure to Environmental Chemicals . * Not calculated: proportion of results below limit of detection was too high to provide a valid result. see Data Analysis section) for Survey year 03-04 is 0. population from the National Health and Nutrition Examination Survey.S.6.Metals Urinary Arsenocholine Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. which may vary for some chemicals by year and by individual sample.S. * 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 Limit of detection (LOD.

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.Metals Urinary Arsenous (III) Acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. see Data Analysis section) for Survey year 03-04 is 1. Survey years 03-04 Geometric mean (95% conf.76) < LOD 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. which may vary for some chemicals by year and by individual sample.29) < LOD 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.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 2.2.44) 2.S.95 (<LOD-2.40 (<LOD-1.08 (<LOD-4. Fourth National Report on Human Exposure to Environmental Chemicals 187 .00) 1.20 (<LOD-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.00 (<LOD-3. Urinary Arsenous (III) Acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th < LOD 90th < LOD 95th < LOD Sample size 2568 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1.S. Survey years 03-04 Geometric mean (95% conf.00 (<LOD-2.80) < LOD 621 725 1078 Limit of detection (LOD. < LOD means less than the limit of detection. population from the National Health and Nutrition Examination Survey. population from the National Health and Nutrition Examination Survey.

00-11. Survey years 03-04 Geometric mean (95% conf.70-3.30 (7.45) 8.85 (3.7-16.60-7.00) 4.00-4.20) 11.8) 7. 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) 6.00) 7.00-5.95 (4.0 (14.14) Selected percentiles ( 95% confidence interval) 50th 3.37 (2.74) 90th 9.82-5.17 (2.60-3.00-15.19) Selected percentiles ( 95% confidence interval) 50th 3.0 (12.0) 9.38 (3.69 (3.20-4.27 (3.12 (3.00-11.20-12.69-3.91) 75th 5.0 (10.00-3.71 (3.00-7.00-7.0-16.16 (2.16 (4.6-18.00-8.00) 9.69 (3.33-4.5 (11.00) 6.65-6.06) 5.94) 3.0 (13.70-4.00) 3.00 (5.03-6.34-4.00) 75th 6.00-22.70) 5.0) 621 725 1078 Limit of detection (LOD.00 (5.50-15.29-4.67) 9.27 (2.4) 621 725 1078 188 Fourth National Report on Human Exposure to Environmental Chemicals .3 (8.77 (3.92) 3.0-19.39-3.44 (2.0) 9.09 (7.00 (3.0 (10.86-21.00-4.73) 6. Survey years 03-04 Geometric mean (95% conf.00-4.00 (6. interval) 3.95-3.00 (5.1-15.34 (3.9) 12.0-25.86-7.84-18.S. interval) 3.11 (3.18 (6.00-7.74 (2.25 (4.10) 6.0 (11.0-12.Metals Urinary Dimethylarsinic Acid Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.97-3.27-5.61-11.00 (6.69-6.00 (3.13-4.00-3.0 (8.50 (4.90) 2.3 (7.49-4.00-4.00 (3.0) 14.0) 13.0 (10.92-12.34) 3.27-2.30) 3.0) 11.61-16.00) 4.52) 3.60-6.00 (3.78 (4.7.98) 4.80) 2.57 (3.88 (4.72 (4.1-18.10) 3.94-3.0-17.9 (11.17-4.0) 17.7) 13.00 (7.82) 3.49) 10.90 (3.55 (2.00) 6.08 (2.28) 2.95-4.00-7.90) 5.71 (4.34 (3.00 (5.31-4.57-5.0) 292 728 1548 03-04 03-04 4.0) 16.46 (4.0 (13.1-22.71) 3.00-15.48 (3.5) 95th 13.80 (4.03 (3.00-4.9 (7.7) 12.00-12.05) 5.0 (9.0) 12.82-9.00 (5.16-11.24-4.4 (7.44) 5.89 (3.00-9.45 (8.71-4.00-11.00) 12. see Data Analysis section) for Survey year 03-04 is 1.00-10.0-16.00-15.79 (3.5) 12.33) 3.9) 5.45) 3.8) 7.11) 4.0-18.00-12.2) 10.86 (2.3 (8.00 (4.67) 8.00-13.50-5.14) 3.0) 11.22) 4.6) 1284 1284 03-04 03-04 03-04 4.65-8.00 (6.00-4.00) 3.00) 6.0) 95th 16.80-6.24) 3.62) 4.00) 90th 11.32 (4.0) 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 4.0 (8.70-12.6 (9.00 (7.00 (3.73 (3.9) 13.31) 4.84-8.7 (10.0) 13.0) 16.05) 3.32-10.12-4.0-17.8) 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 3.00 (3.05) 10.32 (8.0 (12.0) 17.59 (6.15) 4.60-4.34-4. population from the National Health and Nutrition Examination Survey.7) 1284 1284 03-04 03-04 03-04 4.70 (3.48 (2.80-3.81 (5.0 (10.95-6.S.9) 11.37 (3.42) 3.17-6.1 (8.0) 10.80-5.80) 7.00) 5.0 (9.6) 292 728 1548 03-04 03-04 3.78) 4.0) 9.0 (9. population from the National Health and Nutrition Examination Survey.

50 (1. population from the National Health and Nutrition Examination Survey.10 (1.20 (1.62) 2.82-2.10-1.53) Sample size 2567 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.34) 2.53 (1.30-1. Survey years 03-04 Geometric mean (95% conf.18-1.90) 2.84-3.10 (1.07-3. see Data Analysis section) for Survey year 03-04 is 0.28 (1.77) 1.16 (2.20 (1.10 (<LOD-1.10 (.52 (2.71-2.00) 1.43-3.11-1.40) 1.40-2.86 (2.90) 1.10) 2.05-1.61) 2.10 (. < LOD means less than the limit of detection.70-2.30-2.88 (1.30 (1.50) 621 725 1077 Limit of detection (LOD.50) 1.80) 1.30 (1.28 (1.10-1.816 (<LOD-.79) 2.86) 2.60) 1.20-1.22 (1.07 (1.70-2.20 (1.90 (2.40) 2.96-2.40 (2. Urinary Monomethylarsonic Acid (creatinine corrected) Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.30 (2.60) 292 728 1547 03-04 03-04 * * < LOD < LOD 1.53) 1283 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.30) 1.30-1.40-3.93) .70-2.14-1.45) 3.80) Sample size 2567 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.50 (<LOD-1.75) 621 725 1077 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.80 (2.46-2.60 (2.40-3.00 (<LOD-1.40-2.80 (1.81) 1.900-1.00-1.20 (1.00-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.80) 1.23) 1.60) 2.60) 2.40) 1.80 (1.37 (1.10) 95th 2.60-2.15-1.50-2.00 (1.853-1.58) 2.73-2.30) 1. Fourth National Report on Human Exposure to Environmental Chemicals 189 .60) 1283 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.33 (1.17) 2.82-2.80 (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 1.88 (1.90) 2.53-2.00) 1.00 (2.60 (1.00) 2.33 (1.80-2.61-3.18-1.S.85) 2.46 (1.70-3. population from the National Health and Nutrition Examination Survey.35-3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.50 (2.20 (1.57) 95th 2.36) 1.20-3.00-2.S.9.63 (<LOD-1.80-2. which may vary for some chemicals by year and by individual sample.88-2.00-4.00-2.90 (1.07) 2.20 (1.10-3.86 (2.80 (1.Metals Urinary Monomethylarsonic Acid Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.31-3.54) 90th 2.50 (1.985) 1.70-2.00 (<LOD-1.30) 2.22) 3.00) 1.36 (1.86) 3. Survey years 03-04 Geometric mean (95% conf.85) 1.00 (2.20) 2.30) 90th 1.31 (1.53) 292 728 1547 03-04 03-04 * * < LOD < LOD 1.70) 2.30 (1.40 (1.00) 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.

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

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70 (1.34 (1.26) 2.70) 7.15 (6.30) 4.28) 90th 5.97 (1.49) 8.35-1.05% of the earth’s crust.51 (1.81-3.60-2.88) 4.43) 2.57-7.75-3.65 (5.44-2.06-1.40 (1.53-5.80 (2. Certain foods. 2001).51) 1.50) 2. and food. see Data Analysis section) for Survey years 99-00.70-5.44-5.50 (1. soluble forms of barium.62) 1.25-11.65-5.72) 75th 3. bricks.87-14.30-2. and 0.45) 7.30 (5.56 (2.66 (4.28-1.91) 2.60-6. barium sulfate is used as a contrast medium for taking radiographs of the gastrointestinal tract.65) 3.60-6.70 (5.43) 6.50 (1.10) 5.01-7.70-2.61 (3.61 (2.92) 2.27 (1. The general population can be exposed to low amounts of barium in air.78-2.70) 1.30) 2.90 (4.90-9.53) 2.20-1.88) 7.90-2.9) 5.00 (2. In single dose animal studies.52 (4.49-1.11-1.56 (1.73 (5.41) 1. respectively.30 (5. 7440-39-3 Medically.60-10.48) 1.88) 1.21-2.00) 4.43 (1.40-13. Small amounts of barium can be released into the air during mining and other industrial processes.48) 1.56 (6.15 (1.65-1.90 (6.71 (2.50-6.69 (1.82-6.00 (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 1.40 (1.93-8.4) 6.36-1. 0.27 (1.02 (7.39 (1.60 (1.76-2.11 (3.77) 1.50 (2.S.05-2.71) 2.20-5.87) 7.54) 2.40 (5.80-2.64-3.4) 9.90-13.49-9.46) 1.51) 7.50) 2.39-1. Barium salts have also been available as rodenticides.12 (2.80 (5.8) 9. 01-02.87-7.80) 1.82) 2.14 (6.37) 1.73 (6.37-8. Workers employed by industries that make or use barium compounds can be exposed to barium dust.20-1.95 (4.10-5.15-11.15 (2.21 (1.72) 4.2) 6.98) 1.12) 6.40 (5.30-1.12.59-11.60) 1.74-3.37) 5.99-5.73) 1.51) 2.41-1.78) 1.50-6.90) 2.74-2.57 (5.g.80-5.18-1.50) 1.40) 7.50 (3.00) 6.16) 5.54-8.22) 6.60) 4.61 (1.90) 2.12.21-8.8 (6.04-2.61 (1.50 (4.12 (2.54-1.21 (1.20-8.63 (8. were relatively well absorbed following inhalation (60-80% of a dose) or ingestion (11-32 % of a dose). and 03-04 are 0. In nature.70-6.31-2.Metals Barium CAS No. it combines with other chemicals such as sulfur or carbon and oxygen.90 (1.32-1.85) 1.90) 4.53) 1.54 (6.12-1.80-3.55-3.70-8. Barium compounds are used by the oil and gas industries to make drilling muds.64 (1.50) 4.27) 2.00-76.73-5. Ingested soluble barium General Information Elemental barium is a silver-white metal which comprises approximately 0.91) 6.30 (3.62 (1.78-3.80 (1.36 (4.26-1.62) 1.68 (1.20-6.74) 3.19-1.64) 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 2.40) 3.44 (1.29) 5.30) 5.09 (1.63) 1.60) 3.86-4.47) 4.24-1. whereas others are practically insoluble (e. interval) 1.63) Total 1.40 (4.06-2.32-7.56) 4.61 (5. rubber.30-3.35-1.12) 7.15) 5.08-8. Fourth National Report on Human Exposure to Environmental Chemicals 193 .36) 5.40) 7.50-1.38 (1.50 (6. Barium compounds are also used commercially in paint.4) 7.71) 1.48 (6.65) 1.60-3.96-2.14-1.59) 3.30-1. Urinary Barium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.49 (1.39) 1.70-2.03 (1.87-3.56 (1.95-6.10-4.38) 2.87 (6.50 (5. depilatories.8) 5.65-8.49) 11.15-1.49) 4.86 (4.32) 8.56) 1.00-8.26) 5.93-2.70) 1. are high in barium (Genter.91 (2.33 (1.34 (1.93 (4.76 (3.47-1.50 (4.80-7.38 (1.63 (5.10 (3. and ceramics.31.30) 3.53) 692 683 618 540 667 723 765 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.1) 9.18) 3. fireworks.00) 1.11 (3.85) 1.50 (4.49) 2.75) 2. Some barium salts are freely soluble in water.16 (1.00) 1.99 (4.34) 2.10 (2.30) 8.20-8.30 (1.19) 2.86) 6.20 (3. tiles.26-7.63) 1.50 (1.46-1.35 (1.39 (1.14-6. such as brazil nuts.30 (2.18 (6.81-2.20-1.70) 5.43 (5.29-5.40 (5.47-1.54-1.61-8.11 (2.22-1.30) 5.48-4.76-7.39) 4.50 (1.07 (2.54) 1.43 (1.37 (4.63 (2.29-1.41-3.24 (4.08 (6.87 (5.35 (2.36 (1.20) 2.77-3.20-8.25 (1.72) 1.70) 3.20 (4.94-6.37-1.45 (1.00-3.10) 3.17-1.80 (1.80) 7.76-3. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.25-1.80) 6.86 (4.20 (1.73) 3.30-5.70) 4.20-1.36-1.40 (1.81-2.46) 1.77 (3.35 (3.15-1. barium sulfate and barium carbonate).88 (5.66) Selected percentiles ( 95% confidence interval) 50th 1.30) 5..04-6.35-4.22-1.71) 95th 6.85 (2.86-5. glass.57) 3.50 (1.54) 1. such as barium chloride.78) 1.55-7.76) 1.43) 297 368 290 621 762 725 1262 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 1. water.63 (1.70-3.48-4.30-2.01 (4.31 (2.60 (2.35) 5.09 (2.38) 8.82) 1. population from the National Health and Nutrition Examination Survey.71-9.87-9.65) 1.50-1.90) 1.10 (4.84) 5.42 (1.62 (1.80 (2.24-1.52 (1.60) 1.67) 6.80 (1.54 (2.34 (2.

62) 2.44-2.03-1.36-1.67-6.2) 6.87) 1.97 (5.56 (1.59) 2. a benign condition that may occur among barite ore miners.52) 2.60 (1. The health effects of exposure to barium compounds depend on the dose.19-1.34) 1.73) 2.96 (4.58) 1.64 (1.53 (2.0) 7.91) 2.05-1.39-10.37) 2.36 (1.52-4.31 (4.10) 3.3) 6.26-1. 1994.75) 2.49 (1.19-1.77) Total 1.19-2.34-5.754-1.90-2. Chronic exposures to natural low levels of barium in drinking water have not produced general health effects or evidence of cardiovascular risk (Brenniman and Levy.02) 4.81-6.82) 1.51) 4.81-7.40-1.30) 2.65 (2.44-2.71 (5.66 (1.89 (2.48 (1.04) 5. hypertension.76) 1. about 75 % of a dose of soluble barium was eliminated within 3 days (Reeves.00-1. and route of exposure.47) 1.26-1.915 (.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 1.04 (2.46) 1.20 (1.36 (3.53) .08-2.48 (1.75-3.52-10.881 (.20-1.96) 4.22-4.47) 4.91 (3.06) 2.14-2.41 (1. 1986).34-3.00 (5.3 (6.68 (2.40 (1.76-3.33) 1. vomiting.55 (4.25) 4.60 (1.29-4.49-1.77) 1.38) 4.28-7.76 (2.32) 2.47-8.28) 5.75) 1.24-11.68) 1.62 (2.32) 2.11-2.60 (2. Urinary Barium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.45 (1.32 (2.73-4.57-5.27) 7. in urine.832-1.46-22.55-5.38 (1.75-22.39) 4.45 (3. are not absorbed when administered. Following intravenous injection in animals.47) 1.96) 7.60 (5.29-3.64 (1.64) 7.64) 7.24-6. paralysis. diarrhea.55 (1. Human health effects from barium at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 1984.00 (2.76) 2.29-4.10 (6.63) 1.00 (3. weakness.33 (5.75) 2.28-1.41) 4.62 (1.52 (3.97-3.20) 4.38 (4.29 (1.37-2.47 (2.29-1. 1990).96) 4.24-1.35-1.92 (4.44 (1.08-1.99 (4.76 (4.04) 1.26) 4.89) 90th 4.97) 1.83) 3.37 (1. such as those used in medical radiographic procedures.34-1.41 (2.79-5.18 (1.35-1.51) 4.30 (1.51-3.58 (2.03) 3.84 (3.0) 6.11) .68 (3.40 (1.32 (1.38) 1.55 (1. Symptoms following acute high dose include perioral paresthesias.46 (2.39-1.48-3.24 (3.40 (1.70) 4.39-1.49-1.39 (3.26-4.27) 692 682 618 540 667 723 765 1132 1074 Non-Hispanic blacks Non-Hispanic whites 194 Fourth National Report on Human Exposure to Environmental Chemicals .26-1. population from the National Health and Nutrition Examination Survey.28-6.22-1.23-2.35-3.99 (2.49-1.54) 1. Barium is not rated for human carcinogenicity.56) Selected percentiles ( 95% confidence interval) 50th 1.80-6.03) 2.68) 3.55) .72 (2.703-1.83) 2.54 (1.60 (2.41 (1.02 (3.777-1.38) 1.60) Sample size 2180 2689 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 2.91 (3.921 (.36 (3.76) 2.61 (4.8) 4.28 (1.10-2.82) 1.10) 6.00-7.79) 1.27 (2.01 (5.54) 2.24) 3. Perry et al.33 (1.4) 5.38-1.51 (1.50) 1.23-1.51 (3.01 (4.39-5.23-5.81-6.48-5.905 (. NTP.31-1. Barium blocks cellular efflux of potassium resulting in profound hypokalemia.74 (5.33) 6. water solubility.69 (5.34 (1.Metals was eliminated primarily in feces and to a lesser extent.13-2. interval) 1.88 (6.31-1.33-1.00) 4.78 (2.37-1.52) 1.80) 3.88 (2.84-5.57) 2.97-4.963 (. 2001).50 (4.58-6.70) 10.48 (1.59-7.42 (4.36 (5.21 (1.16 (1.55-6.24-1.57-7.36-2.97 (4..92) 2.77) 1.00) 6.86-7.73-2.45-6.77-5.72) 4.46) 3.70) 1..12) 2.01) 1.20-8.02-5.85-5.84) 2.42) 1.68 (3.84-2.96-6.13-3. Insoluble barium salts.0) 5. Chronic accumulation of inhaled barium dust in the lung tissue may cause baritosis.47 (5.24-6.55 (5.56) 4. 1989).59 (1.02) .75) 1.39 (2.68-3.29-7.47) 10.710-1.62 (4.22-2.00) 1.43-6.33-4.48) 2.2 (3..18 (1.45) 95th 6.96 (4.38-7.4 (5.2) 5.59) 1.39 (2. Chronic high doses in animals resulted in kidney damage (McCauley et al.77) 1.69-9. Wones et al.29) 1.86) 5.65 (5.29 (3.80) 4.03-1. and cardiac dysrhythmias.00 (3.63-4.86 (2.64 (1.06) .58) 75th 2.38-5.880-1. but can occur after intentional or accidental ingestion of barium carbonate in rodenticides (Genter.45) 1.03) 1.42) 1.38 (4.41) 5.11) .45-1.52) 7.58 (4.16) 11.25 (1.74) 1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.36 (1.59) 1.31 (1.10-1.S.61) 2.48-1.00) 4.31-1.37 (1.28-11.76 (3.24 (5.64 (1.19-1.09) 6.27-3.57 (6.33 (1.15-4.31) 5.24-3.32 (1.43) 1. 1985.54 (2.99) 1.49 (1.98 (2.16-1.50) 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 1.22-1.57-10.50) 1.77) 5.46) 2.26-1. Toxicity from soluble barium salts is rare.50) 2.96) 4.30 (1.72) 6.39 (2.45-8.27-1.38 (1.51 (1. chemical form.68-3.20-2.891 (.25-11.58) 4.56-3.53-21.51) 6.56 (1.59 (1.74) 1.36-1.45-1.91-2.

Perry EF. Comparison of representative ranges based on U. p. 1994. 2000) to levels in NHANES 1999-2000 and 2001-2002. Paschal et al. Gallorini M. 2001-2002. National Toxicology Program (NTP). Calabrese EJ. Finding a measurable amount of barium in urine does not mean that the level of barium causes an adverse health effect.cdc.pd f&qt=barium+chloride+dehydrate+1994&col=020rpt&n=3&la= en. environmental levels) and health effects is available from ATSDR at: http://www.html?charset=iso-88591&url=http%3A//ntp. Pirkle JL. Sabbioni E.gov:8080/cs.76(1):53-59. 2005. Investigations into the effect of drinking water barium on rats.. and 2003-2004 (CDC. Inc. Information about external exposure (i. ed. calcium.28(3):373-388. Sampson EJ.niehs. Nordberg GF. Apostoli P.64(1):13-23. 1998). Costa R.S. et al.. ed. the welders had no obvious adverse clinical effects (Zschiesche et al. 2nd Ed. Cohressen B. Clin Chim Acta 2000. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 1986. eds. PS. and a drinking water standard has been established by U. Ash KO. A study of 46 elements in urine. Minoia C.. Wones RG. et al. Minoia et al. [online]. 1990. Epidemiological study of barium in Illinois drinking water supplies. 1992). Sci Total Environ 1990. Howerton K. Zschiesche W. Ting BG. NTP. 231-249. 10326-27-9) in F344/N rats and B6C3F1 mice (drinking water studies).. p. eds. 5th ed... 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. Lack of effect of drinking water barium on cardiovascular risk factor. Studies reporting urinary levels of barium in general populations have found values generally similar to those reported in NHANES 1999-2000.html. Barium levels determined in clinically submitted specimens were broadly comparable (Komaromy-Hiller et al. Vol 2: Specific Metals. J Toxicol Environ Health.Metals Workplace standards for external air exposure to various barium salts have been established by OSHA. Morrow JC. New York: John Wiley & Sons. Welders of barium-containing electrodes had median urinary levels of barium that were 60 times higher than the median levels in this Report. Jackson RJ. Exposure to soluble barium compounds: an interventional study in arc welders. In: Inorganics in drinking water and cardiovascular disease.. Third National Report on Human Exposure to Environmental Chemicals.e. technical report on the toxicology and carcinogenesis studies of barium chloride dehydrate (CAS no. Princeton NJ: Princeton Scientific Publications. Environ Health Perspect 1990.S. Stadler BL.197210. p. Atlanta (GA). New York: Elsevier.. 1989. 84-94. blood. Pozzoli L. Barium. Centers for Disease Control and Prevention (CDC). Vouk VB.85:355-359. 1984. Int Arch Occup Environ Health 1992.296(1-2):71-90.niehs. 4/8/09 Paschal DC. Schaller KH. et al. et al. Urinary concentrations in acute poisonings are often hundreds to thousands of times higher than in this Report.95:89-105.nih.. and radium In: Bingham A. Weltle D.atsdr. Available at URL: http://ntp. Douglas BH. In: Calabrese EJ. Pietra R. Fourth National Report on Human Exposure to Environmental Chemicals 195 . Handbook on the Toxicology of Metals. Frohman. In Friberg L. Reeves AL. and serum of Italian subjects.gov/ntp/htdocs/LT_rpts/tr432. Kopp SJ. LA. Jr. strontium. Powell C. Hypertension and associated cardiovascular abnormalities induced by chronic barium feeding. patient population and literature reference intervals for urinary trace elements. McCauley PT. Environ Res 1998. 1985. Genter MB. Biomonitoring Information Levels of urinary barium reflect recent exposure. Princeton (NJ): Princeton Scientific Publications. Trace element reference values in tissues from inhabitants of the European community I. Advances in modern toxicology. barium. 221-252 Komaromy-Hiller G.nih. Magnesium. Levy. 2001.gov/toxpro2. Laurie RD. Perry HM. EPA. References Brenniman GR. Patty’s toxicology. 2005. pp. Trace metals in urine of United States residents: reference range concentrations.

7440-41-7 General Information Pure beryllium is a hard gray metal. In studies of laboratory animals. nuclear. and dental bridges. aircraft. and machine-parts industries. and 03-04 are 0. which may vary for some chemicals by year and by individual sample. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. In medicine.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 . Exposure to beryllium occurs mostly in the workplace. inhaled insoluble beryllium sulfate was retained in the lungs and nearby lymph nodes. respectively.140 (<LOD-. electrical. < LOD means less than the limit of detection.13.13.13. Burning coal and oil can produce small amounts of beryllium dust that can be released into the air. and 0. soil. and refined beryllium is used in mirrors and special metal alloys for the automobile. and volcanic dust.130 (<LOD-. beryllium is used in instruments. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. bertrandite and beryl. 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 .S. computer.130 (<LOD-. see Data Analysis section) for Survey years 99-00. 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.Metals Beryllium CAS No. and can be found in mineral rocks. 01-02. eating food. are mined for commercial recovery of beryllium. or drinking water containing the metal. x-ray machines. Beryllium is also used in the production of sports equipment such as golf clubs and bike frames. Beryllium compounds are commercially mined. and from breathing tobacco smoke. Low-level beryllium exposure in the general population can occur through breathing air. near some hazardous waste sites. population from the National Health and Nutrition Examination Survey. Two types of minerals.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. the lightest of all metals. 196 Fourth National Report on Human Exposure to Environmental Chemicals . A half-life of 450 Urinary Beryllium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. coal.

which produces pneumonitis. Skin exposure can result in delayed hypersensitivity reactions. including contact dermatitis and subcutaneous nodules. population from the National Health and Nutrition Examination Survey.Metals days has been calculated for beryllium elimination from the human skeleton (IPCS. Maier.S. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th < LOD < LOD < LOD 90th < LOD < LOD < LOD 95th < LOD < LOD < LOD Sample size 2465 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 .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 . EPA. Genetic factors modify individual sensitivity to beryllium and susceptibility to developing chronic beryllium disease (McCanlies et al. Human health effects from beryllium at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 2002). is a granulomatous interstitial lung disease that is caused by chronic beryllium inhalation and the resultant immunologic response.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. NTP considers beryllium to be a known human carcinogen. Air levels greater than 100 µg/m3 can result in erythema and edema of the lung mucosa. 1990). based upon excess lung and central nervous system cancers in studies of workers. or berylliosis. respectively. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.346 (<LOD-. Fourth National Report on Human Exposure to Environmental Chemicals 197 .. IARC has classified beryllium as a human carcinogen. S.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. 2003. 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. The effects of occupational exposure to beryllium depend on the concentration of beryllium in the inhaled air and the duration of air exposure. Workplace air standards and guidelines for external exposure have been established by OSHA and ACGIH.281 (<LOD-. and drinking water and environmental standards have been established by U.231 (<LOD-.

20012002. Sampson EJ. less than 0.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. Paschal et al. Levels of beryllium in urine for the U.. 1998). Paschal DC. Beryllium [online].. Costa R. Available at URL: http://www.Metals (i. Ash KO. and the fact that most NHANES participant levels were undetectable.15 μg/L in workers exposed at the recommended threshold limit value (Apostoli and Schaller.inchem. International Programme on Chemical Safety (IPCS). Minoia et al.e. Sci Total Environ 1994. population are lower than levels in workers. and the 95th percentile for males in NHANES 2001-2002. 2001).S. et al.. Maier L. Morrow JC. Finding a measurable amount of beryllium in urine does not mean that the level of beryllium causes an adverse health effect. Gallorini M. Pozzoli L. VI.76(1):53-59. Urinary beryllium--a suitable tool for assessing occupational and environmental beryllium exposure. 1990.atsdr.e. Andrew M. Environ Res 1998. Centers for Disease Control and Prevention (CDC). Atlanta (GA) 2005. Clin Chest Med 2002.S. Hamilton et al. 0.74:162-166. 3/27/08 Komaromy-Hiller G. Am J Epidemiol 2003. Sabbioni E. blood. Trace element reference values in tissues from inhabitants of the European community I. urinary levels for general populations have been either undetectable or had different detection limits than in this Report (KomaromyHiller et al. Van der Venne MT.1 μg/L). Trace metals in urine of United States residents: reference range concentrations. Apostoli P. Howerton K.. et al.95:89-105.org/documents/ehc/ehc/ ehc106. 1990. and 2003-2004. Hamilton EI. Apostoli and Schaller (2001) stated that detection limits in earlier studies were inadequate to estimate nonoccupational exposures. 198 Fourth National Report on Human Exposure to Environmental Chemicals .html. Ting BG. and serum of Italian subjects. Schaller KH.296(1-2):71-90. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Third National Report on Human Exposure to Environmental Chemicals. They reported urinary beryllium levels ranging from 0.158:165-190. (1994) noted that analytical methods used in several general population studies appeared to have limits of detection that were insufficiently low (i. Given these results. patient population and literature reference intervals for urinary trace elements.12 to 0. References Apostoli P. Environmental Health Criteria. In other studies.. HLA-DPB1 and chronic beryllium disease: a HuGE review. it is likely that urinary beryllium levels in the U. Genetic and exposure risks for chronic beryllium disease. Jackson RJ.htm. 106. Minoia C. Element reference values in tissues from inhabitants of the European community. 2000. Sabbioni E. which approximate this Report’s limit of detection. plasma and urine and a critical evaluation of reference values for the United Kingdom population.13 μg/L. Biomonitoring Information Urinary beryllium levels represent recent and accumulated exposure. Sci Total Environ 1990. environmental levels) and health effects is available from ATSDR at: http://www. McCanlies EC. Pietra R.S. Kriess K.157:388-398. Pirkle JL. Clin Chim Acta 2000. population were generally undetectable in NHANES 1999-2000. Weston A. Review of elements in blood.23:827-839.gov/toxpro2. A study of 46 elements in urine. Comparison of representative ranges based on U. Int Arch Occup Environ Health 2001.

300-.400) < LOD . respectively. 7440-43-9 General Information Cadmium is a soft. population from the National Health and Nutrition Examination Survey.304 (. Other uses include pigment production.600-.400-.800 (.362-.300-.403) .30-1.10 (1.216-. and nonferrous alloys.00-1.00 (.500 (. and 03-04 are 0.300 (.40 (1.300-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.200 (.20-1.400) .800) .400-.400) .400 (.20) 1.900 (.30-1.300 (.10 (1.700) .00 (.10) 1.10 (1.300-.400) .50 (1. see Data Analysis section) for Survey years 99-00.600 (.300-.700-1.500-.S.900-1.14. EPA.400-.00) .300 (<LOD-.50-1.361-.400) .00-1.309-.500-.386-.424) * . and incineration of municipal waste materials.300) .70) 1.600 (.00-1.300-.60 (1.400) . and 0.40 (1.60 (1.10 (1.500) .300 (. Fourth National Report on Human Exposure to Environmental Chemicals 199 .367-.300) .300 (.426-.300) .00-1.20-1.900-1.500-. 01-02. bluish-white metal that is obtained chiefly as a by-product of processing zinccontaining ores (principally sphalerite.800-1.600-1.00 (.10) 1.300) .400) < LOD .30) 1.00-1.20) 1.300 (.40) 1.30-1.368-.400 (.600 (.700) .300) .300) .20) .400 (.337) .40 (1.60) 1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. which may vary for some chemicals by year and by individual sample.70) 2742 2268 2085 1842 2219 2292 2716 3806 3478 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.304 (.366) * * .700) .427) * .300-.300-.400 (.500 (.10) 1.300-.500) . Important sources of airborne cadmium in the environment are burning fossil fuels such as coal or oil.300) .333 (.50) 1.800) .00 (.gov/minerals/pubs/commodity/cadmium).400-.90) 1.296-.00) .00 (.400 (.800-1.00-1.40) 1.400 (.275-.20 (1. or copper smelters (U.500-.412 (.300) 75th .200-.10) 1.200 (.500) .50) 1.00 (1.400 (.331) . plastic stabilizers.266-.80) 1.300-.300) .20) 1.400) .400 (.304-.600) .452) .600) .700) .40 (1.10 (.400-.393 (.900-1.50-1.00 (.376-.00-1.00 (.378 (.500 (.320) Sample size 7970 8945 8372 Age group 1-5 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * .20) 1.20-1.80 (1.60) Total * .460) .20) .40 (1.200) .40 (1.300-.300-.300 (.500-.400 (.300-.900 (.400 (.300 (.300-.425 (.500) .300 (.700-1.700) 1.300-.00 (.420 (.600 (.600 (.20) 1.900-1.326 (.600) .421 (.300) .500-.800 (.200 (<LOD-. Since 2001.60-1.400 (.344) .600 (.70) 1.300-.200 (<LOD-.10) 1.900-1.400-.10) 1.500) .500-.600) .500 (.50 (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 .500-.400) .300) .80) 1.usgs.600 (.00 (.300 (.300 (.600) .30 (1.400-.50 (1.235 (.500-.500-.400) < LOD .470) * .400 (.300-.900-1.300) .400-.500 (.500 (. Blood Cadmium Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U.600 (.395 (.40 (1.400 (.468 (.500-.30) 1.300-. 0.500) .600) 1.Metals Cadmium CAS No.300 (<LOD-.60 (1.400) .50-1.500 (.400) .20-1.359-.20 (.00 (1.3.400) < LOD < LOD < LOD .3.600 (.900-1.600 (.30-1.283 (.00-1.200-.10) 1.600) .600) .20) 1.500-.313 (.600-.500-.300 (.300 (<LOD-.70) 1.60 (1.441) * .300-.600) .200) .400) .600-.400) .900-1.600) 90th 1.500-.40-1.10) 1.700 (.513) .255) .400) .600) .500) .400 (.00 (.200-.300-.200-.10 (1.449) Selected percentiles ( 95% confidence interval) 50th .60 (1.400 (. Cadmium also may be emitted into the air from zinc.378-.600 (.500-.700-1.300 (.382 (. U.50 (1. interval) .S.200-.400-.300 (.10 (1.400-.500-.20-1.403 (.900-1.500 (.600 (.300) .400 (. during refining of lead and copper from sulfide ore.300 (.300-. cadmium use has declined in response to environmental concerns (http:// minerals.30) .70) 1.500-.400) .289-.300) .400 (.300) 1.S.700) .800) 1.30-1.40-1. malleable.20) 1.20-1.600 (.700) .200 (. lead.400-. The predominant commercial use of cadmium is in battery manufacturing.700) .60) 1.30) 1.398) < LOD < LOD < LOD < LOD < LOD < LOD .500-. < LOD means less than the limit of detection.900-1. coatings and plating.50) 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 .400) .600 (.700) . as zinc sulfide) and to a lesser extent.300-.20-1.300 (<LOD-.20) 1.50-1.00-1.500 (.10 (1.60) 1.20) 95th 1.

705-.19) 1.214-.220 (.500) 90th .280 (.179-.199 (.153-. individual values vary and are affected by factors such as dietary intake of essential nutrients (iron.30-1.455 (.52 (1.219 (.310) .800-.15 (.177-.284) .38) .57) 1.493-.221 (. 2003).09-1.72) 1.227 (. calcium.160 (.492 (.090) .265 (.400-.972 (.210 (.436-.741-1.37) 1121 1335 1277 1136 1355 1266 Females 99-00 01-02 03-04 Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 .82) 1.231) .210 (. drinking water is a source for cadmium intake.980-1.134) .394-.** Survey Geometric mean (95% conf.090) .990) .426 (.22 (1.22 (.326) .06..203) .450 (.061 (<LOD-.02-1.191-.530 (. ingestion through food is the largest source of exposure.820-1. wheat.839 (. The kidney is a critical target and shows the earliest sign of cadmium toxicity.295) .190-.273 (.880) ..202 (.06.858 (.207-.875 (.200-.092 (.255) .813 (.170-.07-1.456-.766 (.960 (.204 (. 200 Fourth National Report on Human Exposure to Environmental Chemicals . 2003).322 (.220) .235) .299) .462 (.223 (.700-.148-.580) .540) .17 (.551 (.229) .240) .820) 1.189-.886-1.06-1. 0.193 (.24) 1.15) 1..963-1.390-.115-.519) .48 (1.855-1.360) . a factor that may contribute to the higher absorption of cadmium by women (Diamond et al.233) .289-.211 (.476-.423-..633-1.320) .980-1.300 (.262) .490) 1.445 (.061-.330-.180 (.200 (.977) . zinc.232) .160) .261-.980 (.329 (.194-. Diamond et al.171-.32 (1.430-.836-1.550 (.202-.249-.01 (.210 (.04 (.500) .820 (.38) 1.498-.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.713) .201 (.130 (.216 (. potatoes.470-.440 (.272-.733) .190-.251) .20 (1.918-1.960) 1.520-.151-. Urinary Cadmium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.700-. and 0.232 (.200-. 2001). and 03-04 are 0.187 (.20 (1.680 (.210 (. 01-02.310 (.38) 1.077 (.211-.870) .110-.175 (.240-. With chronic exposure.610) .277 (.733-.230) 75th .989-1.226) .067-.25 (1.308) .128 (.450 (.800 (.892-1.195-.393-.221) .193-.17 (.354) .445 (.175 (.233) .539) .184-.381-.480) . The gastrointestinal absorption of dietary cadmium is about 5% in adult men and 10% or higher in women (Diamond et al.189) .279 (.12-1.157-.700-.790 (.41 (.241) .13 (.763-.919) .10 (1.219 (.362) .210) .198) .257-. cadmium accumulates in the liver and kidneys where it is bound to metallothionein.06.366-.263) .519) .06) .169-.20 (1.607) .350 (.15) . and various seeds.Metals 2000).196-.452 (.173) .065-.160-.234 (.28) 1.596) .316 (.192-.440-.339) .191 (. For nonsmokers who are not exposed to cadmium in the workplace.078 (.327 (. respectively.20-1. including many food crops such as cereal grains.390-.714-1.387) .623) .74) 1.875) .080 (.372) .20) 1.246) .06-1.551) .717-.238-.510) .12 (.285-.239 (.351-.388-.479) .109-.748-1.229-.257) .530) .247) . Cadmium absorption may be increased with iron deficiency (Berglund et al.107-.135 (.220-. 2003).170 (.121 (. however.157) .255) .077 (.281 (.120 (.206 (.13) .886) .753-.220-.114-.283 (.810-1.167-.336) .34) 1.060-.38) . To a lesser extent. Renal tubular and glomerular damage.390 (.433-.253-.13-1.366-.141 (.300) .366) . Kikuchi et al.290-.17) .260 (.806) .170-.208-.51 (1.109 (.980) .559 (.313) ..261-.229) . **All results are corrected for molybdenum oxide interference in the ICP-MS method. rice.17 (. copper) and protein.092) .S. Cadmium is absorbed via inhalation and ingestion.01-1.848 (.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 .36) 1.640) .01) .447 (.181 (.230 (.206) .28-1.249) .165-.490) .843-1.892 (.730-.817 (.440 (.818 (..101) .507) .260-.126) .260-.510-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.412) .860) 1.482) .28 (1.265) . About one-third to one half of the total body burden accumulates in the kidney tissues (Nordberg and Nordberg. interval) . see Data Analysis section) for Survey years 99-00.545 (.940-1.270 (.203 (.26) size 2257 2690 2543 Total years 99-00 01-02 03-04 50th .087-.466 (.686-.150) . Cadmium in soil is absorbed by plants. population from the National Health and Nutrition Examination Survey.136) .270 (.222) .25) 1.400-.890 (.191-. 1994).243-.790 (.219 (. Inhalation of cigarette smoke is a predominant source of exposure in smokers.140 (.633 (.220) Selected percentiles ( 95% confidence interval) Sample 95th 1.980) .589 (.817 (. 1999.03) . whose body burdens of cadmium can be approximately twice that of nonsmokers.890-1.430) .458 (. The estimated half-life of cadmium in the kidney is from one to four decades (ATSDR.190-.183-.160) .210) .148) .210 (.238) .112-.43) 1. an inducible metal binding protein.230) .067-. Horiguchi et al.200 (.178-.192-.475 (.209 (. 2004a.150-.100-.306 (.135-. 2003.04 (.47) 1.081) .189-.255) .302 (.481) .237-.83) 1.226) Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 * .282 (.

479 (.884) .338 (.187-. 2002.147-.201-.438) 90th .507-.143-.678 (.700) ..181 (.518) . a condition known as “itaiitai” (“ouch-ouch”) affected postmenopausal women living in a cadmium-polluted region of Japan.783) .168 (.196 (.247-.830-1.181-.725-1.839) .227-.07 (.084 (.182) .05) 1.940-1.190 (.101) .708-1.184-.691-. 2002.645-. most often a result of occupational exposure (Roels et al.239-.176 (. 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.727-.170-.906) .687-.183 (.198) .181) .157-.364) .261 (.352) .491-.159 (.387 (.075-.224 (.148 (.232) .242) .690-.147 (.184-.536 (.235) .795) 1.289) .490 (.209) Selected percentiles ( 95% confidence interval) Sample 95th .533) .159 (.187) . Most studies of relatively low level environmental exposure to cadmium have demonstrated associations between higher urine or blood cadmium levels and an increased prevalence of various biomarkers of renal tubular effects (Alfven et al. 2004b).200 (.288-.229) .210 (. 2004).074-.154 (.300-.622 (.176 (.223) .607) .097) .696-.985 (.122 (.267 (.678-.267 (.250) .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 .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 .156) .421 (.100 (.931 (.140-.197-.106) .256-. **All results are corrected for molybdenum oxide interference in the ICP-MS method.185) .091 (.412 (.174-.873 (.686 (.434 (.091 (.199 (.090 (.094) .562-. Noonan et al.281) .140-.078 (.288) .051-.340) .154-.143) .927-1.04) size 2257 2689 2543 Total years 99-00 01-02 03-04 50th .185 (.137-.476) .211 (.112) .560-.647-.02 (.181 (.433-.418-.202 (.377-.979 (.208 (.919 (.38) .084-.245 (.207) .126 (.130-.225) .158-.329 (.630-.850) .316 (.470) .531 (.929) .240) .147-.446) .208-.350) .143-.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.253 (.767 (.856 (.431) .175 (.162 (.432 (.** Survey Geometric mean (95% conf.144-.874-1.802 (.204-.631) .806-1.189-.091) . interval) .484 (.381-.545) .113-.085-.998) .438-.813-1.220 (.740 (.690 (.718 (.336-.297) .398-. 1996.303) .501 (.962) .163) .07) .168-.240) .668-.729 (. 2003.712 (. During the 1950’s and 1960’s.722-.173-.206-.308 (.833-1.318 (. two studies in Japan did not find an association between cadmium in urine and renal biomarkers (Ezaki et al.688-.234) .107) .08) .757 (.111-.470) .067-.247-.10) 1.098) .830) .538) . Jarup et al.325 (.391-.135) .00 (.917 (.280 (.266) .418) . 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.783 (.178-.178) .444-.096) .850) .228-.266-.161-.813-.283 (.191 (.263-. However.516-.650-.123-.719 (.666-.335 (.146-.182) .210) .876-1.828) .423 (.171-.500-.190 (.236-.16) 1.13) .207-.288 (.789 (.941 (.163 (.404 (.261) .137 (.075 (<LOD-.716) .415) .818) .382-.156-.191-.182) .150-.473 (.826-1.414-.282 (.191) .083-.487 (.175 (.767) .826-1.387-.818) .674-1.856) .131-.077-.663 (.Metals manifested by irreversible proteinuria and progressive reduction in glomerular filtration rate.304) .865 (.225) .827) .123-.071 (.441-.252 (.950) .274) 1.218) .078-.940 (. Olsson et al.219 (.700 (.212 (.226) 75th .. 2000.104) .331 (.316) .273 (.293-..779 (.559-.551) . Staessen et al.093 (.170 (.255-. 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.449) .292) .16) .209) .537-.136-.104) .06 (.687 (.716-.219 (.388-. 1999). 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.792 (.917) . population from the National Health and Nutrition Examination Survey.667) .222-.234 (. 2002.085 (.09 (.591 (.693 (.263 (.261-.481 (.241) .769 (.614) .. can result from high dose chronic exposure. Horiguchi et al.278) .754) .321) .784) .690-.156 (. At lower environmental exposures.00 (.234-. Fourth National Report on Human Exposure to Environmental Chemicals 201 .233 (..289) .177) .253) .210 (..157-.247-. 1999).192) .268 (.232) .216-.304-..238-.909-1.086 (.205 (.404) .308) .063-.423-. 1999).221-.17) ..343-.166 (.183) .426-.757) .199-.S.440) .382) .617 (.194-.281) .414 (..311) .238) .270 (.541) .215 (.221 (.219) Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 * ..440) .168-.472) .173 (.12) 1.175-.653) .136-.184) .296 (.

2002..Metals greater urine cadmium levels may have an increased risk for bone fracture and diminished bone mineral density (Alfven et al.. Horiguchi et al.. 2005. Blood and urine cadmium levels are typically higher 202 in cigarette smokers.. Becker et al. Jarup et al. Komaromy-Hiller et al. Friedman et al.1 mg/L (Alfven et al. 2002).. 2002). Jin et al.. 2000). Staessen et al.. Further research is needed to address the public health consequences of such exposure in the United States. 2004). However... Workplace exposure to airborne cadmium particulates was associated with decreases in olfactory function (Mascagni et al. Chronic inhalation exposure to cadmium particulates was associated with changes in pulmonary function and chest radiographs that were consistent with emphysema (Davidson et al. 2003. For NHANES 19992000. and drinking water and environmental standards have been established by U. Staessen et al. 2006). Women had higher blood and urine cadmium levels compared to men of similar ages. Suwazono et al. 2003. 2003. CDC. has resulted in severe. 2005. 2005). 2002) and length at birth (Nishijo et al. 2006. Olsson et al.. 2002. Ezaki et al. 2003.. 2004.S.. 1996. Zhang et al. 2002).cdc. intermediate in former smokers and lower in never-smokers (Becker et al. 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). 2002). 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. 2006. Noonan et al.. Salpietro et al.. 2000. 2004. 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.. 2003). 2003.. Blood cadmium levels are about twice as high in smokers compared to nonsmokers (Becker et al. Cadmium can produce lung... as may occur from welding cadmium-alloyed metals. Becker et al. Acute and heavy exposure to airborne dusts and fumes. Ezaki et al. 2002.46 mg/gram of creatinine) (Ezaki et al. respectively..atsdr. 2003.gov/ toxpro2. Olsson et al. Wilhelm et al.. Information about external exposure (i. In adults aged 60 years and older... environmental levels) and health effects is available from ATSDR at: http://www.26 and 3.. decreased bone density was correlated with mean urinary cadmium levels of approximately 1 mg/gram of creatinine (Staessen et al. Both IARC and NTP consider cadmium a human carcinogen..S. the risk of low bone mineral density increased by nearly three-fold when the blood cadmium exceeded 1. urinary cadmium reflects both cumulative exposure and the concentration of cadmium in the kidney. maternal blood or maternal urine and birth weight (Nishijo et al.. Becker et al. 2005. pituitary gland and kidney tumors in animals and has been associated with lung cancer in humans in occupational epidemiologic studies. data (CDC. 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. 2002. In the typical environmental exposure. Creatinine-corrected urine cadmium values in U. 2005. blood cadmium was also slightly higher in Mexican Americans and participants 20 years and older (CDC. People who are occupationally exposed may have blood and urine cadmium levels that are higher than those of the general population. 2004b. Subtle increases in markers of renal tubular effects have been associated with urine cadmium levels as low as approximately 1 mg/gram of creatinine (Akesson et al. 2002.S. Olsson et al. 2002. 2002)... Workplace standards and guidelines for air exposure to cadmium have been established by OSHA and ACGIH.. Small epidemiologic studies have noted an inverse relationship between cadmium in cord blood.. Horiguchi et al. Occupational standards are provided here for comparison only. Staessen et al. respectively. In postmenopausal women. 1999). not to imply a safety level for general population exposure. 1996).. approached these values associated with subclinical changes in renal function and bone mineral density. 2004... 2000. Biomonitoring studies on levels of cadmium provide physicians and public health officials Fourth National Report on Human Exposure to Environmental Chemicals .. Animal studies have demonstrated reproductive and teratogenic effects. 2006).. potentially fatal pneumonitis (Fernandez et al. 2000. Surveys of populations not known to have increased cadmium exposure have reported similar urine and blood levels (Becker et al. 2004b). Moriguchi et al. EPA.html. Mannino et al. Waalkes (2003) provides an overview and summarizes potential mechanisms for carcinogenicity. 1988).. In this Report the urinary and blood cadmium levels at the 95th and 90th percentiles.. 1999.. 2004. Jarup et al.. Wennberg et al.e.. 1999). Biomonitoring Information Blood cadmium reflects both recent and cumulative exposures. Finding a measurable amount of cadmium in blood or urine does not mean that the levels of cadmium cause an adverse health effect.. with peak values observed in the fifth to sixth decades (CDC. Wennberg et al...

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Mueller PW. Occup Environ Med 2002. Lundh T. Liu QF. dietary intake. Tanebe K. Public health implications of environmental exposure to cadmium and lead: an overview of epidemiological studies in Belgium. Lundh T. Nakagawa H. Cadmium concentration in maternal and cord blood and infant birth weight: a study on healthy non-smoking women.S.30(5):395-399. Roels HA. Stegmayr B. et al. pp.21(3-4):251-262.100:330-338. Emelianov D. Kathman SJ. eds.3:26-41. J Environ Sci Health B 2004. Nakagawa H. Effect of environmental exposure to cadmium on pregnancy outcome and fetal growth: a study on healthy pregnant women in China. 204 Fourth National Report on Human Exposure to Environmental Chemicals .Metals Nishijo M. Kido T. Environmental exposure to cadmium. Campagna D. Nordberg GF. Schultz C. Wennberg M. Gallmans G.533(12):107-120. Saito S. et al. lead. Oskarsson A. EPA). Kobayashi E. Ren Fail 1999. Bruiglia S. Relationship between newborn size and mother’s blood cadmium levels.epa. Biological monitoring of cadmium. Kuznetsova T. Staessen J. Jansson J-H. Roels HA. Schwenk M. or cadmium in controlling occupational and environmental risks of nephrotoxicity. Zhang YL.gov/ttn/atw/ hlthef/cadmium. Tanebe K. Wilhelm M. Lybarger JA.110:1185-1190. Honda R. United States Environmental Protection Agency (U.59(1):22-25. Renal effects of cadmium exposure in cadmium nonpolluted areas in Japan.209:301305. Environ Res 2006. Gangemi S.59:394-397. cadmium. New York: Plenum Press. 151-168. age. Thijs L. In: Clarkson TW. Int J Hyg Environ Health 2006. forearm bone density. iron status. 2004. Cadmium compounds. Cadmium carcinogenesis. created 1992. Buchet JP. Ginucchio G. Environ Health Perspect 2002. Nordberg GF. Lauwerys R. lead. Arch Environ Health. Environ Health Perspect 2002. Bergdahl IA. Skerfving S. Effects of maternal exposure to cadmium on pregnancy outcome and breast milk. Suwazono Y. Toyama. Revised 2000 [online]. Noonan CW. and risk of fractures: prospective population study. J Perinat Med 2002.110:151-155. Tawara K. 2001. Sager PR. J Cardiovasc Risk 1996. Effects of exposure to low levels of environmental cadmium on renal biomarkers. 4/8/09 Waalkes MP. Cadmium in blood and urine – impact of sex. Olsson IM. Hazard Summary. and former smoking – association of renal effects. et al. Lancet 1999. Minciullo PL. 2000. Zhao YC. Zhu HD. Japan. Lison D. Hoet P. Sarasua SM.353:1140-1144. Biological monitoring of toxic metals. Available at URL: www. et al. Honda R.39:2507-2515. Roels H. Nogawa K. lead. and mercury in blood or urine of children: Basis for validation of human biomonitoring data in environmental medicine. et al. Salpietro CD. Time trends in burdens of cadmium. Usefulness of biomarkers of exposure to inorganic mercury. Environ Res 2000. Fan YG.84 (Section A):4455. Stelitano A. Ottosson H. and mercury in the population of northern Sweden. Vangronsveld J.html. Lijnen P. Nishijo M. Wang JX. Friberg L. Okubo Y. Staessen JA. Bensryd I. Revised and new reference values for arsenic. Merlino MV. Nordberg M. Nakagawa H. Mutat Res 2003. et al.

12) 5.70 (8.76-6.1 (11.26-11.36 (6.00-8.54) 4.3-13.60-12.9 (11.87-7. infrared lamps.3) 10.62 (5. and as polymerization catalysts.54-11.49 (4.62) 4.81-14. see Data Analysis section) for Survey years 99-00.30) 5.00 (7.4) 10.50 (6.35 (4.10-5.2) 11.6 (9.70 (6.08) 7.90) 5.57-5.03 (4.90) 4. photographic emulsions.9 (11.74-5.00) 6.60-6.0-15.0) 9.43-8.20-5.7) 884 683 618 568 667 723 821 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.1-12.6) 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 4.20-8.0) 12.4 (9.49) 4.5) 10.10-7.5 (10.90-8.6 (11.17-6.05-5.40) 5. Most human exposure to cesium occurs through the diet.4) 9.9) Total 4.10-9. although cesium was generally of low toxicity when given to animals.1-13.22 (4.9 (11.80-10.71 (8.3) 10.4) 11.80-10.4) 95th 11.49 (5.70 (6.77 (9.61) 7. soil.7 (9.60 (8.10-8.05) 5.99) 7.4) 10.99) 9.86 (7.26) 7.16-6.2-13.39) 7.13 (8.12-11.4) 12.27) 4.43 (5.0) 12.08-5.13-8.2 (9.40) 7.01-8.7 (8.67 (4.94 (4.55 (7.10 (6.2-13.84) 5.30) 7.9) 8.08 (6. Little is known about the health effects of this metal.87 (4. However.04) 7.49) 75th 7.1 (9.68) 9.99-11.7 (9.38) 5.97 (7.01-6.70-5.60-7.0) 11.14.9 (10.33 (5.59) 7.56-11.63) 6.3) 12.50) 5.71) 4. nausea.3-15.50) 9.62 (5.87 (4.4) 12.6 (9.7) 10.2-13.36 (3.40-5.8) 9.1) 9.50 (4.45-8.8) 11.88 (8.5-14.80 (4.50 (4.80 (8.8 (11.90-10.2-14.91-8.0) 10.70 (4.77 (9.90) 7.17 (6.03-4.7-14.53 (6.83) 6.81) 9.70) 5.20 (4.10 (8. Human health effects from cesium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.99-6.05) 5.37) 7.42-7.61-6.3) 10.50-7.40) 5.3-13.94 (4.33 (6.7 (10.Metals Cesium CAS No.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 4.10 (8.00-9.90-12.00) 7. interval) 4.74 (4.16-6.55-11.63-4.89) 4.72) 4. semiconductors.29) 4.07-11.52-9. and 03-04 are 0.50 (4.59 (5.94) 4.32-5.90-12.70 (9.7) 11.5) 12.7) 11.10 (6.09-5.0) 12.8) 12.3) 9. Inorganic cesium compounds are used in photomultiplier and vacuum tubes.23) 9.80) 7.79 (4.20-7.93 (4.84) 8.55 (4.0 (9.90 (6.20 (6.90-10.59-5.64) 5.80-13.09) 5. 7440-46-2 General Information Cesium is a silver-white metal that is found naturally in rock.92-13.95-4.30 (6.60-7.22-4.24) 4. 2004).53-11.97) 4.40-5.64-10.95 (3.20-4.0) 11.87) 5.1-12.81 (4.35-5.60 (7.70-8.26 (3. and cardiac arrhythmia (ATSDR.80 (8.90-10.12-5. For absorbed cesium salts.98 (7.84-9.66 (7.46) 7.9) 12.30-10.89-5. diarrhea. Whether cesium compounds are carcinogenic is unknown.04 (4.80-10.13 (7.81) 4. 0.80-6.90) 9.01) 7.40-5.8) 11.27-5.2 (9.37) 5.0 (10.95) 5.3 (8.5-14.6 (9. Workplace guidelines for cesium hydroxide are available from ACGIH and NIOSH.40 (4.96 (6.81) 4. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.45-5.3 (8.60) 7.1) 10.74) Selected percentiles ( 95% confidence interval) 50th 4.56 (4. the body half-life is estimated to be 70-109 days based on 137Cs exposures.8) 12.97-7.91 (7.02 (4.20) 5.00-4.84-5. Urinary Cesium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.86-12.7 (11.21) 90th 9.5) 9.98 (7.80 (8.S. respectively.4 (9.5-13.30-5.6 (9.14.4 (10.8) 9.71-8.08-5.25 (3.68 (7.8 (10.64-5.12 (4. and high-power gas-ion devices.99-11.07) 4.56 (4.71 (4.6) 10.90 (4.08 (7.94-4.70) 7.64) 4.9) 11.80 (4.00) 4.69-6.82-4.84 (4.20) 4.77 (4.71-9.59-5.0-13.73-11.35 (4.97) Sample size 2464 2690 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 4.05-5.21 (4.71-5.60) 7.80-11.72-7. Case investigations of ingestions of large doses of cesium chloride have reported decreased appetite.87 (4.34) 9.36) 3.6 (11.13 (5.15-8.47-4.40-7.70 (5.34 (4.27 (7.26) 4.52) 7.17) 4. Fourth National Report on Human Exposure to Environmental Chemicals 205 .2-12.33-5.20) 8.64) 5.00-10. 01-02.60-6.70) 5.03 (4.30 (6.60-5. scintillation counters.9 (10.1) 11.42) 6. and 0.50 (7.59-5.2.9 (11.6) 11.32) 4.90) 5.89) 5.3) 10.83-4. cesium hydroxide is corrosive and irritating at high concentrations.42) 7.7) 10.44 (8.64 (4.1 (10.77-8. and clay.7 (10.47-8.29 (4.80 (4.73-5.40-11.40-11.14 (4.1) 11.63 (4.20) 7. population from the National Health and Nutrition Examination Survey.23-4.39-4.1) 9.32 (3.8 (10.2) 12.56) 5.00-8.60) 5. Radioactive 137Cs has been used medically to treat cancer.86-11.7 (10.8-13.5 (8.25-5.40-5.70 (8.7 (9.25) 4.31-8.82) 5.5-16.8) 12.4-13.

98) 5.90 (7.47) 6.31 (4.41) 4.17) 4.70) 7.63 (6.78) 4.14) 4.13-9.14-6.05) 6.7) 10.41-7.92) 3.61-3.53 (6.85-4.33 (5.99-9.31 (4.24-10.99 (3.06) 4.55) 4. Urinary cesium levels were similar in a group of forest fire fighters and residents living near the fire area (Wolfe et al.00-8..31-4.39 (5. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.60-20.67 (6.27 (8.09) 8.91-7.3) 11.99-4.51 (7.96-4.05-3.43 (3.10 (3.38-12.24 (3.82) 7.88-10.67 (5.08) 4.63) 6.15-4.11 (5.S.20) 5.68-11.14) 4.77) 4.96 (4.96) 4.06 (3.56) 3.79) 4.84-9.36-6.95 (3. Komaromy-Hiller et al.18-6.75 (6.0 (7.5) 7.00-5.5) 9.73 (3.87) 5.16-8.77 (4.65 (6.41 (4.03) 5.67) 5.95) 4.79 (5.09) 4.63-6.40) 7.9) 10.46-8.87) 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 5.02 (5.70 (7.42-6.53 (4.30 (3.12 (3.18) 8.29) 4.52-5.94) 7.14-7. population from the National Health and Nutrition Examination Survey.43-6.47) 7.3 (8.72-5.51 (4.01-8.06 (5.45 (4.74) 75th 5.21 (2.84-11.47) 6.22 (3.96) 4.13-9.56 (4.17 (6.64-6.27-4.26-6..8) 6.16-8.05-3.15) 95th 8.93-9.59) 4.95-6. population.62-8.50) 8.50) 4.40) 6.60 (3.91 (5.90-8.04) 5.17) 9.38-7.95 (5.60-10.90-8.63 (7.65-3.88-4.43-11.9 (9.2) 340 368 290 718 762 725 1406 1559 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 3.77-5.03-5.9 (10. Urinary Cesium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.46) 6.64 (4.42-4.55-5.27) 4.03-6.26 (3.1) 11.08 (5.22-11.51 (3.72) 4.47) 4.08 (3.39) 5.10 (3.41-4.16) 5.2 (8.8) 10.75 (7.23 (7.0) 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 .20-4.50 (7.74) 3.27-6.19-6.72 (4.25) 4.99-9.15-11.27 (6.84-7.44-5. 1990).13 (3.74 (4.74 (5.18-7.Metals Biomonitoring Information Urinary cesium levels reflect recent exposure.93-7.84-7.91) 5.3 (10.43 (4.33-3.66 (6.44 (4.73-4.54 (3. Two small studies of European populations reported urinary cesium levels similar to U.10) 7.75-11.48) 7.91-6.81 (4.64) 9.79) 9.71) 6.12) 3.89-4.74-11.60) 3.78 (3. and were also roughly similar to those in this Report.35-7.18 (7.51) 4.30 (4.6) 6.2) 11.70) 6.10-4.24-4. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.56) 4.80) 6.47 (7.66 (5.41 (8.37-3.54 (4.58 (4.06) 5.83-7.S.36-10.38 (3.08 (6.64) 4.08-7.58) 3.35 (3.99) 4.58 (6.51 (3.30) 10.68 (4.00 (8.00-4.28 (5.38 (3.92 (5.4) 10.17-4.55 (3.64) 5.05) 3.87 (5.95-12.43 (8.86 (4.36-3.56-10.3 (9.29) 4.21-4.21-5.98 (6.97-5.41 (5.05-4.08) 4.50 (6.11 (5.91-9.40-5.43) 8.08) 3. interval) 4.51 (4.0) 7.07) 8.42 (5.04-11.35) 3. 2005.15 (7.50) 4.02-4.35 (4.08-3.44-9.14-4.44 (8.94 (5.61 (7.54 (4.96-4.27 (6.50-5.8 (9.04) 6.00) 6.54 (5.77 (7.78 (3.48-6.87-4.07) 8.16-5.30-4.98) 5.90-3.3-15.30) 10.58-5.5 (9.78) 4.00-5.25) Selected percentiles ( 95% confidence interval) 50th 4.28 (4.63 (4.19-3.68) 4.04-5.98 (7.6 (9.49) 3.76-9.21-3.05 (4.2 (8.68) 6.46-4.20-4.37) 4.5) 9. Finding a measurable amount of cesium in the urine does not mean that the levels of cesium cause an adverse health effect.3) 9.85) 5.83) 8. Minoia et al.7-12.09 (4.44) 3.62) 5.91) 5.30-4.60 (5.46 (8.64 (8.50 (5.57) 3.7) 10.66 (5.20-8.58) 8.07 (5. 2004).71 (7.56) 4.79) 6.42-4.66-6.63-6.45-6.29-3.20-4..29) 5.79-5.53) 6.07-4.29-3.31-6.28) 7.50) 4.28) 8.39) 8.14 (6.26 (4.91) 4.00-9.65-4.95) 10.6 (9. 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.38) 10.77 (6.10 (5.3) 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 3.03) 6.59-8.41) 9. population results shown in this Report (Alimonti et al. Using clinically submitted specimens.53) 3.47 (4.97-4.95) 8.43 (4.83-6.85) 4.76-6.42 (4. (2000) found urinary cesium levels that were slightly lower than those reported for the U.30 (7.13) 7.35-11.12-6.68) 3.46 (7.91 (5.S.00-10.8) 5.33-8.81 (4.97) 8.34 (5.84-9.33 (5.48) 90th 7.0) Total 4.22) 6.82-4.

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

04-1.310 (.340-.64) 1.03) 1.520 (.26-2.330) .450) .450-.390 (.900) .740-.48) 1.350 (.24 (1.530) .380-.870-1.590-.930 (.610-.14) .470 (.650 (.890-1.285 (.316 (.380 (.08) . population from the National Health and Nutrition Examination Survey.359 (.05 (.410-.540-.900-1.355-.660) .590 (.259-.428-.370-.01 (.20 (1.900) .340) .980) .502) .700) .460-.410 (.393-.373) . Cobalt compounds are used as catalysts in producing oil and gas.03 (.460 (.890) 95th 1.900-1.12) 1.610 (.910-1. Among its many uses are manufacturing superalloys used in gas turbines in aircraft engines.410-.05) 1.400-.710 (.870 (.360-.820 (.16 (1.294 (.600) .650 (.570 (.424) .660-. hard metal (alloys of cobalt and tungsten carbide).580 (.26) Total .640) . 7440-48-4 General Information Cobalt is a magnetic element that occurs in nature either as a steel-gray.338-. Cobalt occurs naturally in airborne dust.800-.37-1.364-.620-.348-.960-1. It is also a component of porcelain enamel applied to steel bathroom fixtures.370-.386) . automobile airbags.581) .26-1.28-2.414) . 01-02.430) . seawater.690-.430-.45 (1.431) .740 (.390 (. and fertilizers.398) .435 (.410 (.450) .930) .03-1.13) 1.430 (.410) .810) .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 .405-. 0.520-. 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 (1.03 (.350-.Metals Cobalt CAS No.75 (1. The cobalt used in U.270-.394) .470) .540-.800) .06-1.950-1.373-.830-1.410 (.620-.820 (.02-1.08-1.450) .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 .850-1.630 (.336-.790-.280-.19) .600-. and in synthesizing polyester and other materials.375 (.530 (.44) 1.670 (.450-.16) 1.343 (.410 (.560 (.440-.12) 1.580 (.890-1.380 (.610) .950-1.770) .650-.334) .372) .320 (.670 (.42) 1.418 (.398 (.410-.26) 1.17 (1.490-.460) .32 (1.730) 1.17-1.370) . and 0.680) .810-.25-1.520-.750 (.291-.300-.690-.379 (.03) 1.416) .04-1.16 (.350-.790) .03) .367 (.710) .900) .850) .331-.09 (.33-1.22 (1.68 (1.417) .980-1.313) .04 (.452 (.670 (.850-1.640) .28 (1.310-.420 (.23-2.487) .419) Selected percentiles ( 95% confidence interval) 50th .14-1.04) 1.16 (1.39) 1.520) .360-.319) .327-.S.360-. steel-belted radial tires.499 (.59 (1.454 (.515 (.06 (.950) .32-2.17 (1.480-.99) 1.870 (.463-.370 (.620-.316-.570) .05 (.540) 1.01-2.465) .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 .340) .850) 1.760) .430 (.520-.820 (.700) . varnishes.370-.930-1.47) 1.550-.940-1.940 (.15 (1.06 (.520 (.950 (.430 (. shiny.07 (.420) .920-1.670-.300 (.404) .16) 1.07-1.50 (1. respectively. hard metal or in combination with other elements.810) .15-1.01-1.46 (1.301 (.840) .92) 1.330-.710) 1.950 (.660) .590-.33 (1.610) .26) 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.800-.390 (.16-1.305-. industry is imported or obtained by recycling scrap metal that contains cobalt.22) 1.760 (. and magnetic recording media.340 (.09 (.330 (.350-.640) .352 (.680 (.16-1. 208 Fourth National Report on Human Exposure to Environmental Chemicals .340-.73) 1.940-1.690 (. and inks.04-1.308-. and kitchenware.550 (.583) .680) .460) .620) .469-. interval) .540-.410 (.750 (.540-.28 (1.461 (.32) 1.388-. Usual human exposure is from food sources.270-.67) 1.520 (.339 (.490-.333-.570-.09) .32 (1.564) .270-.47 (1.369 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. It is emitted into the environment from burning coal and oil and car and truck exhaust.81) 1.590) . blue-colored pigments.53) 1.570) .47) 1.920) 1.410) . Medical uses include joint and dental prostheses and radioactive cobalt in cancer chemotherapy.390) .08.890-1.890) .580 (.350) 75th .750-.21) 1.431) .630 (.460) . large appliances.348-.430) .460 (.496) .81) 1.32) 1.434 (.379 (.17 (.740-.420) .28 (1.36) 1.50) 1.65) 1.520-.01 (. Cobalt compounds are also used in manufacturing battery electrodes.520 (.24 (. and soil.374 (.52 (1.427-. see Data Analysis section) for Survey years 99-00.519 (.333-.390-.543) .47 (1.377-.450) .670-.570-.60 (1.550) 90th . Cobalt is used as a drying agent in paints.07-1.371 (. and 03-04 are 0.860 (.290-. diamond-polishing wheels.480 (.680 (.510) 1.880 (.500 (.630-.523) .530-.56) 1.S.790 (.880-1.07.22-1.48) 1.520) .23) .07.500) .600 (.380 (.380-.750 (.399) .00) .480 (.

707) .738 (..372) .324-.16 (.368) .290 (.11-1.44 (.380-.251-.821 (.368) .06 (.753) 1.352 (. Cobalt constitutes 4% by weight of vitamin B-12 (cobalamin).306 (.12 (.667-1.290 (.323) .615) .990) .700 (.10-1. using hard metal cutting tools.272-.337) .409) . Cobalt is absorbed by oral and pulmonary routes. cobalt is excreted predominantly in the urine.481) 90th .449) .744) 1. respectively. interval) .513 (.327 (.850 (.309) .297-.833-1.500-.753-.33) .471-.391 (.900-1.29 (1.353 (.19) .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 .407) .455 (.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 .792-1.429) 1.278 (.382-. 1972).428-.632-.00) .487-.479-.396) .425-.872 (.513) .329 (.983) .361 (.54) 1.634-.296) . Recent inhalation exposure to soluble cobalt compounds can be monitored by measuring cobalt in urine or blood (Lison et al.733-1.303-.60) 1.277-.457 (.12-1.365-.388 (.638-1. Workplace standards and guidelines for external air exposure to cobalt and several of its compounds have been established by OSHA and ACGIH.647) .57) 1.582-.417) .294-.04-1. 1994). an essential human nutrient.975 (.280-.. 2003).606 (.560-.286) .239-.365) .306) 75th .369 (.689 (.851 (.452-.378-.35) .469-.609) .826-1.929) .03 (. with pulmonary clearance half-lives of from one to two years (Hedge et al. Elimination reflects a multi-compartmental model dominated by compartments with half-lives on the order of several hours to a week.361-.425) .327-.33) 1.667-1.291 (.952 (.593) .830 (.691 (.660-.937 (.304-.740-1.317 (.83) 1.296-.333 (.16 (.302-.895-1.669) .479) .547 (.257-.861 (.738 (.23 (1.426 (.529 (.964 (.Metals fabricated from cobalt alloys (Lhotka et al.400 (.00 (.475 (.630-.11-1. refining or processing alloys.361-.352) .543) .342-.673-.314 (.35) 1.523 (.274-.304) .15) 1.50) 1.585) ..500-.49) 1.850-1.548 (.932-1.00 (.598 (.829-1.387) .352 (.471 (.581) .333-.963-1.301-.16 (1.626-.343-.595) .278-.777-.824 (.562) .917) .842) .635 (.29 (1.895-1. but with a minor fraction (10-15 %) exhibiting a half-life of several years (Mosconi et al.963) .552 (.00) .313-.237-..331-.683-.513-. Smith et al.708) .562) .616-.736-.522) .273 (. or using diamond-polishing wheels that contain cobalt metal.343 (.829) .644 (.27) 1.381) .297) .353-.467-.861-1.495 (.04 (.561) .234 (.476-.737 (.438) .404-.388 (.378 (.433) .259 (.630-..03-1.36) 1.319-.983-1.55) .955) .333-.750-.392 (.15 (.313-. Human studies with 60Co administered as soluble cobalt chloride have reported oral absorption ranging from approximately 1 to 25 % (Smith et al. 1972).346 (.337 (.376 (.256-.550-.282-.407 (.960 (.533 (.608 (.537 (.394) .268 (.16) .27) 1.349) .393-.02 (.461) .785) .00-1. Once absorbed and distributed in the body.339-.591 (.243-.563-.355) .50) 1.488) .419) . in the feces.534 (.10 (.599) .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 .990-1.25 (.611) .313 (.396) .554 (.500 (.09) 1.700 (.756 (.703-. Lung retention of relatively insoluble cobalt compounds such as cobalt oxide may be prolonged.348) .00 (.298 (.471-.360) .257 (.728 (.363) .328 (.362) .289) .449-.60) 1.727 (.611) .435 (.457) . Urinary Cobalt (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.847) .408 (.462) .293 (.508-.554 (.574-.301) .248-.73) 1.316 (.792 (.963-1.378-. A portion of cobalt retained for long periods is concentrated in the liver.368 (.328) .386 (.781-1.329-.444 (.326-.774 (.402 (.S.344-.786-.468) .259-.259) .838 (.694) .281) .25 (.938-1.421) .781) 95th 1.29) 1.335 (.358 (.911-1.821-3.487-.393 (.955) .391) Selected percentiles ( 95% confidence interval) 50th .29) . 1994.282 (.757-1.313-.439) .848 (.723 (.750) .534-.247 (.362-.378-.976 (.728) .938) .250) .600-.334) .14 (.324) .898 (.362 (.361 (.29 (1.271 (.760-1.963) .515 (.503-.844 (.10) Total . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.279) . and to a lesser extent.28) 1.36) 1.313-.24) .640) .457-.275-.463-.417 (.662) .279 (.505) . A nutritional requirement for cobalt other than that contained within dietary cobalamin has not been established.857-1.310) .300) .384) .879-1.313-.30 (1.949) .328 (. population from the National Health and Nutrition Examination Survey.17) . 1979).333-.248-.704-.50 (1.905) .290 (.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 .215-.435-.10) .804) 1.275-.523 (. Exposure in the workplace may come from electroplating.594) .542 (.442-.00 (.434-.679-..

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

Arch Intern Med 1990. Cannon SR. Four-year study of cobalt and chromium blood levels in patients managed with two different metal-on-metal total hip replacements. Kraus T. Salvatori S. Metal-on-metal versus polyethylene in hip arthroplasty: a randomized clinical trial. Exposure assessment in the hard metal manufacturing industry with special regard to tungsten and its compounds.50(9):835-842. Leghissa P. McMinn DJ. Robinson C. Schramel P. Sci Total Environ 1997. Pradhan C. Sci Total Environ 1998.87(5):628-631. Science 1988.20(1):25-31. Clin Orthop Relat Res 2003. Fourth National Report on Human Exposure to Environmental Chemicals 211 . Buchet JP. Meier R. Diepgen TL. Health Phys 1979. Wild P. Barnaby CF. Absorption and retention of cobalt in man by whole-body counting. Moulin JJ. Alessandrelli M. 1985. Stanescu D. Industrial Chemical Exposure: Guidelines for Biological Monitoring. Hedge AG. Vitali MT. Lisi P.45:246-247.150.242:1412-1415. White MA. Cresti R. Dunstan E. Blunn G. Lison D.28(5):1121-1128.95:29-37. Edmonds CJ. Oksa P. Biological monitoring of cobalt exposure based on cobalt concentrations in blood and urine.157:117121. J Rheumatol 2001. Sabbioni E.36:732-734. Kristiansen J.88(4):443448. Zhuber K. Unwin P. Occupational asthma from cobalt sensitivity in workers exposed to hard metal dust. Swennen B. Sabbioni E. Rorabeck CH. Goto S. Chess DG.204:147-160. HoffmannB. Falcone G. Palmroos P. Kusaka Y. Gross RT. Sci Total Environ 1994. Int Arch Occup Environ Health 1997. Ghat IS. a study of 13 elements in blood and urine of a United Kingdom population. Tilley S. Sabbioni E. et al. Respiratory health of cobalt production workers. Lauwerys R. Sci Total Environ 1994. Hoet P. Molders J. Radulescu M. Heki S. Iversen BS. Buchet JP. Smith T. Weber A. 3rd ed.21(2):189-195. Schaller KH. J Orthop Res 2003. J Occup Med 1992. Goto S. McCalden RW. Hoher T. cobalt salts. Lison D. Bozec C. Linnainmaa M.58(10):631-634. Epidemiological survey of workers exposed to cobalt oxides. Occupationallyinduced “isolated cobalt sensitization. J Bone Joint Surg Br 2006. Mutat Res 2003. Laippala P. salt. Zedda S. oxides. Angerer J.150(1-3):167-171. Boca Raton (FL): Lewis Publishers. Meyer zum Buschenfelde K-H. Hypothyroidism and thyroid hyperplasia in patients treated with cobalt JAMA 1955. Roto P. Contact Dermatitis 2003. The release of metals from metal-onmetal surface arthroplasty of the hip. A report of two cases from mineral assay laboratories and a review of the literature. The effect of the diameter of metal-on-metal bearings on systemic exposure to cobalt and chromium.55(4):269-276.216:253-270. Urinary cobalt as a measure of exposure in the wet sharpening of hard metal and satellite blades.148:241-248.Metals effects of cobalt. Uitti J. Ichikawa Y. Shirakawa T. et al. Kiilunen M. Romazini S. Thomassen H. Cobalt-specific T lymphocytes in synovial tissue after an allergic reaction to cobalt alloy joint prosthesis. Lasfargues G. Weyher I. Int Arch Occup Environ Health. Am J Ind Med 2003. and hard metal dust. Cobalt cardiomyopathy.22:359367. Toxic trace element reference levels in blood and urine: influence of gender and lifestyle factors. Bunn HF. Ziaee H. Health Phys 1972.69(3):193-200. Regulation of the erythropoietin gene: evidence that the oxygen sensor is a heme protein.406:282-296. Iavicoli I. Metal ion levels after metal-on-metal proximal femoral replacements: a 30-year follow-up. Long-term clearance of inhaled 60Co. Lhotka C. Lison D. Dunning SP. et al. Br J Ind Med 1993. et al. Goldberg MA. Bourne RB. Sanghrajka AP. Zobelein P. Mosconi G. et al. Daniel J. Swennen B. et al. Christensen JM. Linna A. Thakker DM.34:620-626. Peltier A. Kirsch-Volders M. Dickel H. 2001. Occup Environ Med 1994. Kato M. Fujimura N.533:135-152. Jarvis JQ. Cleland D. J Bone Joint Surg Br 2005.44:124-132. X. Cobalt excretion in urine: results of a study on workers producing diamond grinding tools and on a control group. Outcome of occupational asthma due to cobalt hypersensitivity. Lauwerys RB. DeSantis V. Hammon E. Steffan I. Cobalt and antimony: genotoxicity and carcinogenicity.(1-3):133-139. Lung cancer risk in hard-metal workers. Zweymuller K. Salama A. Kuska Y.51(7):447450.48:172-173. Schank M. and cobalt metals.” Contact Dermatitis 2001. Trace element reference values in tissues from inhabitants of the European Union.150:177-183. De Boeck M. Kriss JP. Occup Environ Med 2001. Szekeres T. Biological monitoring of workers exposed to cobalt metal. Chest 1989. Bacis M. Carnes WH. Thabe H. Am J Epidemiol 1998. MacDonald SJ. J Trace Elem Med Biol 2006. Lauwerys R. Pisati G. Co-sensitivity between cobalt and other transition metals.

leaded glass.60 (3.50 (2.90 (3.90) 2.20 (3.86) 1.50) 2.69) 1.50) 2.00-5.00) 3.02) 1.10-2.00 (5.40 (2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.00 (2.66 (1. such as lead phosphate and tetraethyl lead.90-4.70-1.20 (3.37-1.90-3.43-1.40 (1.10) 3.10 (1.62 (1. Lead was used in plumbing for centuries and may still be present.90 (4.899-.70 (2.90) 2.10) 1.40 (1.80 (1.70 (1.20 (3.10-6.37 (1.20) 5.60 (2.90) 2.946 (.10 (3.20 (2.30) 1.70) 4.53) 1.942 (.66) 1.71-1.10) 4.30-1.55 (1.60) 3.77 (1.40-1.00) 2.60-2.30 (2.10-1.90-2. ceramic glazes.30 (2.80-3.10-2.60) 1.60 (4.800-1.75-1.900-1.50 (4.80) 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 1.60-4.50) 7.52-1.50) 4.25 (1.60 (3.30) 2742 2268 2085 1842 2219 2293 2716 3806 3478 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.10-4.14-1.90) 1.70 (1.80 (1.14-1.60) 1.10-2.20) 1.45 (1.40-5.10-3.40-3.90 (3.00) 5.50) 1.60 (2.00) 2.50 (1.20) 90th 3.50 (1.50-2.90) 3.10-1.90 (3. and 0.50) 1. respectively.01 (1. interval) 1.30-1.00-6.00-4.80) 1.60-2.60) 4.30 (3.20 (1.70) 4.60) 4.50-4.40) 3. Lead has a variety of uses in manufacturing: storage batteries.50-1.19 (1.30-1. ammunition.60-6.60-1.10-2.50 (2.55-1.30 (2.80 (1.50) 4.40-1.90 (2.30 (1.80) 1.80) 2.80 (1.30-1.60 (1.70) 1.50 (2.30 (2.20-1.60 (3.60) 4.40) 1.91) 1.50 (1.43 (1.46 (1.40 (1.900 (.60-1.20-3.90 (1.80 (4.36-1.70 (5.60) 5.80) 2.80-4.00) 1.65 (1.60-1.80-2.S.40-4.40) 2.80 (1.20) 4.48) 1.30) 95th 5.20-2.83 (1. solders.90 (3. population was aerosolized lead emitted from combustion engines that used leaded gasoline.20) 2.90-2.70-2.70 (3.10) 5.10-8.3.20-3.10 (1.50-2.43 (1.95) 1.50 (3.20) 3.50) 1.60 (1.00 (1.90) 5.50) 5.70-6.40-2. Before the 1980’s.90-2.20 (2.00) 2.60) 3.10-3.10 (2.00) 4.40) 2.80-3.60) 2. blue-gray metal that occurs naturally in soils and rocks.3.30-2.00) 1.00) 1.Metals Lead CAS No.55-1.50-1.60 (1.50-4.75) 1.62) 1.20 (4. 7439-92-1 General Information Elemental lead is a soft.40 (3.60) 3.72) Selected percentiles ( 95% confidence interval) 50th 1.70) 3.90-6.90 (1.81) 1.40-3.62-1.30-2.60) 2. lead was added to gasoline and residential paints and used in soldering the seams of food cans.80-3.80) 1.10 (2.40) 5.60) 1.10) 3. see Data Analysis section) for Survey years 99-00.70) 4.10 (1.87 (1.70 (3.30) 2. bronze). 212 Fourth National Report on Human Exposure to Environmental Chemicals .70-2.43) 1.00-1.32-1.80) 2.30) 2.30-6.40-1.00) 1.60 (1.60 (2.20) 4.52-1.20) 3.50-5.28. plastics.80 (5.40) 1.70-1.50-3.14-1.10) 2.30 (4.20) .60-3.900 (.37 (1.70-3.20 (3.80-4.20 (3.10-3.60) 1.93-2.30 (4.80) 3.90 (2.30-1. and for radiation shielding.70-4.00-1.60 (2.04-1.30) 5.70) 1.09) 1.30 (1.70 (2. the main source of lead exposure for the general U.30 (4.986) .50 (4.50-6.90) 1.68-1.70) 3.80 (4.40-2.80 (1.00) 6.69) 1.40 (4. Lead is most often mined from ores or recycled from scrap metal or batteries.75-2.40) Total 1.50 (3.90) 2.22 (1.10) 3.20 (1.56 (1.60) 2.80 (2.12-1.80-5.00 (3.69 (1. 01-02.78 (1.30 (1.20-3.30-5.878-1.50-1.70-5.50 (1. Elemental lead can be combined with other elements to form inorganic and organic compounds. adult lead exposures tend to be limited to Blood Lead Geometric mean and selected percentiles of blood concentrations (in µg/dL) for the U. malleable.40) 4. metal alloys (e.10) 2.39-1.00 (4.40-1.20-6.50) 75th 2.50 (2. In the past.60 (2.40-3. Aerosolized lead is either inhaled or ingested after it is deposited on surfaces and food crops.40 (2.80-3.60 (1.30 (2.60 (1.00) 1.40-6.00 (6.60 (2.20 (1.36-1.S.90-4.70) 1.25) 1.50-3.90-2.40) 2.60-1.60) 5.87) 1.60 (1.00) 2.17) .00-4. population from the National Health and Nutrition Examination Survey.00 (1. antique-molded or cast ornaments.20) 3.60) 4.90 (3.20) 3.30 (2. 0.20 (1.70 (2.50-1.50 (2.20-4.10-4.80) 2.20-2.40-2.90) 2.30) 2.10 (4.70) 1.10) 1.70 (1.00 (4.50) 3.80 (2.60-4.80) 1.36) 1.34-1.30-1.20-1.40-1.20 (3.00-2.51) 1.80 (2.31) 1.30-2.00) 4.50) 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 2.60) 1.40) 1.00) .70) 2.40) 2. brass. Since lead has been eliminated from gasoline. and 03-04 are 0.g.20 (3.96-2.50-1.52 (1.20-3.40 (5.40-1.70) 1.70-2.60) 3.90-4.50-5.50-2.30-2.90-4. dense.49-1.40-6.60) 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 2.43) 1.60) 2.00-4.90) 3.70-1.80 (5.90) 1.30 (1.30-4.50) 1.70) 3.70) 4.10-2.89) 1.45-1.00) 3.69 (1.10-1.23 (1.10 (2.80 (3.32-1.80) 1.51 (1.30 (2.10-6.40 (1.60) 2.60 (3.10-2.39) 1.10) 1.70 (1.80-4.75 (1.25 (1.50-2.10-3.50) 5.20 (1.

80) 2.51) 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.41) 2.960-1.20) 1.20 (1.72) 1.749) .70-3.80-2.600 (.540-.986) .840 (. and contact with soil.78-2.940 (. dust.00) 2.700 (.10) 1.535-.91) 2.50) 2.60 (1.480-.50 (2.80) 2.920 (.700 (. the primary source of exposure in children is from deteriorated lead-based paint and the resulting dust and soil contamination (Manton et al.20) .14 (1.700-.90 (2.800 (.03 (1.80) 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 .808 (.40 (1.40-1.80) 2.595-.80) 1.990) 2.800) .82 (1.27) 1.1.07 (.00 (1.800) .70) 3.40-1.30) 1. respectively.558 (.810-1.20 (1.640-.931) .40 (1.20 (1.20) 1. absorbed lead is bound to erythrocytes and then is distributed initially to multiple soft tissues and eventually into bone.752 (. bullet fragments retained in human tissue.00) 1.941) .04) .630 (.07-1.591 (.729-.70 (2. Less common sources of incidental or unique lead exposure are numerous: lead-glazed ceramic pottery.90) 2.29) 2.790 (.18-1.35 (.20) 1.60-1.10-5.60) 2.642 (.80 (1.11) 2.828) Selected percentiles ( 95% confidence interval) 50th .40) 2.757-.50) 1. population from the National Health and Nutrition Examination Survey.990) 1.30) .800-.80 (1.604 (. interval) .24-1.00 (1. older plumbing systems with leaded pipes or lead soldered connections.21 (2.50-2.970-1.795 (.680-.1.49 (1.62) Total .613) .00 (.731 (.00-2.960-1.90 (1.86-2.540 (.40 (1.78-2.90-3.70) 1.820-1.10 (1. Approximately half of the absorbed lead may be incorporated into bone.60 (1.641-.20 (2.580-.00) .691-.40-5.600-.14 (1.30-1.650) 1.900 (.862) .30-1.20-1.935) 1.12) 90th 2.78-2.70 (2.610 (.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 1.661-.785) .605) .09) 1.900-1.90 (2.90-2.848 (.30) 2.620 (.20 (1.90) 1.700) 1.66 (2.62-4. battery and radiator manufacturing) and recreational sources.40 (1.773) .636 (.00) .10 (1.90-4.766 (.677 (.50) 1.700 (.31-3.600) .701) .833-1.30 (1.20-2.10-3.90) 2.50 (2.800 (.60-2.30-1.637-.90-2.506-.70 (1.97) 4.800-.960 (.30) 1. 01-02.800-1.570-.23-4.910-.50) 2.800) .20 (2.680-.600-.60-2.628) 1.700) .20-2.86 (1.560-.50 (1.589-.60 (2.40 (2.20) .10 (1.14-1.04 (.40-3.700-1.600-.40) 1. Absorption of ingested lead can be as much as five times greater in children than adults and even greater when intakes of dietary minerals are deficient.31 (1.660) .700 (.10-3.20) .59) 1.22) 1.40) 1. However.700 (.70) 2.82 (2.00) .20-1.850 (.30 (2.815 (.90-2.900) .13) ..923 (.33-2.659 (.00-2. and 03-04 are 0.19 (1.710-1.29 (2. lead-contaminated dust in indoor firing ranges.66 (2. Fourth National Report on Human Exposure to Environmental Chemicals 213 .640 (.20) .590 (.718) .g.23) .700-.800 (. 2000).40) 2. stained glass framing.80-2.04 (. imported children’s trinkets and toys. 1991).40 (2.10) .04) 2.40-2.40 (1.75) 4.10-1.90-2.30) 1.20 (2.04-2.40) 1.86) 95th 2.10 (.80) 2.900-1. 0.70) 1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.30 (3.700-. which is the site of approximately Urinary Lead Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.10 (. Small amounts of environmental lead also may result from burning fossil fuels (ATSDR.40-1.10-1.30) 1.33.500-.20 (1.579-.680) .700 (. In the blood.80) 3.02 (.40) 2. see Data Analysis section) for Survey years 99-00. lead-containing folk remedies and cosmetics.625 (.02) 1.89) 2.90) 2.700-.900) .40) 3.32 (1.800-1.50) 3. and 0.900 (.710-.30-3.10) .600 (.10-1.20-1.572-. Lead is absorbed into the body after fine lead particulates or fumes are inhaled.00 (1.40) 1.90 (1.579-.40-1.20 (1.00-1.59-2.688 (.70-2.90 (1.651) .708-.833 (.00) .90 (2.620) 1.90-3.600-.564 (. CDC.03-2.10 (1.10-1.900) .690) 75th 1.60 (1.40) 1.680) Sample size 2465 2690 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.73 (1.80) 1. lead-based painted surfaces undergoing renovation or demolition.52-1.674) 1.10) 2.00-2.33 (2.625-.857) .553-.700-.526-.64) 2.60 (1.671-.800) .745-.30-5.600-.30) 2.S.10) 2.900) .11 (1.573 (.00-1.900 (.50 (2. or after soluble lead compounds are ingested.800) .616) .30) 2. 2007.818) .10 (.52-1.600) .50) 1.40 (2.800 (.52 (1. Children may also be exposed to lead brought into the home on the work clothes of adults whose work involves lead.80 (2.900) .27 (1.86) 1.80) 3.80) 1.10-1.50 (1.50-1.920 (.50-3..40 (2.44-2.00 (2.30-2.17 (1.556-.10-3.60-3.695 (.13-3.822-1.80-3.06) .Metals occupational (e.00 (1. pewter utensils and drinking vessels.50-2.900-1.70 (2.60-3.30-1.70) 1.900-1. or water contaminated by mining or smelting operations.70 (2.900) .915-1.00-1.00) 2.50-2.40) 2.730 (.75) 3.738) .30) 1.70) 3.20 (3.753 (.955-1.

72-2.38 (2.18) 2.22-2.731-.569 (.18 (1.07 (.38 (2.404 (.742) Selected percentiles ( 95% confidence interval) 50th .87) 1. with a half-life of years to decades.44 (1.594-. Approximately 70% of lead excretion occurs via the urine.61) 3.725) .492-.404 (.17 (.541-. Large amounts of lead in the body can cause anemia.25-1.700-.36-2.551-.608-. The skeleton acts as a storage depot.609 (.28) 2.08) .898) .571-.698) . For instance.851) .681-.51) 1.887 (. 1995). 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.09-1.03) 2.20-3.83 (2.535) .971 (. hair.622 (.841-1.23 (1.33-1.18) .644) .09-1.790) .04) 2.73) 2.667-.658 (.98-2.828) .56-3.Metals 90% of the body lead burden in most adults.52 (1.618 (.621 (.914 (.01 (.86 (1.632 (.37-1.02) 1. 2004.529-.11-1.43 (1.739) .82) 1.862-.03 (1.662) Sample size 2465 2689 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1. kidney injury.645-.612-.03 (.606-.652 (.06 (.893) .755 (.47 (2.75 (2.702) . scant amounts are lost through sweat.89-2.78 (2.12-1.28-1.24 (1.774 (.11 (.432 (.763) .85 (1.62-2.62) 2.S.933) .05-1.78-4.41) .781-1.33) 1.15) 1.04-3.03 (.71 (1.682) .375 (. and paralysis.33) 2. 1995.588-. Lead is cleared from the blood and soft tissues with a half-life of 1 to 2 months and more slowly from the skeleton.01) .926 (.722 (.645-.667-.89-5.63) 1.03) 90th 1.0) 3.753) .51 (1. Equilibrated blood lead levels (BLLs) after chronic intake are associated with certain toxic effects.408-.19-5.63) 4.667) .97-18.07) .18) 1.870 (. abdominal pain.66 (1.97) 1. BLLs near 10 µg/dL can affect blood pressure in adults and neurodevelopment in children (Bellinger.720 (.85-2.428) .15-3.603-.681-.05-1.838) . 1996).587-. and through binding to ion channels and regulatory proteins. 1993).615 (.990 (.709 (.03-2.85-2.11 (.693 (.649 (. Additional mechanisms include generating reactive oxygen species and altering gene expression (ATSDR.68 (1.696 (.37-1.06) .461) .44) 1.64) 2.20) .31) 1.436) .44 (1.15) 1.12) 340 368 290 719 762 725 1406 1559 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .997-1. O’Flaherty.18) 1.718) 1.746) .50 (1.41-1.655) 75th 1.00 (1.64-2.98 (1.654) .09) 1. Lead can cross the placenta and enter the developing fetal brain.55 (1.62-1. and iron.50-1.957-1.03) .11) .677) .655-.900 (.765) .14 (1.79 (1.00 (1.641 (.10) 1.810 (.94-2. 2003.22) 1.496 (.853-1.22-1.594-.79) 2.00 (1.981-1.800-. Staessen et al.66 (1.29 (1. encephalopathy.400) .03) 1.615 (. Schwartz.469 (.88) 1.38 (2.963-1.659-.988 (.657) 1.938-1.22) 1.648 (.758) .586-.604-.75-2.946-1.617-.33 (1.688) .703) .00) .635 (..11 (1.975-1.40-1. interval) .812-1.14) 1. with lesser amounts eliminated via the feces. The toxic effects of lead result from its interference with the physiologic actions of calcium.638 (.977) 1.72-2.639 (.712 (. through the inhibition of certain enzymes.07-1.601-.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 .97 (1.43 (2.06) 1.559-.796-1.725) .61) 1.03) 2.623 (.28) .08) .742) .52) 1. In 1991.603-.02-1.34-1.676) .710) .677-.708 (.65 (1.655) .53-1.561-.579-.988-1.920-1.940 (.88-2.404-.342-.679-.96 (1.43-1.06 (1.793-1.707 (.00 (.671 (.510-.56) 3.603 (.47 (1.15-2.92) 2.625 (.639) .979 (.701) .718) . CDC.31 (1.11) 1. seizures.50) 1.03 (. based on prospective population studies.72) . population from the National Health and Nutrition Examination Survey.77) 2.85) 1.69 (1.720 (.27 (1.673) .639 (.03) 1.83) 1.20) .39-1.10) 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 .992-1.605-.64) 95th 2.11 (1.79) 1.08-2.56 (1.31 (2.88 (1.49 (1.383-. 1993.670) 1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. BLLs and associated toxic effects differ in children and adults.876-1.97) 1.26) 2.722 (.914 (.53) 1.98) 2.730) 1.61) 1.62-3.66) 2.679) 1.17-1.50-2.962 (.644 (.61) 1.15-2. and approximately 40 to 70% of lead in blood comes from the skeleton in environmentally exposed adults (Smith et al.933-1.571-.65-2.55 (1.508) .686) .702-.734) .03) .31) 1.09-1. Nash et al.721 (.43) 2.588-.94 (1. 1991.917-1.918 (.88) 2.74 (1. zinc.70 (1.10 (1.46 (1. and nails (Leggett.05 (.593 (.59-3.938 (.43) 1.882-1.668-.31 (1.35) 2.. 2007).47) 1.460-.380-.702) .67-4.623 (.05 (1.71-2.592-.61) 1.58) 1.46 (2.608 (.50-2.19) 1.56-2.698) .73-2.64 (1.26) Total .50-2.25-1.45 (1.48 (1.583-..607-.633 (.88) 2.918-1.22) .828-1.992-1.701 (.914-1.639 (.677 (.10 (.41 (1.683-.

6%) were lower than those from NHANES 1991-1994. 1995. usually with BLLs greater than 40 mg/dL.g.. adults in the 19992000 NHANES sample (Apostoli et al. and organic lead compounds not classifiable with respect to human carcinogenicity. 2003. the geometric mean BLL was 3. 2009). 2005b.S. Telisman et al... Low level environmental lead exposure may be associated with small decrements in renal function (Kim et al. 1991.. subtle or nonspecific neurocognitive effects have been reported at BLLs as low as 20-30 µg/dL (Mantere et al. urban residence. 2002. 1996. 2005a).000 adults. 2005b).S..S. 2003). More recently. Payton et al.. Data submitted through state public health programs from 2006 showed that 1.... approximately 11. Surveillance data reported by U. and spontaneous abortion (Baghurst et al..7 µg/dL and 4. higher than 100-200 µg/dL). including minority race or ethnicity. the prevalence rate has declined annually since 1994 (CDC. Information about external exposure (i. Fourth National Report on Human Exposure to Environmental Chemicals 215 .5 per 100. Muntner et al. Overall. NTP considers lead and its compounds reasonably anticipated to be human carcinogens. when the geometric mean BLL was 2.75 µg/dL in U. A decrease in BLLs is evident also in adult NHANES results reported over past decades (CDC..html... Korrick et al. 1995) and associations between increased bone lead concentrations and blood pressure (Hu et al. adult population has similar or slightly lower BLLs than adults in other developed nations (CDC.. though there is greater individual variation in urine lead than in blood and greater potential for contamination. 2003.. Staessen et al.. Borja-Aburto et al. Both drinking water and ambient air standards for lead have been established by the U.atsdr. and peripheral neuropathy generally occurring at much higher levels (e. 1984. 2000).cdc. environmental levels) and health effects is available from ATSDR at: http://www. In NHANES 1999-2002 in children 1-5 years old. 1996.Metals µg/dL or higher as the level of concern in children. respectively. Schwartz et al. Many animal studies have established the multiple neurotoxic effects of lead (ATSDR. Urine levels may reflect recently absorbed lead. Jones et al. almost double the geometric mean of 1. 1999). Biomonitoring Information Blood lead measurement is the preferred method of evaluating lead exposure and its human health effects.S. However.gov/nceh/lead/surv/database/State_ Confirmed_byYear_1997_to_2006. residing in housing built before the 1950’s. premature delivery.0 µg/dL in females (Soldin et al. Bellinger 2005.3 million children tested had BLLs of 10 mg/dL or higher (http://www.. which is an 84% decline. 1998). Schwartz. 1987. the national prevalence rate for adults with BLLs 25 mg/dL or higher was 7. 2002a). 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. seizures.07 µg/dL (Becker et al. 2002). Recent studies have suggested that neurodevelopmental effects may occur at BLLs lower than 10 µg/dL (Canfield et al. 2000).4% in NHANES 1999-2004. 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. 1996. The U. EPA. lead in women may be associated with hypertension during pregnancy.xls). 2006).gov/toxpro2. adult residents. 2001).. Jones et al (2009) showed that the prevalence of BLLs of 10 µg/dL or greater decreased from 8.. BLLs greater than 10 µg/dL continue to be more prevalent among children with known risk factors.. 2003. Workplace standards and guidelines for lead exposure and monitoring have been established by OSHA and ACGIH. A general population survey of adults in Italy tested in 2000 found BLLs slightly more than double those reported for U. reduce sperm count. In occupationally exposed adults.4% of children had BLLs of 10µg/dL or higher (CDC. 2006). both the geometric mean (1.. may alter sperm morphology.9 µg/dL) and percentage of children with BLLs greater than 10 µg/dL (1. 1994).S. IARC considers inorganic lead compounds probable human carcinogens. A general population survey of adults Germany in 1998 reported a geometric mean blood lead concentration of 3. particularly in the skeleton. and decrease fertility (Alexander et al.cdc. 2007).S. Lanphear et al.2 µg/dL in males and 3. 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. For example. with overt encephalopathy. 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. CDC. BLLs reflect both recent intake and equilibration with stored lead in other tissues. adults in the 1999-2000 NHANES sample.. Temporal declines in children’s BLLs have been found in other developed countries (Wilhelm et al.e. 1999).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. At low environmental exposures.21% of approximately 3.6% in NHANES 1988-1991 to 1. Pirkle et al.. and low family income (CDC.

JAMA 1996. 4/14/09 Centers for Disease Control and Prevention (CDC). et al. Acquisition and retention of lead by young children. Environ Health Perspect 1993. Schulz C. 1988-2004. McMichael AJ. Lepom P. Korrick S. Available at URL: http://www.348:15171526. et al.htm.205:297-308. Pediatrics 2009. Public Health Rep 2000. A longitudinal study of low-level lead exposure and impairment of renal function: the Normative Aging Study. 2005.gov/nceh/lead/publications/ books/plpyc/contents. Cox C. doi:10. et al. Blood lead reference values: the results of an Italian polycentric study.275(15):1171-1176. Pirkle JL. Cory-Slechta DA. Rojas LM. Muntner P. Seiwert M. Farias P.cdc. Semen quality of men employed at a lead smelter. Kaufman JD. Jones RL. The Port Pirie cohort study: lead effects on pregnancy outcome and early childhood development. Coresh J. Atlanta. Apostoli P. Batuman V.gov/nceh/lead/ CaseManagement/caseManage_main. Becker K. gov/mmwr/preview/mmwrhtml/mm5420a5. Homa DM.53:411-416. Ewers TG. Auinger P. 4/14/09 Centers for Disease Control and Prevention (CDC). Luukkonen R. et al. 2002 [online]. Available at URL: http://www. Korrick SA. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans.gov/mmwr/preview/mmwrhtml/ mm5532a2.cdc. MMWR Morb Mortal Wkly Rep 2005a.atsdr. Bavazzano P. Lead. Hernberg S. Scand J Work Environ Health 1984. Ronchi L. Lanphear BP. Ga. Jacobson JL. Available at URL: http://www.82:60-80.htm. IARC Monogr Eval Carcinog Risks Hum 2006. N Engl J Med 2003. Krause C. Hertz-Picciotto I. Toxicological profile for lead. Aro A. Borja-Aburto VH. Rios C. Available from URL: http://www. Rotnitzky A. Henderson CR. Leggett RW. Bellinger D. Chiodo LM. Sparrow D. Am J Public Health 1999.htm. Brody DJ. 1991 [online]. Hunter DJ. A prospective follow-up study on psychological effects in workers exposed to low levels of lead.101(7):598-616.73:409-420. Baghurst PA. Canfield RL. Trends in blood lead levels and blood lead testing among US children aged 1 to 5 yeas. Blood lead levels—United States. Neurodevelopmental effects of postnatal lead exposure at very low levels. Intellectual impairment in children with blood lead concentrations below 10 µg/dL. Jusko TA.8(3):395-401.cdc. Pediatrics 2004. 1999-2002. Roberts RR. Wigg NR. Checkoway H. Kim R. Neurotoxicol Teratol 2004. Environ Res 2000. Teratogen update: lead and pregnancy. Int J Hyg Environ Health 2002. Manton WI. Dietrich K. Cognitive deficits with blood lead concentrations < 10 µg/dL in US children and adolescents.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. Meyer PA. Angle CR. CDC.55(32):876-879.275:1177-1181. Neri A.1542/peds:2007-3608. van Netten C.htm. References Agency for Toxic Substances and Disease Registry (ATSDR). Cox C. Birth Defects Research (Part A). Adult blood lead epidemiology and surveillance—United States. Third National Report on Human Exposure to Environmental Chemicals. Weiss ST. MMWR Morb Mortal Wkly Rep 2006. Vupputyuri S.cdc. Blood lead levels measured prospectively and risk of spontaneous abortion.gov/toxprofiles/tp13. Am J Epidemiol 1999. Kaus S. Baj A. Managing Elevated Blood Lead Levels Among Young Children. Muller CH. 2005b.cdc. Blanco J. Vimpani FB. Blood lead and chronic kidney disease in the general United States population: 216 Fourth National Report on Human Exposure to Environmental Chemicals . Occup Environ Med 1996.html.123:e376-e385. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Aug 2007 [online]. Stanek KL.287:1-11. Reese YR. Wager C.26:359-371. Atlanta (GA).87:1-471. et al. Hu H. Bellinger D. Available at URL: http://www. Ganzi A. 2003-2004. 4/14/09 Centers for Disease Control and Prevention (CDC). Speizer FE. Age-specific kinetic model of lead metal in humans. Rotnitzky A. Sparrow D. Hu H. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. 4/14/09 Alexander BH. Caldwell KL.115:521-529. Robertson EF. Weiss ST.113(4):1016-1022. Payton M. Lanphear BP. 4/14/09 Centers for Disease Control and Prevention (CDC).150(6):590-597. Recommendations from the Advisory Committee on Childhood Lead Poisoning Prevention. Hu H. Neurotoxicol 1987. Hänninen H. The relationship of bone and blood lead to hypertension. Atlanta (GA).10:43-50.54(20):513-516. Mantere P. JAMA 1996. Inorganic and Organic Lead Compounds. Sci Total Environ 2002. Jacobson SW. Lead and hypertension in a sample of middle-aged women. Centers for Disease Control and Prevention (CDC). Preventing Lead Poisoning in Young Children. Kuehnemann TJ.89:330-335.

Weiss ST.327:109-113.118:16-29. Use of endogenous. Schulz D. and copper in men. Int J Hyg Environ Health 2006. Revised and new reference values for arsenic.63:1044-1050. Blood lead concentrations in children: new ranges. Lee SS. Lee GS. Arch Environ Health 1995.9:303-327. Semen quality and reproductive endocrine function in relation to biomarkers of lead. J Hum Hypertens 1995. Fourth National Report on Human Exposure to Environmental Chemicals 217 . stable lead isotopes to determine release of lead from the skeleton. et al. blood pressure. Payton M.S. 50:31-37. cadmium. Kidney Int 2003. Osterloh JD. Pirkle JL. cadmium. Blood lead. Hickman T. Kaufmann R. Rubin R. Toxicol Appl Pharmacol 1993. Roels H. Schwartz BS. Lee BK. Schwenk M. Soldin SJ. Pizent A. Rocic B. Physiologically based models for bone-seeking elements. Hanak B. Low-level lead exposure and renal function in the Normative Aging Study. Hwang KY.209:301305.104(1):60-66.140:821-829. and tibia lead with neurobehavioral test scores in South Korean lead workers. Clin Chim Acta 2003. dimercaptosuccinic acidchelatable lead. Telisman S. and hypertension in perimenopausal and postmenopausal women. Lauwerys RR. Low-level lead exposure and blood pressure. blood pressure and cardiovascular disease in men. Smith DR. O’Flaherty EJ. Lustberg M. population to lead: 1991-1994. zinc. Jurasovic J. Sherwin R. et al.289(12):1523-1531. Hu H.106:745-750. Gunter EW. Schwartz J.153(5):453464. Cvitkovic P. Brody DJ. Kinetics of lead disposition in humans. Staessen JA. Kaufmann RB. Amery A.Metals results from NHANES III. Gavella M. and mercury in blood or urine of children: basis for validation of human biomonitoring data in environmental medicine. lead. JAMA 2003. Stewar WF. IV. Am J Epidemiol 2001.108(1):45-53. Paschal DC. Soldin OP. Wilhelm M. Am J Epidemiol 1994. Environ Health Perspect 1996. Association of blood lead. Lead. Flegal AR. Nash D. Magder L. Environ Health Perspect 2000. Sparrow D. Environ Health Perspect 1998. Exposure of the U.

2002). solid-waste incineration.700-.00) 1. mercuric chloride).900) 1.500) . and dental amalgam.500-. have often required public health intervention (Zeitz et al.80) 4. 1998. 2007). Elemental mercury is a shiny.50) 2. and mining and smelting.00-1.60 (1.30) 4132 4241 03-04 03-04 03-04 ..20-4.800-1. In addition. which can bioaccumulate in aquatic and terrestrial food chains.700-.S.00) 1.20 (2.20-4. Also. thermometers. to form inorganic mercury compounds or salts. 1993).700-.S.40) 3.40-2. After elemental mercury is absorbed.30 (1. IARC.40) 1. 1999 .40 (3.700 (. Elemental mercury is used to produce chlorine gas and caustic soda for industrial applications.40 (4. Poorly absorbed from the gastrointestinal tract. and mercury compounds are still used as preservatives (e.50) Total Age group 1-5 years 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites Sample size 8373 03-04 03-04 03-04 03-04 . 7439-97-6 General Information Mercury is a naturally occurring metal that has elemental (metallic). Atmospheric elemental mercury can be deposited on land and water.484) . Some cosmetic skin creams from countries other than the U.60) 1.20) 2. Inhalation of elemental mercury volatilized from dental amalgam is a major source of mercury exposure in the general population (Halbach.70) 911 856 2081 4525 03-04 03-04 .40 (3.90 (1.60-6.30) 1.00 (.490 (..400-.30-5.60 (2.10-3.419 (.800-1.90 (4.400-. and is distributed to most tissues.50) 4.886) .655-.00 (2.418-. The kinetics of the different forms of mercury vary considerably.700-. thermostats and switches).800 (. population from the National Health and Nutrition Examination Survey.800-1..00-5.60) 1. Accidental spills of elemental mercury.472-. water can be contaminated by the direct release of elemental and inorganic mercury from industrial discharges.40 (4. Elemental mercury is released into the air from the combustion of fossil fuels (primarily coal).90) 90th 3.70-2. 1980.30) 3.500 (.30) 1.30) 3.00 (2.40-2.40-1.877 (.563 (. may contain inorganic mercury.g. phenylmercuric acetate) or topical antiseptics (e.70 (4. electrical lamps.90) 3.714-.326 (..776 (.g.900) .300 (.30 (2.2.00 (1.900 (.30-6.700-.00 (. or oxygen.40-3.300-. Survey years 03-04 Geometric mean (95% conf. sulfur.689-.02) .60-6.800 (.500 (.12) .979 (.60-2. interval) . Woods et al.700) .70 (3. an organic form of mercury.90 (1.60-5.285-.90) 95th 4.60-3. and organic forms.900) 75th 1.60 (1.860-1.00) 3.80 (1..g.80 (1. elemental mercury is used in rituals practiced in some Latin American and Caribbean communities.753-1.00 (2.70 (1. Imported folk and alternative medicines occasionally are contaminated with inorganic mercury. it is oxidized in Total Blood Mercury—2003-2004 Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U.700) .797 (.672) .80) 3.814 (. Inorganic mercury exists in two oxidative states (mercurous and mercuric) that combine with other elements. see Data Analysis section) for Survey year 03-04 is 0. Metabolism of mercury by microorganisms in aquatic sediments creates methyl mercury. elemental mercury is absorbed mainly by inhaling volatilized vapor. such as chlorine (e.70 (1. 1994.00 (. thimerosal.00) 4.30-2. The ingestion of methyl mercury.500-. Apart from methyl mercury. synthetic organomercury compounds were once used in pharmaceutical applications.919) . sphygmomanometers and barometers.. merbromin).00) .50-3. with the highest concentrations occurring in the kidneys (Barregard et al.400 (.800 (.40-1.Metals Mercury CAS No.703-.50) 5.10) .800 (.600 (.800-1.300) .903) Selected percentiles ( 95% confidence interval) 50th .50) 1.50-1.363-. Inorganic mercury compounds such as mercuric oxide are used in producing batteries and pigments and in synthesizing many organic chemicals.00 (.781 (..30-4.50-2.. 218 Fourth National Report on Human Exposure to Environmental Chemicals . Hursh et al.800-1.60) 2085 2293 3478 Limit of detection (LOD.372) .. predominantly from fish and other seafood.80) 1. Other major uses include electrical equipment (e. which create an episodic potential for volatization and inhalation of mercury vapor.20-3. silver-white liquid (quicksilver) obtained predominantly from the refining of mercuric sulfide in cinnabar ore.g.900) 1.80 (3.600) 1. Kingman et al.30) 5.90-3. constitutes the main source of dietary mercury exposure in the general population.80 (1.927) .900) 1.574) . inorganic.

297-.944 (. The slow-phase half-life may be several weeks longer in persons with chronic occupational exposure (Sallsten et al.30-4.00-2.700 (. 1993).60 (3.700-1. 1998).10-3.60 (2.30) 1.50) 1.900 (. excretion of mercury occurs predominantly through the kidney (Sandborgh-Englund et al.50-2. Sandborgh-Englund et al..541-.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. and the newborn’s levels decline gradually over several weeks (Bjornberg et al.833 (. thereafter.10 (.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 .400-. Transplacental transport of methyl mercury and elemental mercury has been demonstrated in animals (Kajiwara et al.20) . 2005).14. Geometric mean Survey years (95% conf. Methyl mercury is incorporated into growing hair. 1994).30 (1.200-.500 (.60) 2. 1995.90) 5.299-.00) 6.800) .407) .70-5.317 (.10 (1.00) 1.800) 1..80-3.00) . 1973).800) 75th .73) 1.10) .800-1.30-6.300 (. McDowell et al.329 (. Vahter et al.90 (1.30-4.40) 2.300) .20-2.800) . 1998). 1992 and 1999. 2003).369) 1. 1999).919) .200-.90 (4.500 (.500-.825-1.30-3.40) 1..90) 2.01) .800 (.10 (. 1999-2002..27) .300) .300 (. 2004.06 (..200-.30-6.80 (3..00-3.90 (3.. Methyl mercury enters the brain and other tissues (Vahter et al.30 (1.23) .50) 95th 2. Suzuki et al.820 (. 16-49 years) Mexican Americans Non-hispanic blacks Non-hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .700-.10-1.871-1.700 (.00 (2.20) 1.00-1.800-1.269-.80) 1..40-1. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.60) 1.00) 2..00 (1.200-.900-1.50 (2. 1990). 1971).10) .20-3.30-11.30-6.800-1.30) 3. Smith et al.824) 1. Inorganic mercury and methyl mercury are distributed into human breast milk in relatively low concentrations.500-.500-. Less than 15% of inorganic mercury is absorbed from the human gastrointestinal tract (Rahola et al.70-6. 1969.600 (..7) 4.20-3. The half-life of inorganic mercury in blood is similar to the slow-phase half-life of mercury after inhalation of elemental mercury.500-1.475) ..343 (.50-3.20) . 1992).00-6.70 (1. 1993).377) .800 (.0) 4.70) 4.70 (1.Metals the tissues to mercurous and mercuric inorganic forms. Excretion occurs by renal and fecal routes.900 (.200-.700 (.00-2.00 (3. Fourth National Report on Human Exposure to Environmental Chemicals 219 . a measure of accumulated dose (Cernichiari et al.374) .700 (.00-2. and a useful marker of exposure in epidemiologic studies (Grandjean et al.300) .300) . 1984.20-3.377 (..50) 3.500-.300 (. Smith and Farris. Human pharmacokinetic studies indicate that methyl mercury declines in blood and the whole body with a half-life of approximately 50 days.268-..738-.S.60) 1.20 (2.60 (1.35 (1.50 (1.900-1..200-.800 (.30 (.3) 4.70) 4..70) 1.70-5.940) Race/ethnicity (females.00 (2. Lesser penetration of inorganic mercury occurs through the bloodbrain barrier than occurs with either elemental or methyl mercury (Hattula and Rahola.60 (1.20-11. The fraction of methyl mercury absorbed from the gastrointestinal tract is about 95% (Aberg et al..00) 7..395) .700-1.06-1.800) 1.80) 579 527 370 436 588 806 Limit of detection (LOD.50) 1.30-2.02 (.50-12.90) 3.90) 2. After exposure to elemental mercury.10 (1. 1992.300) .40 (1.70-3.600) .20 (. 2003). interval) Selected percentiles (95% confidence interval) 50th . urinary mercury levels decline with a half-life of approximately 1-3 months (Roels et al.90 (4.900 (.80 (1.300) .726-1. population.00 (2.40-2.300 (.265-.10 (3.30 (1. Mercury levels in the cord blood are higher than in the mother’s blood (Stern and Smith. Miettinen et al.200 (. and peak urine levels can lag behind peak blood levels by days to a few weeks (Barregard et al.10) 1.00) 4.90 (1. 1991. Vimy et al.70-3.200 (.00) 1. Myers et al. for both acute and chronic exposures..697-..30-5.60 (1.664-1.700-.30) 1. National Health and Nutrition Examination Survey.40 (1. 1975.29) ...40-2.60 (3.90) 90th 1. 1994. 1996.600) .10 (1.50) 2.667 (. Jonsson et al.700) 2.500-.40) 5. with most elimination occurring through in the feces (Sherlock et al. 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..318 (.14 and 0.256-.60) 3.10 (5. 1994) and then undergoes slow dealkylation to inorganic mercury. 1996).307 (.

Overt poisoning from methyl mercury primarily affects the central nervous system. Factor-Litvak et al.700 (. and progressive constriction of the visual fields. The constellation of findings may include anorexia. Stern 2005.600 (. Survey Geometric mean (95% conf. 2000). < LOD means less than the limit of detection.500-. Oskarsson et al.500-..500-.600-. Rice.600) .600 (. the existence of a causal relation is unresolved (Chan and Egeland..600 (. Low-level exposure from dental amalgams has not been associated with neurologic effects in children or adults (Bates et al. 1987). 2000. insomnia..500-. Smith et al. 2002.. 2006..600) . irritability. maculopapular rash.600) . typically after a latent period of weeks to months. limb deformities. 2004). At levels below those that cause acute lung injury..700) .600) * 03-04 03-04 03-04 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . the most prominent effect is on the kidneys where mercury accumulates and may lead to renal tubular necrosis.500 (<LOD-.500-.700) 2007 2240 3406 Limit of detection (LOD. short-term memory loss. hypertension. ataxia. and sleep disturbance (Bidstrup et al. 2005.600 (.500 (<LOD-. and cerebral palsy (NRC.700-. 2004.600 (. population from the National Health and Nutrition Examination Survey.. 1993).600 (. particularly irritability.500 (. 1995. Workplace standards for inorganic mercury exposure have been established by OSHA and ACGIH. depression.500-.. Occupational exposure to elemental mercury vapor has been associated with subclinical effects on biomarkers of renal dysfunction (Cardenas et al. 2003).600) .700 (. Inorganic mercury exposure usually occurs by ingestion. 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. and a drinking water Inorganic Blood Mercury Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U.42. dysarthria... Rissanen et al.600-. altered physical growth. In recent epidemiologic studies. dysarthria.600 (. 1970. High-level prenatal exposure may result in a constellation of developmental deficits that includes mental retardation. Bellinger et al.600) .. Once absorbed.700 (.500 (.800) . 1996)..600 (. DeRouen et al.. pain in the extremities. 1951.. 220 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. 2000. cerebellar ataxia.600) . 2004). 1998. Although recent investigations have suggested a possible link between chronic ingestion of methyl mercury and an increased risk for cardiovascular disease. overt signs and symptoms of chronic inhalation may include tremor.S. 2005).800) 792 842 2060 4453 03-04 03-04 * * < LOD < LOD < LOD < LOD . Sakamoto et al. Acute.600-. Vupputuri et al.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 . anorexia. 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. high-dose exposure to elemental mercury vapor may cause severe pneumonitis. fatigue. and neurocognitive and behavioral disturbances. Large amounts may cause irritant or corrosive effects on the gastrointestinal tract (Sanchez-Sicilia et al. Mercury levels in breast milk also decline in the weeks after birth (Bjornberg et al. and pinkish discoloration of the hands and feet (Tunnessen et al. 1995.600) .600) . Acrodynia is a sporadic and predominantly pediatric syndrome historically associated with calomel (mercuric oxide) in teething powders and occasionally other inorganic forms of mercury.500-.500-.700 (. hearing impairment. Sakamoto et al. 1963).600) .600-.800) 4015 4132 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD .500) .500-. 1983).700 (. which may vary for some chemicals by year and by individual sample. Salonen et al. 2006.800) .700-. interval) Selected percentiles ( 95% confidence interval) Sample 95th . Smith et al. gingivitis. causing parasthesias. 2004.. Drexler and Schaller.. see Data Analysis section) for Survey year 03-04 is 0...Metals may be more efficient for inorganic mercury (Grandjean et al. sensory impairments.700 (.700-.

Among the three racial/ethnic groups. (2000) studied 1216 blood donors in the Czech Republic (896 men and 320 women.8 years.441 (.67-3.254 (.cdc.14-2.39-3.60) 619 713 1066 Limit of detection (LOD. 2006).61) 1.396-.360-.480) 75th 1.840-1.420 (.495 (.290-.960 (.330-. the developing fetus may be the most susceptible to the effects of ongoing methyl mercury exposure (NRC. IARC considers methylmercury to be a possible human carcinogen and elemental and inorganic mercury to be unclassifiable with regard to human carcinogenicity.89) 3.31) 2. 1997. 2009). 2004.330-.555) .. 1995.34-3. Information about external exposure (i.930-1.54 (2.05) 1. EPA.29) 1.63-2.42) 95th 3.840) 1.09 (2. the median concentration of blood mercury was 0.76-3.19 (2. total blood mercury increased with age.580) . Fourth National Report on Human Exposure to Environmental Chemicals 221 . Urinary mercury consists mostly of inorganic mercury (Cianciola et al.S.313-.463) .03-4.76-3.770-1.30) 3. and the age-related changes differed across the groups (Caldwell et al.250) .304) .67-2.700 (.28) 1.00) 1.08 (1.530-.530) .13-2.870-1.350-. total blood mercury levels declined slightly in non-Hispanic black and Mexican American children.S.400 (. 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.480 (. and increased slightly in non-Hispanic white children (Caldwell. range 40 years to 78 years) had an average total blood mercury concentration of 2.90) 2.93 (1. who participated in a 1998 representative population survey (Becker et al.14.460) .549) .07 (..76-4.46) 3.23) .610-1. Schober et al..430 (.460 (.520) .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 .68 (2. EPA at: http://www.Metals standard for inorganic mercury has been established by U.31) 1266 1272 03-04 03-04 03-04 .58 µg/L for 4645 adults.570) .88-3.66) 3.890 (.atsdr. military veterans (mean age 52. see Data Analysis section) for Survey year 03-04 is 0. 2001.S. 758 children.534) .420 (. Urinary Mercury—2003-2004 Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.213-.406-..epa.358 (. 2003).. However.05) 3. Sanzo et al.23) 2.85-2.88 (1.60 (1.530) .00 (.340-. 2002). Mahaffey et al.9 years). adult women in several ethnic subgroups (Hightower et al. slightly higher total blood mercury levels were found in U. 2003). Total blood mercury levels increase with greater fish consumption (Dewailly et al.55 µg/L.24 (2.840-1. Clinically observable signs of ataxia and paresthesias may occur when blood mercury levels increase to approximately 100 µg/L after methyl mercury poisoning.940 (. Over the NHANES 1999-2006 survey periods.442-.509) .26 (1.20 (1.408) . These distinctions can help interpret mercury blood levels in people.S.12 (.416 (. total blood mercury geometric mean levels in females aged 16-49 years did not change.01 (.410-. 2000).413-.360-.gov/mercury and from ATSDR at: http:// www.88) 287 722 1529 03-04 03-04 . Survey years 03-04 Geometric mean (95% conf.430 (. et al.96 (1. Urine mercury levels increase as more occlusal surfaces of teeth are filled with mercury-containing amalgams (Becker et al. aged 18 to 69 years.509) .492) Selected percentiles ( 95% confidence interval) 50th .96 (1.405-.08 (1. average age 33 years.476 (. 2009). Benes et al.370) . Grandjean et al. 2001. A cohort of 1127 U..382-.200 (..78-2.447 (.33 (2.430) .330 (.24) 1.77-2. Kingman et al.18) 2..78 µg/L for adults and 0. interval) . average age 9.433 (.60-2. the total blood mercury concentration is due mostly to the dietary intake of organic forms.160-.440 (. particularly methyl mercury.. During the same survey periods. 1998).65) 1. These men had no occupational exposure to mercury but previously had received dental amalgams at military facilities (Kingman et al.97) 2.700-1. In NHANES 19992002.99-6. although non-Hispanic black females had higher levels than non-Hispanic white or Mexican American females. 1998).52) 2.280-.16 (.330-.e.870-1.. population from the National Health and Nutrition Examination Survey.16 (1. Biomonitoring Information In the general population. environmental levels) and health effects is available from the U.360 (.gov/toxprofiles.19 (1.46 µg/L for children.S. From 1996 through 1998..14) 90th 2. In Germany the geometric mean for blood mercury was 0....

76 (1. et al.196-..67 (1. Biomonitoring studies provide physicians and public health officials with reference ranges so that they can determine whether people have been exposed to higher levels of mercury than are found in the general population. not to imply a safety level for general population exposure.40-1.79 (1.545 (.31 (1. Blood mercury levels of women and children in NHANES 19992006 were also below levels established as occupational exposure guidelines (Caldwell.404-. the urine mercury increased by approximately 0.784) 1. 2006). Biomonitoring data will also help scientists plan and conduct research on exposure and health effects.297 (. et al.. Urinary Mercury (creatinine corrected)—2003-2004 Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.400-.532 (.990) . 2002) adult population surveys were similar to those in a U.455-.333-.480) . mean urinary mercury was 3.44) 1. among workers with urinary mercury concentrations of 25-35 µg/L or greater (Barregard et al.522-.301-.392-.16) 1.39) 1. Information about the biological exposure indices is provided here for comparison.28 (.358) . representative sample of women aged 1649 years reported in NHANES 1999-2006 (Caldwell.32-2.463 (.472-.455-.476 (.464 (. In the study of U.06 (.40 (1.619-.347) .208-. 2009).64-2.276 (. DeRouen et al.25 (.652) . An expert-panel report recently prepared for the U. Finding a measurable amount of mercury in blood or urine does not mean that the level of mercury causes an adverse health effect. Levels in U.04-3.S.696 (.23-2. interval) .289) .S.280-.969-1.246-. 2009).11) 2..13 (1.486) Selected percentiles ( 95% confidence interval) 50th .Metals 2000).03) 2.587 (.909 (.443 (.62 (1.88-2.S.508 (.447 (.225-.65 (1.384 (.46-2.620-.362 (.51-2. and on average.417) .79) 1.265-.87 (1.365 (. 1988.309-.18-1.255 (.537) .275) ..67 (1..687) .875-1.86) 95th 2.88 (1.365 (.588) . ACGIH recommends that the blood levels due to inorganic mercury exposure in workers not exceed 15 µg/L.61) 1.970 (.525 (.77 (2. Czech (Benes et al.785-1.63) 1.217 (.21) 1.599) .368) .87) 2.498) 75th ..56) 1266 1271 03-04 03-04 03-04 .30) 1.616) .13-2.11-2. Survey years 03-04 Geometric mean (95% conf.35 (1. 2002).400) .768 (. and Italian (Apostoli et al.S..90) 618 713 1066 222 Fourth National Report on Human Exposure to Environmental Chemicals .667-1.306 (.88-2.485 (. women of childbearing age have generally been much lower than these levels (CDC. reversible increase in urinary N-acetyl-glucosaminidase.447-. The ACGIH (2007) currently recommends that urinary inorganic mercury in workers not exceed 35 µg/g of creatinine.. Urine mercury and the number of dental amalgams were correlated.376-..1 µg/L for each surface with a dental amalgam (Kingman et al.535) 1.32 (1. population from the National Health and Nutrition Examination Survey.800-1.964-1. Langworth et al. military veterans with dental amalgams.391) .12-3.06 (.00) 286 722 1529 03-04 03-04 . 1992).07) 1. a biomarker of perturbation in renal tubular function.307-.78-4. 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.343 (.714-1.00 (.455) . Department of Health and Human Services noted that several studies have observed a modest.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 .385-.630) ..1 µg/L. 1998). 2003). 2006.01) 2. 2005).S.30) 2.09) 1.54 (2.566) . Urinary mercury levels in recent German (Becker et al.00) 90th 1.11) 1.391-.41-2.

27-1.92) 2.508-.99-2.77) 2.670) 75th 1.624-.664) Mexican Americans Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .637) .742-1.17) 95th 5.79) 3.870) .41 (2.55) 90th 3.03 (.92) 3.592 (.846) .516 (.47) 1.540 (.00 (2.13 (2.76) 2.37 (1.55-3.719 (.07-5.502-.85) 4.61-6.610-.15-1.92) 4.710 (.22-3.05 (3.772 (.30 (1.61) 1.632 (.709) 75th 1.30 (2.569-.72) 1.S.37) 1.15 (2. 16-49 years) 99-00 01-02 .658 (. interval) Selected percentiles (95% confidence interval) Survey years 50th .43-1.27 (2.54) 595 531 381 442 594 826 Limit of detection (LOD.655 (. 16-49 years) 99-00 01-02 .46) 3. National Health and Nutrition Examination Survey.16-5.724 (.62 (4.07-2.91-7.540-.56) 3.25) 2.38) 4.582-.03-2.930) .69 (1.46 (1.32) 2.520-.62 (1.560-.426-.00) 2.656-.14) 3.23-1.97 (1.18) 3. 1999-2002 Geometric mean and selected percentiles of urine concentrations (in µg/L) for females aged 16 to 49 years in the U.892) .47) 1.636-.580 (.966) .760 (.578-.23-1. Urinary Mercury (creatinine corrected)−Females Aged 16-49 Years Old.387-.16) 5.622-.18 (3.84 (2.410-.699) 1.665) .650) 1.744) 1.450-.95 (2.799) .89 (2.06 (.50-4.850-1.65) 1.21 (1.824) .650 (.600 (. population.87-4. 1999-2002.21 (2.76 (1.31 (1.85-3.615 (.909-1.685 (.27 (1.565 (.S.686) .51 (3.691) .24) 6.30-2.65-4.631-.831) .21-3.45-3.3) 5.14. Geometric mean (95% conf.14-1.97) 2.710) 1.475-.97) 2.53-3.09-1.639 (. National Health and Nutrition Examination Survey.740 (.553-.41-6.24-1.44) 3.68) 3.99) 1.59-5.05 (2.806) .721 (.35 (1.97) 2.42-3.48 (2.45 (1.70 (2.51) .94) 1.04-1.03 (.596 (.500-.53) 595 531 381 442 594 826 Fourth National Report on Human Exposure to Environmental Chemicals 223 .99 (2.501-.50 (1.14 and 0.790) .657 (.91 (2.28 (1.99 (3.83-3.46-4.10-4.522 (.580-.664) .520-.39-3.606 (.32-3.45-2.620 (. 1999-2002.42) 90th 2.84 (2.45) 2.13-4.77) 1.706 (.45) 95th 3.Metals Urinary Mercury−Females Aged 16-49 Years Old.56 (1.56) 4.45) 2.774) .42) 2.32 (1.39) Sample size 1748 1960 Age group (females) 16-49 years Race/ethnicity (females.832-1.52) 3.57-4.69-3. 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.31-1.00 (3.68-3.526-.07) 1.30 (2. interval) Selected percentiles (95% confidence interval) 50th .809) .10-2.710 (.560 (.41 (1.62 (3.605-.81-6.41 (1.09-1. population.50 (2.81 (3.98 (5.579-.68 (3.03) 1.723 (.63) Sample size 1748 1960 Age group (females) 16-49 years Race/ethnicity (females.14-2.616-.833) .420-.79) 1. Geometric mean Survey years (95% conf.35) .557-.910) .650 (.22 (. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.810) .04-10.709) .76-5.831) .665) Mexican Americans Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .

Subrt P. White RF. Lebel G.72:169-173. Schaller KH. Kaus S. Barbon R. Jones RL. Environ Health Perspect 2003. Persson G. Application to workers exposed to mercury vapour. Cerna M. Int JHyg Environ Health 2002. Grandjean P.8(2):117-119. Cutress T. Greitz U. Roels H. Bernard AM. mercury exposure. et al. and heart diseases. Jorgensen PJ. Budtz-Jorgensen E.61:65-69. Levallois P. Elia G. Assessment of reference values for mercury in urine: the results of an Italian polycentric study. Osterloh JD. Becker K.50:17-27. Lepom P. Aposian HV. Kaus S. Third National Report on Human Exposure to Environmental Chemicals. Sallsten G. Brewer R.47(3):185-195.S. Ekman L. Schulz C. Epidemiologic assessment of measures used to indicate lowlevel exposure to mercury vapor (Hgo). Barregard L. Seiwert M. 52:19-33. Townes BD. Bjornberg KA. Leitão J. Luis H. Arch Environ Health 2001. Jarvholm B. Based on the Documentation of the Threshold Limit Values for Chemical Substances and Physical Agents and Biological Exposure Indices.Metals References Aberg B. Schulz C.149:301-305. Rosenbaum G. DeRouen TA. and Se in blood of the population in the Czech Republic. Smid J. Drago I. Debes F. JAMA 2006. 206:15-24. Myers GJ. Arch Environ Health 1992. ACGIH. Becker K. Factor-Litvak P. Markers of early renal changes induced by industrial pollutants. Trachtenberg F. Mangili A. Drexler H. Spevackova V. Bonnell JA. Pb. Bates MN. Jacobs D. Int J Epidemiol 2004. Barregard L. Atlanta (GA). Impact of maternal seafood diet on fetal exposure to mercury. 2005. Kline J. Weihe P. Environ Health Perspect 2005. 2007 TLVs and BEIs. Health effects of dental amalgam exposure: a retrospective cohort study.295(15):1775-1783.113(10):1381-1385. I. Berglund B. Sallsten G. Echeverria D. Bidstrup PL. Bellinger DC. McKinlay S. Weihe P. Leroux BG. Nutr Rev 2004. Niklasson B. Cernichiari E. Cincinnati (OH): Signature Publications. et al. Neuropsychological and renal effects of dental amalgam in children: a randomized clinical trial. Ayotte P. Tissue levels of mercury determined in a deceased worker after occupational exposure.2:856-861. Lauwerys RR. Cardenas A. Sandborgh-englund B. Lancet 1951. Cianciola ME. Martin MD.289:1324. Am J Epidemiol 1999. Videro T. Fawcett J.16(4):705-710. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Clarkson T. Jorgensen PJ. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Schutz A. Skerfving S. Woods JS. et al. Attewell R. Benes B. Krause C. Tavares M. Harvey DG. Total blood mercury concentrations in the U. Grandjean P. Begg M. The concentration levels of Cd. Bernardo M. Cu. Locket S. The mercury concentration in breast milk resulting from amalgam fillings and dietary habits. Garrett N. population: 19992006. Conradi N.56(4):350-357. Chan JM.295(15):17841792. Vahter M. Martin MD. Mortensen ME. Hultberg B.111:719-723. Martins IP. Environ Res 1998. JAMA 2006. Chronic mercury poisoning in men repairing direct-current meters. Arch Environ Health 1969. Kinetics of mercury in blood and urine after brief occupational exposure. Hg.33:1-9. Hasselgren G. Metabolism of methyl mercury (203Hg) compounds in man. Cox C. Seifert B. Methylmercury exposure biomarkers as indicators of neurotoxicity in children aged 7 years. Sci Total Environ 2002. Snihs JO. Falk R. Cernichiari E. Int J Hyg Environ Health 2003. Cejchanova M. Daniel D. Weber JP. Biennow M. Caldwell KL. Centers for Disease Control and Prevention (CDC). Neurobehavioral effects of dental amalgam in children: a randomized clinical trial. selenium. Kjellstrom T. Seiwert M. Buchet JP. Exposure of the Inuit population of Nunavik (Arctic Quebec) to lead and mercury. Zn.19:478-484. Neurotoxicology 1995. Geier J.62(2):68-72. Arch Environ Health 1992. Int Arch Occup Environ Health 1999. 224 Fourth National Report on Human Exposure to Environmental Chemicals .77(2):124-129. Monitoring methylmercury during pregnancy: maternal hari predicts fetal brain exposure. Woods JS. Br J Ind Med 1993. and lead. Sallsten G. et al.7(3):176-184.205:297-308. et al. Egeland FM. Caudill SP. Int Arch Occup Environ Health 1988. Cernichiari E.. Barregard L. Cent Eur J Public Health 2000. Dewailly E. Enzymuria in workers exposed to inorganic mercury. Fish consumption. Lapham LW. Schuzt A. Transport of methylmercury and inorganic mercury to the fetus and breast-fed infant. Int J Hyg Environ Health 2009. Mercury derived from dental amalgams and neuropsychologic function. Apostoli P. et al. Bruneau S. Cortesi I. et al. Marsh DO. Barregard L.212:588-598. J Toxicol Environ Health 1997. Gagliardi T. Castro-Caldas A.

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Turner MD. Aguinagalde FX. 1999-2000. Topping G. Guo S.110:129-132. Smith PJ.4(5):981-988. Toxicol Appl Pharmacol 1994. Amurrio A. Vupputuri S. Maternal-fetal distribution of mercury (203Hg) released from dental amalgam fillings. et al. Kaye WE. Sinks TH. Arch Environ Health 1993. 226 Fourth National Report on Human Exposure to Environmental Chemicals . Lorscheider FL. Goldberg J. Tunnessen WW.2:117-131. McMahon KJ. Leitao JG. A review of the studies of the cardiovascular health effects of methylmercury with consideration of their suitability for risk assessment. Smith JC. Methyl mercury pharmacokinetics in man: a reevaluation.Metals Sanzo JM.97(2):195-200. Elevation of mercury in human blood from controlled ingestion of methyl mercury in fish. Osterloh J. Toxicol Appl Pharmacol 1994. Burbacher T. Orr MF. Environ Health Perspect 2007. Stern AH.37:245-252.115(10):1527-1531. Stern AH. Smith AE. Sandler DP. DeRouen TA. Toxicol Appl Pharmacol 1996. 1993-1998. Hum Toxicol 1984. et al. Smith RG. Vahter M. JAMA 2003. The contribution of dental amalgam to urinary mercury excretion in children. Effects of occupational exposure to elemental mercury on short term memory. Takahashi Y. Daniels JL. Hislop D. et al. Am J Physiol 1990.111(12):1465-1470.48(4):221229. Effects of exposure to mercury in the manufacture of chlorine. Leroux BG.128(2):25125-25126. Bolger PM. Farris FF. Estimation and validation of mercury intake associated with fish consumption in an EPIC cohort of Spain. The kinetics of intravenously administered methyl mercury in man. The hair-organ relationship in mercury concentration in contemporary Japanese. Schober SE. Matsuo N. Pediatrics 1987. Vimy MJ. Lind B. Zeitz P. Woods JS. Newton G. Longnecker MP. An assessment of the cord blood: maternal blood methyl mercury ratio: implications for risk assessment. Fisher HL. Blood mercury levels in US children and women of childbearing age. Public Health Nutr 2001.31:687-700.98(1):133-142. Baser M. Langolf GD. Speciation of mercury in the primate blood and brain following long-term exposure to methyl mercury.79:786789. Environ Health Perspect 2002. Environ Res 2005. Acrodynia: exposure to mercury from fluorescent light bulbs. Amiano P. Am Ind Hyg Assoc J 1970. Shen DD. Most B.258(4 Pt 2):R939-945. Hongo T. Nakazawa M. Sherlock J. Bernardo MF. Public health consequences of mercury spills: hazardous substances emergency events surveillance system. Vorwald AJ. Mooney TF. Hall LL. Martin MD. Mottet NK. Yoshinaga J. Blood mercury level and blood pressure among US women: results from the National Health and Nutrition Examination Survey 1999-2000. Environ Health Perspect 2003. Patil LS. Allen PV. Imai H. Suzuki T. Dorronsoro M. Jones RL. Br J Ind Med 1983. Smith JC.40:413-419. Friberg L. McDowell M. Azpiri MA.124:221-229. Whittle K. Environ Res 2005.289(13):1667-1674.

9-55.5 (74.8-46.3) 83.3) 90th 135 (125-146) 124 (117-130) 111 (105-118) 95th 180 (154-216) 165 (145-176) 138 (133-146) Total 45.9 (44.9 (52.3-91.2 (49.4-52.3 (53.3 (84.4 (48.4) 56.9) 34.0-62.5 (49.5-68.8) 40.5-66.7) 75th 84.0 (42.7-96.9-109) 97.5) 44.5-52. and xanthine oxidase (Kisker et al.2) 37.1) 46. interval) 45.1-48.8 (67.3 (55. and 03-04 are 0.2-79.6) Selected percentiles ( 95% confidence interval) 50th 50.9-83. population from the National Health and Nutrition Examination survey.4 (79.9-55.3 (37.0) 45.6 (73.2) 52.6) 51.6) 71.0-100) 63.8) 44.7-73.1-55.1 (91.6) 53.8) 48.5.3 (46.8 (42.5 (43.0 (41. hard metal widely used to add strength and hardness and retard corrosion in metal alloys.0) 55. Compounds of molybdenum are also used as corrosion inhibitors. More recently.6) 71.6 (55.8) 46.7) 86.8 (82.2 (63.9-56.5 (41.1) 82.5 (41.7-92.1-52.7 (51.8-94. and 1.7 (44. In humans.1 (71.Metals Molybdenum or ore deposits.3 (73.7-84.5-65.7) 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 78.0-110) 90.8.9 (78.1) 59.2 (49.3 (47.2 (69.1 (34.7) 45.0) 84. Gastrointestinal absorption of molybdenum averages 8893% for dietary intakes of 22-1490 µg/day.4) 45. Molybdenum occurs in natural waters and may be present in concentrations of several hundred micrograms per liter or higher in ground and surface water near mining operations Urinary Molybdenum Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.7-47.6-72.5) 80.0 (76. lubricants.0 (46.9-82. Fourth National Report on Human Exposure to Environmental Chemicals 227 .5) 60.1-59.6 (52.3) 65.9 (40.2) 40. inks.1 (38.0) 60.5-41.4) 52.6-96.8) 39.0 (81.0) 54.0-101) 82.6) 93.2-59.3-47.0 (48.2-53.2) 53.6-42.1) 57. 2001.3) 54.7-68. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.9) 62.6-62.0-38.4-82.0-65.8-106) 88.3 (71.7) 57.2 (40.8-49.7 (50.1-44.9) 67.7 (45.0 (42.5 (48.0-77. molybdenum is a cofactor for three enzyme classes— sulfite oxidase.3 (79. 0.5-91.2-37.6-82.2-42. chemical reagents in hospital laboratories.0-56.3-108) 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 47.0) 39.4 (72. 7439-98-7 General Information Elemental molybdenum is a silver-white. 01-02.7-39. and the average dietary daily intake of molybdenum is approximately 100 µg/day (IOM.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.. 2001).1-63.7-51.2) 41. hydrogenation catalysts.8-90.1) 35.3) 47.4) 76.0-53.4) 49.5) 80.9 (32.6 (55.7) 77.7) 78.7-41. The recommended dietary allowance for adult men and women is 45 µg/day (IOM.2 (55.7) 46.1-52. see Data Analysis section) for survey years 99-00.1-51.7-122) 93.7-50.2) 150 (128-187) 130 (120-141) 119 (112-130) 119 (105-138) 115 (104-128) 101 (97.0-71.7 (37.5) 47.2 (83.8-108) 87.2) 48.2-70.1) 60.5) 85. which exert homeostatic regulation over molybdenum balance.4-61.9 (73.3) 85.0-85.5 (81.6-46. urinary excretion over six days CAS No.2 (61.6 (40.9-85. and in pigments for ceramics.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. semiconductor and battery industries have begun to use molybdenum.7-105) 69.6 (43.8) 75.0 (43.3-44.9 (37.8 (85.2-91. aldehyde dehydrogenase.4 (80. Excretion occurs predominantly via the kidneys.7 (36.3 (64.9 (33.0) 97.3) 41.6 (40.3-115) 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. respectively.4 (48.7-60.3-75. 1997).4) 42.4) 41.9 (34.7) 51.7 (73.6) 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 (99.7 (71.S.7-91.2-59.3 (55.5 (67.2 (56. and paints.1-88.3 (38.0) 62.1) 126 (106-147) 109 (94. At a daily oral molybdenum dose of 24 µg. 1996).5-52. WHO.7) 78.4-75.5-46.5 (37.4 (34.2) 79.7 (58.2 (38.6-55.3) 37. Molybdenum is a nutritionally essential trace element that enters the body primarily from dietary sources.6-58.8.5-124) 108 (92.

4) 58.0) 36.4 (55.7) 112 (95.1-38..1) 56.6 (36.4) 60.4-66.9-96. Biomonitoring Information Molybdenum is an essential element for health.9) 40.1 (54.3 (53.5 (41.4) 116 (101-126) 104 (88.0) 88.2 (36.3-59.0) 95th 144 (125-171) 130 (120-149) 120 (107-135) Total 42.4 (37.2 (69.5-35.9) 79.9) 92.3) 41.3) 57.1-39.8) 39.1-100) 86.3 (71.4) 89.9) 173 (130-243) 159 (129-170) 132 (107-158) 85.0-103) 103 (90.4) 40.8-118) 81.6 (38.0) 39.4 (59.6-78.2-96.8-47..6) Selected percentiles ( 95% confidence interval) 50th 41.5-45.7-93.1 (38.Metals was 18% of the ingested dose.9 (39.2) 58.4-39.8 (36.8 (56.3-45.9-68.3) 44.1-127) 90.0-133) 119 (88.2-47.5) 73.7-44. Based on studies finding adverse reproductive effects in rats and mice.8) 71.6) 48.9-117) 57.8) 61.2-80.3 (37.3 (83.8-46.4 (56.4-106) 85. and molybdenum has not been systematically evaluated for carcinogenicity by IARC.5-92. 2001).0-46.6) 43.7-40.5) 90th 108 (97.4 (78.9) 41.9 (36.3-115) 98.5-46.5) 71.6 (36.3) 64.8 (57.0-41.2) 42.1-67. EPA. Human health effects from molybdenum at low environmental doses or at biomonitored levels from low environmental exposures are unknown.6 (57.6 (59.4 (40.2 (73.8-42.1) 65.9-45.2) 39.9 (35.1 (42.7-100) 77.2) 37.4-120) 101 (84.5 (35.. and urinary levels reflect intake from all sources.3) 56.5 (39.3-46.2 (37.1-40.1) 37.3-141) 109 (81.4-107) 85.1 (37.7) 45.5 (34.2-65.4 (53.4) 48.7-62.6-45.5-44. population from the National Health and Nutrition Examination survey.3 (51.6-63. 1997).9 (39.3-52.2 (57. In industry.8-52.2) 43.7-43.6-61.2-46.3) 61.5 (59.0 (35.8 (37.3 (71.5 (79.5 (37.9 (79.8-47.1-112) 78.9-71.7 (66.8) 37.8-66.4-185) 106 (94.1-43.4 (44.6 (42.5 (40.9-42.4) 47.4) 122 (107-133) 109 (99.6) 36.9 (40.2) 39.1-41.3-44.6-41.1-39.7) 115 (93.1-81.8-67. Chronic exposure to very high levels may result in higher serum uric acid levels and a gout-like illness (Koval’skiy et al.6-61.9-45.3-68. and clinical or epidemiologic evidence of adverse effects is limited.8) 38.2) 38.3 (58.6-76.1 (39.0) 38.5 (78.2-96. A long term inhalation bioassay of molybdenum trioxide in mice yielded “some evidence” of carcinogenicity (NTP. the Panel on Micronutrients of the Institute of Medicine identified a no observed adverse effect level (NOAEL) of 0.9-118) 91.0) 53.0 (58.8-65.8 (90.4) 61. Levels of molybdenum Urinary Molybdenum (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.2) 55.7-52.0) 44.0 (80.9 (64.3) 43.9) 44.8) 79.9 (64.2 (33.2) 37.5 (38.7-38.8) 38.5-119) 90.7) 62.4-76.5 (40.3-56.4-42.5 (35.1 (44.1-79.1 (38.9-87.5 (83.2 (40. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.5-70.5 (36.5-48. dust and other fine particles produced during refining or shaping of molybdenum or molybdenumcontaining alloys are inhalational pathways of exposure.0-120) 85.1-45.1 (30.5-69.4-118) 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 (75.1 (33. of the ingested dose (Turnlund et al.5-62.3) 40.3) 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 85.0 (74.8 (75.7 (77.7-120) 87.6-63.5-97.0-46.3 (37.1) 43.7) 41.1 (40.2 (40.9 mg/kg/day and established a tolerable upper intake level of 0.5 (65.1-43.8) 45.5 (37.1-109) 89.1) 37.2-40.7-137) 129 (109-155) 112 (97.S.4-41.0) 33.5 (39.03 mg/kg/day in humans (IOM.5-50.2-121) 107 (92.5) 72. respectively. at daily oral doses of 95 µg and 428 µg.5 (41.2) 42.4 (67.6 (71. 1995).5) 63. but available epidemiologic data are scant. One case-control study suggested a possible link between occupational exposure to molybdenum and lung cancer (Droste et al.7) 53.5) 60.2-49.0) 62.0-56.5-60.9 (49.8-84.7) 57.1 (82.0-38. Molybdenum is generally considered to be of low human toxicity.S.5 (50.2 (43. 1993).7) 42.3-43.1 (49.8) 62.1) 101 (83.1-34.9) 31.1) 40.9 (73.3 (36.4) 44. 1961.4) 77.2 (52.9-40.2 (50.7) 75th 63.0) 72. U.3 (36.5 (65.2 (40.5 (80.3-102) 122 (116-147) 123 (109-139) 118 (101-134) 310 368 290 648 762 725 1299 1559 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 40.0) 39. interval) 43.2-41.5 (54. 1999).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 42.5-99.6) 39.9-41.7 (30. urinary excretion over six days rose to 50% and 67%.9-61.5) 214 (154-1040) 185 (165-219) 160 (129-257) 112 (78.6-88.3 (55.3) 37.6) 39.

. White and Sabbioni. molybdenum. copper.php?record_id=10026&page=420.Metals in urine for the U. National Toxicology Program (NTP). Molybdenum-cofactorcontaining enzymes: structure and mechanism. these levels were comparable to those reported for adults in smaller European population surveys (Iversen et al..epa.niehs. Third National Report on Human Exposure to Environmental Chemicals. pp. Menne C. 420-441. Molybdenum. Toxicology and carcinogenesis studies of molybdenum trioxide (CAS No. Ann Rev Biochem 1997. et al. Food and Nutrition Board. Inductively coupled plasma mass spectrometric determination of molybdenum in urine. 1996.15(2-3):149-154. 2002. Turnlund JR. J Trace Elem Med Biol 2001. and zinc: a report of the Panel on Micronutrients. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 4/14/09 White MA. Institute of Medicine (IOM). vanadium. Occup Environ Med 1999. Atlanta (GA).216:253-270. Changes of purine metabolism in man and animals under conditions of molybdenum biogeochemical provinces. Geneva: WHO. Yarovaya GA. 2005. Available at URL: http://ntp. Trace element reference values in tissues from inhabitants of the European Union.62(4):790-796. Shmavonyan DM. Droste JHJ. (DC): National Academy Press.66:233-267. Koval’skiy GA.S.22(3):179-191. Molybdenum 1993 [online]. Finding a measurable amount of molybdenum in the urine does not mean that the level of molybdenum causes an adverse health effect. Fourth National Report on Human Exposure to Environmental Chemicals 229 . edu/openbook. Dietary reference intakes for vitamin A.gov/iris/ subst/0425. van Sprundel MP.S. World Health Organization (WHO). Environmental Protection Agency (U. Minoia et al. Christensen JM. cfm?objectid=070A72C6-E9C1-AE67-4BFAB97AD0F427E8. and retention studied with stable isotopes in young men at five intakes of dietary molybdenum. Weyler JJ.nih. Schindelin H. Am J Clin Nutr 1995. Ronchi A. Available at URL: http://www. Occupational risk factors of lung cancer: a hospital based case-control study. arsenic. Van Meerbeeck JP. 144-154. Urinary molybdenum concentrations in infants may be slightly lower than those in other age groups (Sievers et al. White MA. Schaub J. Minoia C. Keyes WR. Molybdenum absorption.htm. excretion. In: Trace elements in human nutrition and health. Available at URL: http://books. population were well characterized in NHANES 1999-2000 and 2001-2002 (CDC. TR-462. Rapid Comm Mass Spectrom 2002. pp. iodine. 2001. Zhurnal Obshchey Biologii 1961. References Centers for Disease Control and Prevention (CDC). Washington. nickel. 16:1313-1319. 1998. boron. Sabbioni E. Schleyerbach U.nap. 2001). manganese. Inductively coupled plasma mass spectrometric determination of molybdenum in urine from a Danish population. iron.123(1):81-85. Rees DC. Standing Committee on the Scientific Evaluation of Dietary Reference Intakes. Sci Total Environ 1998. Gatti A. Analyst 1998. chromium. EPA). silicon. 4/14/09 Iversen BS. 2005). Sciarra G. A study of 13 elements in blood and urine of a United Kingdom population. Molybdenum in infancy: methodical investigation of urinary excretion.gov/index. 56:322-327.. 1998). Aprea C. X. 1313-27-5) in F344 Rats and B6C3F1 Mice (inhalation studies) 1997 [online]. vitamin K.S. U. 4/14/09 Sievers E. Peiffer GL. 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. Kristiansen J. Kisker C. Sabbioni E. Vermeire PA. Turci R.

S. Higher environmental soil concentrations of platinum from vehicular emissions have been found near roadways (Farago et al.04. copper.. and iron. 230 Fourth National Report on Human Exposure to Environmental Chemicals . and 03-04 are 0. 0. 7440-06-4 General Information Platinum is a silver-gray. Platinum-rhodium and platinumpalladium crystals are used as catalysts in petroleum refining and in vehicular catalytic converters to control exhaust emissions. and 0. population from the National Health and Nutrition Examination Survey. which may vary for some chemicals by year and by individual sample. as oxidation catalysts in chemical manufacturing. 01-02. Platinum compounds are used in electrodes.g. jewelry. lustrous metal found naturally in extremely low amounts in the earth’s crust and is typically associated with sulfide-ore bodies of nickel. 1998). Important properties of platinum are resistance to corrosion. see Data Analysis section) for Survey years 99-00. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th < LOD < LOD < LOD 90th < LOD < LOD < LOD 95th < LOD < LOD < LOD Sample size 2465 2690 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 340 368 290 719 762 725 1406 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1227 1335 1281 1238 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.. Platinum-rhodium compounds are also used in glass and glass-fiber manufacture and in hightemperature thermocouples. dental alloys. thick-film circuits printed on ceramic substrates. cisplatin.Metals Platinum CAS No. respectively. 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. 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. carboplatin) in the treatment of cancer. < LOD means less than the limit of detection. Human health effects from platinum at low environmental Urinary Platinum Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.04. strength at high temperatures. however. and as drugs (e.07. and high catalytic activity.

or recommended for the metal form by NIOSH (Czerczak and Gromiec. and duration of exposure. cutaneous. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. When ingested or inhaled.. Most absorbed platinum accumulates in the kidneys and is excreted in urine (Moore et al.e. inhalational. Toxicity is determined by the type of compound (e.. Saindelle et al.g. 1975b). oral).. 1969). inorganic salt.. intravenous medicinal use. 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. Fourth National Report on Human Exposure to Environmental Chemicals 231 . population from the National Health and Nutrition Examination Survey. 2000). whereas soluble platinum compounds (e. or organometallic). The pharmaceutical cisplatin is an animal carcinogen and reasonably anticipated to be a human carcinogen as determined by NTP.Metals doses or at biomonitored levels from low environmental exposures are unknown. metallic. Workplace air standards for external exposure are established for soluble salts of platinum by OSHA and ACGIH. 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 are very poorly absorbed (<1% of a dose) and cleared from the body within a week after a single dose.g.. Platinum metal is biologically inert. Animals exposed to cholorplatinate salts used in industry have demonstrated severe hypersensitivity with asthma-like symptoms and anaphylactic shock (Parrot et al. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Information about external exposure (i. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th < LOD < LOD < LOD 90th < LOD < LOD < LOD 95th < LOD < LOD < LOD Sample size 2465 2689 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 340 368 290 719 762 725 1406 1559 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1227 1334 1281 1238 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 884 682 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.g. 1975a.S.. 1969.. The carcinogenicity of other platinum compounds remains uncertain. route of exposure (e. Platinum metal and insoluble salts can produce eye irritation.

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. Hysell D. Biomarkers 1999.35:313-321. Schierl R.. References Becker K. J Expo Anal Environ Epidemiol 2003. Br J Pharmacol 1969. Kazantzis G. Seifert B. Grimm CH. Arch Environ Health 2001. Wilhelm M. Schierl R. Turfeld M. 289-380.inchem. 2000.01 µg/L (Becker et al. 2003..org/documents/ehc/ehc/ehc125. International Journal of Hygiene and Environmental Health 2003. et al. Biomonitoring of traffic police officers exposed to airborne platinum. Environ Health Perspect 1975b. Urinary excretion of platinum from platinum-industry workers. Neuendorf J. Fruhmann G. and platinum. 2004) or less than 0..55(2):138-140.. Biomonitoring studies on levels of platinum provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of platinum than are found in the general population. Herr et al. Biological monitoring of hospital pharmacy personnel occupationally exposed to cytostatic drugs: urinary excretion and cytogenetic studies. Ensslin AS.. Stara J: Preliminary studies on the toxicity and metabolism of palladium and platinum.inchem. New York: John Wiley & Sons. Several studies have shown that background concentrations in general populations were usually less than 0. Occup Environ Med 2004. Jankofsky M. Nowak D. 2003. Duneman L:Long-term urinary platinum.. Carelli G. 1997. Hauff K. Revised and new reference values for some trace elements in blood and urine for human biomonitoring in environmental medicine. Int Arch Occup Environ Health 1997. Powell CH. Nickel. Boos KS. Pethran et al. Hall L. Occup Environ Med 1998. Part 1: monitoring of urinary concentrations. and in blood and urine in the United Kingdom. Schierl R. 1998). Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Kuster W.htm. 5th ed. Kaus S. pp. 232 Fourth National Report on Human Exposure to Environmental Chemicals . Czerczak S. Pethran A. Gieler U. Stilianakis NI. Ruff F: Platinum and platinosis. Ruff F: Histamine release by sodium cholorplatinate. Finding a measurable amount of platinum in the urine does not mean that the level of platinum causes an adverse health effect. Arch Environ Health:1969. 1991 [online]. Uptake of antineoplastic agents in pharmacy and hospital personnel. Schierl R.56(3):283-286. van de Weyer C.htm.. Stara J: Biological fate of a single administration of 191Pt in rats following different routes of exposure. Int Arch Occup Environ Health 2003. eds. et al.005 µg/L (Iavicoli et al. and gold excretion of patients after insertion of noble-metal dental alloys. Hysell D.4(1):27-36. Begerow J. Schierl. Fries HG. 2003. which elevate urinary platinum by five to twelve-fold (Begerow et al. Crocker W. 1999.9:152-158. Saindelle A.Metals the International Programme on Chemical Safety at http:// www. Wilhelm et al. Farago ME. Herr et al. 3/31/08 Moore W Jr. 2003). In: Bingham E. et al. et al.org/documents/ehc/ehc/ ehc125. Herr CE. Moore W Jr. palladium.19:685-691. Blanks R. Available at URL: http://www. Platinum-industry and precious-metal workers had urinary concentrations about one-thousand times higher than general populations (Schierl et al.. Influences on human internal exposure to environmental platinum. Platinum. Senofonte O. Schierl et al. Thornton I. 2004. Environmental Health Criteria 125. Hebert R. Urinary platinum levels associated with dental gold alloys. Patty’s Toxicology. Int J Hyg Environ Health 2004.70(3):205-208. Gromiec JP. Schulz C. Angerer J. Saindelle A. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. 2004). Huber R.207(1):69-73. Platinum concentrations in urban road dust and soil. One study found that traffic-control officers had no greater urinary platinum concentrations than office-based control subjects (Iavicoli et al. Raab W. Alimonti A. Levels of platinum in urine for the U. 2001). International Programme on Chemical Safety (IPCS). ruthenium.04 µg/L) in this Report. Seiwert M.S. Allergy and histamine release due to some platinum salts.123(3):451-454. Iavicoli I. Rommelt H. Cohrssen B. palladium. Environ Res 1975a.61(7):636-9.10:63-71. Schulz C. Gold-platinum dental restorations were correlated with increased urinary platinum concentrations. osmium... Campbell K. Kulka U. population were below the limit of detection (0. 206:15-24.13(1):24-30. 1998).. Kavanagh P. Petrucci F. Analyst 1998.76(1):5-10. Ewers U. rhodium. Kelly J. Parrot JL. Bocca B. Biomonitoring Information Urinary platinum levels reflect recent exposure. Pethran A.

450 (.310-.171 (.170-.145 (.230-.220) .270 (. Fourth National Report on Human Exposure to Environmental Chemicals 233 .410-.450 (.290) 90th .370-.225) .201 (.239) .243) .590) .260 (.410 (.181-.250-. In addition.183) . 0.640) .260 (. it has not been specifically mined or refined in the United States since 1984.420-.380-.200-.230) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.206) ..200 (.187-.135-.340 (.350) .350-. Thallium exposure occurs primarily from industrial processes such as coal-burning and smelting.500) .410) .02.440-. 7440-28-0 General Information Elemental thallium is a blue-white metal found in small amounts in soil and in sulfide-based minerals. From these and other sources. interval) .390 (.170 (.179-.250 (.240-.370 (.200) . thallium was obtained as a by-product of smelting other metals.300) . population from the National Health and Nutrition Examination Survey.190 (.330-.270 (.460-.180 (.440 (.270-.410-.430 (.560) .280-.250-.470 (.300) . and 0.200-.170) . Elimination from the body tissues occurs slowly through urine and feces (Blanchardon et al.147-.201 (.300 (.300 (.400-.480) .290) .380) .240-.200) .350 (.02.230) .196) .180-.191 (.500) .180 (.280) . 2005).350-.330) .410 (.430-.220 (.167 (.360-.260-.270-.320) .440 (.430-.S.200) .250-.360 (.410 (.173) .430 (.220 (.176 (.190 (.330-.175) . Thallium disappears from the blood with a half-life of several days.190 (.200) .202) .430) .197-.480) .340-.230 (.215) .200 (.360 (.250) .380 (. Human health effects from thallium at low environmental CAS No.200) .260-.170-.220) .180-.185-.250-.300) .400) .170-.137-.330-.02.150-.156) .290 (.160-.470) . 01-02.340-.310 (.450 (.400-.250-.360 (.157-.400 (. see Data Analysis section) for Survey years 99-00.217) .420) .410 (.510) .390-.450 (.300-.420) .170) . 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.480) .160 (.470) .200) .167-.270 (.330-.220-.310 (.430 (. It is still used in relatively small amounts in pharmaceutical and electronics manufacturing.490) Total .350 (.380-.165 (.370 (.460 (.430-.160-.360-.420-.170 (.230-.350-.134-.290 (.400) .290) .390-.410-.210) .156-.Metals Thallium depilatory cosmetics.390) .240) .280-.370) .230-.480) .300) .230) .400) 95th .144 (. In the United States.280 (.360 (. and 03-04 are 0.440) .350-.380 (.490) .370 (.290 (.330) .160 (.410-.180 (.190 (.183) .350-.200 (.146 (.218) .158) .450 (.170-.340-.145-.200 (.520) .390-.370) . however.390) .440) .340) .370 (.250 (.280 (.149 (.360) .170-.270) .185 (.147-.340) .410-.156) .310) .173-.400) .210-.154-.230) .390 (.220 (.400-.210 (.370-.200-.390-.440 (.500) .240-.159 (.250-.147-.260-.400) .480) .218) .270) . the latter being the current major industrial consumer of thallium in this country.300 (.270 (.133-.210 (.420 (.172 (.162-.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 .400 (.320-.202 (.340-.450 (.260-.290) .390) .250-.470) .510 (.160-.440 (.170) .590) .470 (.550 (.400-.290 (.420) .440) .490) .290-.290 (.200 (.360-.280 (.178) .170-.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 .330-.460) 861 675 618 561 657 723 801 1114 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.260) .350-.630) .520 (.450 (.270-.188) .172 (.153-.150-.159 (.420-.290-.370 (.270 (.390) .182-.177) .220) .184 (.200 (.420) .430 (.160 (.420-.330) .155 (.500 (.173) .290 (.160-.150-.192) Selected percentiles ( 95% confidence interval) 50th .400 (.320) .220 (.320) .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 .260-.160 (.196) .690) .330-.400 (.370 (.145-.180) 75th . In the past.370 (.520) .520) .360-.170 (.240) .490) .217 (.202 (.350) .450) .310 (.180) .450 (.180-.190 (.200-.172) .410-.450 (.240) .490 (.280) .420) .370-.163) .220 (.460) .400 (.180-.140-.170-.148-.150-.220) .370-.430) .150-.250-.420) . thallium is produced in a fine particulate form that can be absorbed through inhalation or ingestion.197 (. representing distribution into other tissues.220) .330-.400-.320 (. thallium readily crosses the placenta and also distributes into breast milk.190 (.420) .160-.160 (.290) .167-.260 (.150-.190-.280) .410 (.360-.330) .220) .410 (. respectively.159 (.

200) .198) .160) .137-.170) .S.281-. Chronic high-level exposures have been associated with weight loss.346) .287-.143) .194 (.215) . (ATSDR.364 (.161 (.224 (.422) .231-.235 (.282 (.148 (.158 (.149-.172) .162 (.333-.200-.317) .412 (.266-.214 (.271-.278 (.148-.333 (. neurologic injury.153-.200-.233 (. Peripheral neuropathy and alopecia are well-documented effects of acute and chronic exposures.142 (.167 (.260-.293) .156 (.154 (.307) .162) .271-.356) .167 (.280-.272 (.402) . and a drinking water standard has been established by U.237) .327) .146 (.150) .149) .254 (.162-.289) .153-.167) .267-. IARC and NTP consider the evidence for the carcinogenicity of thallium as inadequate or unclassifiable. 1992) Workplace air standards and guidelines for external exposure are established by OSHA and ACGIH.238-.387) .263-.223) .197-.205 (.346-.198-.301-.258-.152) .Metals doses or at biomonitored levels from low environmental exposures are unknown.141-.244-.338 (.159 (.333) .312 (.154 (.297 (.304) .153 (.169 (.306-.215-.167 (.383 (.389) .365) .342) .278) .424 (.321) .321 (.364 (.256 (.213 (.297) .377) .164) . Relatively high-dose intentional or accidental ingestion can result in gastrointestinal symptoms followed by multiorgan failure.184-.192 (.170) .313-.html.326-.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 .181) .307 (.210 (.197) . and death.389) .208-.286 (.313 (.222) 90th .300) .198-.178 (.153) .167) .349 (.184-.180) .300 (.237-.217) .208-.145-.299-.135-.153 (.313 (.202 (.153-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.356-.147-.167-.248) .287 (.122-.140-. population from the National Health and Nutrition Examination Survey.241) .143-.255 (.119-.146) .135-.227 (.184-.171) .363) 861 674 618 561 657 723 801 1114 1074 Non-Hispanic blacks Non-Hispanic whites 234 Fourth National Report on Human Exposure to Environmental Chemicals .271-.143 (.260 (.162) .147-.259) .125-.203-.167-.cdc.368 (.192-.278-.149 (.364) .306 (.191-.462) . respectively.378 (.469) .161) .292 (.200-.286 (.158-.364) .148-.273-.222 (.243) .188 (.324) .128 (.219) . arthralgias.146) .142 (.140 (.238) . Biomonitoring Information Urinary thallium levels reflect recent exposure.231) .. environmental levels) and health effects is available from ATSDR at: http://www.208) .383) .412) 1200 1312 1281 1213 1340 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .333 (.136 (.173 (.148-.286) .204 (.329) .216 (.389-.246-.189) .221) .377) .230) .160 (.156) .128-.214) .458 (.304) 95th .157-.185 (.196-.162-.456) .215 (.319) .286-.304) .159-.222 (.133-.148-. Information about external exposure (i.280) .264 (.254-.143 (.140 (.265-.375 (.155-.300-.144-.157 (.156 (.167 (.S.340-.350) .169) .214 (.269) .402) .156 (.223 (.154 (.207 (.155) .e.350 (.gov/toxpro2. interval) .293 (.282-.154 (.286 (.221 (.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 .343 (.250) .161) .250-.400-.155 (.159) .170-.148 (.145 (.297 (.217-. Levels of thallium in urine for the U.366) .133 (.412 (.187-. Severe accidental thallium poisonings from ingesting of rat poisons that contained water-soluble thallium salt have occurred.160-.258 (.180-.306-.236) .221) .173) .226-.146 (.348-.156 (.176) .192-.283 (.134-.333-.152) .304 (.131-.212) .362) .145-.250-.146-.194 (.278-.370 (.278 (.217-. although additional mechanisms of action are possible.222) .286-.196 (.155-.361 (.233) .323 (.153) .333-.313-.234-.343 (.177) .304) .348) .207) .164) .273-.171) .328 (.369 (. 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.152) .146-. EPA.532) .222-.153 (.204) .169-.206 (.143-.151) .366 (.330-.333) . Thallium produces toxicity by replacing intracellular potassium in the body.214) .218 (.168 (.145) .149-.272-.157) .387) .278) .338-.166 (.269 (.S.348 (.226) .273 (.160) 75th .424) .458) .244 (.144-.153 (.142-.229-.146-.138 (.207-.179-.317 (.214-.240) .176) .600) .211 (.147-. and polyneuropathy.176) .369) Total .325-.176) .151-.161 (.191-.380 (.198-.179) .182 (.211 (.271-.171-.200 (.atsdr.291-.328-.229) .150) .153 (.300) .162) .173) Selected percentiles ( 95% confidence interval) 50th .166 (.317 (.235-.278) .462) .286 (.274-.289) .318-.129-.337-.135-.160) .

Available at URL: http://www.76(1):53-59.1 mg/m3 (Marcus. Investigations of thallium-exposed workers in cement factories. blood.gov/toxprofiles/tp54.html. Trace metals in urine of United States residents: reference range concentrations. Challeton-de Vathaire C. Schmidt M. Sci Total Environ 1990.S..95:89-105. Trace element reference values in tissues from inhabitants of the European Union. Trace element reference values in tissues from inhabitants of the European community I. Marcus RL.. Celier D. Apostoli P. Schaller KH. Ewers U. Valentin H.216:253-270.48(4):375-389. Manke G. Third National Report on Human Exposure to Environmental Chemicals. X. 1998. Pirkle JL.5 μg/L. Intake and health effects of thallium among a population living in the vicinity of a cement plant emitting thallium-containing dust. Buhlmeyer G. Environ Res 1998. Nearby residents were exposed by eating garden plants that had been contaminated by the thallium. These urine levels are generally comparable to levels observed in earlier studies of general populations (Brockhaus et al. Toxicological profile for thallium. Ting BG. Soddemann H. Long term retention and excretion of 201Tl in a patient after myocardial perfusion imaging. 2005) and are shown with results from NHANES 2003-2004 in this Report. 1992 [online].atsdr. There was no increase in the prevalence of symptoms at levels less than 20 μg/L and only a slight increase in nonspecific symptoms greater than 20 μg/L. Martin J-C. 7/15/09 Blanchardon E. Kramer U. Wiegand H. and serum of Italian subjects. 1981. Boisson P. 1985). Radiat Prot Dosim. Sampson EJ. Minoia C. J Soc Occup Med 1985. Pozzoli L.. population) are thought to correspond to workplace exposures at the threshold limit value of 0. Sabbioni E. Gallorini M. Morrow JC. Seventy-eight percent of the urine specimens in that study contained greater than 1 μg/L. White and Sabbioni.. 2005. Centers for Disease Control and Prevention. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Int Arch Occup Environ Health 1980. Paschal et al. Brockhaus A. Minoia et al. A study of 13 elements in blood and urine of a United Kingdom population. Sci Total Environ 1998. Schaller et al. Brockhaus et al. Urinary concentrations of 100 μg/L in asymptomatic workers (500 times higher than median levels in the U. et al. 1990.cdc.47(3):223-231. et al. White MA. Atlanta (GA).113(1):47-53. A study of 46 elements in urine. 1998). Jackson RJ. Int Arch Occup Environ Health 1981. Sabbioni E.265 people living near a thallium-emitting cement plant in Germany. et al. Cassot G. Fourth National Report on Human Exposure to Environmental Chemicals 235 . Raithel HJ. Finding a measurable amount of thallium in urine does not mean that the level of thallium causes an adverse health effect.Metals (CDC. 2005. (1981) studied 1. References Agency for Toxic Substances and Disease Registry (ATSDR). with concentrations ranging up to 76.35(1):4-9. Dolger R. 1980. Investigation of a working population exposed to thallium. Pietra R. Paschal DC. 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.

430 (.180 (.180) .120) .113 (.260-.650) .100 (.370-.080) .135) .260-.070 (.230 (.250) .076 (.122) .101-.250-.070-.180-.068) .082) .180-.230) .170) . interval) .270 (.320 (.350 (.400-.310-.105 (. 7440-33-7 General Information Tungsten is a steel-gray to tin-white metal that occurs naturally in the earth’s crust.370-.00) .130 (. and 0.430-.095-.260) .090) .160) .550 (.113 (.130) . Although workers occupationally exposed to tungsten carbide may develop serious lung disease (“hard metal disease”). their illness may stem from exposure to cobalt mixed with tungsten carbide rather than to tungsten alone.090-.090-.260-.126) .500 (.071 (.210-.066-.190) .060 (.080 (. Little information is available on the toxicity of tungsten.080-.250) .220) .070) .100) Selected percentiles ( 95% confidence interval) 50th .430) 320 363 290 679 744 725 1339 1545 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .060-. Urinary Tungsten Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.270 (.430 (. bronzes in pigments.300 (.360-.290) .160 (.830) .070) .250) .204) .120-.096 (.520) .130) .280 (.160) .060 (.058-.330-.110-.440) .092 (.100-.800) .130-.420-.220) .800) .073-.190-.110-.151) .530 (.140-.400) .420-.150) .350) . which is used in the steel industry.470-.220) .370 (.140 (.240 (.170) .400 (.500) .320-.340-.080) .090-.070-.360-.350) .100) .080) . filaments for incandescent lamps.109) .123-.Metals Tungsten CAS No.060-.290) .310-.200-.060-. Human health effects from tungsten at low environmental doses or at biomonitored levels from low environmental exposures are unknown.092 (.100 (.071-.620) .082 (. Tungsten is used mainly for producing hard metals.130-.620) .070) .130) .170 (.120-. mainly as scheelite (CaWO4).105) .095-.180 (.120) .310-.360) .310-.050-.077-.310 (.370 (.320) .150 (.210 (.580) .120-.490 (.100) .070-.470) .111-.130) .180) .220-.S.070) .290-.300 (.270-.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 .078-.060-.110-. 0.210 (.060 (.530 (.170 (.090-.090-.110) .069) . population from the National Health and Nutrition Examination Survey.090) .060-.370 (.100) .550) .092) .110 (.550) .270-.310) .200) . and as catalysts in the petroleum industry.230-.180-.090-.380-.400 (.080 (.350-1. see Data Analysis section) for Survey years 99-00.084) .070-.53) .210 (.120) .290-. which are used in rock drills and metal-cutting tools.370) .050-.230-.130-.400 (.160-.100) .081 (.550) .140 (.100 (.080 (.073) .270-.132) .113 (.380) .140 (.090) .570 (.084 (.120) .220 (.950) .091) .084-.330-.250) .101 (.340-.670) .088 (.110 (.250-.158 (.270 (.180) .064-.230) .310-.570 (.090 (.110) .090-.270-.120) .160 (.350) .400 (.790) .090 (.110 (.300 (.190-.130-.500 (.380 (.056-.260 (.140) 90th .260 (.170-.04. Most background environmental exposures to tungsten are from the soluble forms such as tungstate salts that may occur in drinking water.280 (.160-.810) .060 (.360 (.062 (. Occupational exposure is from dusts released during grinding or drilling of hard metals.050-. Tungsten compounds are used as lubricating agents.340) .410) 790 680 618 562 649 723 802 1117 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.460) . and it has not been classified with respect to its carcinogenicity by either IARC or NTP.300) .190 (.087-.190 (.087) .160-.450-.250) .460 (.060 (.130) .510-.090 (.240-.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 .530 (.080-.410 (.160 (.470 (.320 (.620 (.120-.180) .330 (.160-.090-.430) .062 (.120-.230-.630) .093 (.050-.520) .430-.560) .113 (.520) .390 (.210 (.290-.590) .770 (.074-.170) .200 (.070 (.100 (.093) .510 (.137 (.090) . and for producing ferrotungsten.100) .290 (.140-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.430 (.133) .080 (.100-.450 (.470 (.116) .510-1.380-.082-.300) 95th .150 (.490) .065-.390) .190-.073 (.690) .190-.330) .560 (.340-.360 (.300-.070-.320-.070 (.360 (.130 (.170) .076 (.460 (.120-.082 (.380 (.210) .160 (.380-.140 (.560) .04.250) . respectively.080) 75th .470) .110 (.560) .080-.560) .060-.107 (.150-.093-.480) Total .100-.410-.640 (.460 (.280-.097-.110 (.380-.096-.120) .330) .104) .060 (.086 (.120 (. 236 Fourth National Report on Human Exposure to Environmental Chemicals .150 (. Evidence is lacking for the carcinogenicity of tungsten. 01-02.460) .080 (.065 (.230-. and 03-04 are 0.210 (.073-.056-.088) .069-.180-.160 (.04.

098-.727) .148) .267-. interval) .201) .067 (.094) .880) .217-.065-.214-.S. Using neutron activation analysis to 2000.053-.148 (.075-.078 (.109 (.094) .240-.108-.381) .217-. measure urinary tungsten.201 (.054-.358) .133) .093) .157) .122-.071-.119-.054-.462) .410-.484) .084 (..340 (.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 .161) .326) .144-.339 (.465) .086) .098 (.216 (.085-.098-.124 (.103-.105 (.139-.329 (.258 (.347 (.169 (.079 (.634 (.096) . 2001-2002.089) .071) .069 (.176-. population (CDC.150 (.302-.188-.300-.167) .136-.150-.124-. Biomonitoring Information median urinary levels were as much as 15-fold higher than median levels in the U.200-. and 2003-2004 (Paschal et al.203-.190) .063-.179-.180-.200-.216-.538) .126-.431) .250 (.317 (.091) .452-.071) .222-.169) .109-.375) . Nicolaou et al.075-.170-.092) .081-.079) .293 (.081 (.055-.253-.085) .131-.106 (.111 (.198-.154) .386) .074-.392) .063-.083) .279 (.255-. 2005).333 (.122 (. (1987) found possibly due to methodologic.100) . 1998).057-.267) .049-. 2001).272-.(Kraus et al.302-.285) .116-.167) .100 (.093-.354) .359 (.255 (.255 (..174) .081 (.077) .069-.184 (.084) .181 (.28) .333 (.139) .078) .077-.S.082 (.353 (.333 (.079 (.146) .063 (.083 (.739) .125 (.359 (.412 (.237) .333 (.308) .105 (.098-. population from the National Health and Nutrition Examination Survey.231 (.075 (.070 (.317) .333-.199 (.216-.294 (.082) .107-.436) .308) .075 (.364 (.152-.136-.120) .500) .555 (.179-.133) 90th .144 (.071 (.078 (.077) .074) 75th .198) .136-.222) . A were more than 900 times higher than the overall geometric nonrandom subsample from NHANES III demonstrated mean of the U.080-.215 (.084 (.065 (.431) .071 (.065 (.069 (.065) .211 (.095) Selected percentiles ( 95% confidence interval) 50th . population in the NHANES 1999-2000 slightly higher values than those found in NHANES 1999.279 (.484 (.136-.158) .341 (.287) .439 (.146 (.209-.261-.300-.605) .258-.354-.554) .306) .067-.079) .074-.116 (.216 (.108) .080 (.153) .080-. 1997).250-.151 (.068-.121 (.079) .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 .064-.146 (.078-.283) .333-.278-.360 (.071) .168 (.206-.158 (.174 (.158) .497 (.057-.439) Total .301) .068 (.237-.059 (.Metals Workplace air standards for external exposure have been established by ACGIH and recommended by NIOSH.094-.300) .199 (.250 (.329-.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 .299 (.090-.071 (.117) . or exposure that a control group of non-metal workers had mean levels differences.059-.090-.060 (.150-. In whereas the tungsten-worker group had mean urine levels a Nevada community where tungsten was measured and 35 times higher.426) .139 (.253 (.385 (.339 (.081) .164 (.214) .S.344-.231-.091 (.098) .270 (.122-.138 (.085 (.245-.279 (.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 .086-.095-.237) .154) .224) .082) .823) .138 (.061-.091) .143 (.066 (.059-.301) .073 (.155-.453) .197-.084) .086) .414) . A study of 14 unexposed adults yielded values that were similar to the 95th percentiles in this Report.186 (.078) .063-.153-.091) .275 (.116) .233-.218 (.582) .065-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf..253) 95th .136 (.176-.100) .158) .099-.145 (.197 (.079) .060-.197) .073 (.333) . Workers involved in grinding operations that released tungsten metal into the air had elevated urinary levels that Levels of urinary tungsten reflect recent exposure.133) .119 (.167-. Patients with medically-inserted tungsten found at increased levels in drinking water.070 (.072 (.426) .104-.125) .086) .089 (.075) .167-.072-.063-.087) .083-.465) .087 (.197) .121-.088) .088) . population.063 (.058-.143-.138) .436-1.205-.300 (.073 (.056-.187) .083 (.383 (.074 (.431) .353 (.216-.379 (.667) .333) .130 (.091 (.074) .208-.062 (.165) .317-.061-. 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.059-.265 (.331-.056-.120) .064-.215) .286-.060-.667 (.077-.067 (.073 (.130-.075) .482 (.284) .301) . 2003.459) .117 (.072-.065-.797) .439 (. similar to those in this Report (Schramel et al.315-.083) .091) .061-.066 (.080 (.

Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Angerer J. Schramel P. Environ Res 1998.58(10):631-634. The determination of metals (antimony. Trace metals in urine of United States residents: reference range concentrations. Wendler I. Exposure assessment in the hard metal manufacturing industry with special regard to tungsten and its compounds. thallium. bismuth. et al.htm. References Bachthaler M. Occup Environ Med 2001. Zobelein P. cadmium. and hair (Bachthaler et al. lead. Churchill County (Fallon). Catheter Cardiovasc Interv 2004. [online] 2003. 2004). Ting BG. Third National Report on Human Exposure to Environmental Chemicals. 4/15/09 Centers for Disease Control and Prevention. Paschal DC. Pirkle JL. Mosconi G. Nevada Exposure Asssessment. 238 Fourth National Report on Human Exposure to Environmental Chemicals .62:380-384. Morrow JC. Centers for Disease Control and Prevention. Angerer J.Metals blood.76(1):53-59. Schaller KH. Jackson RJ. Available at URL: http://www. Nicolaou G. platinum. Cancer Clusters. Multielement determination of metals in biological specimens of hard-metal workers: a study carried out by neutron activation analysis. Seghizzi P.69(3):219-223. Pietra R. 2005. Feuerbach S. palladium. National Center for Environmental Health.gov/nceh/clusters/Fallon/study. Atlanta (GA). Sampson EJ.cdc. mercury. Link J. tellurium. Lenhart M. Finding a measurable amount of tungsten in the urine does not mean that the level of tungsten causes an adverse health effect. Paetzel C. J Trace Elem Electrolytes Health Dis 1987. Weber A. tin and tungsten) in urine samples by inductively coupled plasma-mass spectrometry. urine. Int Arch Occup Environ Health 1997. Kraus T. Sabioni E.. Cassina G. Urinary tungsten levels in many patients were hundreds-fold higher than observed in this Report.(2):73-77. Corrosion of tungsten coils after peripheral vascular embolization therapy: influence on outcome and tungsten load. 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. Manke C. Schramel P.

009-.007 (.007-.039) . Fourth National Report on Human Exposure to Environmental Chemicals 239 . see Data Analysis section) for Survey years 99-00.027) .011 (.009) .017-.011 (.013 (.062) .018-.023 (.020) . In workplaces that involve uranium mining.036) 883 683 618 568 667 722 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.012-.011) .035-.030 (.030 (.026) 95th .006 (.022) .055 (.034) .009-.021 (.051) .012) .015) .007-.017-.021-.007 (.010 (.021) .021 (. the primary exposure sources for nonoccupationally exposed persons are dietary (especially root vegetables) and drinking water.030 (.011-.012-.012) .011) .022-.S. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.008 (.005-.034-.009-.026 (.054-.031 (.038) .007-.033 (. Variable concentrations of uranium occur naturally in drinking water sources.014 (.022-.016) .017) . 7440-61-1 General Information Uranium is a silver-white metal that is extremely dense and weakly radioactive.011-.023-.006-.037) .015 (.018) .037) .017) .012-.027 (.023) .006-.005.031 (.011-.009) . 0.007) .046-.013) .010) .012 (.008 (.007-.065) .018) .007-.012-. DU has been used by the military in armor-piercing ammunition and as a component of protective armor for tanks.009-.020-.039) .010) .013 (.010) .010-.029-.041 (.011) .020-.006-.010 (.009 (.056) .015 (.007-. 01-02.016) .027-.009 (.018 (.009) .007 (.017-.009 (.009-.012-.035) .067) .018) .015 (.007 (.017 (.027 (.043) .020 (. Thus.030-. milling.016) .016-.012) . 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.007) .035) .029 (.046 (.040-.031 (. Uranium has many commercial uses.009) .016 (.048 (.020-.008-.021-.008) .009) .049) .007-.006-.007) 75th .014 (.007 (.026-.008 (.012 (.017) .017-.033) .006-.007-.009 (.036 (.008) .028 (.037) Total . in some ceramics.006 (. and as an aid in electron microscopy and photography.007-.007) .010) * .023-.033 (.008 (.060 (.009) . 235U (about 0.008 (.010) .037-. Since the 1990’s.009) * .024-.018) .063) .016-.036) .040-. or processing.042 (.036-.008 (.009 (. and 0.027 (.007-.010 (.022 (.040 (.008) .047 (.013-.005-.007-.013 (.024-.006-.009 (.005-.040 (.031 (.009 (.006-.008) .014 (.010-.036-.114 (.023 (.007-.073) .014 (.069) .045) .007 (.019-.023-.009) .010 (.019-.015-.028 (.017) .009-.012 (.038 (.009) .009) .064 (.020-.007) .053 (.023) .049) .026) .008 (.011-.028-.008-.008 (. population from the National Health and Nutrition Examination Survey.027-.054) .007 (.Metals Uranium CAS No.026-.016-.046 (.046) .028 (.022-.012 (. and 03-04 are 0.011) .027) .009 (.007 (.030) . and 234U.013 (.007 (.010) .011-.052 (.017 (.014 (.015 (.010) * .006 (.034-.007 (.013 (.010) .006-.009) .006-.009 (.008 (. nuclear fuel.010-.006 (.066) .072) .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 .008-. including nuclear weapons.027-.006-.009) .028-.009-.065) .016) .012 (.032 (.031-.037 (.021 (.017) .026 (.008-.027 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.007-.008-.021) .012-.023 (.008 (.005-.127) .045) .009-.007-.008 (.025-.007-.010) .018 (.041 (.72%).008 (.019-.009) Selected percentiles ( 95% confidence interval) 50th .009) .006-.008 (.053) .158) .008-. 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.013-.008-.042) .010-.009-.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 .046 (.017-.033-.054) .050) .017-.019 (. Natural uranium is a mixture of three isotopes: 238 U (greater than 99%).027) .011) .008 (.011) .008) .026 (.004. respectively.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 .067) .023-.009) .010 (.016) .013-.006-.004.011-.024-.027) .006-.010) .009 (.010-.050) .009-.011-. It usually occurs as an oxide and is extracted from ores containing less than 1% natural uranium.044 (.007) .007-.043 (.020) .279) .013) 90th .008 (.039-. interval) .020-.040) .029-.024 (.010-.088) .040) .007 (.026) .008 (.007-.031 (.023) .011) .048) .056) .015) .016) .013 (.021) .036 (.046 (.008 (.012 (.013 (.012) . human exposure occurs primarily by inhaling dust and other small particles.007-.005-.037) .008-.014 (.036) .019-.

019-.006-.008) 75th .010 (.010) * .019 (.008 (.034 (.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 .035 (.056) .011-.020-.012 (.014) .012 (.006) . After long term or repeated exposure.015-.S.005-.007 (.015 (.019-.008 (.029) .042) .017-.010-.016-.027-.008 (. 2003).018 (.007 (.006-.005 (.050 (.010-.026 (.018-.009) .010) .004-.019 (.005 (.011-.010-.019-.007 (.007-.010 (. population from the National Health and Nutrition Examination Survey.024) .008-.006-.009 (.050) .022-.010) .010-.028) . liver.009) ..034 (.012-.018-.007 (.009-.012 (.059 (.034) .022 (.040 (.012 (.027-.008) . 0.020 (.033 (.024) .039) .006-.014-.058) .034-.016) .006-.044) .011-.010) .033 (.006-.024 (.009) .015 (.007 (.006-.011) .027 (.016) .007 (.054) .009-.025-.010) .016) .013 (.043 (.006) .008) .006-.014-.030 (.007) .030-.010-.008) .031 (.014 (.008 (.009) .270) . 240 Fourth National Report on Human Exposure to Environmental Chemicals .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 . Radiation risks from exposure to natural uranium are very low.009 (.015) .045 (. Depending upon the specific compound and solubility.039) Total .013 (.009-.006-.012 (.080) .053) .033 (. After inhalation.010-.010-.017-.016-.024) .017 (.030 (.016) .005-.006-.006 (.006 (.024-.009) .009) .008) .015-.050) .021-.020) .009) .028) .020 (.009) .019) .013 (.009) Selected percentiles ( 95% confidence interval) 50th .012 (.013 (.006-.022 (.034-.017) .019 (.047) .013 (. with much slower elimination from bone.011-.029 (.008) .061) . 2005).017 (.005 (.058) .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 .006-.063) .009 (.146) .007-.018-.007-.007 (.030) .028) .015) .021 (.007 (.010) .021) .009) .007 (.016 (.042) .033 (.009-.006-.026-.009 (.009-.006-.012 (.006-.051) .010 (. Human health effects from uranium at low environmental doses or at biomonitored levels from low environmental exposures are unknown. In cases of retained DU shrapnel.Metals impact.013 (.009) .012) .024 (.015-.008) .008 (.007-. Inhaled uranium-containing particles are retained in the lungs.021 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.005-.010-.006-.015-.010 (.027) .004-.021 (.011 (.016-.016) .013-.013 (.025 (. and bones can accumulate uranium with the largest amounts being stored in bones (Li et al.013 (.006 (.005-. 1992).006 (.007 (.027-.027 (.008) . After exposure to soluble uranium salts.006) .017) .013 (.019-.027-.030-.010 (.027 (. Uranium is eliminated in feces and urine.006-.051) .067) .016-.006-. Studies of persons with chronic exposure to soluble uranium salts in drinking water have not shown kidney Urinary Uranium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.005-.007 (.039) .051) .011-.025) 95th .031-.008-.008) .025-.011) .005-.028-.014) .023-.015) .007-.010-.016) .039) .051 (.013 (.005-.009 (.008 (.022) . where limited absorption occurs (less than 5%).006-.008 (.042-.029) . the initial half-life of uranium is about 15 days (Bhattacharyya et al.033) .007 (.074) .006 (.008 (.019-.011-.006-.010-.025-.007 (.029 (.008) .011-.011-.077) .008) .006-.014 (.024 (.014) .032) .016) .021 (. Health effects from uranium exposure result from chemical toxicity to the kidney.025-.008) .011-.007-. kidneys.010) .013) .024) .016) .015 (.007 (.053) .028 (.020-.018-.013) .018-.015) .009) .007 (.011) .011 (.029) .007) .. low level exposure.034 (.006-.009-.022-.019) .007-. Soluble forms of uranium salts are poorly absorbed in the gastrointestinal tract.006 (.1%-6% of an ingested dose may be absorbed.037 (.012-. the shrapnel acts as a source of chronic.032) .030 (.007 (.017) .012) .026) .027) .024) .007-.012) . interval) .100 (.008 (.020 (.007 (.007-.014) 90th ..017-.028) .020-.029) . the half-life of insoluble uranium in the lungs is several years (Durakovic et al.009) * .006-.015-.008-.040) 883 682 618 568 667 722 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites * Not calculated: proportion of results below limit of detection was too high to provide a valid result.006-.034 (.013) .005 (.008 (.020-.018) .010-.007 (.011) * .024-.006) .014-.026 (. which represents distribution and excretion.007 (.048) .035 (.007 (.028 (.025 (.041) .022 (. which can occur occasionally from high occupational exposure.007 (.022-.015 (.006) .030) .007-.024-.026 (.034 (. about 50% of the absorbed dose is eliminated in the urine within the first 24 hours.007) .008-.008-.029 (.017-.008-.048) .

78:143-146. et al. Karpas et al.atsdr. respectively. Tolmachev et al.. Horan P. in that the levels were below their respective detection limits (Byrne et al. the median urinary uranium concentration was 2.S.. Galletti.066 μg/g creatinine (Gwiazda et al. McDiarmid et al. NRC. IARC and NTP have no ratings for uranium human carcinogenicity.. 2006..107:143-157. Eighty-five percent of those levels were above the 95th percentile of the NHANES 1999-2000 population. Guidebook for the treatment of accidental internal radionuclide contamination of workers. 2006).011 μg/L (McDiarmid et al. Komaromy-Hiller et al. Uranium content of blood. In a study of 105 persons exposed to natural uranium in well water. Drinking water and other environmental standards have been established by U.. 2006).. 41 (1). The U. ingestion. soldiers evaluated before. In: Gerber GB. eds.S. 2000). Boyd P. 2004)... Benedik L. Pullat VR. 1999) and other small populations have shown urinary concentrations that are similar to those in NHANES 1999-2000. Hamilton et al. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Older studies have demonstrated urinary uranium concentrations that are consistent with levels in the U. population.1996. 2004). Six workers in a depleted uranium program showed concentrations of 0.. In the same study. 2003.62:562-566. Stradling GN. Nuclear Regulatory Commission (NRC) has set an action level of 15 μg/L urinary uranium to protect people who are occupationally exposed (U. 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.168(8):600-605. 2006).. 2005. Byrne AR. 2004). with emphasis on quality control. 1994. and 2003-2004 (Dang et al. Finding a measurable amount of uranium in urine does not mean that the level of uranium causes an adverse health effect.S. Breitenstein BD.html. Atlanta (GA). pp.S. Information about external exposure (i.S. 1991. Health Phys 1992. Carmichael AJ. References Bhattacharyya MH. the median urinary concentration was 0. urine and hair of exposed and non-exposed persons determined by radiochemical neutron activation analysis. 2004). 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.. Dang HS. A previous nonrandom subsample from NHANES III (n = 499) (Ting et al. 2001-2002. Thomas RG. 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. soldiers who had been injured and had embedded DU shrapnel for as long as eight years.162 μg/L) (Orloff et al. during. Hamilton MM.e. 28 soldiers who may have been exposed to DU by inhalation. Sci Total Environ 1991. Vol.. the geometric mean urinary uranium concentration was 0. Metivier H. 2002). but in whom no shrapnel was embedded. In a much larger study of 446 Gulf War veterans who were concerned about past exposure to DU. (Kurttio et al. Biomonitoring Information Levels of urinary uranium reflect recent and accumulated exposure. EPA. Determining the normal concentration of uranium in urine and application of the data to its biokinetics.S. Squibb K. Durakovic A. 2002. although slightly increased during and after deployment. 2000). 1978). Health Phys 2000. Mil Med 2003. Pillai KC. Ejnik JW. (May 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.1992. Fourth National Report on Human Exposure to Environmental Chemicals 241 . In two studies of a Finnish population with high natural uranium concentrations in their drinking water. Recent studies of veterans have been conducted to examine concerns about DU exposure during military conflicts. Volf V.55 μg/L (median 0. or wound contamination.110 to 45 μg/L (Ejnik et al. 1992. environmental levels) and health effects is available from ATSDR at: http://www. had a mean urinary uranium concentration of 0. Muggenburg BA.078 μg/L (ranging up to 5.Metals injury associated with elevated urinary uranium levels (Kurttio et al. Centers for Disease Control and Prevention (CDC).61 μg/g creatinine.65 μg/L). Radiation protection dosimetry. 1-49.gov/ toxpro2. Zimmerman I. Urinary uranium measurements in 103 Canadian military personnel showed mean urinary levels slightly less than geometric mean in this Report (Ough et al. Dietz LA.cdc.. 2006). Determination of the isotopic composition of uranium in urine by inductively coupled plasma mass spectrometry. and no consistent effects on multiple endpoints of kidney function were found. A cohort of 46 U. In 17 U... Third National Report on Human Exposure to Environmental Chemicals... Workplace air standards and guidelines for external exposure to soluble and insoluble uranium compounds have been established by OSHA and ACGIH. Kent (England): Nuclear Technology Publishing. urinary levels of uranium were as high as 9. McDiarmid M..

Makelainen I.47(6):972-982. Health Phys 2003.S. Karpas Z. Jackson RJ. Shelly T. Health Phys 1996.67(8-10):697-714. 242 Fourth National Report on Human Exposure to Environmental Chemicals . Int Arch Occup Environ Health 2006. et al.22–Bioassay at uranium mills. Pinto V. Environ Res 1999. Jarrett JM. McDiarmid MA. Biologic monitoring for urinary uranium in Gulf War I veterans. Harmionen A. McDiarmid M. et al. Environ Health Perspect 2002. D’Annibale L. VI.S. Element reference values in tissues from inhabitants of the European community. et al. Biokinetic modeling of uranium in man after injection and ingestion. Pirkle JL. Gucer P. Renal effects of uranium in drinking water.87:51-56.S. Katorza E. Kane R. Washington (DC): NRC. Military deployment human exposure assessment: urine total and isotopic uranium sampling results. Nuclear Regulatory Commission (NRC) Guide 8. Wahl W. Comparison of representative ranges based on U. Oeh U. Metcalf S. Review of elements in blood. Ejnik J. Auvinen A. Sampson EJ. McDiarmid MA. Environ Res 2004. Kidney toxicity of ingested uranium from drinking water. Auvinen A. Hollriegl V. et al. Ting BG. Komaromy-Hiller G. Squibb K. Van der Venne MT. Kurttio P. Bennett LG. Marino R. Hancock RG.81:45-51. Oberbroekling KJ.71(6):879-85. U. Hamilton EI. Lewis BM.85:228-235. Biological monitoring and surveillance results of Gulf War I veterans exposed to depleted uranium. Noguchi H.91(2):144-153. Roiz J.158:165-190. Roth P. Halicz L. Costa R. Kuwabara J. Tolmachev S. Charp P. Inductively coupled plasma mass spectrometry as a simple.86:12-18. et al. Health Phys 2004. Smith D.110(4):337-342. An examination of uranium levels in Canadian forces personnel who served in the Gulf War and Kosovo. Cordero S. patient population and literature reference intervals for urinary trace elements. May LM.94:319-326. Radiat Environ Biophys 2005. July 1978.79(1):11-21. Paretzke HG. Paschal DC. Wilson PD.S.82(4): 527-532. Marko R. Salonen L. Uranium daily intake and urinary excretion: a preliminary study in Italy. Salonen L. Pekkanen J. Heller J. Ash KO. U. Saha H. Komulainen H. Karpas Z. Scott K. Saha H.296(1-2):71-90. Ough EA. Health Phys 2006. Am J Kidney Dis 2006. Oliver M. Li WB. Squibb K. Engelhardt SM. Health Phys 2002. Sabbioni E. Human exposure to uranium in groundwater. Sci Total Environ 1994.44:29-40. plasma and urine and a critical evaluation of reference values for the United Kingdom population. Health Phys 2004. Uranium and thorium in urine of United States residents: reference range concentrations.Metals Galletti M. Howerton K. Englehardt SA. Andrews WS. Detection of depleted uranium in urine of veterans from the 1991 Gulf War. and inexpensive method for determination of uranium in urine and fresh water: comparison with LIF. Nuclear Regulatory Commission (U. Kalinsky V. Clin Chim Acta 2000. Kurttio P. Lorber A. concentration and daily excretion of uranium in urine of Japanese. et al. Cremisini C. NRC). Mistry K. rapid. Gwiazda RH. J Toxicol Environ Health A 2004. Orloff KG.

Other manufactured uses include fireworks.0-17. interval) 3.0 (12.0) 374 314 828 721 1618 1487 01-02 03-04 01-02 03-04 4. Animal and human studies have shown that perchlorate can inhibit thyroid hormone production (NAS.0) 1335 1229 1485 1293 01-02 03-04 01-02 03-04 01-02 03-04 4.80-12.0) 10.22-5. 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.10) 3.0-17. 2007).40-4.80) 3.20 (2.0 (9.40 (4.76 (3.0) 13.0) 9.. Perchlorate has been characterized as a mobile and persistent ground and surface water contaminant.40) 3. or ammonium salt.93 (4.0 (11.0) 11.50-4.51 (3.90) 6.80) 12.0 (12. 2005).EPA.0) 9. but has strong oxidant properties in the presence of concentrated acids. 2002).20 (5.0) 13.38) 5.10 (6.08-3.50) 5.00) 7.20) 7.20-4.40) 3.12) 3.0 (11.0) 708 617 681 652 1228 1092 Limit of detection (LOD.0) 15.70 (3.80 (3.00-6. fabric dyeing.0 (8.30-17.90-3.00-5.40-5.20-11.62 (3.0) 15.90-11.10 (5.75 (3.00) 3.0 (9.00) 3.60 (7.19 (3. 1998).30-7.35 (3.40) 4.90-12.90 (2.31) 2.80 (6.90-3.56) 3.0) 13.40) 2.30) 6.50-4.70-3.80) 7.10-7..50 (8.0) 11.60 (4.50) 6.0 (12.02 (3.0 (8.50 (3.20-3.0 (11.47-4.0) 9.20-4.60) 5.0) 9.0 (9.Perchlorate Perchlorate (Urbansky.20 (4.60 (4.05 and 0.0) 13.70-11.96 (3.80-6.19-4.18-3. The ammonium salt of the perchlorate ion has been manufactured in the military defense and aerospace industries primarily for use as an oxidizer in solid propellant systems for rockets and missiles.0-23.90-10.07-4.0) 13.0) 13. lettuce) can be the main sources of intake for humans (FDA.0-29.79 (2.50) 5.87-3.51 (3.32 (3.45-4.0 (11.90-9.0 (12.89-3.50 (5.10 (6.0-17.90-11. and certain plants with high water content (e.40 (5.68) 4.10-4.0 (8.70) 3.S.40-11.0) 9.60) 3.70-7.84) 14.50) 3. Perchlorate is stable under most environmental and physiological conditions.40 (5.0) 16.40) 6.10 (7.00-6. and reducing agents. 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.88) 3.30 (2.0 (11.00) 5.40) 90th 10.60-6.90 (4.40 (3. matches.0 (8.93-4.16) 3.30-6.0-17.10) 3.40) 3.29-3.74-3.66) 3.0 (11. and electroplating.20 (6.44-4.50) 11. Perchlorate was added to the U. laboratory analysis.0) 9.0-20.90 (3. see Data Analysis section) for Survey years 01-02 and 03-04 are 0.0) 12.0-15.30) 6.S.50-11.10-12.70 (3. population from the National Health and Nutrition Examination Survey.20) 4.0) 10.60) 8. Survey years 01-02 03-04 Geometric mean (95% conf. 2005).30 (2.90 (5.10) 5.20-12.40 (5.26 (2.0) 14.80 (7.0-18.80) 75th 6. It is normally found and produced as the anion of a sodium. Large doses of perchlorate have been used as a medicine to treat hyperthyroidism and to diagnose disorders related to thyroid or iodine metabolism.70-5.0) 95th 14.0) 19.0) 13.39-4.90-6.80-4. milk. In addition.60-7.30-7.81-16.65) 3.0 (11.40-13.54 (3.0 (13.0 (11.0) 11. leather tanning. Perchlorate is excreted unchanged from the human body with an estimated elimination half-life of about 7.0-18.0 (11.90 (5.0-18.50-7.0 (9.0) 8.0) 10.80-15.0-14.10-11.40 (3.70 (3.0) 8.09) 3.S.0) 13.30-19. 7601-90-3 General Information Perchlorate is an inorganic chemical containing one chlorine and four oxygen atoms. Drinking water.g.80-4.40-4.0) 14.0 (10.50-3.10-11.21 (2. certain catalytic metals.81) Selected percentiles ( 95% confidence interval) 50th 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 3.05.0 (9.90-9. and limited applications in pharmaceutics.0 (9.11) 3.40-6.90 (5.5 hours and has a small estimated volume of distribution (Crump and Gibbs. small amounts of perchlorate can form naturally in the atmosphere (Dasgupta et al.22 (2.80-8.30 (5.67-5.40 (4. 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.55) Sample size 2820 2522 01-02 03-04 01-02 03-04 01-02 03-04 4.75-3.40-7. potassium.05 (2.49-3.10 (2.0-17.20 (8.20 (4.70-9.90) 5.10) 5.70-3.03) 3.70-12.00) 4.0-15.20 (2.76) 4.20 (7.0-17.93-3. 2001-2002 performed on surplus samples (variable unavailable of NHANES website) Fourth National Report on Human Exposure to Environmental Chemicals 243 .0-19.0 (8.11) 4.40 (8.30 (5.01 (2.0 (9.80 (3.0 (11.10) 12.46) 3.0) 14.70-6.20) 3.

10) 6.50) 9.7 (11. levels.0 (10.70-4. Steinmaus et al.90-15.10 (2.54 (3.1 (11.20) 8..S.35) 3.70-15.61-10.16-3.46-13. suggesting its tumorgenic effect is a result of a chronic increase in thyroid stimulating hormone indirectly resulting from iodine uptake inhibition.42 (3.EPA.32) 5. dietary iodine intake.76 (3.95 (2.93-7.35 (2.60-15.80 (7..00 (4.04-3..02) 3.0) 10.30 (5.25) 5.36 (8.00-2. population from the National Health and Nutrition Examination Survey.40 (7.30 (6.0) 12.22 (2.0-44.90-11.0) 374 313 827 715 1617 1476 01-02 03-04 01-02 03-04 3.80 (7.50) 6.82 (5.Perchlorate inhibition (RUI).1-14.50) 2.56 (3.60 (3. chronicity of exposure.60) 8.05 (4. Lamm and Doemland.03 (2.50-5.0) 13.77 (3.73) 3.89 (2.93) 3.20-10. Li et al.1 (8.30) 3. although iodine intake was higher than U.50 (3.90 (2.10-3.54 (2.81-3.2) 8.g.12 (6.93-5.89-3. menopausal status. During gestation and infancy. Also. congenital hypothyroidism is a condition for which nearly all newborn blood is screened. nitrate.3 (10.0) 12.60-11.24 (4.00-11. However. but without effects on serum levels of thyroid stimulating hormone or thyroxine (Braverman et al.67) 5.6) 20.20 (2.66) 3. Survey years 01-02 03-04 Geometric mean (95% conf.80-3. 2001.25) 5.00 (6.80) Selected percentiles ( 95% confidence interval) 50th 3.50-3.20 (4. 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. 2007).18-3.45-2.51 (3.08 (3.72 (3.04-3.87 (5.0) 6.40) 5.0) 9. 1999.3) 11.0) 12. up to 68% RUI has been demonstrated.6-17.30) 90th 9.90-9.41) Sample size 2818 2504 01-02 03-04 01-02 03-04 01-02 03-04 5.34-3.10-7. 2003.22-4.70-5. interval) 3.3-14.00) 4.0 (8..10 (4.33-6.93-5.25) 5.61 (5.4) 8.20 (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.0 (9.90-3.80 (4.41-9.4) 13.30-5.S.20-9.90) 5. urinary perchlorate at environmental exposure levels were inversely associated with thyroxine levels and positively associated with levels of thyroid stimulating hormone (Blount et al.S..0 (9.29) 2.0 (11.60-3. 2006.4-16.40) 3.70) 10.22-6.60-5.58) 2.52-9.93-8.0-14.60) 10.64) 5. 2002.40 (3.51-4. levels and sufficient in most participants (Tellez et al.87) 7.0 (11.14 (2.37-13.S. in a representative sample of U.84) 2.87) 2.40) 17..0) 11.52 (8.10 (6.0) 14.0) 12.30 (3. 2005).50) 95th 12. 2002.90 (7.00-3.5) 8.4 (10.99 (5. 2005.09 (7.59) 3. Short term human studies of the effect of perchlorate on RUI have been used for risk estimation (Greer et al.26) 4.20-3.60-6. Lawrence et al.20 (3.35 (4.60-5.0) 7. 2005).1-22.15-12.0 (9.46-4.86) 4.6) 12.71 (5.S.46 (3.60-11.44-6.00 (2.39-4. thiocyanate.3) 8.0-14.90-2.4 (11..20-3.60) 3.19-10.07 (2. 2005.33 (7.10 (4.74) 7.0) 1335 1220 1483 1284 01-02 03-04 01-02 03-04 01-02 03-04 3.08) 3.70 (4.S.50) 2.3) 12.60-8.64-3. NAS.. 2000).40 (4. 2005).19-6.09) 3.44) 3.56-3.26 (3.21 (2.0) 13.33-12.60-8.45) 3.87-3. women with urinary levels of iodine less than 100 micrograms per day.30-5.75) 3.50-9.0) 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 . In the U.4 (11.30) 75th 5.90 (4.50) 5.90-20.30-10. it is known that maternal and congenital hypothyroidism adversely effects neurological development and decreases learning capability.1) 8.30) 5.10) 13.20-4. 2002).00) 9.29-6.EPA.70 (2.40-10.10 (1. Though it produces follicular cell thyroid tumors in animal studies at goitrogenic doses. 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.47) 2. Greer et al..10) 4.1-13.0 (8.76-3.00) 3.90 (2. age.5 (13..87 (7.1-16. and the presence of other substances known to affect thyroid function (e.20) 3.83 (5.70) 2.39 (3.91) 4.0 (11. perchlorate is negative in most genotoxic assays (U.50 (6.8 (11.S.97-5.0) 4.96) 2.10) 3.12-2.99-3.98) 3.70-3.0-17. U. 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. medications).4 (8.0) 9.0) 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. Many factors may be important in consideration of perchlorate action on the thyroid: dose.39) 2. gender.0-19.61-5.53 (2.22-4.24-2.70 (2.37 (4.80-3.20 (6.40 (3.25 (3.2) 8.02-4.43) 6.

The effect of perchlorate.113(8):10011008.fda. Cross M.46(5):509. most of the population is considered to be below the U.42(2):200-205. Dasgupta PK. Daaboul JJ.gov/toxpro2. Has perchlorate in drinking water increased the rate of congenital hypothyroidism? J Occup Environ Med 1999.45(10):1116-1127.html. and nitrate on thyroid function in workers exposed to perchlorate long-term. Abarca CR. Health effects assessment for environmental perchlorate contamination: the dose response for inhibition of thyroidal radioiodine uptake in humans. Pleus RC. Blount BC. thiocyanate.. References Blount BC. Byrd D. Mauldin JP. The effect of short-term low-dose perchlorate on various aspects of thyroid function.S.htm. 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. et al. the women in the community with the highest drinking water levels had mean urinary perchlorate levels about 40 times greater than the geometric mean for participants in NHANES 2001-2002 aged 20 years and older (Tellez et al. Page Last Updated: 05/28/2009. Neonatal thyroxine level and perchlorate in drinking water. Food and Drug Administration (FDA). Biomonitoring Information Urinary perchlorate levels reflect recent exposure. Magnani B. He X. Health Implications of Perchlorate Ingestion. Lamm SH.. Blount BC. Pino S.113(11):A732. 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. Braverman LE.atsdr.115(9):1333-1338.S. population. Miller MD. Dyke JV. Primary congenital hypothyroidism.11(3):295. Finding a measurable amount of perchlorate in urine does not mean that the level of perchlorate causes an adverse health effect. Environ Sci Technol 2006. Doemland M. Sesser DE. 2005).html and from ATSDR at: http://www. Pirkle JL. Crump KS. Environ Health Perspect 2002. The levels seen in NHANES 20032004 show a similar pattern to NHANES 2001-2002. 2007). EPA reference dose (Blount et al. Pino S. Thyroid 2001.cdc. Urinary perchlorate and thyroid hormone levels in adolescent and adult men and women living in the United States. Thyroid 2000. Perchlorate Exposure of the US Population.S. Goodman G. Howd R. Steinmaus C. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.90(2):700-706. Gibbs JP. Landingham CB. J Occup Environ Med 2000. National Research Council of the National Academies. Lau EC. Li FX.EPA at: http://www. Impact of smoking and thiocyanate on perchlorate and thyroid hormone associations in the 2001-2002 national health and nutrition examination survey.gov/safewater/ccl/perchlorate/perchlorate. J Occup Environ Med 2003. Caldwell KL. Valentin-Blasini L. Analysis of relative source contributions to the food chain. Lamm S. et al. Braverman LE.gov/Food/FoodSafety/ FoodContaminantsAdulteration/ChemicalContaminants/ Perchlorate/ucm077653. Low dose perchlorate (3 mg daily) and thyroid function. Blount et al. Kirk AB.10(8):659-663. (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. and environmental perchlorate exposure among residents of a Southern California community. et al. Pirkle JL. Crump KS.110(9):927-937.40(21):6608-6614. Kelsh MA. epa. Additional information about exposure and health effects is available from the U. 2005). Richman K. newborn thyroid function. et al. 6/2/09 Greer MA. When these NHANES 2001-2002 urinary levels of perchlorate are used to calculate daily oral intakes for the U. Barnard JC. Osterloh JD. J Expo Sci Environ Epidemiol 2007. CFSAN/Office of Plant & Dairy Foods.41(5):409-411. Lamm SH. 2005.. Chacon PM. Erratum in: Environ Health Perspect 2005. 2001-2002. Benchmark calculations for perchlorate from three human cohorts. Available at URL: http://www. Environ Health Perspect 2005. Lawrence J.114(12):1865-1871. May 2007. Buffler PA.17(4):400-407. National Academy of Sciences (NAS). Environ Health Perspect 2007. Erratum in: J Occup Environ Med 2004.Perchlorate be unlikely to occur without overt perturbation of thyroid homeostasis. J Clin Endocrinol Metab 2005. Lawrence JE. Greer SE. Osterloh JD. Washington (DC): National Academy Press. Also. Preliminary Estimation of Perchlorate Dietary Exposure Based on FDA 2004/2005 Exploratory Data. Environ Health Perspect 2006. Deyhle GM. Jackson WA. Li Z. Valentin-Blasini L. Compared to a previous study of pregnant women in three Chilean communities with varying perchlorate levels in the drinking water. Braverman LE. Tellez RT. Long-term environmental exposure to perchlorate through drinking water and thyroid function during Fourth National Report on Human Exposure to Environmental Chemicals 245 . Skeels MR. Lamm SH. Rutherford GW. Perchlorate in the United States.

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

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

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

In comparing three separate reports on adults.S.10 (. Harada et al.108 times higher than background serum levels in humans (Butenoff et al.900 (. the median PFCs values tend to be roughly similar in these age categories (Olsen et al.500) . 2005).. 2007b).500) . reproductive. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Olsen et al.00) .. PFOA. Twelve different PFCs were measured in the sera of NHANES 2003-2004 participants.500-1. 2007b.400 (<LOD-.10) * 03-04 03-04 * * < LOD < LOD < LOD .500-1. 2003a).400-. monkeys.10) . Biomonitoring Information Serum levels of PFCs (particularly PFOA and PFOS) tend to reflect cumulative exposure over several years. PFOS. 1999. Effects on serum liver enzymes in limited observational studies of human occupational exposures are unclear. 2003a).80) 485 538 962 Limit of detection (LOD. Due to marked intergender differences in the elimination of PFOA in rats and substantial differences in the half-life of PFOA in rats.500-1. possibly related to lung immaturity (Lau et al. developmental and teratogenic effects were demonstrated in offspring.50) . U. the potential to estimate risks to humans from animal doses is uncertain.400-. 2004). A study of workers chronically exposed to primarily PFOA showed no biochemical evidence of hepatotoxicity or hormonal changes (adrenal.. PFOA. 1992.400-1. 2003)...500) 90th .. animal and human serum PFOA levels have been compared: serum levels associated with toxic effects in animals are 66-11. and no substantial age trends were seen within adults ages 20-69 (Olsen et al.500 (.S. However. population.500-1. Slightly higher levels of PFOS and PFOA in males than females have been noted in several other studies (Calafat et al. Analysis of the NHANES 20032004 subsample demonstrated higher levels of PFOA and PFOS in males and a slight increase in levels of PFOS with age (Calafat et al. or increased cancer rates (Alexander et al. 2007. EPA. 2003a.500-. hepatotoxicity. elderly and children..800 (.400-1.400-1. Serum PFOS levels associated with toxicity in test animals were 310-1550 fold higher than 95 percent of the levels found in a study of adults (Olsen et al. Late gestational exposure to PFOS in animal studies has also demonstrated early neonatal lethality. perfluorohexanesulfonate (PFHxS).10) . and changes in thyroid hormone concentrations (Grasty et al.. Animal studies of PFOS have demonstrated weight loss.00) .600 (.00) .S.. 2004). 2003. 2007a. interval) Selected percentiles ( 95% confidence interval) Sample 95th . 2003). 2004b). Cook et al.40) . Survey Geometric mean (95% conf.400 (<LOD-..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 . < LOD means less than the limit of detection.400 (<LOD-. 2003..500 (<LOD-1. population from the National Health and Nutrition Examination Survey. development in offspring was stunted and hypothyroxinemia was observed.20) .900 (.00 (.300 (<LOD-.400-1..Perfluorochemicals and testicular tumors in high dose animal testing (Biegel et al. which may vary for some chemicals by year and by individual sample.800 (.600-2.600 (..300 (<LOD-. 2007).800 (. Fei et al. and other PFCs have not been classified as to human carcinogenicity by IARC or NTP. 2004. 2004. 2003a... thyroidal). 2007a. 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.S. In such studies. Olsen et al.500) .500 (.500-3. Thibodeaux et al.400-1.. At doses causing maternal toxicity. 2001.600 (.400) . 2003a. PFOS. 2004a. Fourth National Report on Human Exposure to Environmental Chemicals 249 .3. Lau et al.800 (.300-1. and there was no clear evidence of excess all-cause or diseasespecific mortality. At high but non-toxic maternal doses of PFOS. EPA. U..80) 640 1454 03-04 03-04 * * < LOD < LOD .700 (. 2003).300 (<LOD-.. 2003. Kennedy et al. Olsen et al..900 (.800) 1. Serum Perfluorodecanoic acid (PFDeA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U..700) .500) . see Data Analysis section) for Survey year 03-04 is 0.20) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD . 2005).800) 1. Roughly similar levels of PFCs in serum have also been measured previously in other samples of the U.. and humans.

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

population from the National Health and Nutrition Examination Survey. see Data Analysis section) for Survey year 03-04 is 0. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.900) < LOD .600) < LOD .900) < LOD 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD . interval) Selected percentiles ( 95% confidence interval) Sample 95th .Perfluorochemicals Serum Perfluorododecanoic acid (PFDoA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U. < LOD means less than the limit of detection. which may vary for some chemicals by year and by individual sample.600 (. 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 < LOD < LOD 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 .400) .500 (<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 . Survey Geometric mean (95% conf.S.500) 485 538 962 Limit of detection (LOD. Fourth National Report on Human Exposure to Environmental Chemicals 251 .500-. see Data Analysis section) for Survey year 03-04 is 1.300 (<LOD-.300 (<LOD-.400 (<LOD-. population from the National Health and Nutrition Examination Survey.3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.0.S. Serum Perfluoroheptanoic acid (PFHpA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.300-. < LOD means less than the limit of detection.400 (. Survey Geometric mean (95% conf.400 (<LOD-.

80) 3.50 (1.00 (1.Perfluorochemicals Serum Perfluorohexane sulfonic acid (PFHxS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.30 (3.900-1. population from the National Health and Nutrition Examination Survey.900 (.10) 6.90 (4.20 (1.90) 1.17 (1.70) 3.50 (4.90) 3.10 (4.90 (1.50 (1.900-1.80-7.20-2.70 (2.80-7.861 (.20) 03-04 03-04 2.80-12.56-1.0) 8. 252 Fourth National Report on Human Exposure to Environmental Chemicals .30) 3.00 (2.697-1. Survey Geometric mean (95% conf.809) 1.60 (1.54) .90) 1.40 (1.80 (4.80-4.90 (1.60-3.14) Selected percentiles ( 95% confidence interval) Sample 95th 3.86 (1.04) .30 (1.20-1.80-3.S.40) 1.700-1.10 (.70) 1.72 (1.10 (4.40) 2.90-2.26) 2.50-3.60-8.70-2.10) 6.50-6.30 (1.912-1.40-1.70-7.50 (4.50 (1.90-19.00 (5.10) 4.20-3.30-6.40) 640 1454 03-04 03-04 2.27) 1.3.08) 2.60) 3.50) 2.42 (1.721-1.30 (7.10) 75th 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 1.10) 75th 3.51) 1.70) 2.16) .20) 1.30-9.60-2.90) 90th 5.689 (.10 (.60-2. see Data Analysis section) for Survey year 03-04 is 0.30) 3.1.80-6.00 (.03) 1.60-7.00-6.09 (.5) 8.80 (1.92 (1.77-2.966 (.01 (1.60) 2.3 (9.70) 13.50 (2.50) 2.60 (1.852 (.90 (1.10 (1.73-2.20 (1.60-4.900-1.16) Selected percentiles ( 95% confidence interval) Sample 95th 8.90 (4.60) 9.00-1.10-9.30 (1.600-.20) 485 538 962 Limit of detection (LOD.40-1.10 (.91) 2.80-2.20 (1.80) 1.20) 1.1) 485 538 962 Limit of detection (LOD.40 (2.700 (.30 (6.80-8.70) 1.87-2.30) .0) 1053 1041 03-04 03-04 03-04 1.80) 90th 2.90) 1.S.40 (1.93 (1.70-6.60) 1.30-2.900) 1.963 (.44 (2.40 (1. interval) 1.62-2.900-1.30 (2.826-1.586-.72) 1.14 (.90 (2.70) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 1.00) 2.10-9.60-3.80-8.00 (1.60-2.50 (6.00 (1.12) .80-4.60 (6.90) 8. interval) .70) 2.30 (1.90 (1.900 (.800 (.10) 8.40-3.00-7.900-1.67-2.20-1.00 (.00-8.20) 2.00) 1.984 (.05-2.40) 640 1454 03-04 03-04 1.900-1.10) 4.20 (6.50-6.40) 1.10) 1.30 (2.80) 4. see Data Analysis section) for Survey year 03-04 is 0.10) 5.00 (1.40) 4.5) 5.70-2.60-4.80 (1.20) .20 (6.00) 3.90-10.40) .6) 7.00) 1.50) 6.00-1.60 (1.80-3.834-1.50 (6. Survey Geometric mean (95% conf.10) 1.70-5.30) 3.17-1.800-1.20-1.40 (1.80) 5.50 (1.70-10.20 (1.835-1.20-1.70 (1.30-12.80-4. population from the National Health and Nutrition Examination Survey.50-10. Serum Perfluorononanoic acid (PFNA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.10) 1053 1041 03-04 03-04 03-04 .816-1.10-5.30) 03-04 03-04 .

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 4.1 (24.2 (16.9-38.27) 4.20) 10.1-36.8 (34.20) 5.2 (28.9 (19.89 (3.20-9.80 (7.3 (28.50) 7.70) 4.7-49.70-10.80 (6.80 (5.4) 640 1454 03-04 03-04 23.4 (28.20 (4.5 (28.8) 32.60 (5.10-3.11 (2.60 (4.5) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 21.40-14.80-4.30-3.40-10.6) 7.6) 35.0 (27.0-66.90-12.2) 30.10) 5.80 (6.0-70.5) 1053 1041 03-04 03-04 03-04 14.0) 485 538 962 Limit of detection (LOD.5-33.40-6.9 (17.9) 22.0) 23.3) 41.0) 21.53) 3.6) 42.20) 4.7-23.5 (28.27) Selected percentiles ( 95% confidence interval) Sample 95th 9. interval) 20.1-35.3-61.1) 57.9) 22.6) 1053 1041 03-04 03-04 03-04 3.4) 21.07-4.6 (19.70 (5.7 (13.30 (3.0-20.7 (35.1-33.4.1 (19.3) Selected percentiles ( 95% confidence interval) Sample 95th 54.4-25.2 (19.5-23.20) 5.00) 3. population from the National Health and Nutrition Examination Survey.4 (23.6 (42.6) 62.20 (4.30-6. interval) 3.30-11.4 (17.6) 9.9-23.8-22.5) 32.4 (19.60 (7.3) 42. population from the National Health and Nutrition Examination Survey.8-78.20-5.50-6.40-17.60 (6. Serum Perfluorooctane sulfonic acid (PFOS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.0 (20.6-24.20-4.50-13.90 (7.3-22. Survey Geometric mean (95% conf.7) 39.8 (45.0) 03-04 03-04 19.2 (18.6) 21.70-7.2-22.82) 4. Survey Geometric mean (95% conf.5) 9.S.4-17.3 (17.00 (5.3) 485 538 962 Limit of detection (LOD.60) 8.0) 21.10 (3.95 (3.2) 30.80) 8.60 (3. see Data Analysis section) for Survey year 03-04 is 0.Perfluorochemicals Serum Perfluorooctanoic acid (PFOA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.50-4.2) 640 1454 03-04 03-04 4.8-22.1.70 (3.85-4.3 (44.00 (3.70-9.20) 7.91) 3.00 (5. see Data Analysis section) for Survey year 03-04 is 0.18 (3.1-52.90 (5.4) 20.50 (3.8) 46.9-19.47-4.9) 27.3 (35.40) 3.30) 6.40 (4.6 (35.10 (6.5) 7.70-7.65-4.90 (7.8-22.5-62.8) 27.1-24.30-8.7-69.5) 19.79) 4.7 (43.4) 56.90) 6.47 (4.30) 7.7 (7.8-30.80-9.30-5.70) 6.60-9.7 (43.8-35.1-25.90-4.9 (13.35) 3.0-16.40-6.8-81.4) 75th 30.40) 75th 5.2-57.5) 18.60-6.5) 8.40) 90th 7.4-42.96 (3.7-33.7 (19.2 (27. Fourth National Report on Human Exposure to Environmental Chemicals 253 .40 (6.3) 28.40) 5.7-53.21-3.7 (35.70-5.0) 90th 41.60) 03-04 03-04 3.37 (2.6 (44.5) 57.9 (22.6-45.0) 43.60-14.99-3.2 (21.10 (3.9) 9.7-30.70 (5.S.70) 3.6-50.1 (23.67-4.80-12.30 (5.84-3.50) 4.5-21.30 (3.6) 18.50 (4.2) 45.0) 36.90-4.1) 15.8 (37.90 (7.4 (19.60-13.20) 7.60 (6.3 (35.

300 (.500) . 254 Fourth National Report on Human Exposure to Environmental Chemicals .300) .4. 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 .200-. 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. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.300) . Survey Geometric mean (95% conf.300) * 03-04 03-04 * * < LOD < LOD < LOD < LOD .300 (.300-.200-.500) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .200-.2. which may vary for some chemicals by year and by individual sample.300-.200-. population from the National Health and Nutrition Examination Survey.300 (.300) .300 (.200 (<LOD-. population from the National Health and Nutrition Examination Survey. which may vary for some chemicals by year and by individual sample.500) .300 (.300 (.300 (.300 (. Survey Geometric mean (95% conf.300 (.300) .200-.300) .300) .300 (.200-.300 (.200-.Perfluorochemicals Serum Perfluorooctane sulfonamide (PFOSA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.400 (<LOD-.400) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th 90th .400) 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD .200-.300 (. see Data Analysis section) for Survey year 03-04 is 0. interval) Selected percentiles ( 95% confidence interval) Sample 95th .300-.S. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.200-.500) .300 (. < LOD means less than the limit of detection.300 (.300) .500) 485 538 962 Limit of detection (LOD.S. < LOD means less than the limit of detection. see Data Analysis section) for Survey year 03-04 is 0.200-.500) < LOD 485 538 962 Limit of detection (LOD.300-.

700) 1.50) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD 75th . see Data Analysis section) for Survey year 03-04 is 0.80) 1.60) 485 538 962 Limit of detection (LOD.900-1. which may vary for some chemicals by year and by individual sample.70) 1.10-1.900) 1.10-1.40) 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD .700 (<LOD-. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.30) 1.10-1.00 (.50 (1.700 (<LOD-.6.700 (<LOD-2.3.600 (<LOD-.20) 1. Survey Geometric mean (95% conf.S.30 (1.10-1.10) * 03-04 03-04 * * < LOD < LOD .10) .900) .40) 1.80) 1.10 (.900-1. which may vary for some chemicals by year and by individual sample. population from the National Health and Nutrition Examination Survey.700) . Serum Perfluoroundecanoic acid (PFUA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.900-1.700 (<LOD-.20-1.S.800 (<LOD-.10) 1.900-1. population from the National Health and Nutrition Examination Survey.700) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .400 (<LOD-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.400 (<LOD-.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 .00 (. Fourth National Report on Human Exposure to Environmental Chemicals 255 .900 (<LOD-1.10 (.700) 90th 1.900-1.700 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.30) .50 (1.900-1.10-1.700 (<LOD-.900) 485 538 962 Limit of detection (LOD.20 (1.00-1.00 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th .300 (<LOD-1.900-1.90) .00) < LOD .10 (. < LOD means less than the limit of detection.800) . < LOD means less than the limit of detection.30 (1.10) .500 (<LOD-.800) .30) 1.700) 1.10 (1.40) < LOD < LOD .900 (. see Data Analysis section) for Survey year 03-04 is 0.00 (. Survey Geometric mean (95% conf.600 (<LOD-1.10) 1.80) 1053 1041 03-04 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 (<LOD-.600 (<LOD-1.60) 640 1454 03-04 03-04 * * < LOD < LOD .600 (<LOD-1.700 (<LOD-.30 (1.600) .300-2.

Serum concentrations of 11 polyfluoroalkyl compounds in the U. Needham LL. Fei C. Chlorinated.60(10):722729. Olsen J. Sasaki S. population: Data from the National Health and Nutrition Examination Survey (NHANES) 1999–2000. Kannan K.41:2237-2242. Kuklenyik Z. Environ Res 2005. Moore RW. Regul Toxicol Pharmacol 2004. Reidy JA. The influence of time.40:21282134. Crit Rev Toxicol 2004. Katakura M. Calafat AM. Environ Sci Technol 2005. Birth Defects Res B Dev Reprod Toxicol 2003. Kuklenyik Z. Wong LY. Witter FR. Environ Sci Technol 2007a. Kannan K. Mortality of employees of a perfluorooctanesulphonyl fluoride manufacturing facility. Hekster FM. Characterization of risk for general population exposure to perfluorooctanoate. Renal clearance of perfluorooctane sulfonate and perfluorooctanoate in humans and their species-specific excretion. Tully JS. Olsen GW. Frame SR. et al. Reidy JA. Environ Sci Technol 2004. Edwards EA. Toxicol Appl Pharmacol 1995. and perfluorinated contaminants in livers of polar bears from Alaska. Environ Health Perspect 2007. Bookstaff RC.115(11):1596-1602. Moore JA. Inoue K. Calafat AM. Yun SH. Calafat AM. Environ Health Perspect. Calafat AM. Kuklenyik Z. Chemosphere 2006b. in vivo. Peterson RE. Olsen GW. Mechanisms of extrahepatic tumor induction by peroxisome proliferators in male CD rats. Grasty RC. Kumar KS.39(3):363-380. Toxicol Appl Pharmacol 1992. Butenhoff JL. Biegel LB. Arendt MD.104(2):322-333. J Environ Monit 2005.34(4):351-384. Induction of Leydig cell adenomas by ammonium perfluorooctanoate: a possible endocrine-related mechanism. Jarnberg U. de Voogt P. Taniyasu S. Cook JC. Corsolini S. Kuklenyik Z. Holmstrom KE. Perfluorinated organic compounds in human blood serum and seminal plasma: a study of urban and rural tea worker populations in Sri Lanka.7(4):371-377. et al. Environ Health Perspect 2007. O’Connor JC. Seacat AM. Yamashita N. Burris JM. Toxicol Sci 2001. Fluorotelomer alcohol biodegradation yields poly. Frame SR. Perfluorochemicals in pooled serum samples from United States residents in 2001 and 2002. Mandel JH. Laane RW. Perfluorooctanesulfonate and related fluorochemicals in human blood from several countries.S. Watanabe T.60(1):44-55. Chem Biol Interact 2000.115(11):1670-1676. Cook JC. Fillmann G. Tully JS. sex and geographic factors on levels of perfluorooctanesulfonate and perfluorooctanoate in human serum over the last 25 years. Yoshinaga T. Caudill SP. Koizumi A. Needham LL.99(2):253-261. Day RD. Perkins RG. Yamashita N. et al.63:490496.68(6):465-471. Environ Sci Technol 2004. Calafat AM.S. Gaylor DW. Falandysz J. Environ Sci Technol 2005. Herbstman JB. Lau CS.39(1):80-84. Mabury SA.46(2):141-147. Inoue K. Saito N. Evans TJ. Ye Y. Cook JC. and ex vivo studies. Grey BE. et al.113(2):209-217.134(1):18-25. Reidy JA. Liu RC. Murray SM. 256 Fourth National Report on Human Exposure to Environmental Chemicals .124(2):119-132. Rodricks J. Hurtt ME. Mandel JS. brominated. 2007b. Polyfluoroalkyl chemicals in the U. Mandel JH. et al. Needham LL. et al. Kawashima Y. Androgenic deficiency in male rats treated with perfluorodecanoic acid. Seneviratne HR. Rev Environ Contam Toxicol 2003.Perfluorochemicals References Alexander BH.39(23):9057-9063.38(17):4489-4495. Biegel LB. Tarone RE. Keller JM. Olsen GW. Loganathan BG. J Occup Health 2004. Mohotti KM. Caudill SP. Effects of ammonium perfluorooctanoate on Leydig cell function: in vitro. Halden RU.1968--2003. Perfluorinated compounds in the plasma of loggerhead and Kemp’s ridley sea turtles from the southeastern coast of the United States.39(23):9101-9108.115(11):1677-1682. Apelberg BJ.179:99-121. Rogers JM. Induction by perfluorinated fatty acids with different carbon chain length of peroxisomal beta-oxidation in the liver of rats. Kamiyama S. Environ Sci Technol 2006a. Environmental and toxicity effects of perfluoroalkylated substances. Harada K. Toxicol Appl Pharmacol 1990. Kannan K. Butenhoff JL. Temporal trends of PFOS and PFOA in guillemot eggs from the Baltic Sea.38(10):2857-2864. O’Connor JC. Suzuki E. Taniyasu S. Kennedy GL Jr. Environ Sci Technol 2005. The toxicology of perfluorooctanoate. McLaughlin JK. Morikawa A. Aguilar-Villalobos M. Yoshinaga T. Reidy JA. population: data from the National Health and Nutrition Examination Survey (NHANES) 2003-2004 and comparisons with NHANES 1999-2000. Bignert A. Needham LL. Dinglasan MJ. Prenatal window of susceptibility to perfluorooctane sulfonate-induced neonatal mortality in the Sprague-Dawley rat. Guruge KS. Harada K. Wijeratna S.and perfluorinated acids. Perfluorinated chemicals in selected residents of the American continent. Perfluorinated chemicals and fetal growth: A study within the Danish National Birth cohort. Cord serum concentrations of perfluorooctane sulfonate and perfluorooctanoate in relation to weight and size at birth. Hurtt ME.Koizumi A. Occup Environ Med 2003. Bandai N. et al. Ingall GB. Saito N. Kudo N. Hurtt ME.

Moisey J. Hanari N. Coordinate induction of acyl-CoA binding protein. and humans from Japan. Church TR.113(5):539-545. Hansen KJ. et al. Grey BE.68:105–111. van Belle G. Grey BE. Burris JM. Olsen GW. Butenhoff JL. Ellefson ME. Cousins IT. Olsen GW. Horii Y. Biol Pharm Bull 2003. Yamashita N. et al. Lau C. htm. Preliminary Risk Assessment of the Developmental Toxicity Associated with Exposure to Perfluorooctanoic Acid and its Salts. Environ Sci Technol 2003. Froehlich JW. Huang HY. Sterchele PF. Mair DC.gov/opptintr/pfoa/pfoara. fast foods. Zobel LR. et al.Perfluorochemicals Kudo N.41(9):799-806. Subchronic toxicity studies on perfluorooctanesulfonate potassium salt in cynomolgus monkeys. Thibodeaux JR.115(9):1298-1305. Mandel JH.198(2):231-241. Nesbit DJ. Toxicol Sci 2002. Available from URL: http://www. et al. Rogers JM. Induction of triglyceride accumulation in the liver of rats by perfluorinated fatty acids with different carbon chain lengths: comparison with induction of peroxisomal betaoxidation. Burlew MM. Petrick G. Toxicol Appl Pharmacol 2004. Environ Sci Technol 2006. Church TR. Butenhoff JL. Hansen KJ. Helzlsouer KJ. Preliminary evidence of a decline in perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) concentrations in American Red Cross blood donors.37(12):2634-2639. Burris JM. EPA). Chemosphere 2007b. Environ Health Perspect. Prevedouros K. U. Burris JM. Toxicol Sci 2003. Butenhoff JL. Sources. Burris JM. Cao XL et al.1177(2):183-190. Environ Health Perspect 2003a. (Erratum in: Toxicol Sci 2004. and food items prepared in their packaging. Miller JP. Olsen GW. Seacat AM. Serum concentrations of perfluorooctanesulfonate and other fluorochemicals in an elderly population from Seattle.55:3203-3210. et al. Seymour C. Hanson RG.68(1):249-264. II: postnatal evaluation. Exposure to perfluorooctane sulfonate during pregnancy in rat and mouse. 2007a. Chemosphere 2004a.45(3):260-270. J Ag Food Chem 2007. A global survey of perfluorinated acids in oceans. I: maternal and prenatal evaluations. Thomford PJ. Kannan K. Environ Health Perspect 2005. Burris JM.111(16):1892-1901. A survey of perfluorooctane sulfonate and related perfluorinated organic compounds in water. Quantitative evaluation of perfluorooctanesulfonate (PFOS) and other fluorochemicals in the serum of children. 2003.74(2):369-381. Peterson RE. Lundberg JK.74(2):382-392. Reagen WK. perfluorooctanoate andother fluorochemicals in human blood.51(8-12):658-668.54(11):1599-1611. Hansen KJ. Korzeniowski SH. Hanson RG. (Erratum in: Environ Health Perspect. Kannan K. Bronson R.. Ehresman DJ. Richards JH. Exposure to perfluorooctane sulfonate during pregnancy in rat and mouse. Kawashima Y. Larson EB. Mandel JH. Half-life of serum elimination of perfluoroo ctanesulfonate. 2003a.2(1):53-76. and perfluorooctanoate in retired fluorochemical production workers. Case MT. Rogers JM. Olsen GW. et al. Environmental Protection Agency (U. Taniyasu S. fatty acid binding protein and peroxisomal beta-oxidation by peroxisome proliferators.S. Washington. Olsen GW. Dietary exposure of Canadians to perfluorinated carboxylates and perfluorooctane sulfonate via consumption of meat.S. Mandel JH. Yamashita N. Butenhoff JL. fish. Toxicol Sci 2003. Ehresman DJ. Olsen GW. Olsen GW.82(1):359. Pepper K. J Children’s Health 2004b. Seacat AM.111(16):1900) Olsen GW. Mar Pollut Bull 2005. Butenhoff JL. Church TR. Taniyasu S. Stanton ME. Epidemiologic assessment of worker serum perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) concentrations and medical surveillance examinations. birds.epa. Perfluorooctanesulfonate and other fluorochemicals in the serum of American Red Cross adult blood donors.40(1):32-44. Lundberg JK. Biochim Biophys Acta 1993. fish.) Tittlemier SA. Lau C. 1/15/06 Vanden Heuvel JP. The developmental toxicity of perfluoroalkyl acids and their derivatives. J Occup Environ Med 2003b. Mandel JH. Rogers JM. Fourth National Report on Human Exposure to Environmental Chemicals 257 . Olsen GW. Historical comparison of perfluorooctanesulfonate. Horii Y. Hansen KJ. J Occup Environ Med 1999. Serum perfluorooctane sulfonate and hepatic and lipid clinical chemistry tests in fluorochemical production employees. fate and transport of perfluorocarboxylates.26(1):47-51. Hansen KJ. Barbee BD. Butenhoff JL. Thibodeaux JR. Buck RC. Gamo T.perfluorohexanesulfonate.

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

1982). Biomonitoring Information Urinary levels of phthalate metabolites reflect recent exposure to the parent phthalate diester.html.html). Toxicological profile for di(2-ethylhexyl)phthalate update [online]. Jongeneelen FJ. Mackay D. Albro PW and Lavenhar SR.nih. 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. 1982.html. Corbett JT. 2000c. Herbert AR. environmental levels) and health effects is also available for some phthalates from ATSDR at: http://www.. 2002). 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. 2001..Phthalates and metabolites have been tested. Matthews HB. Calafat AM. 2006). Evaluation of a recombinant yeast cell estrogen screening assay. In Staples CA (ed). The Handbook of Environmental Chemistry. but there are known species-related differences in the hydrolysis of diester phthalates. 4/20/09 Albro PW. Massey RC.gov/ toxprofiles/tp9. 2004. Connor C. 1986). 2001). Rhodes et al.atsdr. at very high levels. Variation occurs from person to person in the proportions or amounts of a metabolite excreted after similar doses (Anderson et al. 2007). 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. 1985. NTP-CERHR.. Automated solid phase extraction and quantitative analysis of human milk for 13 phthalate metabolites. In animals. gender. Cousins IT. Silvapathasundaram S. References Agency for Toxic Substances and Disease Registry (ATSDR). The monoester metabolites are thought to mediate toxic effects for some of the phthalates. reducing estrogen production. Environ Health Perspect 1997.18(12):10681074. McDonnell DP. Hauser et al. Coldham NG...45:19-25.gov/toxprofiles/ tp135. Clark K. Springer. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects..805:49-56.niehs. and benzylbutyl phthalate (BzBP) during the fetal period produced lowered testosterone levels. Drug Metab Rev 1989. Kessler et al. Needham LL. Metabolism of di(2-ethylhexyl) phthalate. Food Addit Contam 2001.. Information about external exposure (i. 2003. Hauser et al. Available at URL: http://www. which may be a pathway to the development of liver toxicity and cancers in these animals. and race/ethnicity (Silva et al. Lovekamp-Swan and Davis. 2000a. dibutyl phthalate (DBP). Silva MJ. Castle L. Scotter MJ. Toxicological profile for di-n-butyl phthalate update [online]. 2004. Phthalate urinary metabolite levels in men evaluated at an infertility clinic were associated with several measures of sperm function and morphology (Duty et al. pp. phthalates produced anti-androgenic effects by reducing testosterone production and. effects that may be mediated by inhibiting testicular and ovarian steroidogenesis. High doses of di2-ethylhexyl phthalate (DEHP). testicular atrophy. McKee et al.html. Dirven HA. Vol. ovarian abnormalities in the female animals (Jarfelt et al. Sauer MJ. A biomarker approach to measuring human dietary exposure to certain phthalate diesters. 2002.gov/toxpro2. atsdr. 2004. van der Broek PH. Part Q: Phthalate Esters. J Chromatogr B 2004. 2004).atsdr.. 2005). 2003.. Also.gov/ reports/index. 2000b. 2002). Jordan S.. Available at URL: http://www.e. Peck and Albro. 227-262... Determination of four metabolites of the plasticizer di (2-ethylhexyl) phthalate Fourth National Report on Human Exposure to Environmental Chemicals 259 . These differences may contribute to species-specific differences in toxicity (ATSDR. efficiency of intestinal absorption.cdc. variation also occurs in the same person during repetitive monitoring (Fromme et al. Anderson WA. However. Hoppin et al. but similar findings were not present in young Swedish men with comparable or higher median levels of urinary metabolites (Jonsson et al. 2006). Pharmacokinetics. Schroeder JL. 2004.. Dave M. 2005.New York.. interactions with macromolecules and species differences in metabolism of DEHP. Assessment of critical exposure pathways. 105:734-742..cdc. Springall C. 2001. Slakman AR. and extent of metabolite conjugation to glucuronide (Albro et al.21:13-34. at higher doses. phthalates have been shown to induce peroxisomal proliferation in rodents. Environ Health Perspect 1982. The proportions of each metabolite for a given phthalate may vary by differing routes of exposure (Liss et al.3. 4/20/09 Agency for Toxic Substances and Disease Registry (ATSDR). 2007.cdc.. Population estimates of concentrations of specific phthalate metabolites may differ by age. peroxisomal proliferation may not be a relevant pathway in humans (Rusyn et al. and Sertoli cell abnormalities in the male animals and.

Parker MG. Silva MJ. Int J Hyg Environ Health 2007. Antiandrogenic effects in male rats perinatally exposed to a mixture of di(2-ethylhexyl) phthalate and di(2-ethylhexyl) adipate. Brock JW.html. Wang P. et al. gov/chemicals/dehp/dehp-eval. Mechanisms of phthalate ester toxicity in the female reproductive system. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction.18(1):122.gov/chemicals/ phthalates/dbp/dbp-eval.nih. Reynolds T. Zhang S.html. Giwercman A. Monograph on the Potential Human Reproductive and Developmental Effects of Di(2-ethylhexyl) Phthalate (DEHP).Phthalates in human urine samples. Chahoud I. Pan G.112(17):1740]. Borch J. Harris CA. Hass U.11(5):381-387.382:10841092. Park MG. Richthoff J. Calafat AM.nih. Hoppin JA. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Kalita JC. Decreased serum free testosterone in workers exposed to high levels of di-n-butyl phthalate (DBP) and di-2-ethylhexyl 260 Fourth National Report on Human Exposure to Environmental Chemicals . 2000b [online].105:802-811. Hauser R. Calafat AM.gov/chemicals/dehp/dehp-eval. Scand J Work Environ Health 1985. Sumpter JP. Kessler W. Toxicol Appl Pharmacol 2004.22(3):688-695. Numtip W. Davis BJ. Anal Bioanal Chem 2005. Brock JW. Ladefoged O. Stringer WT.16(4):487-493. 2000a [online].64(8):555-560. et al.103:582-587. Monograph on the Potential Human Reproductive and Developmental Effects of Butyl Benzyl Phthalate (BBP). Available at URL: http://cerhr. Biol Pharm Bull 2003. Fromme H.html.46(11):643-647. Hauser R. 6/2/09 Okubo T. Yokoyama Y. Henttu P. Draft Update Monograph on the Potential Human Reproductive and Developmental Effects of Di(2-ethylhexyl) Phthalate (DEHP).niehs.110(5):515-518. David RM. Jobling S. Lovekamp-Swan T. Tsukino H. Determination of phthalate monoesters in human milk. Mortensen GK. Grote K. McKee RH. Butala JH. Skerfving S. Drexler H. Am Ind Hyg Assoc J 1985. 6/2/09 NTP-CERHR. Temporal variability of urinary phthalate metabolite levels in men of reproductive age [published erratum appears in Environ Health Perspect 2004.19(4):505-515. et al.nih. Milligan SR. Blood burden of di(2-ethylhexylphthalate (DEHP) and its primary metabolite mono(2-ethylhexyl) phthalate (MEHP) in pregnant and non-pregnant rats and marmosets. Kano I. Reprod Toxicol 2005. Urine phthalate determinations as an index of occupational exposure to phthalic anhydride and di (2-ethylhexyl) phthalate. Environ Health Perspect 1995. Gans G. J Androl 2004. Kano K. Environ Health Perspect 1997.25(2):293-302.html. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Int Arch Occup Environ Health 1993.112(17):1734-1740. Environ Health Perspect 1998. Relative potency of xenobiotic estrogens in an acute in vivo mammalian assay. Reprod Toxicol 2004.26(8):1219-24. Koch HM. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. Rylander L. A variety of environmentally persistent chemicals including some phthalate plasticizers are weakly estrogenic. Epidemiol 2005.nih. Ryan L. Duty S.195:142-153. Hanaoka T. Urinary phthalate metabolites and biomarkers of reproductive function in young men. Environ Health Perspect 2003. Sumpter JP. White R.210:21-33. Filser J. Csanády G. Suzuki T. Environ Health Perspect 2002. Meeker JD. Available at URL: http://cerhr.niehs. NTP-CERHR. Phthalate ester exposure—air levels and health of workers processing polyvinylchloride. Baird DD. Available at URL: http://cerhr. Hum Reprod 2007. The estrogenic activity of phthalate esters in vitro.106(1):23-26. Chen Z. Main KM. Research Triangle Park (NC). Available at URL: http://cerhr. Dalgaard M. Duty SM. Park S. Jacobsen H. 2000c [online].gov/ chemicals/phthalates/bb-phthalate/bbp-eval. Boehmer S.111(2):139-145. Leffers H. Jonsson BAG. Meeker JD. Research Triangle Park (NC). Research Triangle Park (NC). 2006 [online]. Jarfelt K. Monograph on the Potential Human Reproductive and Developmental Effects of Din-Butyl Phthalate (DBP). Silva MJ. Angerer J.niehs. and infant formula by tandem mass spectrometry (LC-MS-MS). et al. Yoshimura M. Balasubramanian AV. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. Ryan L. Akesson B. consumer milk. Albro PW.niehs. Bolte G. Hagmar L. Occurrence and daily variation of phthalate metabolites in the urine of an adult population. Hartle RW. Skakkebaek NE. Silva MJ. Liss GM. Davis BJ. 6/2/09 NTP-CERHR. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Singh NP. 6/2/09 NTP-CERHR. Nielsen J. Reproducibility of urinary phthalate metabolites in first morning urine samples. Estimation of estrogenic and anti-estrogenic activities of some phthalate diesters and monoesters by MCF-7 cell proliferation assay in vitro. Research Triangle Park (NC). Andersson A-M. Environ Health Perspect 2004.

Batten PL. Hodge CC. Environ Health Perspect 2004. Caudill SP. Barlow NJ.58:339349. Environ Health Perspect 2006. Rusyn I. Modes of action and species-specific effects of di-(2-ethylhexyl)phthalate in the liver. Environ Health Perspect 1982. Urinary levels of seven phthalate metabolites in the U.114(11):1643-1648.S. Wu ZF. 112(5):A270]. Klinefelter GR. Lambright CR. Toxicol Sci 1998. Meek MD. Cunningham ML.36:459-479. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Ostby JS. et al. Comparative pharmacokinetics and subacute toxicity of di(2-ethylhexyl)phthalate (DEHP) in rats and marmosets: Extrapolation of effects in rodents to man. Bratt H. Silva MJ. Parks LG. Examination of the in vitro and in vivo estrogenic activities of eight commercial phthalate esters. Pratt IA. Peck CC.Phthalates phthalate (DEHP): a cross-sectional study in China.65:299-308. Malek NA. Environ Health Perspect 1986. Barr DB.46:282-293. Zacharewski TR. Toxicol Sci 2000. Matthews JB. Fielden MR. Crit Rev Toxicol 2006. Peters JM. The plasticizer diethylhexyl phthalate induces malformations by decreasing fetal testosterone synthesis during sexual differentiation in the male rat. Reidy JA. Albro PW. Rhodes C.112(3):331-338. et al. Jackson SJ.45:11-17. et al. Orton TC. Fourth National Report on Human Exposure to Environmental Chemicals 261 . Abbott BD. Clemons JH. Toxic potential of the plasticizer di (2-ethylhexyl) phthalate in the context of its disposition and metabolism in primates and man.

.6) 16.9 (12.6-150) 94.9 (12.4) 75th 35.6-38.8 (50.0) 24.6-79. some personal care products. 01-02.8-121) 79.9-14.3-91.2-38.1-15.9) 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.Phthalates Benzylbutyl Phthalate CAS No.7-14.9-16.3) 54. IARC considers BzBP not classifiable with respect to human carcinogenicity.1-15.6) 25.8-41.1-16.4) 12.9) 14.8 (30.8-98.3 (13.5-41.6-43.6 (66.0) 20.3-18.3) 13.5) 214 (108-399) 235 (183-330) 255 (146-365) 125 (93.4) 14.4-15.2 (19.4 (63.6) 95th 103 (94.1-90.0) 23.4 (13. 2000).7 (51.9) 43. it can be released into the ambient air during use or disposal of the products.4 (48.3 (12.1) 68.3-130) 122 (88.4 (10.1) Selected percentiles ( 95% confidence interval) 50th 17.2) 22.0 (23.6) 50.9 (16.2) 66.5 (66.9) 12.5 (61. and 03-04 are 0.5-62. respectively.3-88.1-35.0) 32.6) 13.4 (59.1-61.1 (32. 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.0-85.4) 35.9 (70.2) 14.7 (80.4-62.2 (19.2-183) 101 (78.1-16. 262 Fourth National Report on Human Exposure to Environmental Chemicals .9 (21.2-155) 91. 85-68-7 General Information Benzylbutyl phthalate (BzBP) is a solvent and additive used in products such as adhesives. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.0 (14.4-92.2-16.6) 35.0 (34.3 (12.8 (53.6 (13.7-15.6) 13.6 (13.S.1-18.6 (13.0) 70. car care products.1) 32.4) 81.9) 11.5-18.2-116) 122 (102-143) 101 (84.1) 67.9-62.3 (44.5-94.3-43.0 (27.0) 90th 67.0 (33.6 (41.1) 76.7 (53.1 (58.3) 23.3) 15.3 (29.8-48.6-92.5-97.2-40.5 (55.7 (12.4-120) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 13.7) 40. and 0.8) 28.3-161) 99. Biomonitoring Information The median levels of MBzP in NHANES subsamples from 1999-2000.6-132) 103 (84.6) 14.8-14.3 (29.3-82.7-172) 103 (74.5-145) 138 (106-241) 143 (127-179) 120 (99.2) 13.0 (30.4) 129 (98.6) 67.8 (28.8) 33.8-17.8 (71.4-25.9-27.5 (67.6 (21.2) 69.3-27.2) 78.5-35.2-115) 113 (91.1-120) 52.1 (20.3-12.4) 108 (96.0) 34.8 (12.5-14. and to a lesser extent.7-35.5) 15.4) 38.4) 49.1 (10.3 (33.5 (27.5-84.5) 82.2 (11.6) 29.1-43.1) 29.9-28.0 (43.8 (38.9-47.2 (14.8-133) 89.1-38.8) 24. including MBzP.0) 16.3) 94.9 (13.6-72.3 (22.2) 12.6 (12. 2000). particularly male animals (McKee et al. residents (Blount et al.6-116) 122 (102-142) 101 (85.4 (31.2) 33.8-16.. 0.1) 12.4-127) 80.9 (11.9 (28.0) 33.2 (10.7-17.8 (10.3 (30.8) 14.7-16.1-116) 122 (93.5) 27.5) 23.3) 37.8-72.8-16.2-17. sealants.0 (20.2-16.7-119) 99.2) 15.4) 98.4 (53.8-64.3-34.1.8 (71.6) 63.9-30. can produce developmental and reproductive toxicity in rodents.6) 37.2 (43. 2004.4-16. vinyl tile.0-55.4 (27.5 (13.1 (14.9-49.1-39.0 (15.0 (11.6-39.8) 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 16.9) 13.4) 35.5 (26.2) 32.9-190) 86.6-18.9 (22.8.9) 15.1 (13.6 (13.0 (12.2 (47.5-36.6 (53. BzBP can be released into the environment during its production and.4 (29.8-35. see Data Analysis section) for Survey years 99-00.4 (10.9) 14.0 (55.8-13.5) 65.7-170) 169 (134-198) 152 (99.3-125) Total 15. Food crops take up BzBP.3-18.2-20.7-16.7 (82.9) 18.5) 15.S.8-18.3 (54.5 (76.0-106) 58.2) 17. population from the National Health and Nutrition Examination Survey.6) 15.9) 49.6-29.3-75.7 (13.4 (53.1) 31.4) 65.9 (39.1 (55.5) 30.4) 51.5-25. NTPCERHR.2-33. 2001-2002.4) 33. High dose BzBP and its monoester metabolites.2-31.4 (68.7 (11.9-87.0-130) 101 (86.8-14.4 (32.8-76.5 (47.2 (25.5-33. People exposed to BzBP will excrete mono-benzyl phthalate (MBzP) and small amounts of mono-n-butyl phthalate in their urine.8 (21.6) 24.1 (19.6-17.2-39.3-21.5 (57.7 (15.7-13.7) 38.5) 16.1) 14.1) 13.7-58.8-17.7) 23.1 (13. and diet is the major source for general population exposure.4 (32.0 (15.8 (14.4) 71.7 (70.4) 80.2-19.6) 14.7-25.7-82.6 (32.3.6) 35.3 (12.4-24.0 (30.8 (86.8 (80.3-74.1-214) 166 (116-191) 145 (110-213) 88.3) 13.0 (26.6-92.5) 55.3-122) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.3) 63.8) 63. and 2003-2004 were generally similar those reported in U.2) 14. because it is not bound to products in which it is incorporated.1 (14.7-16.5-36.0-26. interval) 15.5-40.

5) 16.4) 13.8 (10.8-85.73-12.9 (22.9-14.6-81.S.1) 23.4) 50.2) 11.1-35.9-28.4-90.4-60.0 (12.4 (11.1) 27.0 (38.6 (30.8-80.9) 11.5) 78.8) 24. Hoppin et al.1) 39.1-29.7-31.7) 46.2) 12.8) 16.6) 53.3 (24.5) 41.2-26.5-29.1 (11.5 (10.3) 90.5) 17.2) 11.1 (23.1 (13.0 (41.0 (33.8-48.3-34.0-48.4) 13.9) 52.3) 67..1 (21.8-42.6-40..9 (12.6) 12.8) 33.2-13.5) 95th 77.8-60.3-73.8-64.0-26.1) 24.8-14.0 (11.6-99.5-213) 49. 2003).9-83.5-58.7-15.6 (30.1 (34.7-69.4-14.2-15.0-90.5-61.4-142) 134 (116-176) 136 (85.7 (12.5-99.1 (14.0 (13.3) 14.8) 11.3) 21.0 (49.3) 73. and in a small sample of German residents (Koch et al.1-12.4) 60.5-16.5 (10. population from the National Health and Nutrition Examination Survey.0 (67.3) 18..7 (14.9-13.9-69.4 (10.3) 29.5 (49.6) 12.8-13.6-20.4 (11.2) 15.2-15.4) 21.7-14.8-34. 2004.6) 75th 25.3) 16.7) 19.5-26.8-69.1) 17.6) 13.2-21.9 (24.0) 24.7-397) 70.2-51.4 (46.4 (11.9) 42.3) 37.4) 44.7-90.8) 53.2) 32. 2005.7 (54.1) 142 (99.1) 80.4-15.7-20.4) 104 (89.4-116) 73.8) 13.0) 60.2 (41.6 (57. In NHANES 1999-2000.2) 11.7-12.6-15.1 (19.0) 15.4) 51.9 (9.8-13.9-40.6 (24.5-13. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.6) 58.4 (12.8) 54.1 (18.2 (56.4 (13.5-57.4) 17. in men attending a Boston infertility clinic (Duty et al.8-13.4-14.8-27.6) 73.8 (30.4) 14.5) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Fourth National Report on Human Exposure to Environmental Chemicals 263 .7 (23.9-62.4-19.9) 24.9-115) 57. 2006).7 (19.7 (13.3-16.8-15.1 (53.3) 13.2-57.4) 90th 50.9 (10.7) 25..8) 68.2-78.7 (11.3 (12.8 (50.4) 25.1-14.7-14.1 (13.7 (21.69-11.1 (46.5-23.3) 13.1 (21.5 (12.6 (19.4) 328 393 342 752 742 729 1461 1647 1534 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 12.2-13.1) 24.0) 49.9-16.5) 20.7-56.7-19.7) 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 40.1-27.6-86. 2002.6 (11.1-79.2-117) 95.4-99.7-20.6 (51.3-64.4) 28.4 (34.2-49. adolescents compared with adults.8 (11.0-53.3 (60. 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.6-12. 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.7) 11.9) 12.6-13.8 (12.5) 10.6 (22.8 (13. Hauser et al.7 (18.8 (64.5) 14.6 (34.5 (48.7-19.1 (9. 2007).7) 56.4-102) 70.5) 46.4 (26.2-17.0-15. A small study of African-American women in Washington.5-42.5-79.7 (59.3) 14.2 (69.7-29.0-51..3-38. and females compared to males (Silva et al.0 (12.5-26.0 (41.1 (15.1-12.1-58. Weuve et al.5-38.6 (11.1-125) 86.4) 12.3-11.3) 89. 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) 24.4-93.5-58.0 (62.4 (74.9 (54.9) Total 14.3 (23.95-14..3 (39.3) 12.1-120) 77.8) 26..5-31.7 (13.8 (49.Phthalates York City (Adibi et al.1 (43.3) 36.8-173) 195 (121-305) 229 (99. 2005).3) 13..8) 34.9 (29.6 (15.4 (60.9 (39.8) 46. 2007).3 (13. DC reported median urinary MBzP levels that were about twice the levels of adults and females reported in NHANES 1999-2002 (CDC.8) 71.9 (51.8 (57.8) 33.4-23.0-109) 65.5 (42.9) 12.1) 12.1 (25.4-79.6-116) 74.4-42.6) 38.2 (27. 2004).8-14.8 (69.9 (43.7 (55.8-15.7-123) 77.8 (46.4 (25.8-16.6) 25.9) 100 (80.9) 11.4-27. interval) 14.9 (15.6 (11. in young Swedish men (Jonsson et al.0) 13. 2002).6-47.7 (11.4 (63.4) 15.6 (14.6 (36.7 (11.4-17.7) 38.4-18.8) 108 (75.0) 12.5) 23.1 (21.2-12. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.7 (38.9) 12.5 (35.6) 30.4 (21.3) 55.8) 56.8) 53.8) 15.1 (21.8-39. 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.5-76.5 (11.6-26.7-61.3 (35. In an annual sample of German university students.4 (69..5) 13.5 (9.9 (24.7-15.9 (12.0 (10.2) 67.9 (10.8) 80..2 (40. the adjusted geometric mean levels of urinary MBzP were significantly higher in several subgroups: children compared to adolescents and adults.1) 35.0) Selected percentiles ( 95% confidence interval) 50th 13.0-27.1 (41.0) 11.9-13.5 (56.3 (15.2) 26.9 (55.3 (38. median urine levels of MBzP were about one-half the median levels in NHANES subsamples from 1999-2002 (Wittassek et al.9-23.9 (15.4 (33.2) 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 12.9) 64. 2003).9-104) 62.

Environ Health Perspect 2003. Exposure to phthalates in neonatal intensive care unit infants: urinary concentrations of monoesters and oxidative metabolites. Sampson EJ. Davis BJ. Camann DE. McKee RH. Malek NA. Caudill SP. Wittassek M. Phthalate monoesters levels in the urine of young children. Angerer J. Calafat AM. Urinary levels of seven phthalate metabolites in the U. Hum Reprod 2007. Barr D. Environ Res 2003. Giwercman A. Prenatal exposures to phthalates among women in New York City and Krakow. Duty S.112(3):331-338. Jonsson BAG. Eckard R.niehs. Silva MJ. Wiesmuller GA. Environ Health Perspect 2004. Available at URL: http://cerhr. Hauser R. Green RA. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine.93:177-185. Jedrychowski W. Environ Health Perspect 2002. 112(5):A270]. Koch HM. Perera FP. Reproducibility of urinary phthalate metabolites in first morning urine samples. Atlanta (GA). Research Triangle Park (NC).68:309-314. Silva MJ. et al. Hu H. Meeker JD. 2005. Bull Environ Contam Toxicol 2002. Chen Z. Calafat AM.gov/ chemicals/phthalates/bb-phthalate/bbp-eval. et al.22(3):688-695.S.18(1):122. Environ Health Perspect 2006. Jacek R. Internal phthalate exposure over the last two decades—a retrospective human biomonitoring study. Singh NP.210(3-4):319-333. Hilborn ED. Brock JW. et al. Caudill SP. Third National Report on Human Exposure to Environmental Chemicals.16(4):487-493. Blount BC. Brock JW.110(5):515-518. Brock JW. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Hoppin JA.111(14):1719-1722. Helm D. Butala JH. Duty SM. Reprod Toxicol 2004. Monograph on the Potential Human Reproductive and Developmental Effects of Butyl Benzyl Phthalate (BBP). Hagmar L. et al. Rossbach B. Poland. 4/20/09 Silva MJ. Weuve J. Silva MJ. Needham LL. Schettler T. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Environ Health Perspect 2000. J Androl 2004.114(9):1424-1431. Pirkle JL. Centers for Disease Control and Prevention (CDC). Dobler L. Koch HM. et al. Silva MJ. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. Caudill SP. Int J Hyg Environ Health 2007. Needham LL. Ryan L. 2000 [online].html. Ryan L.25(2):293-302. Levels of seven urinary phthalate metabolites in a human reference population. Gans G. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. 264 Fourth National Report on Human Exposure to Environmental Chemicals . Reidy JA. et al. Drexler H. Barr DB. Urinary phthalate metabolites and biomarkers of reproductive function in young men. Richthoff J.Phthalates References Adibi JJ. NTP-CERHR. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. et al. Sanchez GN. Rylander L.nih. Baird DD. David RM. Hodge CC.108(10):979-982. Epidemiol 2005.

about 65% to 80% of a dose is eliminated in urine within 24 hours.40 (2.0) 12.7-20.40) 5.68 (2.1) 22.6-20.7 (7.30 (1.6) 10.6) 17.40 (2.55) 2.4 (14.5) 23.80) 75th 5.5 (11.Phthalates Di-n-butyl Phthalate CAS No.97-7.9-23. Median MBP levels in two European studies were about two to six times higher than median levels in this Report (Jonsson et al.6 (14.2 (11.40-17. In addition.44-2.5) 18.80 (5. see Data Analysis section) for Survey years 01-02 and 03-04 are 1.73 (2.3 (18.0) 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 2.3-30.56-4.3-18.50) 5.5-29. 84-69-5 General Information Dibutyl phthalates (both di-n-butyl and di-isobutyl phthalates.40 (3.10) 11.6) 26. 2007).6 (9.1 (13.07 (3. 2005.63) 3.0 (13. NTP-CERHR.3 (13.3 (16.6 (13.20-12.40-3. mostly as MnBP (Anderson et al.60 (5.20 (6.20) 7. Neither IARC nor NTP has evaluated dibutyl phthalates with respect to human carcinogenicity.80 (3.82-3. Following oral administration of DBP to humans.50-4.22) 3. Fourth National Report on Human Exposure to Environmental Chemicals 265 .1-25.55 (3.10) 3. 2000.0) 24..2-22.20-2.4) 12.20-9.5) 19. and in a small sample of Japanese adults (Itoh et al.0 and 0.90) 12.10-2.40-12.5 (20.5 (10.8) 21.4-27.90-4.3 (19..3-20.56 (5.7-31.97) 2. referred to as DBP) are industrial solvents or additives used in many personal care products such as nail polish and cosmetics.6-18.56 (3. in a small sample of pregnant women in New York City (Adibi et al..0) 9.5) 18.0-25.3-19.00 (7.3. population from the National Health and Nutrition Examination Survey.30-7.80 (5.84) 4.1) 16.50) 2.6 (10. 2003).91) 4.70-4.5-24. residents (Blount et al.80-5.00) 4.7-31.4) 22.50) 8.60 (2.24-8. Compared with the median for 6 to 11 year olds in NHANES 1999-2004 (CDC.60 (4.30) 2.90-4.46 (2.6-14.26 (2.25) 01-02 03-04 01-02 03-04 01-02 03-04 4.10 (4.73-5.8 (9.30-3.85-6. 84-74-2 Di-isobutyl Phthalate CAS No. interval) 2. pharmaceutical coatings.40 (7.5) 14. NIOSH and ACGIH have established guidelines for workplace air exposure to di-n-butyl phthalate.0) 13.5-16.60) 3.70) 5. 2005).90-2. When total DBP metabolites have been measured.S.6) 16..46-5.6) 17.20) 4.46 (3.30-11.9 (16.70-8.7 (18. Survey Geometric mean (95% conf.30) 10.4-12.00) 10.7) 14.00) 7.0 (19.60 (8.66) 2.6-26. exposure to benzylbutyl phthalate (BzBP) will also result in small amounts of mono-n-butyl phthalate appearing in the urine.4 (20.30) 10.6 (14.1-20.56) 3.3-48.9 (16..7) 18. DBP can produce reproductive toxicity in male rodents (McKee et al.1-17..70 (2.30-2.7 (16.00-4.1) 25.97) 4.20-12. 2005).19-3.6-34. and insecticides.7 (9.00 (5.0) 20.30) 5.. People exposed to dibutyl phthalates will excrete mono-n-butyl phthalate (MnBP) and mono-isobutyl phthalate (MiBP) in their urine.00) 4.80 (2.50) 7.9) 10.43) 6.6 (11.90 (6.50-10.3) 3.3 (11.00-6.50 (3. 2000).0-18. CDC.9) 15.5) 22.60-6.48 (2.30 (4.3) 18.10-9. Studies of children found age-related differences in urine MBP levels.10) 2.8) 677 652 703 699 1216 1088 Limit of detection (LOD.10) 8.90-7.2-33.40 (6.33 (2.30-13. 2003).3) 33.7) 4. Small amounts of mono-3-carboxypropyl phthalate are also produced from di-n-butyl phthalate.2 (12.1-12.S.17) 4.20-6.3-43.7 (17.90 (3.81 (3..70 (5.10-9.30-6.0-14.7-18. Hauser et al.00-6.6) 16.80 (2.50) 18.22 (3.0) 393 342 742 729 1647 1534 01-02 03-04 01-02 03-04 2. in men attending a Boston infertility clinic (Duty et al.6 (29.6) 12. Koch et al. 2004..90 (4.10 (3.17 (2.9-14.50-6.5-16.40-4.50-2.20 (7.5) 25.0) 1371 1250 1411 1355 01-02 03-04 01-02 03-04 01-02 03-04 3.72-3. they have been referred to as monobutyl phthalate (MBP). 2005).2-14.1 (8.46) 2.40-3.30) 6.5 (27.0 (13.10 (4.3 (16.8) 40.70-4.7) 7.3-24. 2001).50) 90th 12.02) 4. 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.00-9.10) 9.2) 5.49-2.20 (3. Biomonitoring Information Median concentrations reported in the NHANES 19992000. OSHA has established a workplace air standard for external exposure to DBP.96) 3.40-4.5) 12.00-11.71 (2.30 (3.37) 6.80-5.0-38.3 (13.59) 3.6 (13.11-3.40-5.6 (10.30-6.94) Selected percentiles ( 95% confidence interval) Sample 95th 17.90 (4.4) 5.28-5.50 (6.7) 15. and also in some printing inks.0 (11.00) 6.7 (17. 2004.70) 3. 2001-2002 and 2003-2004 subsamples were similar to MBP levels reported in U.5 (17.2 (8.40-9.67 (5.

2005).69-7.7-28.1) 7.8 (9. 2006).6-19.26-2.95) 2.5 (11.and gender.66 (8..53-4.68) 5.04) 7.05) 2. Weuve et al.94-12.52-3.3) 16.8) 10.31) 2.73 (5.72) 5.00-7.35) 3.9-16.45) 3.15) 3.3) 13.0) 15.9 (15.02-10.39-3. Differences in urinary MBP population estimates by gender have also been shown (Silva et al.25) 5.55-6.97-2.24) 3.4) 23.15-4.79-8. to about two to fourfold higher (Fromme et al.41 (2. the students’ median values for MiBP levels remained relatively unchanged.4 (12. ranging from more than one-tenth the NHANES median (Itoh et al. interval) 2.47-12.20-3.78) 8.14 (4.18 (4.94 (5.2) 9.7) 11.31 (7.08-2.0-18.20 (2.54 (2. 2002.4-16.18-10.19 (2.1) 13.66) 2.56-15.7) 3.6 (10.2-15. Studies measuring urinary MnBP have reported variable median values compared to the NHANES 2001-2002 and 2003-2004 subsamples.8-18.36-7. 2005). 2007).S.51) 15.20 (2.32 (7.46 (2.33 (3.51) 5.28 (4.88 (2.74 (4.2 (11.62 (6.76-3.61-3.81) 9.95-3.18 (1.68 (2.30) 2.1) 677 652 703 699 1216 1088 266 Fourth National Report on Human Exposure to Environmental Chemicals . 2004).99-4.33 (2.54) 2.84 (4.7 (11.9-26. respectively.3) 13.31 (2.84 (8.00-3.5 (9.80 (3.5-19.0) 7.26 (2.3 (13.78-8.47-5.39) 5.11) 5.00) 01-02 03-04 01-02 03-04 01-02 03-04 4.3 (17.04-5. Finding a measurable amount of MnBP or MiBP in urine does not mean that these levels or the parent compound cause an adverse health effect.17) 90th 8.7) 10.51) 2.27-12.13-6.8-13.1) 4.00 (3.02 (7.5) 13.0 (10.81 (6.6 (9.46-11.03-7. 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.85 (2.03-11.69) 6.8-18.96 (3. 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.6) 11.7) 1371 1250 1411 1355 01-02 03-04 01-02 03-04 01-02 03-04 3. population from the National Health and Nutrition Examination Survey.8-36.43) 3.11-2.57 (3.94) 6.20-2..1 (10.20 (7..09-2.81) 4.1-15.32 (3. Survey Geometric mean (95% conf.8 (10.17 (2.93-6.1-24.2-13.54 (4.81 (3. 2004). An analysis of NHANES 2001-2002 showed similar age.0 (12.52 (2.56) 5.56) 2.13 (2.57 (3.53-3.1) 15. In an analysis of NHANES 1999-2000.18-4.0) 11.99) 7.7 (13.64-10.65-11. than adults in NHANES subsamples during the same time period.38-10.6-19.9) 12. while MnBP declined (Wittassek et al.29-3.80-3.21) 10. 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.1) 10.6 (8.78) 9.8 (8.30 (6.29-8. Between 1998 and 2003.79 (4.6 (15.58-3..08) 75th 4.75 (6.42) 2.9 (9.2) 8.75 (4.2 (10.82 (4.76-3. samples from German university students had consistently higher median urine levels of MnBP and MiBP.38 (6.37) 3.76-15.32) 7.Phthalates for neonates was lower (by about half) and the median for toddlers was higher (by about sixfold) (Brock et al.03 (5.86) 6.44 (3.79-6.33) 3.20-4.76 (3..04) 3.00-3. Over this time.98 (2.57-4.89 (3.6) 13.69) 4.10-5.80) 7.6 (12.95) 10.65 (4.1 (11.58-4.1) 11.66) 4.07 (2.86-4.0) 393 342 742 729 1647 1534 01-02 03-04 01-02 03-04 2.7) 19.36-2.72-7.01-2.1-12.9-40.43) 3.69 (2.56-4.0 (8.7 (21.6 (8.89) 6.83 (2.59 (4.65-4.1-25..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 2.9 (11.64-7.28-13.11 (5..91-6.52) 3.22 (2.21 (5.34 (3.4) 15.92 (7.07-5.73) Selected percentiles ( 95% confidence interval) Sample 95th 12.3) 28.4) 7. 2007).67-5.5) 15.17-12.64-7.82) 4.31) 2.89-5. up to four and 13 fold.74-3.related differences in the adjusted geometric mean levels of urinary MiBP and MnBP (CDC.52-20.2) 24.0) 3.66) 10.18) 4.46) 3. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.62-12.47 (3.3) 18.43) 3.7 (9.18) 3.68) 3.33-9.53-5.

2 (74.0 (15.2 (21.1) 25.5) 37.4 (19.3-79.5) 24.1 (21.3 (51.2) 32.7-117) 118 (108-143) 93.3) 23.4 (71.3 (37.6) 17.8) 58.6-31.5) 19.9) 29.1-82.4-44.2 (25.0 (25.9) 26.1-20.0) 117 (104-131) 112 (84.9-101) 77.5-47.9 (17.9) 46.5) 20.2 (20.6-36.5) 31.7) 42.0 (18.0) 27.6 (19.8 (57.5 (30.8-42.4 (35.1) 30.5) 36.5) 65.7-127) 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. respectively.5-117) 95.8-132) 95.2 (21.6 (61.0 (31.2) 62.6) 20.4 (35.6 (90.2) 90th 98.2 (75.1-122) 122 (104-137) size 2541 2782 2605 Total years 99-00* 01-02 03-04 50th 26.1) 23.8-25.6 (32.1-27.1) 17.2) 26.5) 26. and 0.7) 74.3 (30.3 (23.3) 24.7 (28.1.3-136) 137 (107-162) 119 (90.2-24.8-165) 167 (143-197) 138 (110-184) 144 (115-168) 142 (111-161) 107 (89.2) 38.1 (16.1) 46.3) 19.4-159) 107 (84.9-114) 116 (97.4) Selected percentiles ( 95% confidence interval) Sample 95th 150 (121-169) 108 (94.0 (17.2) 68.2-49.9.4-42.7 (38.9 (17.5) 78.3 (56.1 (19.2-56.7) 124 (98.4 (84.4 (35.9-87.1 (19.8-119) 90.1) 36.5-43.6-40.6 (44.1 (34.2-63.7-34.1) 47.0 (23.4.7-24.2 (59.4 (23.5) 47.5 (59.1-51.2 (79.5 (74.3-40.5) 17. 01-02.4-18.3-96.7-26.6) 38.3) 21.4-60.3 (17.7-106) 69.7-91.7 (24.8) 62.0-73.5 (29.0) 21.0) 30.2 (58.Phthalates Urinary Mono-n-butyl phthalate (MnBP) Metabolite of Dibutyl phthalate (DBP) and Benzylbutyl phthalate (BzBP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.7 (43.9-42.4) 64.8) 19.7-124) 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.3 (36.7-111) 64.6-33.2-21.0 (20.6-44.1 (26.1 (54.1 (17.2-159) 92.5) 95.9-92.1) 19.6-20.0-19.3) 36.2-23.4 (21.1) 23.6 (65.3) 18.8) 48.8-22.6) 46.9) 21.1 (28.5) 36.7 (51.2-22.6 (22.5) Age group 6-11 years 99-00* 01-02 03-04 99-00* 01-02 03-04 41.9 (79.2 (17.6-37.1) 20.5-42.9 (20.3-24.1 (62.2-87.7 (22. population from the National Health and Nutrition Examination Survey.5-27.1 (19.2 (19.5) 85.9-28.7 (19.0 (72.6) 21.0) 20.5-47.6) 35.1-24.6 (16.6-69.0 (78.0) 31.0-32.8) 43.9-33.3-76.S.7-53. *In the 1999-2000 survey period.3) 26.4) 22. 1.5 (59.3-21.7) 92.1-75.5-44.9) 36.1 (19.3 (42.0-21.0 (30.7-92.5) 40.5 (28.1) 23.4-31.4 (25.4 (35.2) 20.4-20.4 (36.6) 80.6-29.6-143) 127 (99.6) 71.9-79.1 (36.0-24.9) 18.3-145) 85.2-33.9-22.5) 21.4) 20.9 (79. see Data Analysis section) for survey years 99-00.8-29.1-29.0) 84.7 (70.9) 71.7-42.4-26.7-121) 97.8) 23.0-19.5-53.3-85.0-24.9) 75.3 (30.8-123) 101 (90.7 (33.1-80.1 (51.8-111) 167 (143-223) 121 (106-136) 137 (122-156) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00* 01-02 03-04 99-00* 01-02 03-04 23.7-42.6-49.1-22.2 (78. concentrations of mono-isobutyl phthalate and mono-n-butyl phthalate were measured together and expressed as a combined value. Fourth National Report on Human Exposure to Environmental Chemicals 267 .0) 38.9-22.0-26.6 (26.7-34.5) 34.7-116) 95.2) 42.7 (64.6-24.1 (18.0 (45.1 (58.2-93.6 (55.6) 39.8) 75th 51.6 (48. interval) 24.3-60.3-67.4 (72.4 (38.7 (16.9-53.0 (36.4-25.4) 59.7) 52.2-114) 73.2-32.1) 31.7) 28.3 (60.7 (18.1 (41.1 (31. referred to as monobutyl phthalate (MBP).1-92.6-113) 108 (90.3 (23.0-58.6-29. Survey Geometric mean (95% conf.6) 166 (127-279) 159 (110-290) 191 (150-243) 165 (121-227) 148 (106-185) 134 (110-158) 143 (117-161) 95.6-48.0-51.7-20.3) 40. and 03-04 are 0.7 (18.0) 120 (98.5-121) 106 (94.2 (18.5-60.4) 52.8 (19.

8) 20.2-28.5) 84.4) 16.0-47.5-30.7-26.3-21.0-113) 104 (83.6-32.3 (46.1) 61.6-24.0 (20.4-47.4-76.0) 75.2-86.6) 65.3 (17.9-68.6-155) 91.8) 35.6) 23.6 (74.7 (28.9-14.8) 75th 38.7 (27.5-22.2-73.2 (38.4-164) 96.S.6) 31.1) 35.1-128) 97.5-37.6-119) 63.0) 25.6-24.7-78.2-106) 64.0 (26.3 (28.0) 53.7-28.5 (30.5) 134 (93.9-49.5) 91.5-18.3) 35.9 (19.7 (73.4) 19.3-23.1-18.2-48.8) 17.5 (18.0 (34.8 (22.3 (76.4 (45.6-28.2-108) 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.4) 62.1-23.3) 67.4-135) 71.0) 28.4) 15.4-24.6 (19.8 (17.3) 52.5-64.4 (31.3 (17.6 (27.3 (19.6 (41.9) 19.6) 34.1) 44.1) 53.9 (30.4-103) 117 (83.7-21.4 (16.8) 17.6 (72.8) 63.7 (81.3 (42.6 (31.6 (25.3) 33.3 (16.4 (53.8 (25.5) 21.3-17.6) 39.4) 53.0) 59.6) 14.0) 81.1-62.1-83.7 (60.4 (20.3-21.0-92.7-42.0) 29.3 (21.4) 15.2-22.5) 60.7 (57.8 (18.3) 18.2-179) 84.0 (43.2-16.7 (20.2) 159 (102-263) 147 (93.9 (20.3 (71.3-106) 74.0) 41.6 (57.4 (37.4-131) 81.9) 24.9-68.8 (16.8 (65.3 (60.9) 91.5-41.4 (13.8-24.3-39.7 (14. concentrations of mono-isobutyl phthalate and mono-n-butyl phthalate were measured together and expressed as a combined value.2-22.5) 90th 68.6-74.3 (52.1) 20.1 (32.5-142) 81.9 (39.4 (68.6) 38.0 (52.8) 34.6) 37.1 (29.3 (48.0 (50.4 (17.4 (19.5) 39.1-99.8 (18.4 (17.7-51.4-65.9-38.4-34.0-17.0-90.6-44.2-85.1) 22.8) 17.5-23.4 (23.3) 19.8) 13.3-32.1-21.9 (30.4-61.9 (35.3-78.5-142) 89.8) 28.2) 31.7 (16.5-76.9 (64.1 (61.7) 19.3) 33.7 (12.8 (50.3) 21.5-21.8 (18.5 (64.6) 24.1 (15.8-235) 137 (108-198) 88.5 (15.4-72.0 (18.0-60.4) 21.4 (16.3 (69.1 (46.1 (21.6) 64.7-37.6-16. interval) 22.7 (43.Phthalates Urinary Mono-n-butyl phthalate (MnBP) (creatinine corrected) Metabolite of Dibutyl phthalate (DBP) and Benzylbutyl phthalate (BzBP) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.0) 108 (71.9) 14.9) 28.6-19.4 (47.3-81.9-34.0 (61.1 (34.0) 19.7 (19.4) 20.4) Selected percentiles ( 95% confidence interval) Sample 95th 97.2) 65.2-22.2 (19.8 (13.0) 94.9-70.6-23.1-115) size 2541 2782 2605 Total years 99-00* 01-02 03-04 50th 21.7-19.9) 39.2) Age group 6-11 years 99-00* 01-02 03-04 99-00* 01-02 03-04 41.9-56.6-27.8-24.7-39.2) 21.0 (71.0 (16.5 (81.9-36.3-40.4 (50.8-32.7-19.0 (70.3 (24.9) 20.0-19.9-26.6-139) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00* 01-02 03-04 99-00* 01-02 03-04 21.3-71.6 (61.5) 82.6) 18. 268 Fourth National Report on Human Exposure to Environmental Chemicals .0 (69.0) 70.8) 19.6-92.3-18. population from the National Health and Nutrition Examination Survey.2 (83.3) 19.0-38.9-105) 85.6-50.3-49.6) 25.8-43.0 (27.8-23.7-20.1-32.9 (37.2-61.0) 26.4 (33.6-53.7) 20.1) 20.2) 16.9) 52.6 (29.2 (19.0) 55.1-99.1) 42.6-43.6-26.9 (58.2 (16.2) 59.9 (30.6 (25.2 (35.6) 83.5) 17.4) 51.8) 23.6-42.4 (31.3) 17.4 (50.5 (14.1) 37.6-44.5 (18.9 (35.6-22.7) 42.0 (15.3 (55.9-100) 86. Survey Geometric mean (95% conf.5-70.1) 50.8 (33.2-27.7 (60.9 (21.2) 74.7-80.5-16.0 (18.1) 21.7 (54.9 (56.8) 20.9) 30.3-114) 328 393 342 752 742 729 1461 1647 1534 12-19 years 20 years and older 99-00* 01-02 03-04 Gender Males 99-00* 01-02 03-04 99-00* 01-02 03-04 17.3 (52.4 (56.8) 34.8) 22.2-21.0) 35.8) 30.3-26.6-23.9-84.0-41.1 (56.6) 24.6 (17.9 (73.2-18.4 (31.3) 20.4 (18.1) 17.3) 59.8) 40.0-75.7) 36.0 (19.9) 49.3-38.5-15.3 (17.9 (16.3-20.7-23.9) 62.6-128) 96.

Phthalate monoesters levels in the urine of young children. Environ Health Perspect 2003. Food Addit Contam 2001. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Pirkle JL. Masunaga S. Environ Health Perspect 2004.111(14):1719-1722. Jedrychowski W. Silva MJ.html. Sampson EJ. Environ Res 2003. Green RA. Jonsson BAG. Helm D. Dobler L. Fromme H. Ryan L. Internal phthalate exposure over the last two decades—a retrospective human biomonitoring study. Caudill SP. Centers for Disease Control and Prevention (CDC). J Androl 2004. Giwercman A. Schettler T. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction.gov/chemicals/ phthalates/dbp/dbp-eval. Ryan L. Meeker JD. Butala JH. 4/20/09 Silva MJ. Int J Hyg Environ Health 2005. Itoh H.210:21-33. Hodge CC.16(4):487-493. Malek NA. Silva MJ. Wittassek M. Blount BC. Drexler H. Boehmer S. Barr DB.25(2):293-302. Rylander L. et al.112(3):331-338. Bull Environ Contam Toxicol 2002. Occurrence and daily variation of phthalate metabolites in the urine of an adult population.niehs. Massey RC. Koch HM. Eckard R. Richthoff J. et al. McKee RH. Duty S. 2000 [online]. Yoshida K. Exposure to phthalates in neonatal intensive care unit infants: urinary concentrations of monoesters and oxidative metabolites.22(3):688-695. Silva MJ. Koch HM. Calafat AM. et al. Bolte G. Hum Reprod 2007.93:177-185. Environ Health Perspect 2006. Caudill SP. Epidemiol 2005. Reidy JA. Urinary levels of seven phthalate metabolites in the U. Camann DE. et al. et al. Brock JW. Poland.68:309-314. David RM. Angerer J. Barr D. Rossbach B. et al. Fourth National Report on Human Exposure to Environmental Chemicals 269 .108(10)979-982. Hagmar L. et al. Environ Health Perspect 2000. Perera FP. Wiesmuller GA. NTP-CERHR. Angerer J. Atlanta (GA). Hauser R.18(1):122. Caudill SP. Gans G. et al. Needham LL. Monograph on the Potential Human Reproductive and Developmental Effects of Di-n-Butyl Phthalate (DBP). Needham LL. Chen Z. Koch HM. Drexler H. Jacek R. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. Research Triangle Park (NC). Castle L.18(12):10681074.208:237-245. Brock JW. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. Reprod Toxicol 2004. Levels of seven urinary phthalate metabolites in a human reference population. Urinary phthalate metabolites and biomarkers of reproductive function in young men. 112(5):A270]. Silva MJ.S. Int J Hyg Environ Health 2007. Hilborn ED. Third National Report on Human Exposure to Environmental Chemicals. Anderson WA.114(9):1424-1431. Hu H. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review].210(3-4):319-33. Sanchez GN. Evaluation of the effect ofa governmental control of human exposure to two phthalates in Japan using a urinary biomarker approach. Duty SM. Scotter MJ. Calafat AM.nih. 2005. Prenatal exposures to phthalates among women in New York City and Krakow. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004.Phthalates References Adibi JJ. Springall C. Available at URL: http://cerhr. Weuve J. Int J Hyg Environ Health 2007. Singh NP. A biomarker approach to measuring human dietary exposure to certain phthalate diesters.

270 Fourth National Report on Human Exposure to Environmental Chemicals . Neither IARC nor NTP has evaluated DCHP with respect to human carcinogenicity.500) < LOD 1.300 (.00 (<LOD-1.00 (<LOD-1.500 (.300 (.400) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. 84-61-7 General Information Dicyclohexyl phthalate (DCHP) is used to stabilize some rubbers.10 (<LOD-1.400 (<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.600) .50) .300 (. resins.500 (.70 (1.700) .400) < LOD 1. and 0.400 (.600) .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. 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) 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 . including nitrocellulose. < LOD means less than the limit of detection.300-.300 (.400-.10 (<LOD-1.400 (. 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 .00) .50) .600 (.3.400 (.700) .300-. and polyvinyl chloride.20) .400-.400-.500) . respectively.400) < LOD < LOD .400 (<LOD-. 0.70) .500) .400 (<LOD-.500) 1. which may vary for some chemicals by year and by individual sample.300-. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.Phthalates Dicyclohexyl Phthalate CAS No.300-.300-.500) 1.300 (.00 (<LOD-1. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.500) < LOD < LOD .300-.500 (.300 (. In this Report.600) .9.200-.200-.400 (. only levels at or above the 90th percentile could be characterized. and 03-04 are 0.500 (.10) .80) .10 (.600) .500) < LOD < LOD .400) 1.500) .500) . and polymers. Survey Geometric mean (95% conf.500 (. People exposed to DCHP will excrete mono-cyclohexyl phthalate (MCHP) in their urine.500-.500) < LOD * * * Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1.400-.300-.200-.400 (.200-.70) .300) < LOD .300-.400) 1.400) size 2541 2782 2605 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th . see Data Analysis section) for Survey years 99-00. Urinary Mono-cyclohexyl phthalate (MCHP) Metabolite of Dicyclohexyl phthalate (DCHP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.400 (.S.500) 1.200-.500 (.70 (1.2.400-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.90) .300 (.600) .400 (.400-.400-.200-.300-. 01-02.500 (.10 (<LOD-2.00-3.900-1.400 (<LOD-.00-2.300-.300) < LOD .200 (<LOD-. polyvinyl acetate.500 (.500 (.700) .300 (<LOD-.

260-.800-1.82 (1.360-.690 (.910 (.220 (<LOD-.310-.16 (<LOD-3.410 (.500) 3.530) 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.170-.82) .33 (<LOD-3.S.74) .510 (.12-1.770) < LOD 2.54-6.630 (<LOD-.420-.53) .240-.660) < LOD < LOD .330 (.620) < LOD .660) .770-1.310) < LOD .420-.490) .740) < LOD < LOD .610 (.350-.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 .710) .400-.54 (<LOD-2.14 (<LOD-3.470) 3.11) .560) 1.18) .670 (<LOD-.790-1.00 (<LOD-3.380-. population from the National Health and Nutrition Examination Survey. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.54) .910 (. Survey Geometric mean (95% conf.590 (.530 (.16) .880 (.940 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th 3.510-.950 (.34) .670-1.500-.17) .770-1.400-.530) 1.530-1.290-.450 (.630 (<LOD-.05) .690-1.530-.270) < LOD .380 (.830) 1.770-1.00) .67 (1.590 (<LOD-.500) size 2541 2782 2605 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .10) .690) < LOD < LOD .22 (<LOD-1.Phthalates Urinary Mono-cyclohexyl phthalate (MCHP) (creatinine corrected) Metabolite of Dicyclohexyl phthalate (DCHP) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.910 (.06) .740) . Fourth National Report on Human Exposure to Environmental Chemicals 271 .250 (.390 (.770 (.500 (.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 .06) .420-.33) .690) < LOD 2.910 (.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 1.470 (.370 (<LOD-.330 (.44) .43 (1.53) .480 (.36-1.450 (.

. People exposed to DEP eliminate mono-ethyl phthalate (MEP) in their urine.7) 71.3-110) 211 (160-278) 197 (159-243) 225 (187-270) 190 (164-219) 191 (171-214) 205 (176-238) 75. population from the National Health and Nutrition Examination Survey. colognes. 2003) and African-American women in Washington. 01-02. shampoos.8-111) 85. 84-66-2 General Information Diethyl phthalate (DEP) is a solvent used in many consumer products.2-102) 95. and hand lotions.1-93. soaps. Biomonitoring Information MEP levels in the NHANES 1999-2000. and 0. 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.2. 2001-2002.3 (82.9-92. 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.9. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. 2002).3 (74. and also in men attending a Boston infertility clinic (Hauser et al.4. respectively. see Data Analysis section) for Survey years 99-00. 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. deodorants. 272 Fourth National Report on Human Exposure to Environmental Chemicals . 2007).9 (61. Products that may contain DEP include perfumes. In contrast. 0. Neither IARC nor NTP has evaluated DEP with respect to human carcinogenicity.S.5) 81.4 (62.Phthalates Diethyl Phthalate CAS No. particularly those containing fragrances. DC (Hoppin et al.7 (70. and 03-04 are 1.3-103) 193 (141-256) 184 (148-227) 221 (165-294) 180 (140-221) 181 (152-212) 188 (158-219) 197 (129-249) 183 (142-217) 196 (170-241) 564 (419-818) 479 (387-651) 557 (432-695) 482 (390-590) 498 (441-567) 533 (471-629) 378 (290-730) 451 (315-636) 521 (295-571) 1510 (1050-2150) 1260 (983-1480) 1250 (973-1560) 1340 (1010-1660) 1350 (1060-1660) 1590 (1220-2070) 756 (379-1070) 808 (572-1090) 827 (542-1440) 3260 (1550-4420) 2070 (1470-3050) 2310 (1360-3310) 3480 (2230-4640) 2720 (2160-3670) 2980 (2250-3800) 328 393 342 752 742 729 1456 1647 1534 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 179 (149-215) 182 (157-211) 197 (173-224) 178 (154-206) 174 (153-198) 189 (160-225) 154 (119-197) 171 (139-199) 171 (148-201) 174 (138-210) 167 (139-194) 182 (138-219) 523 (372-650) 502 (419-603) 536 (449-654) 425 (350-508) 427 (387-498) 478 (392-564) 1440 (1020-2280) 1450 (1060-2110) 1520 (1210-2070) 988 (880-1230) 1050 (879-1310) 1260 (969-1640) 3500 (2130-4560) 3100 (2110-4390) 2910 (2210-3480) 2230 (1370-3880) 1860 (1490-2500) 2590 (1800-3420) 1214 1371 1250 1322 1411 1355 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 181 (157-209) 226 (195-262) 267 (239-298) 322 (275-377) 352 (324-384) 357 (310-412) 152 (133-175) 158 (141-178) 167 (145-193) 174 (146-210) 220 (190-264) 249 (212-307) 306 (256-350) 357 (290-407) 306 (253-414) 134 (108-157) 147 (119-177) 148 (125-175) 441 (390-541) 530 (444-660) 597 (523-688) 789 (635-949) 853 (709-1090) 948 (769-1150) 367 (287-482) 413 (366-451) 418 (366-477) 1280 (851-1510) 1490 (1050-2110) 1640 (1320-2180) 1890 (1410-2270) 2160 (1620-2470) 2500 (1840-2980) 986 (798-1340) 1020 (905-1230) 1210 (954-1480) 1720 (1460-2130) 2630 (1540-4460) 3050 (2230-4300) 3610 (2130-4640) 3540 (2810-5070) 4370 (2780-5910) 2470 (1590-3880) 2320 (1560-2720) 2250 (1590-3290) 813 677 652 603 703 699 908 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.. a sample of young Swedish males entering the military had median urinary MEP levels that were somewhat higher than males in the NHANES subsamples. Workplace air guidelines for external exposure to DEP have been established by ACGIH and NIOSH.1 (71..

2003) were slightly lower than levels found in NHANES 2001-2002. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. In an analysis of NHANES 1999-2000.Phthalates 2002 (Brock et al. with adjusted geometric mean levels of urinary MEP that increased with age (CDC. 2005).6 (77.9 (82. 2004).6 (65. This age-related trend is opposite the direction seen for other phthalates. Median MEP levels found in a small sample of German residents (Koch et al. 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.. 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. 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.S.2 (66. 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. population from the National Health and Nutrition Examination Survey.0 (66.9-110) 96.5-113) 122 (93.5-114) 101 (87.0-117) 142 (119-169) 152 (126-184) 168 (141-201) 179 (161-199) 181 (164-200) 197 (174-223) 79.7-110) 81..3-105) 87.0-156) 140 (111-180) 150 (123-184) 154 (136-177) 160 (146-182) 177 (147-202) 165 (127-208) 177 (135-224) 180 (145-203) 364 (275-495) 330 (249-409) 363 (292-485) 390 (336-452) 419 (363-486) 512 (423-632) 341 (219-554) 512 (290-802) 470 (310-596) 879 (676-1260) 808 (590-1100) 791 (589-1080) 1010 (803-1460) 1060 (884-1320) 1230 (989-1610) 625 (400-784) 843 (512-1320) 719 (470-1330) 1760 (1000-2000) 1330 (868-1840) 1470 (987-2220) 2170 (1790-3350) 2120 (1520-2790) 2290 (1770-3200) 328 393 342 752 742 729 1456 1647 1534 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 141 (124-159) 148 (130-168) 154 (139-171) 187 (165-211) 187 (166-210) 211 (180-248) 120 (107-134) 126 (110-147) 127 (108-150) 158 (142-179) 171 (148-188) 181 (148-217) 324 (249-415) 352 (282-425) 390 (341-465) 377 (307-495) 407 (355-473) 508 (379-634) 1000 (693-1480) 1100 (839-1480) 1070 (852-1360) 822 (697-1170) 860 (712-1100) 1120 (889-1400) 1950 (1460-2900) 2120 (1490-3030) 2000 (1610-2410) 1930 (1170-3410) 1430 (1190-2010) 2250 (1440-3330) 1214 1371 1250 1322 1411 1355 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 164 (142-190) 213 (182-249) 241 (213-271) 208 (183-236) 247 (226-271) 254 (225-287) 149 (135-165) 157 (142-173) 165 (144-189) 154 (136-174) 199 (164-242) 233 (202-270) 196 (166-228) 227 (185-270) 212 (188-246) 128 (111-142) 136 (124-150) 135 (120-158) 382 (314-472) 461 (396-572) 533 (417-665) 443 (390-505) 557 (478-618) 619 (476-791) 313 (239-387) 338 (288-402) 386 (338-485) 814 (673-974) 1080 (860-1650) 1230 (956-1610) 1030 (762-1700) 1240 (961-1480) 1530 (1200-1970) 856 (655-1390) 919 (712-1160) 989 (831-1330) 1330 (974-1920) 1940 (1410-2630) 2270 (1810-3140) 1920 (1230-2590) 2090 (1550-2800) 2590 (2160-3500) 1950 (1480-2740) 1590 (1320-2170) 1920 (1400-2780) 813 677 652 603 703 699 908 1216 1088 Non-Hispanic blacks Non-Hispanic whites Fourth National Report on Human Exposure to Environmental Chemicals 273 . 2002). Survey years 99-00 01-02 03-04 Geometric mean (95% conf. Analysis of NHANES 2001-2002 showed similar findings. Other population estimates also differed by sex and race ethnicity (Silva 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..

Hodge CC. Malek NA. Koch HM. Caudill SP.112(3):331-338. 274 Fourth National Report on Human Exposure to Environmental Chemicals . Barr DB. Camann DE. Environ Res 2003. Centers for Disease Control and Prevention (CDC). Reidy JA. Angerer J. Silva MJ. Baird DD.Phthalates References Adibi JJ. Prenatal exposures to phthalates among women in New York City and Krakow. Hum Reprod 2007. Atlanta (GA). Barr D. Perera FP. Phthalate monoesters levels in the urine of young children. Jacek R. Meeker JD. Urinary levels of seven phthalate metabolites in the U. Silva MJ. Caudill SP. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. Poland. et al.68:309-314. Environ Health Perspect 2002. Jedrychowski W. et al. 2005. Rossbach B. et al.93:177-185. Brock JW. 112(5):A270]. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Davis BJ. Bull Environ Contam Toxicol 2002. Environ Health Perspect 2004. Hauser R. Third National Report on Human Exposure to Environmental Chemicals.110(5):515-518. Ryan L. Duty S. Drexler H. Needham LL. Hilborn ED.S. Silva MJ. Reproducibility of urinary phthalate metabolites in first morning urine samples. Hoppin JA.111(14):1719-1722.22(3):688-695. Brock JW. Singh NP. Environ Health Perspect 2003.

1 (11.92-2.7) 19.5) 31.3) 13.90 (4.10) 3.6-38.0-29.19-3.40) 9.S.50-11. and blood product storage and intravenous delivery systems.0 (14.00) 1.3-25.12 (4.92-5.7-32. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.5) 37.0 (21.9-28.23 (2.6) 5.2-17.1 (10.80 (1.6 (16.5-40.92-2.4-42.60-11.0 (18.23) 3.40 (4. 01-02.50-16.68 (3.6-25. and in humans.30 (7.5) 40.6) 14.70) 7.6-28.40) 4.40) 4.00 (7.90) 3.2 (10.40) 8.4-20.00) 2.40-9.6 (12.92) 4.60) 90th 14.3 (11.70 (1.80-9.1-48.00) 5.6-23.4) 13. DEHP has been removed from or replaced in most toys and food packaging in the United States.90) 7.50 (3.10-4.9 (7.1-29.9) 15.70) 16.90 (1.10-2.5 (30.0 (17.00 (5.4-53.80) 13.2-28.34 (2.2.56 (2.70 (3.00) 19.60-7.50-8.2) 42.9 (29.50 (7.40-8.75-4.70-4..50-5.9-26.10-11.51) 4.4) 20.60) 4.30-6.6-130) 31. 1982.5-27.80) 6.0) 11.3 (10.5 (18.23 (3.9-55.15 (1.16-3.49 (3.5 (18.70-5.7) 35.96-5.83) 2.82 (3.90 (3.3 (15.1-27.8 (19.70 (3. interval) 3.70-6.37-4.7) 27.9) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.20 (3.2 (11.8 (17.80-27.60) 4.6 (9.4) 5.0-19. Four metabolites were measured in this Report: mono-(2-ethyl-5-hexyl) phthalate (MEHP).60) 9.14 (1.39) 3.00) 3.80) 9.70-3.90-4.50-2.27) 2. as glucuronide conjugates (Albro et al. Following ingestion.90-5.96) 4.00-3. which is used for many consumer products.40-1.50 (3.3 (19.6 (41. 1989.00-3.5-28.2-39.10) 4.84 (2. After parenteral administration.75 (3.10-5.5 (20.40) 75th 7.10) 2.6 (20.10-3.70-8.6 (11.24-4.90-8. MEHP is primarily formed by the hydrolysis of DEHP in the gastrointestinal tract and then absorbed.50-2.0) 39.00) 2.10 (3.54) 4.80-4. Fourth National Report on Human Exposure to Environmental Chemicals 275 .10 (3.2-35.8-47.2) 6.50 (3.89-3.5-28.1 (8.1-17.70 (8.00) 9.0) Total 4.69) Selected percentiles ( 95% confidence interval) 50th 3.10-5.50-5.40 (6.50 (2.5 (12.07-4.80-8.90) 4.31 (3.8-50.5-17. toys.4) 15.43 (3. respectively.60) 10.30-8.42-5.10) 3.00-5.6 (10. DEHP is metabolized to more than 30 metabolites which are rapidly eliminated in urine.0 (13.9 (16.27 (3.0) 23.50-6.10) 3.90) 4.00) 1.0 (19.3-64.7) 8.9 (15.9-48.5 (12.40-8.10-3.9) 13.6) 15.10 (4.60) 3.86) 2.10 (4.20 (1.8) 15.7) 22.50-3.9 (17.10) 2.40-11.9 (29.20 (3.0-18.7) 6. 117-81-7 General Information Di-2-ethylhexyl phthalate (DEHP) is primarily used to produce flexibility in plastics.2 (29.60 (5.9) 5.