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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2-Trichloroethane Trichloroethene (Trichloroethylene) m.4'-Tetrabromodiphenyl ether (BDE 66) 2.2'.2'.1-Trichloroethane (Methyl chloroform) 1.2.1.4'.2'4.5'-Tetrachlorobiphenyl (PCB 44) 2.2-Dichloropropane 2.What’s New in this Report What’s New in this Report In this Fourth Report.5'.2'. 2009 Acrylamide Adducts Acrylamide Glycidamide Total and Speciated Arsenic Arsenic.2'.1-Dichloroethane 1.3.4.4.5'-Hexabromodiphenyl ether (BDE 153) 2.6-Pentabromodiphenyl ether (BDE 100) 2.4.1.2-Dibromo-3-chloropropane (DBCP) Dibromomethane 1.2-Tetrachloroethane Tetrachloroethene Tetrachloromethane (Carbon tetrachloride) Toluene 1.2'.5-Dimethylfuran Ethylbenzene Hexachloroethane Methyl-tert-butyl ether (MTBE) Nitrobenzene Styrene 1.6. Paradichlorobenzene) 1.5'-Tetrachlorobiphenyl (PCB 49) 2. 75 new chemicals are added for the 2003-2004 survey period and are listed in Table 1.2’.4.4'.4'-Tetrabromodiphenyl ether (BDE 47) 2.4.3.and p-Xylene o-Xylene 2 Fourth National Report on Human Exposure to Environmental Chemicals . Total Arsenic (V) acid Arsenobetaine Arsenocholine Arsenous (III) acid Dimethylarsinic acid Monomethylarsonic acid Trimethylarsine oxide Disinfection By-Products (Trihalomethanes) Bromodichloromethane Dibromochloromethane (Chlorodibromomethane) Bromoform (Tribromomethane) Chloroform (Trichloromethane) Environmental Phenols Benzophenone-3 (2-Hydroxy-4-methoxybenzophenone) Bisphenol A (2.4'.html.3’.4'.1.2-Dichloroethene trans-1.2-Dichloroethene Dichloromethane (Methylene chloride) 1. Table 1.5.2-bis[4-Hydroxyphenyl] propane) 4-tert-Octyl phenol (4-[1.5'-Hexabromobiphenyl (BB 153) Volatile Organic Compounds (VOCs) Benzene Chlorobenzene (Monochlorobenzene) 1. The process for selection is described at http://www.4-Tribromodiphenyl ether (BDE 17) 2.gov/exposurereport/chemical_selection.2'3.2'.5-Pentabromodiphenyl ether (BDE 99) 2.5.3.3'.4.cdc.6'-Decachlorobiphenyl (PCB 209) Perchlorate Perfluorinated Compounds Perfluorobutane sulfonic acid (PFBuS) Perfluorodecanoic acid (PFDeA) Perfluorododecanoic acid (PFDoA) Perfluoroheptanoic acid (PFHpA) Perfluorohexane sulfonic acid (PFHxS) Perfluorononanoic acid (PFNA) Perfluorooctane sulfonamide (PFOSA) Perfluorooctane sulfonic acid (PFOS) 2-(N-Ethyl-Perfluorooctane sulfonamido) acetic acid (Et-PFOSA-AcOH) 2-(N-Methyl-perfluorooctane sulfonamido) acetic acid (Me-PFOSA-AcOH) Perfluorooctanoic acid (PFOA) Perfluoroundecanoic acid (PFUA) Phthalate Metabolite Mono-(2-ethyl-5-carboxypentyl) phthalate (MECPP) Polybrominated Diphenyl Ethers (PBDE) and Polybrominated Biphenyl 2.3-Tetramethylbutyl] phenol) Triclosan (2.5.4'.2'.4.4.4’.2'.1-Dichloroethene (Vinylidene chloride) cis-1.6'-Hexabromodiphenyl ether (BDE 154) 2.4’.3-Dichlorobenzene (m-Dichlorobenzene) 1.6-Heptabromodiphenyl ether (BDE 183) 2.4.4'-Pentabromodiphenyl ether (BDE 85) 2.2-Dichlorobenzene (o-Dichlorobenzene) 1.5’.4.3.2-Dichloroethane (Ethylene dichloride) 1.4.4-Dichlorobenzene (p-Dichlorobenzene.1.4. Chemicals reported for the first time in the Fourth National Report on Human Exposure to Environmental Chemicals.5.4’-Trichloro-2’-hydroxyphenyl ether) Non-dioxin-like Polychlorinated Biphenyls 2.2'.4'-Tribromodiphenyl ether (BDE 28) 2.

Some results reported previously have been changed or removed due to improvements in analytical measurement or recognition of an analytical issue (e.g.1). 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. 2003-2004 data for these other pesticides will be provided on this website as soon as they are available. Fourth National Report on Human Exposure to Environmental Chemicals 3 . Data for other pesticides are included only for 1999-2000 and 2001-2002.g. Percentiles for all three NHANES survey periods (1999-2000. the presence of an interference) that produced results of inadequate quality.5-dichlorophenol for the 1999-2002 survey periods. and polycyclic aromatic hydrocarbons (PAHs) for one or more of the 1999-2002 survey periods. 2003-2004 data for the organochlorine pesticides and the dialkyl phosphate organophosphorus insecticides are included in the Report. five results that all have the value 90.4-dichlorophenol and 2.. 2001-2002. and these data will be included in the next release of the Report. Explanations for each change are provided in Appendix B. 2003-2004) have been re-computed by use of this improved procedure. urinary 2. Affected analytes were serum beta-hexachlorocyclohexane for the 2001-2002 survey period.. Details of this procedure are provided in Appendix A.

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

Data Sources and Data Analysis metabolites in blood. stratified. gender. Data Analysis Because the NHANES is a complex. Geometric means were calculated by taking the log of each concentration and then computing the weighted mean of those log-transformed values using SUDAAN software. race/ethnicity is categorized based on the sample design as Mexican American. 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. 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.cdc. serum. PCBs. and race/ethnicity as defined in NHANES. These compounds are lipophilic and concentrate in the body’s lipid stores. results are given for the total population as well as by age group.htm. Age groups are as described for each chemical in each data table. levels are presented two ways: per volume of urine and per gram of creatinine. Data were analyzed using the statistical software package Statistical Analysis System (SAS) (SAS Institute Inc. Results are reported here using standard units. including tolerance limits for operational parameters. serum levels are presented per gram of total lipid and per whole weight of serum. This type of distribution is common in the measurement of environmental chemicals in blood or urine. References for the analytical methods used to measure the different chemicals are provided in Appendix C. Urinary levels are expressed both ways in the literature and used for different purposes. For dioxins. non-Hispanic black. or urine levels for each environmental chemical. Units: For chemicals measured in urine. Table 2. Acrylamide and glycidamide adducts are expressed as the picomoles per gram of blood hemoglobin to which the adduct is bound. the measurement of quality control samples in each analytical run to detect unacceptable performance in accuracy or precision. and urine were based on isotope dilution mass spectrometry.. Levels per gram of creatinine (i. The geometric mean is influenced less by high values than is the arithmetic mean. or graphite furnace atomic absorption spectrometry. Statistics include unadjusted geometric means and percentiles with confidence intervals. and verification of traceable calibration materials. SUDAAN uses sample weights and calculates variance estimates that account for the complex survey design. if one person has consumed more fluids than another person. creatinine corrected) adjust for urine dilution..e. Census Bureau estimates of the U. This design does not permit straightforward analysis of exposure levels by non-targeted strata such as locality.S. Other racial/ethnic groups are sampled. The Report presents descriptive statistics on the blood. and nonHispanic white. population. furans. 2001). Gender is coded as male or female.gov/nchs/nhanes/ nhanes2003-2004/analytical_guidelines. probability-cluster design. his or her urine output is likely higher and the urine more dilute than that of the other person. or region.g. state. Ninety-five percent confidence intervals around this Fourth National Report on Human Exposure to Environmental Chemicals 5 . Sample weights also are used to adjust for possible bias resulting from nonresponse and are post-stratified to U. or by use of particular products. inductively coupled plasma mass spectrometry. micrograms per liter). Serum levels reported per gram of total lipid reflect the amount of these compounds that are stored in body fat. including the lipid in serum. sample weights must be used to adjust for the unequal probability of selection into the survey.S. Other racial/ethnic groups are included in estimates that are based on the entire population sample. For example.. Guidelines for the analysis of NHANES data are provided by NCHS at http://www. generally conforming to those most commonly used in biomonitoring measurements. but the proportion of the total population represented by other racial/ethnic groups is not large enough to produce valid estimates. serum. seasons of the year. 2002) and the statistical software package SUDAAN (SUDAAN Release 8.0. multistage. and organochlorine pesticides. In each table. Units of measurement are important. 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. proximity to sources of exposure. Other mostly non-lipophilic chemicals measured in serum are expressed per liter of serum (e. Useful unit conversions are shown in Table 2. Laboratory measurements underwent extensive quality control and quality assurance review. For these analyses.

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

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

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

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

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

Fourth National Report on Human Exposure to Environmental Chemicals 11 . (NTP-CERHR.9 (60.5 (52. EPA. such as potatoes and some grains..3 (55.0-115) 156 (120-203) 146 (129-163) 149 (125-179) 218 (172-271) 197 (172-223) 1792 1874 2994 Limit of detection (LOD.7 (65.1) 101 (95.0-58.6-75. Estimated intakes in children are about twice that of adults (DiNovi and Howard. FDA.2 μg/kg/day (U.7 (63.0 (57.7) 54. soil conditioners. 1990. smoking. Smaller scale applications of polyacrylamides include additives to paperboard used for food packaging. ocular and dermal irritation from direct contact with acrylamide containing materials.7-64.6-66. 1994). but can covalently bind to form adducts with proteins.4 (54. are heated at temperatures used for frying and baking.5-85. or to glutathione conjugates (Calleman et al.4 (51.3) 63. FAO/WHO.7-64. in permanent press fabrics.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. glycidamide.2-93. 2002). 2006.9-52. 2005). see Data Analysis section) for Survey year 03-04 is 3.0 (69.S.0. Since acrylamide has limited volatility and high water solubility.3) 70.1 (73.1-61.8 (81.5 (79. and in the synthesis or compounding of dye materials. and binding agents. and peripheral neuropathy following chronic Acrylamide Geometric mean and selected percentiles of hemoglobin adduct concentrations (in pmol/g hemoglobin) for the U. 217 million pounds of acrylamide were produced commercially in the U.1) 55.5 (44.1 (52. it was discovered that acrylamide is formed when starch-rich foods.2-114) 163 (147-191) 96.8 (52.7) 58. environmental releases of acrylamide can enter aquatic systems and soils where it degrades within days and does not bioaccumulate (U.5) 66.3-71. and from dermal contact with products that contain residual acrylamide. acrylamide is synthesized and used in the production of polyacrylamide polymer.1) 46.5 (74. Polyacrylamides are useful water-compatible polymers used in water treatment. the main source of exposure is from the diet.0 (53.0-108) 152 (139-175) 126 (111-142) 108 (86. in some sealing grouts. Survey Geometric mean (95% conf.1 (88. acrylamide has produced upper airway irritation following inhalation of high levels.0-66.9) 57.1 (47. gels.6 (56. 2004).2) 57. widely distributed in tissues. and is either metabolized to the reactive epoxide.2-91.4-76.2) 57.4-89.8 (57.6) 73.7 (58. Tareke et al. In the general population.0) 85. 2005).4) 57.3 (53.5-80. Natural substances in the food are converted to acrylamide.0 (67.0-104) 132 (115-151) 223 (194-243) 141 (120-152) 220 (189-237) 164 (147-191) 350 769 1889 2570 1523 3509 3592 03-04 03-04 03-04 61.7) 73. EPA.8-55.7) 75th 79.2 (62.9-61.2-77.1-64.4) 57.9) 58.Acrylamide Acrylamide CAS No. In humans. Elimination occurs mainly in the urine as mercapturic acid conjugates. drinking water.9) 63.1) 62. as an absorbent in disposable diapers.4 (59. and well below doses known to cause nerve damage or carcinogenicity in animals. pulp and paper production. interval) 61.1 (83. These estimated intakes are hundreds of times lower than occupational exposures.9 (54..2-59.2-70.0 μg/kg for adults (FAO/ WHO.0) 57.9) 75.S. 2005). and in some cosmetics. 2005). although additional exposures from cosmetic products could add a similar amount (NTP-CERHR.7) 96.1) 53. Fennell et al. 2005). 2004.6 (51. population from the National Health and Nutrition Examination Survey.1-57. People may be exposed to acrylamide from foods.6-65.9-105) 86.6-104) 82. and an average daily intake is estimated as 0. 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. Commercially.4-83. Acrylamide is not thought to accumulate in the body at environmental doses. 79-06-1 General Information Acrylamide is a small organic molecule existing as a white crystalline powder in its pure state.4) 100 (89.6-108) 61.6) 90.6) 50.7 (55.6) 71.2 (75.6 (81.4 (53. Recently.4-60.2-67.4-60.S.2 (58.6) 90th 141 (124-155) 03-04 03-04 03-04 03-04 03-04 03-04 03-04 59. EPA reference dose of 0.2-118) 98.S.7-60.3) 86. mineral processing.6-61.5) 58.3-2. and cosmetics (NTP-CERHR. but are generally above the U.0-49.9 (69. 2006). In 1997.. 2005. Animal studies indicate that acrylamide is well absorbed.8 (91.1-64.S.4 (54.8-57.

6-62.8-49.1) 56. fetal death.. 2002. Animal studies have shown that acrylamide can cause nerve damage (neuropathy). 2008).3) 59.1 (56. although different analytic methods can affect results. and neuronal DNA reactivity (Doerge et al. Several of these studies have shown that smokers have adduct levels that are three to fourfold higher than non-smokers.5) 75th 85.6 (66.6 (90. AHA levels have been shown to increase with dietary intake (Hagmar et al.. presynaptic nerve terminal binding (LoPachin.2) 65.1 (82. 2005.5) 87.9-64.2 (72.1-70. 2006) have been demonstrated after acrylamide dosing. most non-smokers had levels less than about 100 pmol/gram hemoglobin. 2005..4 (90. 2006.8) 45. 2009).7 (57.9 (58.9-138) 143 (130-159) 96. interval) 59. Rice.0 (70. Biomonitoring Information Acrylamide and glycidamide hemoglobin adducts (AHA and GHA.8-61.3) 59. 2006). Younger children may have slightly higher levels possibly due to increased intake of acrylamide-containing foods relative to body size (Dybing et al.9-62.4-59.5) 71..3) 59.1) 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 59.5-92.0 (52.7 (61.9) 75. Glycidamide has been shown to react with DNA (Doerge et al.2-91..5 (42.5 (83.0) 118 (103-126) 121 (112-134) 113 (94.0 (75.2) 55.2-68. Mucci et al. 1997. 2005). uterine. Maniere et al.3-101) 95. reproductive effects (reduced litter size.5-66.....9) 87. 2005. population from the National Health and Nutrition Examination Survey. probably through its epoxide metabolite. 2005) have been demonstrated in animals.1) 62.S. male germinal cell injury. adrenal. Schettgen et al.who.5-64. EPA at: http://www. 12 Fourth National Report on Human Exposure to Environmental Chemicals .epa.7) 74. Additional information is available from U. Axonal degeneration. 2005.1-62. 2005. see Data Analysis section) for Survey year 03-04 is 4.7-64.9) 59.8-48.5) 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. 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.7) 61. Schettgen et al.5 (59. 2004.7 (84.. 2001). Klaunig et al.S. and other sites) (FAO/WHO.7 (87.0 (80.1-60. Acrylamide is clastogenic and can produce dominant lethal mutations.7) 60.Acrylamide occupational exposures. scrotal. 2005. 2005).9) 65. After exposure ceases.1) 60. 2005.9-77. 2006).1 (57.. U.8) 60.. respectively) are markers of integrated acrylamide exposure over the preceding few months.. 2005.7-86.0) 94.7) 90..2 (56. In addition.4 (57. Vesper et al.4 (56. IARC classifies acrylamide as probably carcinogenic to humans.4) 53.4 (61. Adducts are formed when either acrylamide or glycidamide react to form a permanent covalent bond with hemoglobin in the blood.6-90. dominant lethality).0-93. Puppel et al.2-90.. 1997.2) 87. 2002. gov/iris/ and from the Food and Agriculture Organization of the United Nations and WHO at: http://www.1-56. NTP-CERHR.8 (44.S. and cancer (mammary.9-78. Survey Geometric mean (95% conf.4-65.S. 2005). EPA.4-103) 79. 2005) and sperm DNA adducts (Xie et al. and to increase DNA reactivity when glutathione availability is reduced (Klaunig et al.3-78.1 (66.5-94..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.. glycidamide (NTP-CERHR.pdf. EPA. 2005. U. 2008).0-62. 2005. Hagmar et al. to increase the unscheduled synthesis of DNA in tumor susceptible tissues (Klaunig et al.4) 46. Vesper 2005) and smoking (Bergmark.4 (81. The degree of formation of the more toxic glycidamide and levels of GHA can be influenced by polymorphisms in several of the enzymes that metabolize acrylamide (Duale et al.1 (70.2 (63.3 (56. 2005.9 (81. thyroid. levels of AHA adducts decline but may remain detectable for several months (Hagmar et al.4) 83. altered gene expression in testicular tissues (Yang et al. 2003.4 (51.9 (57.0. Glycidamide Geometric mean and selected percentiles of hemoglobin adduct concentrations (in pmol/g hemoglobin) for the U. 2005). Puppel et al....8 (51.int/ ipcs/food/jecfa/summaries/summary_report_64_final.3) 85.4-98.5) 90th 130 (120-141) 03-04 03-04 03-04 03-04 03-04 03-04 03-04 71.9-76.6-64.5 (56.7-62. 2004).

Duale N. symptoms of numbness or tingling in the extremities did not occur in exposed workers whose AHA levels were below 510 pmol/gram hemoglobin.56. J Agric Food Chem 2008. and 39% of workers with levels above 1000 pmol/gram hemoglobin had these symptoms (Hagmar et al. et al. Mechanisms of acrylamide induced rodent carcinogenesis. Doerge DR. Simultaneous analysis of hemoglobin adducts of acrylamide and Fourth National Report on Human Exposure to Environmental Chemicals 13 . Determination of hemoglobin adducts in humans occupationally exposed to acrylamide. Tian G. Fennell TR.cfsan.pdf. Costa LG. Alexander J. 8-17 February 2005. Mucci LA.85:447-459. 2004 Acrylamide in Food Workshop: Update Scientific Issues. Illinois. Bergmark E. Acrylamide intake through diet and human cancer risk. Fennell TR. Calleman CJ. Toxicol Appl Pharmacol 1993. National Toxicology Program.580(1-2):157-165. Hagmar et al. Monograph on the Potential Human Reproductive and Developmental Effects of Acrylamide. Differences in hemoglobin adduct levels of acrylamide in the general population with respect to dietary intake. April 13-15. Wilson KM. NIH Publication No. Health effects of occupational exposure to acrylamide using hemoglobin adducts as biomarkers of internal dose. Axmon A. Chem Res Toxicol 1990. References Bergmark E. Mutat Res 2005. Malmberg B. Human exposure and internal dose assessments of acrylamide in food. In another study. Acrylamide is metabolized to glycidamide in the rat: evidence from hemoglobin adduct formation. Acrylamide neurotoxicity: neurological. Biomarkers of human exposure to acrylamide and relation to polymorphisms in metabolizing genes. Cheong HK. 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.gov/chemicals/ acrylamide/Acrylamide_Monograph. Aprea P. Osterman-Golkar S. Bergmark E.fda.120(1):45-54. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. et al.561:21-37. 1993. Italy. Calleman CJ. 1994). Bjellaas T. Food and Drug Administration (FDA). Mutat Res 2005.who. 2005.pdf. Available at URL: http://www.10(1):78-84. et al. Scand J Work Environ Health 2001.. 054472.Acrylamide In occupational settings. Adv Exp Med Biol 2005. 2001).3:406-412. Available at URL: http://www. Hemoglobin adducts of acrylamide and acrylonitrile in laboratory workers. Farmer PB.561:49-62.126(2):361-371. He F. The Updated Exposure Assessment for Acrylamide. da Costa GG. Godard T. Snyder RW.43:365–410. Uncertainties.580(1-2):131-141. Toxicol Sci 2005. Twaddle NC. Spicer R.Toxicol Appl Pharmacol 1994. 1999). [Epub ahead of print] Dybing E. Andersen M. Churchwell MI. 2004. Toxicol Sci. Churchwell MI. Bergmark E. AHA levels were several fold to several hundredfold higher than levels in non-exposed non-smokers (Bergmark et al. Mutat Res 2005. Doerge DR. Costa LG. DNA damage and DNA adduct formation in rat tissues following oral administration of acrylamide. Yang JS. Calleman CJ. Laurentie M. Chicago. Center for the Evaluation of Risks to Human Reproduction (NTP-CERHR). LoPachin RM. 2/3/09 Hagmar L. 2006. Wirfalt E. Joint FAO/WHO Expert Committee on Food Additives. smokers and nonsmokers. Survey data on acrylamide in food: individual food products. Perez et al. and Research Strategies. Guffroy M.. Maniere I. 2/3/09 Klaunig JE. Burgess J. Tornqvist M. Kamendulis LM. et al.html#u1004. 2/3/09 Perez HL. 2001. CFSAN/Office of Plant and Dairy Foods.niehs. Rosen I. Becher G.27(4):219-226. Bridson WE. Adv Exp Med Biol 2005. gov/~dms/acrydata. Rome. et al. Zhang S. morphological and molecular endpoints in animal models. 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. Tornqvist M. Nordander C. Beland FA. Kautiainen A. Available at URL: http://cerhr. 64th Meeting: Summary and Conclusions (FAO/WHO). DiNovi M and Howard D. Metabolism and hemoglobin adduct formation of acrylamide in humans. smoking habits and gender.int/ipcs/ food/jecfa/summaries/summary_report_64_final. Paulsen JE. Magnusson AL. McDaniel LP.580(1-2):119-129. Hagmar L. He F. Paulsson B. Haugen M. 2009 Jan 8. Summer SCJ.. DNA adducts derived from administration of acrylamide and glycidamide to mice and rats. 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..nih. Toxicol 2005. July. Wu Y.. Food Chem. 6013-6019. February. Bruze M. Relationships between biomarkers of exposure and neurological effects in a group of workers exposed to acrylamide. Chem Res Toxicol 1997 Jan. Granath F.

September. Tornqvist M.163(2):101-8.S.561:89-96. Rapid Commun Mass Spectrom 2006. revised 1/3/06. Analysis of acrylamide. U. J Agric Food Chem 2008. Int J Hyg Environ Health 2004. Sun H. acrylonitrile and acrylamide-biomarkers in occupational and environmental medicine.gov/chemfact/s_acryla. Hemoglobin adducts of ethylene oxide. The carcinogenicity of acrylamide. Chae C. Kutting B. Fueller F. Anal Biochem 1999. Weiss T. a carcinogen formed in heated foodstuffs. Adv Exp Med Biol 2005.20(6):959-64. Office of Pollution Prevention and Toxics. Letzel S. Hallmans G. Mutat Res 2005 Feb 7. Lee SH. EPA). Meyers T. Mutat Res 2005. Ding X. 2/3/09 Vesper HW. Ingham L. Xie Q.S. Ospina M. Benetou V.gov/iris/subst/0286. Schettgen T.580(1-2):71-80.274(1):59-68. Ospina M. Acrylamide. Pilot study on the impact of potato chips consumption on biomarkers of acrylamide exposure. Liu K. 14 Fourth National Report on Human Exposure to Environmental Chemicals . et al.epa. Han DU. Smith A. et al. Rice JM. Agudo A. Drexler H. Rossbach B.580(1-2):3-20. Gray JG. A first approach to estimate the internal exposure to acrylamide in smoking and non-smoking adults from Germany. Angerer J. Fu D.50(17):4998-5006. 1994. Tjaden Z. Automated method for measuring globin adducts of acrylamide and glycidamide at optimized Edman reaction conditions. Toxicol Lett 2006. EPA).S. Choi JH.207(6):531-9. Adduction of biomacromolecules with acrylamide (AA) in mice at environmental dose levels studied by accelerator mass spectrometry. Integrated Risk Information System (IRIS). Yang HJ. Licea-Perez H. Karlsson P.epa. Tareke E.S. Lee MH. Broding HC. Toxicological effects of acrylamide on rat testicular gene expression profile. Angerer J. Washington (DC). Environmental Protection Agency (U.Acrylamide glycidamide by gas chromatography-mass spectrometry.htm.56(15):6046-53. Marko D. Schettgen T. Myers GL. Determination of haemoglobin adducts of acrylamide and glycidamide in smoking and non-smoking persons of the general population. Meyers T. 2/3/09. Available at URL: http://www. Available at URL: http://www. Jin Y. U. DNA strand breaking capacity of acrylamide and glycidamide in mammalian cells. Liu Y.txt. Toxicol Lett 2002. Puppel N. Schettgen T. Vesper HW. Tjønneland A. Drexler H. Environmental Protection Agency (U. Drexler H. J Agric Food Chem 2002. Han CH. Int J Hyg Environ Health 2003. Slimani N.206(1):9-14. Reprod Toxicol 2005. propylene oxide. Eriksson S. Chemical Summary for Acrylamide. Rydberg P. Angerer J. Cross-sectional study on acrylamide hemoglobin adducts in subpopulations from the European Prospective Investigation into Cancer and Nutrition (EPIC) Study.134(1-3):65-70.19(4):527-34. Vesper HW.

21-1. and 03-04 are 0.23 (2.570 (.S.50) 3.060 (<LOD-.197) .137-.790) .92 (1.770-1.540 (.150) .43 (1.16) .216 (. DHHS.99) 2.77 (1.120-. and various other disorders (U.860 (.96 (1. respectively.310) 90th 1.990 (.63-2.40) .88 (.44) 2.066 (.058 (.060 (.S.30) * .130 (.190-.00) .620-1.087 (.180 (.260) 1. and 17% had an LOD of 0.050 (<LOD-. acute respiratory infections.080-.470-.850 (.080-.063) .54) 1.050-.11) .84-3. population from the National Health and Nutrition Examination Survey.960-1.280 (.20) . and exacerbated asthma (U.030-.310-1.49) 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.01) 3.160 (.510 (.670) .23 (1.77 (2.350 (.110) .060 (<LOD-.54) size 5999 6819 6320 Total years 99-00 01-02** 03-04 50th .95) 1.080-.260-1.220) .060) .625) .080) < LOD < LOD .300) .726) .120 (.060-.580) .900-1.104-.070 (<LOD-.53-4.068) .075 (.17 (.020-.060 (.630 (.23-2.44) 2.188) .450-.312) .19-2.520 (.050) . Persons exposed to secondhand tobacco smoke (environmental tobacco smoke [ETS]) may have adverse health effects that include lung cancer and coronary heart disease.230) .75) 1.060-.110-.040-.88 (1.428-.110 (.630 (.120 (.65 (1.144 (. 2006).110-.047-.090-.210 (.310) .62) 2. and 0.09-2.070-. Children exposed to ETS are at increased risk for sudden infant death syndrome.68) 2.410) . < LOD means less than the limit of detection.33-2.02) 1.350-.05) 1.047-.15) 2.14) .164 (. ear problems. producing roughly 1–2 mg of bioavailable nicotine per cigarette (Benowitz and Jacob. 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. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.55 (1.148-.17) .47-3.220) .175 (.79) 3.76 (1.106-.190-.062 (.20 (1.28-1.34 (1.17 (1.21-1.950 (.070) . stroke.54 (1.220-.084) .110 (.160) .26-1.086 (.89) 1.115-.20-2.160 (.126) . Fourth National Report on Human Exposure to Environmental Chemicals 15 .93) . ** In the 2001-2002 survey period.071) .997-3.040-.740-1.800 (.030-.180) .78) 2.12 (1.22) 2.840) 3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.70) 2.910-1.19) .68) .320) .00) 1.770) . maternal exposure during pregnancy can result in lower birth weight.09-3.089) Age group 3-11 years 99-00 01-02** 03-04 .32) 1.193) .180) .53 (1.060-.040 (.088-.01 (1.068) .63 (2.050) .430-1.730 (.153-.213) .66-3.140-.350-.030-.190-.22) 2789 3152 2937 3210 3667 3383 Females Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 * .120 (.066-.02 (.87-3..059-.02) 1.570-1.052 (<LOD-.187) .110 (. emphysema.820) .66) 1.087) < LOD < LOD .094) .Cotinine Cotinine CAS No.050 (<LOD-.19) 1.076-.505 (.198) * .62 (2.180) .28) .180) . 2004). which may vary for some chemicals by year and by individual sample.066) .500 (. see Data Analysis section) for Survey years 99-00.32-2.60-2.506 (.052 (<LOD-.100-.145) .600-1.040 (.05 ng/mL.120 (.480-1.12 (2.99) 2.080) < LOD .140 (.201) .42-4.92) 1174 1415 1252 1773 1902 1783 3052 3502 3285 12-19 years 99-00 01-02** 03-04 99-00 01-02** 03-04 20 years and older Gender Males 99-00 01-02** 03-04 99-00 01-02** 03-04 .050 (<LOD-. 2004).45) 1.49) 1.18-3.360) .55-2.20) 1.110 (.660) .94) 1.124 (.308 (.68 (1.077) . 1998).043-.015.30) 2.180 (.66 (1.12-4.131 (.30) 2.370-.090-.950-1.180) .234) .57) 2.85 (1.S.240 (.163 (.302) .077) .050 (<LOD-.163) .057-.167 (.070) 75th .44 (2.990) .05.059-.96-4.39 (1.090-.54 (1.073) < LOD .070) .061) < LOD .04 (1.142-.087-.09-3.040 (.130) .110 (.230 (.50-4.540-.111-.38-2. The smoke produced by burning tobacco contains at least 250 chemicals that are toxic or carcinogenic.14-1.160) .150) .053 (<LOD-.35 (2.015 ng/mL. DHHS.160 (.930 (.5% nicotine by weight (Kozlowski et al.50 (1. and more than 50 compounds present in ETS are known or reasonably anticipated to be human carcinogens (NTP.920 (.400-.580-1. Cigarettes contain about 1.120 (.710 (.533-.050-.071 (.080 (.83-2.70-2.080 (.630 (.20 (.140 (.42 (1.12) 1.580 (. The consequences of smoking and of using smokeless tobacco products are well known and include an increased risk for several types of cancer.48-3.200) 1.770) .44 (1.77 (1.030 (.137 (. cardiovascular disease. 83% of measurements had an LOD of 0.81-2.50-1.96) 2.480-.21 (. Survey Geometric mean (95% conf.690 (.108) * .32-2.054 (.23 (.49) 1.120-.164 (.050 (.110) .48-2.310-1.110-.15 (2.620 (.160-.621-1.080-.154-.14) .120) .140-.139) * . acute respiratory illness.740-1. 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.39) 3.

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

fr/ENG/Monographs/ allmonos90. Giovino GA. 4/13/09 National Cancer Institute (NCI).56:483-493. Jarvis MJ. Pirkle JL. Epidemiol Rev 1996.php. National Center for Chronic Disease Prevention and Health Promotion. Benowitz NL. June. Tobacco Smoke and Involuntary Smoking. Centers for Disease Control and Prevention. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Aiba M. Vol 83.niehs. Health Effects of Exposure to Environmental Tobacco Smoke: The Report of the California Environmental Protection Agency. Department of Heath and Human Services. International Agency for Research on Cancer. Strauss WJ. JAMA 1998. Cotinine as a biomarker of environmental tobacco smoke exposure. Benowitz NL. Brody DJ. Benowitz NL.niosh. Lewis PJ.4:313-316. 4/13/09 International Agency for Research on Cancer.114(6):853-858. J Pharmacol Exp Ther 1999. Turner DM. Kozlowski LT.S. Jacob P III. 1999. Biomonitoring data can also help scientists plan and conduct research about exposure to ETS and about its health effects. Int Arch Occup Environ Health 1991.15:302-307. Benowitz NL.S. 11th ed. cigarette smokers: the Third National Health and Nutrition Examination Survey. 1999-2002. the United Kingdom. Am J Public Health 2004. Summary of Data Reported and Evaluation [online] 1986.S. Metabolism of nicotine to cotinine studied by a dual stable isotope method. Giovino G. Available at URL: http://www. Decrease in the prevalence of environmental tobacco smoke exposure in the home during the 1990s in families with children.pdf. Department of Heath and Human Services. Herrera B. Jacob III P. available at URL: http://mtn. Available at URL: http://monographs.cancer. Coordinating Center for Health Promotion. Third National Report on Human Exposure to Environmental Chemicals. iarc. Centers for Disease Control. Jacob P. Benowitz NL.pdf. et al. population to secondhand smoke: 1988-2002. References Armitage AK. 4/13/09 U.94(2):314-320.cdc. National Toxicology Program (NTP). Brody DJ. Soliman S. Mehta NY. Coordinating Center for Health Promotion. Caraballo R. Tob Control 2006.gov/ntp/roc/eleventh/profiles/ s176toba.gov/tcrb/monographs/10/. Curtin LR. Mowery PD. Maurer KR. George CF. U. Pirkle JL.S. Hukkanen J. Houseman TH. Racial/ethnic differences in serum cotinine levels among adult U. National Center for Fourth National Report on Human Exposure to Environmental Chemicals 17 . Clin Pharmacol Ther 1994. Herrera B. Pharmacol Rev 2005. Available at URL: http://monographs. Tobacco related exposures. Environ Health Perspect 2006.nih. The Health Consequences of Involuntary Exposure to Tobacco Smoke: A Report of the Surgeon General — Executive Summary. Respiratory nicotine absorption in non-smoking females during passive smoking. 1991. Office on Smoking and Health [online] 2006.280:152-156. and the United States.gov/library/ secondhandsmoke/. Current Intelligence Bulletin 54: Environmental tobacco smoke in the workplace.275:1233-1240. Metabolism and disposition kinetics of nicotine. Bernert JT. Pechacek TF. Trends in the exposure of nonsmokers in the U. Smoke-free laws and secondhand smoke exposure in US nonsmoking adults. Pechacek TF. DHHS). Kira S. 1988-1991.63:139-43. JAMA 1996. Smoking and Tobacco Control Monograph 10 [online]. Tob Control 1998. Tobacco Smoke. Etzel RA. Pickett MA. Vol 38. Flegal KM.fr/ENG/Monographs/allmonos90. Nicotine metabolism and intake in black and white smokers. U. DHHS). Sweeney CT. Perez-Stable EJ. Modin G. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Sosnoff CS.57(1):79115. Warner K. Schober SE. Vogler GP. JAMA 1998.S. IARC Monogr Eval Carcinog Risks Hum. IARC Monogr Eval Carcinog Risks Hum. Schwartz SS. 4/13/09 Centers for Disease Control and Prevention (CDC).S. National Institute for Occupational Safety and Hygiene (NIOSH).iarc. 1988-1991. Filter ventilation and nicotine content of tobacco in cigarettes from Canada.S Department of Health and Human Services (U. Available at URL: http:// cancercontrol. Ethnic differences in N-glucuronidation of nicotine and cotinine. Bernert JT. Pollack HA.7:369-375. [online].291(3):1196-1203. Summary of Data Reported and Evaluation [online] 2004. 2004. Exposure of the U. U. Fong I.surgeongeneral.php.Cotinine and public health officials determine whether people have been exposed to higher levels of ETS than are found in the general population. et al.gov/eid/rmca/critdocs/ criteriadoc/33. BMJ 1975. 4/13/09 Perez-Stable EJ.S. Atlanta (GA): 2005. Jacob P III. In Report on Carcinogens. The Health Consequences of Smoking: The Surgeon General’s Report—Executive Summary. 4/13/09 Iwase A.18:188-204.S Department of Health and Human Services (U.280:135-140. Caudill SP. Absorption and metabolism of nicotine from cigarettes. Available at URL: http://ntp. Centers for Disease Control and Prevention. population to environmental tobacco smoke: the Third National Health and Nutrition Examination Survey. Richter PA. Dollery CT.

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

DEET is not registered for use on agricultural commodities. have been reported as result of self-poisoning by ingestion or excessive dermal application.560) < LOD . Its use is recommended for prevention of several vector-borne diseases. General population exposure to DEET occurs from skin application and from inhalation of aerosol formulations. < LOD means less than the limit of detection. and it has not been rated by IARC or NTP with respect to human carcinogenicity.120-. Survey Geometric mean (95% conf.130 (.130) < LOD .100-.100 (<LOD-. 1998). Exposure can also occur from consuming food contaminated by DEET on hands or that was sprayed nearby.110-. Additional information is available from U. EPA.180 (.130-.110 (. After absorption.100-.EPA.130-. DEET is metabolized via hydroxylation and dealkylation pathways and eliminated in the urine within approximately 24 hours (Selim et al.210) 964 1191 1013 1344 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . see Data Analysis section) for Survey years 99-00 and 01-02 are 0.140-.140 (.gov/pesticides/. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. DEET is also used in combination with dermal sun screens (U.epa.140) < LOD .449 and 0.120-. Most reports of adverse effects from overexposure to DEET involve skin reactions (Bell et al.250) < LOD .110 (<LOD-. Urinary N.S. which may vary for some chemicals by year and by individual sample. About 3-8% of dermally applied DEET is absorbed. DEET is not genotoxic.S.S. 2005).220 (.180 (..130-. 1998). DEET has low acute toxicity.180) < LOD .270) 688 678 518 700 598 956 Limit of detection (LOD. Neurological effects in humans.EPA at: http://www. One survey detected DEET in 74% of sampled streams in the U.110 (<LOD-. 134-62-3 General Information N.140) < LOD . (Kolpin et al.150) < LOD .240) < LOD .100-.140) < LOD .130 (.100-.190) < LOD .220) size 1977 2535 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD 90th . People in outdoor occupations may apply DEET more frequently or use higher concentration formulations resulting in higher levels of exposure.520) < LOD ..N-diethyl-meta-toluamide (DEET) is an insect repellent that was first marketed in 1957. There are over 225 insect repellents brands containing DEET.110-. DEET can be applied to clothing and the skin to repel biting insects.100-.N-Diethyl-meta-toluamide (DEET) N.1.N-Diethyl-meta-toluamide (DEET) CAS No.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 .110 (. 2002). population from the National Health and Nutrition Examination Survey. including seizures and encephalopathy.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 .N.110 (. and they range in concentration from 4% to 100%. 2002). 1995. (U. DEET is not a developmental or reproductive toxicant in animals (U.130) < LOD . 2003)..S.170 (. 2003).170 (. Fourth National Report on Human Exposure to Environmental Chemicals 19 . interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD .110 (.EPA.180 (.130 (.210 (.160) < LOD .S. but higher DEET concentrations and different formulations may result in greater absorption (Sudakin and Trevathan.130-. Sudakin and Trevathan.100-.S. Human health effects from DEET at low environmental doses or at biomonitored levels from low environmental exposures are unknown.

Urinary levels of DEET were characterized only at the 90th and 95th percentiles of the U.440) < LOD .410-.S.410 (. In this survey period. 2007)..N-Diethyl-meta-toluamide (DEET) Biomonitoring Information Urinary levels of DEET reflect recent exposure.200 (. Urinary N.300 (..190 (<LOD-. 20 Fourth National Report on Human Exposure to Environmental Chemicals .320 (.S.320) < LOD .350) < LOD .230-.330 (.250 (.480 (.690 µg/L were measured in eight park employees who applied 71% DEET once a day (Smallwood et al.250-.280-1.490) < LOD .93) < LOD .140-. Biomonitoring studies on levels of DEET provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of DEET than are found in the general population.190 (. population from the National Health and Nutrition Examination Survey.230-. 2005).150) < LOD .240) < LOD .500) size 1977 2534 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD 90th .130 (<LOD-.280 (.630) < LOD .150-. 1992).290-.N-Diethyl-meta-toluamide (DEET) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.390-. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.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 .500 (.270 (<LOD-. representative subsamples from NHANES 2001-2002. Finding a measurable amount of DEET in urine does not mean that the level of DEET causes an adverse health effect.230) < LOD . the limit of detection was lower than for the NHANES 1999-2000 survey period (CDC.270) < LOD .190 (. DEET was detected in 10% of 60 Latino children in eastern North Carolina farm worker households (Arcury et al. Survey Geometric mean (95% conf.350-.190-.N.370-.550) 688 678 518 699 598 956 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.270-. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD .410 (. Urinary DEET levels as high as 5.640 (.370) < LOD .330 (.270 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.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 .350) < LOD .250) < LOD .240-.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 .

Page BC. and excretion of N. Veltri JC. U. Bell JW. Barr DB. Pesticide urinary metabolite levels of children in eastern North Carolina farmworker households.25:95-100. Selim S.2:341352. 1999-2000: a national reconnaissance. Quandt SA. EPA 738-R98-010. Chemical Summary.S.41(6):831-839. Lowry LK. Fundam Appl Toxicol 1995.N-diethyl-mtoluamide insect repellents reported to the American Association of Poison Control Centers. Environmental Protection Agency (U. 2005 Kolpin DW. Hartnagel RE Jr. Furlong ET. Absorption. Diethyltoluamide (DEET). Atlanta (GA).epa.S. metabolism. Int J Toxicol 2002.N-diethyl-mtoluamide following dermal application to human volunteers. and other organic wastewater contaminants in U.EPA).EPA. Sudakin DL. 1-118. 4/9/09 U.N. Barber LB. Available at URL: http://www.S. Osimitz TG. September 1998.gov/oppsrrd1/REDs/0002red.N-Diethyl-meta-toluamide (DEET) References Arcury TA.S. Tapia J. pp.S.S.N’-diethyl-mtoluamide (m-DET): analysis of an insect repellent in human urine and serum by high-performance liquid chromatography. Zaugg SD. 4/9/09 Fourth National Report on Human Exposure to Environmental Chemicals 21 . Washington (DC): U. DEET: a review and update of safety and risk in the general population.115(8):1254-1260. pdf.36(6):1202-1211. J Toxicol Clin Toxicol 2003. Toxicity and Exposure Assessment in Children’s Health.EPA). et al. 1993-1997. EPA. Gabriel KL.gov/teach/chem_summ/ DEET_summary. Pharmaceuticals. Third National Report on Human Exposure to Environmental Chemicals. Environ Sci Technol 2002. Meyer MT.pdf. U. Smallwood AW. Human exposures to N. Centers for Disease Control and Prevention (CDC). Thurman EM. Available at URL: http://www. Chen H. DeBord KE.epa. Environmental Protection Agency (U. 2005.16(1):10-13.S. N. Reregistration Eligibility Decision (RED): DEET. hormones. Schoenig GP. streams. Environ Health Perspect 2007. Trevathan WR. Grzywacz JG. J Anal Toxicol 1992.

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

Endocrinology 2008. 32 Fourth National Report on Human Exposure to Environmental Chemicals . Barton L. Kim CS. Klinefelter GR.europa.14(2):149-157.. Rubin C. Zacharewski TR. 2007. Watanabe C.. NC. Wong LY. November 26. et al.S. Urinary concentrations of bisphenol A and 4-nonylphenol in a human reference population. Timms BG.137(3):353-362. Urinary bisphenol A and plasma hormone concentrations in male workers exposed to bisphenol A diglycidyl ether and mixed organic solvents. Pharmaceuticals. Cha SW. Arakawa C. bisphenol A glucuronide. Department of Health and Human Services. European Commission.eu/ health/ph_risk/committees/sct/documents/out156_en. 2/4/09 National Toxicology Program’s Report of the Endocrine Disruptors Low-Dose Peer Review (NTP).gov/ntp/htdocs/liason/ LowDosePeerFinalRpt. Myers CB. Exposure to bisphenol A from bis-glycidyl dimethacrylatebased dental sealants. Brine DR. Shin HC. Estimation of intake level of bisphenol A in Japanese pregnant women based on measurement of urinary excretion level of the metabolite. hormones. Reidy JA. Available at URL: http://cerhr.780(2):365-370. NTP-CERHR Panel Report on Reproductive and Developmental Toxicity of Bisphenol A. Doull J. and Hardy MP. Bisphenol A prevents the synaptogenic response to testosterone in the brain of adult male rats. Kuklenyik Z. et al. Howdeshell KL. Joskow R. and Hajszan.S.pdf . Chem Res Toxicol 2001. Three-generation reproductive toxicity study of dietary bisphenol A in CD Sprague-Dawley rats.nih. National Toxicology Program. Szigeti-Buck. Matthews JB. Ye X. Biochem Biophys Res Commun 2003. Exposure of the U. Twomey K.113(4):391-395. population to bisphenol A and 4-tertiary-octylphenol: 2003-2004. Estrogenic chemicals in plastic and oral contraceptives disrupt development of the fetal mouse prostate and urethra. Serizawa S. Caudill SP. Needham LL.pdf. Environ Health Perspect 2005. Needham LL. Kiguchi M. Proc Natl Acad Sci USA 2005. Yang M. Richter CA. Reprod Toxicol 2001. Chung MK. Joint Research Centre Institute of Health and Consumer Protection.36(6):1202-1211. Han SY. Life Sci 2001.116(1):39-44. Research Triangle Park. An evaluation of the possible carcinogenicity of bisphenol A to humans. 4. Endocrinology 2004. niehs. Lynch BS. Cohen JT. Harazono A. Rat two-generation reproductive toxicity study of bisphenol A.pdf. Ecotoxicity and the Environment (CSTEE). Ikka T. DirectorateGeneral Health and Consumer Protection. and other organic wastewater contaminants in U. Fujii S.68(1):121-146. Hum Ecol Risk Assess 2004.Environmental Phenols References Akingbemi BT.gov/chemicals/bisphenol/BPAFinalEPVF112607. Weight of the evidence evaluation of low-dose reproductive and developmental effects of bisphenol A.J. Hughes C. Yoshinaga J. N. Marr MC.gov/chemicals/bisphenol/bisphenol. Kroes R. Needham LL. 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. Tyl RW. Gender differences in the levels of bisphenol A metabolites in urine. Kim YH. Park S. Ekong J. Available at URL: http://cerhr. Brussels.pdf .S.149:988-994.nih. Toxicol Sci 2002. Imai H.4’-Isopropylidenediphenol (Bisphenol-A) Summary Assessment Report. Meyer MT. J Am Dent Assoc 2006. Hanaoka T. Hlywka JJ. streams.312(2):441-448. Evaluation of developmental toxicity in rats exposed to the environmental estrogen bisphenol A during pregnancy. Regul Toxicol Pharmacol 2002. Kawamura N. Calafat AM. McConnell EE.10:875-921. Available at URL: http://ntp. Thomas BF.jrc.69(22):2611-2625. Ispra. 2002. 2/4/09 Ouchi K. Belgium. Bisphenol A. Measurement of bisphenol A in human urine using liquid chromatography with multi-channel coulometric electrochemical detection. Furlong ET. Haighton LA. MacLusky. Nippon Eiseigaku Zasshi 2004. Leranth. 2/4/09 National Toxicology Program Center for the Evaluation of Risks to Human Production (NTP-CERHR). Tsugane S. Han SS. Koulova AI. National Institute of Environmental Health Sciences. 2/4/09 European Commission. Barr JR. Occup Environ Med 2002. C. Thurman EM. Italy. Calafat AM. Reidy JA. Calafat AM. Bradley S. Watanabe S. et al.102(19):7014-7019.145:592-603. 2008. August 2001. Zaugg SD. T. U. 5: 505-523.pdf. vom Saal FS. Munro IC.niehs. Gray GM. Keimowitz AR. with estrogen receptors alpha and beta.Scientific Committee on Toxicity. National Institutes of Health.35(2 Pt 1):238-254. Pyo MY. Available at URL: http://ec. Sottas CM. J Chromatogr B Analyt Technol Biomed Life Sci 2002.nih. Kim JC.. 1999-2000: a national reconnaissance. Furukawa M. Environ Health Perspect 2008. Koh WS.59(9):625-628. Available at URL: http://ecb. Cunha G. National Toxicology Program Center for the Evaluation of Risks to Human Production (NTP-CERHR). Human Health. NTP-CERHR Panel Report on Reproductive and Developmental Toxicity of Bisphenol A. K.59(4):403-408. niehs. Ema M. Rhomberg et al. May 22.it/DOCUMENTS/ Existing-Chemicals/RISK_ASSESSMENT/SUMMARY/ bisphenolasum325. Hara K. Kolpin DW. Barber LB. In vitro and in vivo interactions of bisphenol A and its metabolite. 2/4/09 Fujimaki K. 2003. September. Barr DB. Environ Sci Technol 2002.

Csanady GA. Large effects from small exposures. Kawamoto T. et al. Metabolism and kinetics of bisphenol A in humans at low doses following oral administration. Nagel SC. Yang M. An extensive new literature concerning low-dose effects of bisphenol A shows the need for a new risk assessment. Environ Res 2007.44(4):546-51. Morgan MK. Environ Health Perspect 2005. Sheldon LS. Wilson NK. Colnot T. Chem Res Toxicol 2002. Lee SM. Vom Saal FS. vom Saal FS. Food Chem Toxicol 2002. Endocrine mechanisms mediating effects of bisphenol A at levels of human exposure.40(7):905-12. Chuang JC. Lordo RA. Fourth National Report on Human Exposure to Environmental Chemicals 33 . III. Biological monitoring of bisphenol a in a Korean population. Welshons WV. bisphenol-A. Jang JY. Kim SY. Low-dose in utero effects of xenoestrogens in mice and their relevance to humans: an analytical review of the literature. Witorsch RJ.147(6 Suppl):S56-69. Arch Environ Contam Toxicol 2003. Endocrinology 2006. Dekant W. Chang SS.Environmental Phenols Volkel W. An observational study of the potential exposures of preschool children to pentachlorophenol. Filser JG.15:12811287.103(1):9-20. Hughes C. and nonylphenol at home and daycare.113(8):926-33.

pesticides.507) * < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.30 (.60-3.600-1. Nonylphenol ethoxylates are more commonly used than octylphenol ethoxylates.900 (.60-3.400 (.20 (1.50) 1.50 (1. 2000. 2002). 4-octylphenol monoethoxylate was detected in 43.274-.300 (<LOD-.50) 1. and from contact with some personal care products and detergents.3.10) 1. 2002).60) 1. is used to manufacture alkylphenol ethoxylates.30) 90th 1. streams in 30 states (Kolpin et al. and to alkylphenoxycarboxylates. They are biodegraded to the corresponding alkylphenol (octylphenol or nonylphenol).3-Tetramethylbutyl] phenol) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.00) 1229 1288 03-04 03-04 03-04 * .500) .80) 2.g.5% of 139 U. 2004).500-1.477) . 2000. Several alkylphenols.1.. 1996). to shorter chain alkylphenol ethoxylates. over 500.50) .600) 1.389 (. 1995.20) 314 715 1488 03-04 03-04 * * . population from the National Health and Nutrition Examination Survey. Human exposure to alkylphenols and alkylphenol ethoxylates may occur through ingestion of contaminated foods (e.30 (1.500-1. The alkylphenols can bioaccumulate in some fish.700-1. which may vary for some chemicals by year and by individual sample.80 (1.70 (1.600-1.60-3.20-2. fish) and drinking water. and some of their degradation products are toxic to aquatic life.80 (1.30 (1.20-2.70 (1. Laws et al.. industrial cleaners. 140-66-9 General Information 4-tert-Octyphenol. the various alkylphenols have also been used as emulsifiers and modifiers in paints. Commercial formulations of alkylphenol ethoxylates usually contain a mixture of oligomers and isomers.30) 2.60) 613 652 1092 Limit of detection (LOD.60-3. Octylphenols and nonylphenols can also enter the environment directly from manufacturing waste streams. The alkylphenol ethoxylates enter the environment through human use of products containing them.200-. Indoor and to a lesser extent.497) * .500) 75th .20-2.30) 1. impaired steroidogenesis. Saito et al. Ying et al.90) 2.10 (. textiles.400) 1.357 (.400 (..00 (.60) .30-2.900 (.900 (. In 1999-2000.40) 2. Alkylphenols also have been used as plasticizers and antioxidants in plastics and resins.50) .50) 1. In rats.70 (1.30 (1..10 (. and was quickly eliminated from the blood (Certa et al..2.. orally administered 4-tert-octylphenol was well absorbed.40) 2. altered estrus cycles and reproductive outcomes. and the polyethoxy chain may consist of up to 50 ethoxy units. through sewage.500) .40) 1. have demonstrated estrogenic effects particularly when injected at high doses in animals.600-1.00 (1.50-2.600) .40) * 03-04 03-04 03-04 .268-.10) 2.600-1. and some personal care products. Katsuda et al. and impaired spermatogenesis (e.369 (.600-1. leading to inhalation as another potential exposure route (Rudel et al.900 (. and emulsifiers.50-3. Disposition in humans has not been studied sufficiently.g.600) .300-.600-1. testicular atrophy.299-. including 4-tert-octylphenol.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 .30 (1. an alkylphenol.60-3. 2003. < LOD means less than the limit of detection.300 (<LOD-.20) 2. 2006. 34 Fourth National Report on Human Exposure to Environmental Chemicals . During the 1980s and 1990s..00 (. Human health effects from 4-tert-octylphenol or the corresponding octylphenol ethoxylates at low environmental doses or at biomonitored levels from low environmental exposures are unknown.400 (.600) .40 (1.20-2. Survey Geometric mean (95% conf.. see Data Analysis section) for Survey year 03-04 is 0. Less frequently.500) .900 (. Bian et al.300 (<LOD-.60-3. 1997. and through manufacturing waste streams (Warhurst.Environmental Phenols 4-tert-Octylphenol CAS No.300-.40) 1.500 (.20-2.S.90) 2..70 (1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.10-2.300 (<LOD-.20-2. altered neonatal sexual development.. which are anionic surfactants used in detergents. Blake and Boockfor.80 (1.200-.300 (<LOD-.S. did not bioaccumulate.000 tons of alkylphenol ethoxylates were produced annually worldwide. These high dose parenteral effects of 4-tert-octylphenol have included altered sex hormone levels and hypothalamicpituitary suppression.800-1.20) 1. outdoor air may have detectable levels of 4-tert-octylphenol and 4-tert-octylphenol monoethoxylates. several European nations banned the use of alkylphenol ethoxylates in domestic detergents and other uses. Urinary 4-tert-Octylphenol (4-[1. In the 1990s.10 (1.

450) . Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.1.40 (1.59 (1.435 (. IARC and NTP have not rated octylphenol.740 (.337-.65-3.276 (. 2004).76 (2. 1999). population from the National Health and Nutrition Examination Survey.17 (.270 (.470-1..71) 2.560) . Kawaguchi et al.11) 1.53-3.860 (. 2003.00) size 2514 Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th .450) 1.11) 2.10-2.610) .43) 1.270-.400) .500-1.14) 314 713 1487 03-04 03-04 * * .62) .160-.64 (.03-6. Urinary 4-tert-Octylphenol (4-[1.550-1.280-. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.62 (1. 2000.270 (. 2004.Environmental Phenols Myllymaki et al. nonylphenol.640-1. It is unclear if estrogenic or other effects occur in animals through oral dosing. (2008) showed that urinary levels of 4-tertoctyphenol were detectable in slightly greater than half of the participants of the U.22) .00 (.S..18-4. 4-tert-Octylphenol is not considered directly genotoxic.730-1.349) * < LOD .530) .320 (<LOD-. 2001).02-4.3.00) 2.33) 3.68) 2.00) 2.15) 1.770 (. Biomonitoring Information Urinary levels of 4-tert-octyphenol reflect recent exposure.40-4. Calafat et al.29) 2.25-2.25) 2.3-Tetramethylbutyl] phenol) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.00) 1.11-2. Nagao et al.81 (1.68-2.470-1.20 (1.. * Not calculated: proportion of results below limit of detection was too high to provide a valid result..03 (1. In a small number of adult Japanese volunteers.33 (2.850 (.96-4.170-. 2005.470) 75th .31 (1. Sweeney et al.31-2. Survey Geometric mean (95% conf.03 (1. 2001..890-2.269 (.36-3. 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.54) * 03-04 03-04 03-04 .06 (2.85 (1.25) 90th 1. representative subsample of NHANES 2003-2004.41) .370 (<LOD-.60 (1.78) 1228 1286 03-04 03-04 03-04 * .630-1..740 (.620) .73) 2. the urinary concentrations of 4-tert-octyphenol were near or below the detection limit (Inoue et al.43) 1.420) .460 (.570) .78) 3.380 (<LOD-. Yoshida et al.300 (<LOD-.207-.62 (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.43-3.78 (1. or their corresponding ethoxylates with respect to human carcinogenicity.540-1.260 (<LOD-.05-2.24) 612 651 1091 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.620-1.199-.910 (. at lower or environmentally relevant doses (Blake et al.67-2. Fourth National Report on Human Exposure to Environmental Chemicals 35 .08) 1.410 (. Tyl et al.59) 1.00 (.50 (2.384) * .S.

Cooper RL. Wong LY. Brooks AN. Zaugg SD. Thurman EM. Brody JG. Toxicol Appl Pharmacol 2005.141(7):2667-2673. Two-generation reproduction study with para-tert-octylphenol in rats. Taya K. Indoor Air 2004. Watanabe G.799(1):119-125.foe. Karjalainen M. Song L.pdf. Boockfor FR. Pharmaceuticals. Katsuda S.Environmental Phenols References Bian Q. Chronic administration of the environmental pollutant 4-tert-octylphenol to adult male rats interferes with the secretion of luteinizing hormone. Regul Toxicol Pharmacol 1999. Paranko J. Katsuda S. testis size. Environ Sci Technol 2003. Haavisto TE. Onuki A.14(5):325-332.44(8):1355-1361. Yoshimura S. and testosterone. Saito Y. polybrominated diphenyl ethers. McCoy GL. nonylphenol. Maekawa A. Seto H. Fedtke N. et al. Toxicokinetics of p-tert-octylphenol in male Wistar rats. Reproductive effects in male and female rats from neonatal exposure to p-octylphenol.54(1):154-167. Ye X.co. Measurement of 4-nonylphenol and 4-tert-octylphenol in human urine by column-switching liquid chromatography-mass spectrometry. Meyer MT. pesticides. Effects of 4-tert-octylphenol given in drinking water for 4 months on the male reproductive system of Fischer 344 rats. Food Chem Toxicol 2006. Korn LR. Ono H. Nair-Menon JU. Muller AM. Ferrell JM. Inoue K. Toxicol Sci 2000. 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. Indoor air pollution by alkylphenols in Tokyo. Spengler JD. Williams B. An environmental assessment of alkylphenol ethoxylates and alkylphenols. 1999-2000: a national reconnaissance. Roche JF. Nicol L. 2/4/09 Ying GG. Brine DR. 36 Fourth National Report on Human Exposure to Environmental Chemicals . Endocrinology 2000. Camann DE. and other endocrine-disrupting compounds in indoor air and dust. Makino T. Chen J. Kolpin DW.28(3):215-226. Laws SC. et al. Kawaguchi M. Environ Sci Technol 2002.15(6):683-692.116(1):39-44. Biol Reprod 1997.57(2):255-266. Calafat AM. streams. and other organic wastewater contaminants in U. Izumi S. Toppari J. Okada F. et al. 2003. Sweeney T. Tyl RW. Kookana R. Toxicol Appl Pharmacol 2000. Boockfor FR. Horie M. Blake CA.165(3):217-226. prolactin.18(1):43-51. 1995.folliclestimulating hormone. bisphenol A and methoxychlor in rats. Effects of neonatal exposure to a high-dose p-tertoctylphenol on the male reproductive tract in rats. Yoshida M. Barber LB.S. Saito I. Yoshimura Y. Bodman GJ. Environ Health Perspect 2008. Sakui N. J Chromatogr B Analyt Technol Biomed Life Sci 2004. Carey SA. Anal Chim Acta 486:41-50.37(20):4543-53. and sertoli cell number.71(1-2):112-122. Exposure of the U. Certa H. Fail PA. Yoshida M. et al. Phthalates. Takai N. hormones. Inoue K. The toxic effects of 4-tert-octylphenol on the reproductive system of male rats. Wiegand HJ. Reprod Toxicol 2001. Infantile 4-tert-octylphenol exposure transiently inhibits rat ovarian steroidogenesis and steroidogenic acute regulatory protein (StAR) expression. Furlong ET. Rudel RA. Seely JC. Wang X. Warhurst AM. Environmental fate of alkylphenols and alkylphenol ethoxylates--a review. Environ Int 2002.121(1):21-33. Ito R. Myllymaki SA. Toxicol Lett 2001. Reidy JA. Kawaguchi M. Maternal exposure to octylphenol suppresses ovine fetal follicle-stimulating hormone secretion.30(2 Pt 1):81-95. Taya K. Qian J. Myers CB.207(1):59-68. Millette CF. population to bisphenol A and 4-tertiary-octylphenol: 2003-2004. Marr MC. Bolt HM.36(6):1202-1211. Watanabe G. Nakagomi M. Blake CA. Estrogenic activity of octylphenol. alkylphenols. Raychoudhury SS. Reprod Toxicol 2004. Takenaka A. Maekawa A. Xu L.uk/resource/reports/ethoxylates_alkylphenols. Needham LL.S. Arch Toxicol 1996. Available at URL: http:// www. Usumi K. Nagao T. Irreversible effects of neonatal exposure to p-tert-octylphenol on the reproductive tract in female rats.

Triclosan has a low bioaccumulation potential in fish. 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. There is some concern that widespread use of triclosan and other biocides can alter antibiotic resistance in bacteria (Aiello et al. Matsumura et al. toys. 2007). and wound disinfection solutions.... 3380-34-5 General Information Triclosan is a phenolic diphenyl ether used for over 30 years as a preservative and antiseptic agent.. 2006). Calafat et al. 2008). Triclosan can remain present in the oral saliva for several hours after the use of toothpaste containing triclosan (Gilbert et al. General population exposure results from dermal and oral use of products containing triclosan.. triclosan was found in 57. 1969). Triclosan has been added to soaps.S.. but not by race/ethnicity and sex. streams sampled in 30 states (Kolpin et al.2 µg/L) of children 6-11 years of age who participated in NHANES 2003-2004 (Wolff et al. young girls. 2002). Human health effects from triclosan at low environmental doses or at biomonitored levels from low environmental exposures are unknown. In the body it is conjugated to glucuronides and sulfates (Bodey et al. Triclosan formulations may rarely cause skin irritation..Environmental Phenols Triclosan CAS No. IARC and NTP do not have ratings with respect to human carcinogenicity. 2007.2 µg/L was comparable to the median level (8. 2008 has shown higher levels during the third decade of life and among people with the highest household income. Calafat et al. Veldhoen et al. toothpastes. In a U. Some reports show endocrine effects are observed in amphibians and fish (Foran et al.. 1976.. Mezcua et al. mouthwashes.6% of 139 U. Biomonitoring Information Urinary triclosan levels reflect recent exposure. 2007).S. 2005. 2004). representative subsample of NHANES 2003-2004. Triclosan is not considered teratogenic at maternally toxic doses. In animal and human studies. In a study of 90 U. a process that can result in the formation of small amounts of 2. and has not been considered mutagenic or carcinogenic (Bhargava and Leonard. and medical devices. In 1999-2000. It can be photochemically and biologically degraded. and has also been impregnated into some kitchen utensils. 2007. Lyman and Furia.S. acne medications. (Sandborgh-Englund et al. Triclosan can be absorbed across skin into the blood stream. It acts by inhibiting bacterial fatty acid synthesis. 1996.. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 2000.8-dichlorodibenzo-p-dioxin (Aranami et al. it has low acute toxicity.... 1987). it is excreted over several days in the feces and urine as primarily as unchanged triclosan (Kanetoshi et al. Fourth National Report on Human Exposure to Environmental Chemicals 37 . Finding measurable amounts of triclosan in the urine does not mean that the levels of triclosan cause an adverse health effect. Triclosan enters the aquatic environment mainly through residential wastewaters. In animal studies.. Moss et al. deodorants. 1988. the median urinary triclosan level of 7. 2000)..

Urinary Triclosan (2.S.11-11.7-318) 224 (186-272) 236 (115-336) 356 (169-580) 385 (308-506) 314 713 1487 03-04 03-04 13. population from the National Health and Nutrition Examination Survey.2-14.22-10.5-341) 245 (163-334) 597 (372-992) 450 (254-750) 461 (383-527) 613 652 1092 Limit of detection (LOD.21 (6.8) 7.6-111) 33.8-63.10-9.6-14.45 (5.70-16.30-14.6 (30.4) 7.2) 9.6-14.29-12.8-60.9 (33.92-12. Survey Geometric mean (95% conf.50) 10.45-10.0) 9.00-8.5) 20.8 (21.18 (5.0-213) 213 (160-272) 453 (263-1150) 260 (127-513) 358 (276-480) 612 651 1091 38 Fourth National Report on Human Exposure to Environmental Chemicals .6) 31.5 (11. interval) 12.4) 25.55 (4.8) 116 (39.6) 237 (175-294) 182 (138-217) 384 (294-506) 336 (225-480) 1228 1286 03-04 03-04 03-04 13.1) 9.80 (5.38-18.5) 66.9) 75th 47.43-13.20 (7.16 (6.40-17.48-10.1) 13.1-39.5-14.7) 292 (151-432) 132 (78.72-13.0) 65.1) 9.4-18.9-61.50-10.3 (9.4) 317 (231-433) 144 (96.1) 9.20-10.Environmental Phenols Urinary Triclosan (2.2 (27.00 (4.4 (32.0 (36. interval) 13.2 (11. Survey Geometric mean (95% conf.6) 90th 212 (172-241) 03-04 03-04 03-04 9.4) 75th 43.7 (11.1 (45.82 (8.3) 10.7 (9.8-112) 30.2-46.9 (8.5-86.3-31.40-11.10) 84.7) 10.4) 357 (225-456) 203 (87.6) 39.1 (15.1) 50.4.60 (6.3.2) 12.2 (13.6-65.7) 123 (36.60 (8.9) 8.3 (26.4) 90th 249 (188-304) 03-04 03-04 03-04 8.0 (8. population from the National Health and Nutrition Examination Survey.4’-Trichloro-2’-hydroxyphenyl ether) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.32-14.0 (26.6 (9.3-15.9 (50.9-236) 193 (90.7 (39.20-11.0 (34.0-73.4 (12.20-13.0-15.5-250) 574 (461-716) 380 (258-430) 1229 1288 03-04 03-04 03-04 14.54 (8.3 (8.3) 47.6-15.3) 6.93 (7.2-58.1) 9.4 (38.2 (10.20 (7.7 (28.1) 11.86-12.3 (11.2 (25.45-13.1) 14.8-85.1 (8.4-163) 304 (134-566) 261 (198-317) 157 (113-380) 655 (310-890) 472 (406-522) 314 715 1488 03-04 03-04 16.9) 32.6 (10.4) 51.0-15.5) 13.1) Selected percentiles ( 95% confidence interval) Sample 95th 368 (294-463) size 2514 Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 9.7 (14.9 (11.90-10.2) 13.6-20.8) 9.4’-Trichloro-2’-hydroxyphenyl ether) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.74 (5.4 (11.6) 10.6 (12.5) 11.3-35.4-19.89-11.8) 14.0-19.1) 7.9) 7.8-127) 37.2 (37.48 (8.4.0 (11.3-67.0) 49.6) Selected percentiles ( 95% confidence interval) Sample 95th 461 (383-522) size 2517 Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 9.6-37. see Data Analysis section) for Survey year 03-04 is 2.94 (7.6) 12.4) 73.2-58.S.

Wolff MS. Pilot study of urinary biomarkers of phytoestrogens. The oral retention and antiplaque efficacy of triclosan in human volunteers. Hirano M. population: 2003-2004. Odham G. Hong HC. Chemosphere 2007. Pinney SM. Developmental evaluation of a potential non-steroidal estrogen: triclosan.524:241-247. Calafat AM.36(6):1202-1211. Barber LB. and phenols in girls.66:1052-1056. Benson WH.4..7/2. et al.23(5):579-583.116(3):303-307. Ferrer I. 4. Mezcua M. hormones. Howes D. Aguera A. Anal Chim Acta 1004.115:116-121.8-dibenzodichloro-pdioxin as a photodegradation product of triclosan in water and wastewater samples. Veldhoen N. Pharmacokinetics of triclosan following oral ingestion in humans.83(1):84. Thurman EM. Matsumura N. Foran CM. Toxicology of 2. Hernando MD. Percutaneous penetration and dermal metabolism of triclosan (2. Katsura E. J Toxicol Environ Health A 2006. Biol Pharm Bull 2005. phthalates. Adolfsson-Erici M. Photolytic degradation of triclosan in freshwater and seawater. Bennett ER. Kaneshima H.S.24(3):209-218. Am J Infect Control 1996. Environ Sci Technol 2002.69(20):1861-1873. Skirrow RC. Moss T. et al. Ogawa H. Mar Environ Res 2000. J Invest Dermatol 1976. and other organic wastewater contaminants in U. Shiratsuchi H. Triclosan: applications and safety. Wigmore H. et al. Aquat Toxicol 2006.80(3):217-227. Urinary concentrations of triclosan in the U. Sandborgh-Englund G. Meyer MT. The bactericidal agent triclosan modulates thyroid hormone-associated gene expression and disrupts postembryonic anuran development. Effects of nonylphenol and triclosan on production of plasma vitellogenin and testosterone in male South African clawed frogs (Xenopus laevis). Disposition and excretion of Irgasan DP300 and its chlorinated derivatives in mice.17(5):637-644. Levy SB. Kanetoshi A.38(4):361370.45 Suppl 2:S137-S147. Britton JA. Food Chem Toxicol 2000. Ekstrand J. Readman JW. Erratum in: Aquat Toxicol 2007. Zaugg SD. streams. Environ Health Perspect 2007. Teitelbaum SL.38(2):64-71. Williams FM. Furlong ET. et al. Watanabe N. Ebersole R. 1999-2000: a national reconnaissance. Furia T. Consumer antibacterial soaps: effective or just risky? Clin Infect Dis 2007.S. Aranami K.67(4):532-537.28(9):1748-1751. Gunderson MP. Kolpin DW. Windham G. Lyman FL. Br J Clin Pharmacol 1987. Chelimo C. Arch Environ Contam Toxicol 1988.Environmental Phenols References Aiello AE. Wong LY. Gomez MJ. Evidence of 2. Fernandez-Alba AR. Randomized trial of a hexachlorophene preparation and P-300 bacteriostatic soaps. Leonard PA. Fourth National Report on Human Exposure to Environmental Chemicals 39 . Environ Health Perspect 2008. Bodey GP.4’-trichloro-2’hydroxydiphenyl ether). Williams PE. Nagao Y. 4’-trichloro-2’-hydroxydiphenyl ether. Bhargava HN. Gilbert RJ. Ye X. Larson EL. Pharmaceuticals.50(1-5):153-156. Ishibashi H. Needham LL. IMS Ind Med Surg 1969. Osachoff H. Okui T. Reidy JA. Clapson DJ.

75) 2.50) 1.350 (.990-2. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.70) 2.37) .S. 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.510-3.42) 696 680 521 696 603 951 Limit of detection (LOD.01 (<LOD-1.350-.350) < LOD .350-.350-.91 (1.94 (1.350 (.350-2. After a single dose.58-2.350) .350-2.42) 973 1190 1021 1338 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .98 (1.350) < LOD .350-.350) < LOD .10 (<LOD-1.630 (. algaecide and insecticide.960) 1.62 (.33-2.90) 1.350) 90th . PCP is eliminated over a few days (Braun et al.660 (.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. and possibly of lindane (IPCS.10 (1.350-.350-.83 (2.350 (.30 (.350 (. PCP is absorbed rapidly and well by all exposure routes.10) 1.350) < LOD .350 (.350) < LOD .980 (.350-.53) 482 577 681 826 831 1125 99-00 01-02 99-00 01-02 * * * * .350 (.30) 1.350 (.Fungicides Pentachlorophenol inhale it or absorb it through exposed skin.350-..350) < LOD .770 (.350) < LOD . plants.18 (<LOD-1.30 (.350) < LOD .S. and metabolic acidosis were observed in CAS No.g. Human health effects from PCP at low environmental doses or at biomonitored levels from low environmental exposures are unknown.00) 2.350 (.64) 1. high dose exposure to PCP can induce a hypermetabolic state and excessive heat production as a result of uncoupling mitochondrial oxidative phosphorylation.480-2. PCP also may be eliminated in urine as a metabolite of hexachlorobenzene.08-3. mollusicide.350-. and it is used primarily as a preservative for wood to be used outdoors (e.70) .33) .350) < LOD < LOD 75th . bactericide.30 (1. which may vary for some chemicals by year and by individual sample.350 (.10) 1. 1997). herbicide.00 (.350-1.350-. air.350) < LOD .94 (1. PCP cannot be used on wood in residential or agricultural buildings.350 (.5. and dermal contact with PCP-treated products. with repeated or chronic exposure.350-.680-1. hypertension. PCP is degraded by sunlight and metabolized rapidly by microorganisms.76) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .350 (.350) < LOD .890-1.350 (.51) 1.350-. 40 Fourth National Report on Human Exposure to Environmental Chemicals . Survey Geometric mean (95% conf. Kohli et al.350 (.40 (. In the environment.30) 1. Effects including hyperthermia.390 (.350) < LOD . Since 1984. 1979).350-1. utility poles and fence posts).350) < LOD . so it is relatively non-persistent.390 (.350 (.90) 2.00) 1.53) 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 .90 (1. Human exposure to PCP has become less common.590-1.47-3.54-2..350-.58-2.350-.09) . 2002.850-2.350) < LOD . 1986).04) 1. Acute.350-2.350-.500-2.350-2.350 (.350-.00) 1.67) 1..350 (.350 (.48-2.65 (.350 (. PCP is distributed to most tissues and is not extensively metabolized.350-.60) 1. are eliminated in the urine.990 (<LOD-2.350 (. The parent compound and conjugates.350-.860-2. 1976.78) 1.350-2.650) 1..48 (..76) 1.350-.350) < LOD .76) .10 (.350) < LOD . General population exposure to PCP may occur by inhalation of contaminated air.350) < LOD . and animals.350-.650 (. After absorption.60) 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. PCP use in the U. the elimination half-life may be a week or more (Uhl et al.530) 1.350-.350-1. ingestion of contaminated food or water.510-5. along with small amounts of tetrachlorohydroquinone and conjugates.350-.73 (1.25 and 0. population from the National Health and Nutrition Examination Survey.350 (.65 (. To-Figueras et al.80) .45-2. has been restricted.47-5. PCP has been detected in soils.32 (. < LOD means less than the limit of detection.30) .350-1.23 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1. water and sediments because of the large amounts that were produced and used historically.37 (. other polychlorinated benzenes.890 (.

.830) < LOD .S.35-2.52 (<LOD-1.40) 1..800) < LOD 1.40) 1.06 (.40) 1.220-.94 (1.30) 1.510-.99) 482 577 681 825 831 1125 99-00 01-02 99-00 01-02 * * * * .760 (.580-.08) 696 680 521 695 603 951 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.270-. Pentachlorophenol is not mutagenic or teratogenic.320) < LOD . 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 (4.730) < LOD .220-.700-2.650) 90th 1.52 (<LOD-1. inhalation.epa.S.6 and 14.370 (.25-1.30-2.290) < LOD .EPA.40) 1. 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.09-1.90) 1.00-1. and the FDA has established a standard for bottled water.19) 2.26 (1.92) 1.250 (.25) 1.260 (.19) 2.270-. In a small sample of U.300 (.560) < LOD . population from the National Health and Nutrition Examination Survey.420) < LOD .340-.84-4.310-.67 (1.82 (1..0 mg/L. More information about external exposure (i.240-. Fourth National Report on Human Exposure to Environmental Chemicals 41 .500-1. IARC has determined that pentachlorophenol is possibly carcinogenic to humans. 1995).400 (.69 (1.atsdr.590-1.500 (.S. 2003).55) 1.57 (.73 (1.00) 1.290-.30 (.36) . 2003).. 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.560) < LOD . Urinary levels of pentachlorophenol in the general population are far below (hundreds of times lower than) urine levels reported for workplace exposure to PCP or among people living in PCP-treated log homes (Cline et al.910-1.75) 1.380-. Among adults in the NHANES 1999-2000 subsample.21-2.34 (.78) 1.710-1. chronically administered high doses of PCP were hepatotoxic. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1. In NHANES 2001-2002 subsamples.25 (1.56) 1.. the median and 95th percentile urinary PCP levels were approximately three times lower than comparable values in German adults (2.300 (.55) 973 1190 1021 1337 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * ..360 (.35-2.780-1.57 (1.06-3.780) < LOD .html.30) 1.330-. Death can result from seizures and cardiovascular collapse.630 (.25-2.11) 2.94 (1.08 and 5.800-1.00-1.950-1.440 (. In animals. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.360-.79) 1.500-.52 (1.40) 1.40-2.570 (.950-1. children in the 1980’s.83 (1.35) 1.82) 1.320 (. respectively) (Seifert et al.48-2.430) < LOD . 2004.35) 1.e.67 (1.320) < LOD . EPA at: http://www. 1989).650 (. 1989).19 (1. The U.490) < LOD .280) < LOD . van Raaij et al. Survey Geometric mean (95% conf.13 (.S.18) .610 (.67 (1.350) < LOD .250 (.29-3.300 (.560-.cdc.18 (1.510-..52) 1.920 (.gov/ toxpro2..650 (.9 mg/L. respectively) (Becker et al.94-3.67-3.16 (. 1991).67-2.67 (1.75 (<LOD-2. EPA has developed standards for PCP in drinking water and the environment.950-1. the 95th percentile of urinary PCP levels was about fiftyfold higher than that for 6-11 year olds in NHANES 2001-2002 (Hill et al.09 (<LOD-2.290-.25 (1. 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.10 (1.84 (1.470 (. OSHA has established an occupational standard.67 (1.320) < LOD < LOD 75th .850 (.S.310) < LOD .430-.51) 1.Fungicides adults and children severely exposed to PCP through ingestion.67-3.19) 2. or skin absorption.590) < LOD .900-1.06) 1.75) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * . and adversely affected thyroid function (U.gov/ pesticides/ and from ATSDR at: http://www. carcinogenic.21 (.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 .10-2.16-1. 2000).26 (1.25-2.990 (. environmental levels) and health effects is available from the U.84) 1.78) 1.95) 3.

Seifert B. PCP: Human Risk Characterization [online]. Blau GE. Bragt PC. Barrot C. Becker K. htm. 206:15-24. Gregg M. Notten WR. 4/21/09 van Raaij JA.4:289296. Kaus S. van den Berg KJ. et al. Engel R. The German Environmental Survey 1990/1992 (GerES II): reference concentrations of selected environmental pollutants in blood. r e g u l a t i o n s . Fast DM. et al. Lindane. Dev Toxicol Environ Sci 1979. The metabolism/ pharmacokinetics of pentachlorophenol in man and a comparison with the rat and monkey. Effects of hexachlorobenzene and its metabolites pentachlorophenol and tetrachlorohydroquinone on serum thyroid hormone levels in rats. Schulz C. Hill RH Jr. Uhl S. Helm D. Pentachlorophenol measurements in body fluids of people in log homes and workplaces. Int J Hyg Environ Health 2003.105(1):78-83. Environ Res 1995. Schlatter C. Pesticide residues in food-2002-Joint FAO/WHO meeting on pesticide residues. Smith SJ. Arch Toxicol 1986. house dust. Environmental Protection Agency (U. Jones D. Pharmacokinetics of pentachlorophenol in man. Schmid P.58:182-186. Available at URL: h t t p : / / w w w. Chenoweth MB. International Programme on Chemical Safety (IPCS).Fungicides Finding a measurable amount of PCP in urine does not mean that the level of PCP causes an adverse health effect.10:552-65. Arch Environ Contam Toxicol 1989.54(3):203-208. Rodamilans M.org/documents/jmpr/jmpmono/2002pr08. References Becker K. Krause C. Baker S. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children. drinking water and indoor air. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. 2002. Metabolism of hexachlorobenzene in humans: association between serum levels and urinary metabolites in a highly exposed population. Hill RH. Phillips DL. The metabolism of higher chlorinated benzene isomers. Bailey SL. 42 Fourth National Report on Human Exposure to Environmental Chemicals .S. Schulz C.S. To-Figueras J. 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. Toxicology 1991: 67(1):107-16. U. 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. Safe A. J Expo Anal Environ Epidemiol 2000. EPA). Seiwert M. Cline RE. Seifert B. Needham LL.inchem. 4/21/09 Kohli J. Sala M. Arch Environ Contam Toxicol 1989. Biomonitoring data can also help scientists plan and conduct research about PCP exposure and health effects. Shealy DB. Environ Health Perspect 1997. urine. Otero R. Seiwert M. To T. Santiago-Silva M. Can J Biochem 1976. Holler JS.18:475-481.71:99108. hair. Braun WH. 11/30/2004. Pesticide residues in urine of adults living in the United States: reference range concentrations.18(4):469-474. et al. Needham LL. Hill RH Jr. Head SL. available at URL: http://www.

S.30) < LOD 1.09) 2.17 (.930 (.34) 1.3.10 (1.. 1989).860) * 99-00 01-02 99-00 01-02 99-00 01-02 .690-1.20) < LOD 2. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. interval) .33 (. fungicides.3 and 0.90) 2.610-1.. and as a wood preservative.50 (1. Estimated human intakes have been below recommended intake limits (U.800-3.30) 1.590-2. < LOD means less than the limit of detection.450 (<LOD-. SOPP is applied topically to the crop and then rinsed off.760-2.S. OPP is considered to be moderately toxic after acute oral doses in animal studies.364-. Most agricultural food applications have been revoked.19 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 90-43-7 General Information Ortho-phenylphenol (OPP.880-2.466 (. Cnubben et al.770 (.410-. Human health effects from OPP at low environmental doses or at biomonitored levels from low environmental exposures are unknown.00) .88) 1.840-1.490 (<LOD-.497 (.Fungicides ortho-Phenylphenol CAS No.386-.50-3.509 (.950) < LOD .570 (.40 (.00) .23) 480 577 681 827 830 1125 99-00 01-02 99-00 01-02 .630) < LOD .820 (.600-1.790) 2. or 2-phenylphenol) and its water-soluble salt.742) * .670) 2. leaving the chemical residue OPP.645) * . 2006). 1998).402-.EPA.780) < LOD .60 (1.50) < LOD . Available evidence suggests that OPP does not accumulate in the body.550-1.20 (1.560-8. Fourth National Report on Human Exposure to Environmental Chemicals 43 .30) < LOD .600-1.03) 1.638) * .500-2.00 (1.14 (<LOD-3. on ornamental plants and turfs. 2006).696) * .540-2.890) 1. inhalational.90 (1.50 (1.00 (1.90) 1.76) 1.00) < LOD .10) .490 (<LOD-.10) 2.498 (. Survey Geometric mean (95% conf. OPP was detected in 40 of 60 different canned beers at concentrations in the low parts per billion (Coelhan et al. it was used in home sanitizers for surfaces. General population exposure can occur via dermal. however.433-.28 (.610 (.490 (<LOD-.570-.10-1. which may vary for some chemicals by year and by individual sample.07 (. 2006).770 (. 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. in paints.389-.80 (2.50) .750-2.570-1.20 (.370-.496 (.22) 2.10-2.20) 2.10) .80) 1.349-.490 (<LOD-.61) 2. small amounts of OPP have been measured in human adipose tissue (Onstot and Stanley.552 (.508 (.600-1. sodium ortho-phenylphenate (SOPP).890 (.450 (<LOD-.28-3.40-7.EPA.850 (.624) * .710) 3.470 (<LOD-. OPP is still used as a disinfectant fungicide for industrial applications. or oral routes from residential use and by ingesting treated food or food that was in contact with treated surfaces or equipment.830 (.690) < LOD .567 (. and sanitizers.20) < LOD 1.30-7. and it has limited water solubility.90) .20 (1.85) size 1991 2529 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th .493 (.480-1.23) 695 680 520 695 603 953 Limit of detection (LOD. Workers who manufacture.85) 2. whereas SOPP is not volatile and is more water soluble.570 (.60-2.00 (1.02) 1.91) 973 1190 1018 1339 99-00 01-02 99-00 01-02 99-00 01-02 .740 (.00 (1.600) < LOD 75th .890 (.50) 1.90 (1.50 (1.22 (.60 (1.30 (1. In the past.S.860 (.60 (1.370-. such as fruits and vegetables.. but OPP and SOPP are still used on pears and citrus (U.370-.10 (1.600) < LOD 1.570-2.40-5.10) .636) * .00-2.40-5. OPP is volatile. Timchalk et al.92 (.520 (.50) < LOD .S. or apply these chemicals may be more highly exposed than the general population.20-3.632) Selected percentiles ( 95% confidence interval) Sample 95th 2. 2002.600) < LOD . Both have been used in agriculture to control fungal and bacterial growth on stored crops. OPP is efficiently absorbed from the gastrointestinal tract and through the skin.80-3.640) < LOD . are antimicrobial agents used as bacteriostats.621) * .20-2.90) .710-2.389-. EPA.60-3.30-2. population from the National Health and Nutrition Examination Survey.350-1. Both chemicals degrade within hours to weeks in the environment (U. and it is eliminated rapidly from the body as OPP glucuronide and sulfate conjugates (Bartels et al.450 (<LOD-.490 (<LOD-.10) 1.50) < LOD .600) < LOD .27 (.80) 1.10) 1.970 (. 1998. formulate.50-4. 2006).836) * .30) < LOD 90th 1.420 (<LOD-.40-2.580-1.390-.50-2.

270-. U.. by possible genotoxic mechanisms (Hagiwara et al.26) 1.46) < LOD 1. 1998.84 (1.656) * .28 (2..17 (. 1984.32) 3.343 (.93) .11-1.09-6.620-1. 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.860 (.08-1. 2005.791) * .EPA 2006).61 (2.29) 1.510 (<LOD-.S.20) < LOD 3.329-.09 (1.550 (.59) ..88-4.27) < LOD . Nakagawa et al.44 (1.382 (.21-2.810-1.74 (1.570) < LOD 1.558) Selected percentiles ( 95% confidence interval) Sample 95th 2.560-2.91) 695 680 520 694 603 953 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.17) * 99-00 01-02 99-00 01-02 99-00 01-02 . or developmental toxicity was observed (Bomhard et al. or.550-.496 (.670 (.21) 1.38) 973 1190 1018 1338 99-00 01-02 99-00 01-02 99-00 01-02 .33-2.385 (.420 (<LOD-.980 (.06 (1.311-.640-1.950) < LOD .4) 3. Volunteers exposed to 0.43-2.500) < LOD ..410 (<LOD-. and it has classified OPP as not classifiable with respect to human carcinogenicity.28 (<LOD-4.33) . Brusick. interval) .455-.353-. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.06-4.96) 1.epa.17) 2.810) < LOD . ortho-phenylhydroquinone and ortho-phenylbenzoquinone.08-2. OPP was not found to be mutagenic. Pathak and Roy. 2005).06-5.508) * .01) 1.S. population from the National Health and Nutrition Examination Survey. Dermally applied OPP was not carcinogenic in a 2-year experimental study in animals (NTP.43 (1.38) 1. leading to production of two metabolites.510-.18) 2.11) < LOD 90th 1.17 (.880-1.gov/pesticides/.58) 2.Fungicides anemia.29) 1.75 (1. Smith et al. Finding a measurable amount of OPP in urine does not mean that the level of OPP causes an adverse health effect.11 (.38) 2.291-.11 (.EPA 2006).05-2..750-2.52 (.30) 480 577 681 826 830 1125 99-00 01-02 99-00 01-02 .666) * ..320 (<LOD-. U.670) < LOD .453 (.470 (<LOD-. 2000.61 (1.04-4.S.470) < LOD .403-.47) .12-2.81) 1. 1999.38-3.473) * .484) * .900) < LOD . Kwok et al. population in the subsamples from NHANES 1999-2000 and 2001-2002 (CDC. 2002.990) < LOD . 1997.770-2.420 (<LOD-. Additional information is available from U.690 (.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.580-1. 1993. CDC.32) 1.620-1. Bomhard et al.910 (.910 (<LOD-1. 1992.800-1.11) 4.590) * . IARC has classified SOPP as a possible human carcinogen.59) 1.43) 3. less likely. Ito et al.301-.96 (1.96 (1.560) < LOD 75th .750 (.69 (1.93) .514 (.750 (.460-. 2005). Survey Geometric mean (95% conf. OPP or SOPP produced carcinomas of the bladder only after phase II detoxification pathways were saturated.64 (2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.860 (. 2002).S.380 (.610) < LOD 1.480-.13) 1.840 (. Detectable levels were seen in over half the U. but no neurologic.08) 1.75 (1.00 (.650-1.91 (1.940-2. 1999. Murata et al. These metabolites may induce carcinogenicity via nongenotoxic regenerative hyperplasia of the bladder (Appel.910-1.24-2.02 (.12) < LOD 1.97 (2.780 (.900-1.00 (1.EPA at: http:// www.25-6. 1984.78 (2.780-14.S.248-.600-1.410 (<LOD-..550) < LOD . Urinary ortho-Phenylphenol (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.53) 1. 2002.86 (1. Biomonitoring Information Urinary OPP levels reflect recent exposure.361-.21 (.07) 2. 44 Fourth National Report on Human Exposure to Environmental Chemicals .980 (<LOD-1. 1986).568) * .09-3.40-13.31) < LOD .51-3.43-2.96-4.970) 1. In high dose animal studies.580) < LOD .0) 1...33) size 1991 2528 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th .670 (.360 (<LOD-. Zhao et al.24-2.93 (1.440 (.89 (1.444 (.62) .61 (.93) 1. reproductive..

Bartels MJ.EPA).17(8):411-417. Bartels MJ. Available at URL: http://ntp. Ito N. Arnold LL. Kawanishi S. Eastmond DA. Timchalk C.pdf. Moldeus P. EPA). Mendrala AL. Narang A. Roy D. Shibata M. Cano M. Leser KH. J Agric Food Chem 2006. Richter M. Centers for Disease Control and Prevention (CDC).703(12):97-104.20(5):851-857. Eadon G. Ito N. Dose-dependent binding of ortho-phenylphenol to protein but not DNA in the urinary bladder of male F344 rats. Biochem Pharmacol 1992. U. Fukushima S. NTP Technical report on the toxicology and carcinogenesis studies of ortho-phenylphenol (CAS No. Hirose M. Comparative in vitro-in vivo percutaneous penetration of the fungicide ortho-phenylphenol. Oxidative damage to cellular and isolated DNA by metabolites of a fungicide orthophenylphenol.286(2):309-319. Determination of orthophenylphenol in human urine by gas chromatography-mass spectrometry. J Chromatogr B Biomed Sci Appl 1997.150(2):402-413. Hagiwara A. March 1986.S. Smith RA. Hakkert BC. EPA 739 R-06004.Fungicides References Appel KE. Determination and levels of the biocide ortho-phenylphenol in canned beers from different countries. Mutat Res 1993. et al. U. Freyberger A.50(11):3351-3358. Third National Report on Human Exposure to Environmental Chemicals. Identification of SARA compounds in adipose tissue. 4/9/09. Toxicol Appl Pharmacol 1998.gov/ntp/htdocs/LT_ rpts/tr301.nih. Brendler-Schwaab SY. The pharmacokinetics and metabolism of 14C/13C-labeled ortho-phenylphenol formation following dermal application to human volunteers. National Toxicology Program (NTP). O-phenylphenol and its sodium and potassium salts: a toxicological assessment. Xenobiotica 1998. Roberts AL. St John MK. McNett DA. Regul Toxicol Pharmacol 2002. EPA-560/5-89-003. Selim S.45(5):460-481. Long-term toxicity and carcinogenicity study of sodium o-phenylphenate in B6C3F1 mice. Tayama S.74(2):61-71. Moore GA.22(10):809-814. Environmental Protection Agency (U. Nakagawa Y.159(1):18-24. Urinary physiologic and chemical metabolic effects on the urothelial cytotoxicity and potential DNA adducts of o-phenylphenol in male rats. Gierthy J. 2005. Available at URL: http://www. et al. Imaida K. Carcinogenesis 1999. Bartels MJ. Food Chem Toxicol 1984. Shirai T. Environ Mol Mutagen 2005.niehs. Bartels MJ. Environmental Protection Agency (U.S. IARC Sci Publ 1984. Meuling WJ. Arch Toxicol 2000. Buchholz BA. Bormett GA. Analysis of genotoxicity and the carcinogenic mode of action for ortho-phenylphenol.. Detection and characterization of DNA adducts formed from metabolites of the fungicide ortho-phenylphenol. Timchalk C.pdf. Reregistration Eligibility Decision (RED) for 2-phenylphenol and salts (Orthophenylphenol or OPP). 4/13/09 Onstot JD. Kwok ES. Bromig KH. In vivo genotoxicity of sodium orthophenylphenol: phenylbenzoquinone is one of the DNA-binding metabolite(s) of sodium ortho-phenylphenol. 90-43-7) in Swiss CD-1 mice (dermal studies). Murata M. Vogel JS. Hagiwara A. Moriya K. Atlanta (GA). Brusick D.43(7):14311437. Office of Toxic Substances.S. J Agric Food Chem 2002. Turteltaub KW. Elliott GR. Fourth National Report on Human Exposure to Environmental Chemicals 45 .(56):399-407.S.32(6):551-625. Sangha GK. Coelhan M. Relationship between metabolism and cytotoxicity of ortho-phenylphenol in isolated rat hepatocytes. Drugs. Pathak DN. rat and man. Zhao S. Sangha G.gov/oppsrrd1/REDs/ phenylphenol_red. 2006. van de Sandt JJ. Inoue S. food additives and natural products as promoters in rat urinary bladder carcinogenesis.epa. Glas K.54(16):5731-5735. The carcinogenicity of the biocide ortho-phenylphenol. Toxicol Appl Pharmacol 1999. Cnubben NH. Fukushima S. Bomhard EM. Herbold BA.28(6):579594. Comparative metabolism of orthophenylphenol in mouse. Stanley JS. Christenson WR. 1989. July 28. Christenson WR. Hum Exp Toxicol 1998.35(2 Pt 1):198-208. Brzak KA. Crit Rev Toxicol 2002.

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

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

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

Kolpin DW. J Expo Sci Environ Epidemiol 2007. Hodgson E. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. Bravo R. Heederik D. Deddens JA. et al. Davison KL.Herbicides References Ashby J. Sci Total Environ 2000. U. EPA). Environmental Protection Agency (U. Wratten SJ. Centers for Disease Control and Prevention (CDC). Green T. Environ Sci Technol 2005. Federal Register: January 24. Reynolds SJ. Hein MJ. Third National Report on Human Exposure to Environmental Chemicals. Atlanta (GA). Acetochlor (Harness) Pesticide Petition Filing 1/00. Kier L. Feng PCC.17(6):559-566. Barr DB. Environmental Protection Agency (U. J Agri Food Chem 1989. Volume 65. Fourth National Report on Human Exposure to Environmental Chemicals 49 . Curwin BD. and other herbicides in rivers. Environ Health Perspect 2000. reservoirs and ground water in the Midwestern United States.pdf.edu/profiles/herbgrowthreg/24-d-butylate/acetochlor/acetochlor_pet_100. Occurrence of sulfonylurea. EPA). Peter CJ. Alavanja MC.S. EPA 738-R-00-009. Finding minimal herbicide concentrations in ground water? Try looking for their degradates. Linhart SM. Available at URL: http://www. Barr JR. Hum Exp Toxicol 1996. Environ Health Perspect 2003. Barr DB. Lefevre PA. Andrews HF. Whyatt RM. Roberts AL. Chem Res Toxicol 1998. Sci Total Environ 2000. Furlong ET. Ward EM. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. Olsson AO. 2005.11(4):353359. Feil VJ. et al. Hladik ML. Xenobiotica 1994. Thurman EM. Kinney PL. Identification of human urinary metabolites of acetochlor in exposed herbicide applicators by high performance liquid chromatography-tandem mass spectrometry. Coleman S.S. 5/30/06. Hines CJ. Striley CA. Number 15. J Expo Anal Environ Epidemiol 2005. et al.111(5):749-756.S. Casida JE. pages 3682-3690. Rose RL.248(2-3):123-133. Tinwell H. Sanderson WT. imidazolinone.15(6):500-508. Available at URL(non U.24(10):1003-1012. Evaluation of the potential carcinogenicity and genetic toxicity to humans of the herbicide acetochlor.cornell. Comparative metabolism of chloroacetamide herbicides and selected metabolites in human and rat liver microsomes. acetochlor. Quistad GB. 2000. Jefferies PR. Wilson AG.15(9):702-735.html. Linderman R. and metolachlor herbicides in rats. Battaglin WA.39(17):6561-6574.108(12):1151-1157.gov/oppsrrd1/reregistration/REDs/acetochlor_tred. Larsen GL. Comparative metabolism and elimination of acetanilide compounds by rat. March 2006. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns.37(4):10881093. Dialkylquinonimines validated as in vivo metabolites of alachlor. Burkhardt MR. epa.EPA): http://pmep. Camann DE.cce.S. 1998. sulfonamide. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. Barr DB. 5/30/06 U. Report of the Food Quality Protection Act (FQPA) Tolerance Reassessment Progress and Risk Management Decision (TRED) for Acetochlor.248(2-3):115-122. Hsiao JJ.S.

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

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

Shealy DB. Casida JE.44(18):1325. 2007. Hines CJ. 2005.11(4):353359. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. Barr DB. Hill AB. Feil VJ. Thurman EM. International Programme on Chemical Safety (IPCS).43(9):2504-2512.usgs. Biagini R. Driskell WJ.56(6):853-859. 2/27/09 Jefferies PR. Gilliom RJ). Life Sci 1988. Hum Exp Toxicol. Furlong ET. Henningsen G. and metolachlor herbicides in rats. ALACHLOR. Peter CJ. Quantitative assessment of the mutagenic potential of environmental degradative products of alachlor.pdf. Geological Survey (USGS). et al. Hsiao JJ. Heydens WF. 86. Andrews HF. Background document for development of WHO Guidelines for Drinking-water Quality. Wratten SJ. The Quality of Our Nation’s Waters Pesticides in the Nation’s Streams and Ground Water. Casida JE. Available at URL: http://www. 1999. Biological monitoring of commercial pesticide applicators for urine metabolites of the herbicide alachlor. Striley CA. 2/27/00 52 Fourth National Report on Human Exposure to Environmental Chemicals . Supplemental Technical Information (available on-line only). Am Ind Hyg Assoc J 1995. Brown KK. Clark JM. Sacramento. Environmental Protection Agency (U. 1998. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. MacKenzie B. Circular 1291. Xenobiotica 1994. and other herbicides in rivers.56(9):883-889. reservoirs and ground water in the Midwestern United States. Roberts AL.gov/nawqa/pnsp/pubs/circ1291/ supporting_info. Quistad GB. Dialkylquinonimines validated as in vivo metabolites of alachlor. Sci Total Environ 2000. Tessier DM. Wilson AG. imidazolinone. Camann DE. Kimmel EC. Davison KL. Linhart SM. Kier LD.39(17):6561-6574. Hill RH Jr. who. sulfonamide. No. Environ Sci Technol 2005. World Health Organization. Lau H. Bull Environ Contam Toxicol 1996. December 1998. Jefferies PR. Sanderson WT. acetochlor. Kinney PL. Thelin GP. California. Dialkylquinoneimine metabolites of chloroacetanilide herbicides induce sister chromatid exchanges in cultured human lymphocytes. Geological Survey (USGS).S. Kolpin DW. Atlanta (GA). Third National Report on Human Exposure to Environmental Chemicals. Brown MA. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay.S. Available at URL: http://www. 1992-2001. An evaluation of the carcinogenic potential of the herbicide alachlor to man.248(2-3):123-133. Occurrence of sulfonylurea.24(10):1003-1012. Centers for Disease Control and Prevention (CDC). EPA). 1997. Burkhardt MR. Geneva. Available at URL: http://water. Hines CJ. Finding minimal herbicide concentrations in ground water? Try looking for their degradates.111(5):749-756. March 2006. Biagini RE. Thake DC. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. Casida JE.248(2-3):115-122.S. Quistad GB.S. 2/27/09 U. World Health Organization (WHO). 98-4245 (by Barbash JE. Martens MA.395(2-3):159-171. Reregistration Eligibility Decision (RED) Alachlor.47(6):503-517.htm. Feng PCC. Larsen GL. et al.epa. EPA 738R-98-020.org/documents/pds/pds/pest86_e.18(6):363-391. Water-Resources Investigations Report: Distribution of Major Herbicides in Ground Water of the United States Water Resource Investigations Report No. Whyatt RM. Chem Res Toxicol 1998.Herbicides References Battaglin WA. WHO/ FAO Data Sheets on Pesticides. Environ Health Perspect 2003. 2003. 1999.43(25):2087-94. Identification of a major human urinary metabolite of alachlor by LC-MS/MS. DNA adduct formation by alachlor metabolites.37(4):10881093.php.inchem. Ann Occup Hyg 2003. Available at URL: http:// www.int/water_sanitation_health/dwq/chemicals/en/alachlor. Hladik ML. Sci Total Environ 2000. 1996. Comparative metabolism and elimination of acetanilide compounds by rat. Hull RD. 4/2/09 U. U.pdf. Barr JR. Erratum in: Life Sci 1989.gov/oppsrrd1/ REDs/0063. Deddens JA. Mutat Res. J Ag Food Chem 1995. revised February 15. Tolos W. Shoemaker DA. Kolpin DW. J Agri Food Chem 1989. Alachlor in Drinking-water.

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

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

Sanderson WT. Stevens JT.69(2):217-222. Hermaphroditic. Goldman JM. levels of atrazine mercapturate were generally not detectable (CDC. Geneva. Simpkins JW. Determination of urinary residue levels of the N-dealkyl metabolites of triazine herbicides. Pubertal development in female Wistar rats following exposure to propazine and atrazine biotransformation by-products. atrazine was detected in only four children (Arcury et al. Environ Health Perspect 2001. J Toxicol Environ Health 1994. Chen H. 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. Shoemaker DA.76(1):190-200. A risk assessment of atrazine use in California: human health and ecological aspects. Striley CA. Short-term effects of chlorotriazines on estrus in female Sprague-Dawley and Fischer 344 rats. Lucas AD. atrazine mercapturate was infrequently detected at the detection limit of < 1 μg/L. Ferioli A. Lioy PJ. Bradway DE. Tapia J. International Programme on Chemical Safety (IPCS). Tyrey L. In a study of 60 farm worker children. Agency for Toxic Substances and Disease Registry (ATSDR). Collins A. McElroy WK. 2007). Pest Manag Sci 2005. Barbieri F. 2001). No. Aldous CN. Noriega N. Vonk A. et al. Brown KK. Goodrow MH. Ann Occup Hyg 2003. 1996. J Agric Food Chem 1982. Toxicol Sci 2003. Gillis JH. Gillis JH. Lee M. Stoker TE. J Expo Anal Environ Epidemiol 2005..html.inchem. Atlanta (GA). Carr WC Jr. 1993). Pesticide urinary metabolite levels of children in eastern North Carolina farmworker households. Stoker TE. Cottica D. Moseman RF. Stoker TE. Quandt SA. Stuart AA. Laws SC. the urinary geometric mean levels for herbicide applicators in Ohio and Wisconsin were about 6 μg/L (Hines et al.. Toxicol Lett 1993. diamino-S-chlorotriazine and hydroxyatrazine. 2005).cdc. Available at URL: http:// www. Gammon DW. Short-term effects of chlorotriazines on estrus in female Sprague-Dawley and Fischer 344 rats. Bersani M. Proc Natl Acad Sci USA 2002.. Barr DB. Freeman NC. Cooper RL.53(2):297-307. Curwin BD. Toxicol Sci 2000. Third National Report on Human Exposure to Environmental Chemicals.htm. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample. References Adgate JL. Toxicological profile for atrazine. WHO/ FAO Data Sheets on Pesticides. 2000). Wetzel LT. Mendoza M..43(2):155-167. Sanborn JR.. 2001 [online]. Deddens JA. Blewett C. 2005). Maroni M. In a small number of field workers. Finding measurable amounts of atrazine mercapturate in urine does not mean that the levels of atrazine mercapturate cause an adverse health effect.58(2):366-376. Barr DB. 82. demasculinized frogs after exposure to the herbicide atrazine at low ecologically relevant doses. Pfeifer KF. Heederik D. ATRAZINE.47(6):503-517. Cooper RL. 2005. Schmid J. In the NHANES 2001-2002 subsample. 1999) and 83 Minnesota children with multiple urine collections during 1997 (Adgate et al.30(2):244-247.115(8):1254-1260. et al. Hayes TB. Ferrell JM. Biological monitoring of human exposure to atrazine. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. Biagini RE. Barr DB.Herbicides Biomonitoring Information Urinary levels of atrazine mercapturate reflect recent exposure. Extrom PC. Hines CJ. Clayton CA. Hein MJ. Centers for Disease Control and Prevention (CDC). Grzywacz JG. World Health Organization. Fleenor-Heyser DG. urinary concentrations ranged from 5-1756 μg/L (Lucas et al. 3/11/09 Laws SC. In small studies of Maryland residents in 19951996 (MacIntosh et al.109(6):583-590. Reynolds SJ. Determination of atrazine metabolites in human urine: Fourth National Report on Human Exposure to Environmental Chemicals 55 . Available at URL: http://www. Toxicol Sci 2000. Atrazine disrupts the hypothalamic control of pituitary-ovarian function. Perry et al.61(4):331-355.atsdr. Through immunoassay atrazine equivalents (detected mostly as atrazine mercapturate). Cooper RL. Seiber JN. et al. 2003. Eberly LE. Jones AD. The effects of atrazine on female wistar rats: an evaluation of the protocol for assessing pubertal development and thyroid function.99(8):5476-5480. et al.. Eldridge JC.org/documents/pds/pds/pest82_e. et al. Environ Health Perspect 2007. Saiz SG. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models.64(9):672-678. The geometric mean of urinary atrazine mercapturate was 1. Breckenridge CB. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. The mammary tumor response in triazine-treated female rats: a thresholdmediated interaction with strain and species-specific reproductive senescence.gov/toxprofiles/tp153. Steroids 1999.43(2):155-167. Ferrell JM.. et al. Wetzel LT. J Toxicol Environ Health 1994.2 μg/L in 15 farmers studied several days after spraying the pesticide (Curwin et al. Catenacci G. 3/11/09 Arcury TA. Eldridge JC.15(6):500-508.

9(5):494-501.pdf. revised February 15. 0062. Pesticides in the Nation’s Streams and Ground Water.S.10(7):479.epa. March 2006. Kastl PE.6(1):107-116.182(1):44-54.58(1):50-59. Cooper RL. Needham LL. EPA). A review of epidemiologic studies of triazine herbicides and cancer. Washington (DC).pdf. 4/2/09 56 Fourth National Report on Human Exposure to Environmental Chemicals . Wetzel L. Laws SC. The Quality of Our Nation’s Waters.epa. Christiani D. Toxicology 1990. Chem Res Toxicol 1993. Available at URL: http://www. Geological Survey (USGS). Circular 1291. Sanderson JT. Toxicol Sci 2002. Ann Epidemiol 2000.php.67(2):198-206. 1992-2001. Perry M.gov/oppsrrd1/REDs/ atrazine_ired. van den Berg M. EPA). Crit Rev Toxicol 1997. Guidici DL. The effects of atrazine metabolites on puberty and thyroid function in the male Wistar rat. Boerma J. 6/1/09 U.Herbicides development of a biomarker of exposure. 3/11/09 U. 2007. Ryan PB. Dryzga MD.61(1):27-40. Determination of the effect of tridiphane on the pharmacokinetics of [14C]-atrazine following oral administration to male Fischer 344 rats. EPA Office of Pesticide Programs. Interim Reregistration Eligibility Decision For Atrazine. The effect of atrazine on puberty in male Wistar rats: an evaluation in the protocol for the assessment of pubertal development and thyroid function. Pesticides and Toxic Substances. Wood C.S. Dagenhart D. Urinary biomarkers of atrazine exposure among farm pesticide applicators.S. Laws SC. Lansbergen GW. May 2003a. Available at URL: http://water. Delzell E. Breckenridge CB. Office of Prevention.56(2):69-109. MacIntosh DL. White paper on potential developmental effects of atrazine on amphibians. Supplemental Technical Information (available on-line only). Guidici DL.gov/scipoly/sap/meetings/2003/june/ finaljune2002telconfreport. Available at URL: http://www.S. J Expo Anal Environ Epidemiol 1999. A longitudinal investigation of selected pesticide metabolites in urine. Environmental Protection Agency (U. Cooper RL. Environmental Protection Agency (U. Toxicol Appl Pharmacol 2004. Timchalk C. 2003b.27(6):599612. Toxicol Sci 2000. Tortorelli J. Osborne DW. Stevens JT. Environmental Fate and Effects Division. Rayner JL.195(1):23-34. Hammerstrom KA. Toxicol Appl Pharmacol 2002. Induction and inhibition of aromatase (CYP19) activity by various classes of pesticides in H295R human adrenocortical carcinoma cells. Stoker TE. A risk characterization for atrazine: oncogenicity profile.S. Fenton SE. Langvardt PW. U.gov/nawqa/pnsp/pubs/ circ1291/supporting_info. Exposure parameters necessary for delayed puberty and mammary gland development in LongEvans rats exposed in utero to atrazine. J Toxicol Environ Health A 1999. Stoker TE. Case No.usgs. Singzoni B. Sathiakumar N.

10) < LOD 1.230-. nausea.660) 1.4-D) controls broadleaf weeds in residential. As much as 62 million pounds of 2. It was first registered with U.960-1. 1977).952 and 0.930-1..20 (.690 (.24 (.260 (<LOD-.910) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD . 2. and it is often mixed with other chlorophenoxy acid herbicides (such as dicamba.610 (.540-. by direct contact with agricultural and residential areas after applications.30 (<LOD-2.27 (1.27 (. 2004).80) 1.410) < LOD .740 (.250 (<LOD-. and delayed Urinary 2.490) < LOD < LOD < LOD .420-. in 2001 (U.EPA.20 (<LOD-1. Acid and salt forms are much less toxic to fish and aquatic invertebrates than the ester forms.370-.440-1.4-dichlorophenoxyacetic acid (2.550-1. Sauerhoff et al.40) 1. with a half-life of several days to several weeks.13) < LOD .S. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. and mecoprop).66) < LOD 1.420) < LOD . 1989.08) < LOD . Human health effects from 2.810-1. these herbicides can enhance plant growth.EPA in 1948. renal and hepatic injury.S.70) 1. but at higher levels they are herbicidal.400) < LOD .S. it acts as a plant growth hormone.910) 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 . Similar to other chlorophenoxy herbicides. which may vary for some chemicals by year and by individual sample. although dermal exposure may be significant for herbicide manufacturing plant workers exposed to high concentrations of 2. 2.16) < LOD . headache. abdominal pain.730 (. 1974. Intentional overdoses and unintentional high dose exposures to chlorophenoxy acid herbicides have resulted in weakness.21) 1.05-2.210-. It is not well absorbed through the skin.4-D were used in the U. the chlorophenoxy herbicide 2.51 (1.350) < LOD < LOD < LOD . 2.250 (<LOD-.320) 90th .490 (. < LOD means less than the limit of detection.560-.4-D is rapidly absorbed via oral and inhalation routes.4-D can be applied either as an aqueous salt or as oil-soluble esters.4-D has low acute toxicity.02-1.49) 477 546 677 797 823 1070 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD . Kohli et al.4-D have been below recommended intake limits (U.560-1. 4-D. 94-75-7 General Information Widely used throughout the United States. myotonia.48) < LOD 1.330 (. and aquatic environments. Fourth National Report on Human Exposure to Environmental Chemicals 57 .4-Dichlorophenoxyacetic Acid CAS No.210 (<LOD-.4-D may occur during residential applications. MCPA. population from the National Health and Nutrition Examination Survey.690-1. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. dizziness.4-D is eliminated mostly unchanged in the urine with an elimination half-life ranging from 10 to 33 hours (Arnold et al.03) 695 659 520 668 589 892 Limit of detection (LOD.310) < LOD . 2007).EPA.10 (<LOD-1.43) 1. At low levels.4-Dichlorophenoxyacetic acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.610-. It is rarely detected in ground waters (USGS.930 (.Herbicides 2..690 (.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 . 2.890 (.310 (.690 (.680-1. General population exposure to 2. 2005).4-D at low environmental doses or at biomonitored levels from low environmental exposures are unknown.60) 1.670-1.22) < LOD .27-2. Once absorbed. hypotension. Recent estimates of chronic intakes of 2.55 (1.910) < LOD .S.S. and by consuming food or drinking water contaminated with 2. Survey Geometric mean (95% conf.07 (.230 (<LOD-. It is poorly bound in soils.890) < LOD ..760 (.10 (<LOD-1. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 1.32 (1. agricultural.4-D or exposed for prolonged periods.00-2.2.

Survey Geometric mean (95% conf.. eyes.720 (.620-.590 (<LOD-1. other exposures.640 (. 2005).780) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD . 2000).. Knopp et al. IPCS. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 1. 2005.410 (<LOD-.14 (.gov/pesticides/.990-1. Kolmodin-Hedman and Erne. 2003. Hill et al.700 (.550-.470) < LOD .680) < LOD .08 (..39) < LOD 1.390) < LOD < LOD < LOD . 1989). Pearce and McLean.S. developmental. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 2. Frank et al. U. 1996.930-1..670 (<LOD-1.570) < LOD . population from the National Health and Nutrition Examination Survey. IPCS. 2005).980) < LOD 1. 2002. 2005). It is unclear whether these associations are related to the chlorophenoxy herbicides.EPA 2005). 1980.670 (. In previous samples of the U. 1985.890-1.EPA. The acid and salt forms of 2.4-D are eye irritants.810-1. such as soft tissue sarcoma and non-Hodgkin’s lymphoma.490 (. in small samples of children (Hill et al. 58 Fourth National Report on Human Exposure to Environmental Chemicals .560-.4-D reflect recent exposure.08 (..380 (<LOD-.epa.. CDC..7.920) < LOD 1. 1995.380) < LOD .340 (.270-. and evidence of histological injury to the kidneys.380 (<LOD-.330-. or teratogenic effects in chronic rodent studies (Charles et al. or to contaminants in the herbicide formulations (specifically 2. Biomonitoring Information Urinary levels of 2.40) 695 659 520 667 589 892 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.S.410) < LOD < LOD < LOD .810-1. with the exposure to chlorophenoxy herbicides as defoliants or contaminated herbicides. 1995).24) 1.13 (.410) < LOD 1. 2005). Additional information is available from U.Herbicides neuropathy (Bradberry et al. 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. 2001.EPA. Epidemiological studies have reported associations of several types of cancer.EPA at: http://www.890) < LOD 1. 1994).3. U. 1992).27-1.4-D does not have significant reproductive. IARC considers the chlorophenoxyacetic acids group of chemicals as possibly carcinogenic to humans.4-Dichlorophenoxyacetic acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.13 (.19) .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.520-.580-.560-. and of adults and children (Baker et al.4-D had urinary levels several hundred to several thousand times higher than the 95th percentiles of the NHANES subsamples (CDC.780 (.17 (.660) < LOD .26) 962 1135 1015 1277 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD . Acute high doses administered to laboratory animals produced ataxia.850) < LOD .S.610-. U.270 (<LOD-.S.780) .790) < LOD .780-1. liver.380-. thyroid.350 (<LOD-.56) .480 (. IPCS.670 (.4-D was not found to be genotoxic or carcinogenic in animal studies (Garabrant and Philbert.. U.35) < LOD . 1996. 2006. Kutz et al.740 (.EPA.4-D production plant workers and a few forestry workers spraying 2.S.S. 2.440 (. adrenals and gonads (NTP.8-tetrachlorodibenzo-pdioxin) (Garabrant and Philbert.73) .590 (<LOD-1.340-.32 (<LOD-2. 2004).S.610-.16) 1. Average post-application urinary levels of 2. 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 .660 (.410) 90th .. 2002..820-1. population (Hill et al. 2. myotonia.08 (.29) 477 546 677 796 823 1070 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD . IOM.41 (1. 1996.05) .790) 1. 2005. 2005. urinary 2. 2005.4-D levels were detectable in less than a quarter of the individuals studied.

Barr DB.27(1):23-38. Heederik D. Murphy RS. 2005. TOX-63 Peroxisone Project (2. Solomon KR. Stephenson GR. Sanderson WT. Environ Res 1995. Board on Health Promotion and Disease Prevention.51(3):152-159.4-Dichlorophenoxyacetic Acid). Washington (DC): National Academies Press. J Expo Anal Environ Epidemiol 2000. Fast DM. Occup Environ Med 1994. Mandel et al.10(6 Pt 2):789-798. Sircar KP. International Programme on Chemical Safety-INCHEM (IPCS). general population. van Ravenzwaay B. Gupta BN. Carter-Pokras OD. Arch Toxicol Suppl 1980. 1992)..4-D were highest in the farmers who applied the 2. TOX-63: TOXICITY REPORT CURVES.4-dichlorophenoxyacetic acid (2. Pesticide residues in urine of adults living in the United States: reference range concentrations. Dhar MM. Hanley TR Jr. Exposure of homeowners and bystanders to 2. Brody D.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. other family members had levels ranging only slightly higher than the 95th percentile levels in NHANES 1999-2000 and 2001-2002 subsamples (CDC. Bailey SL.15(6):500-508. 2.4-dichlorophenoxyacetic acid in the chemical industry: results of a five year biological monitoring study.37(2):277-291. Selected pesticide residues and metabolites in urine from a survey of the U. Needham LL. Kutz FW. 2005.71(2):99-108. Centers for Disease Control and Prevention (CDC). and the use of protective clothing or equipment (Arbuckle et al. Curwin BD. Updated March 7. Alexander BH.S. Biomonitoring for farm families in the farm family exposure study. Committee to Review the Health Effects in Vietnam Veterans of Exposure to Herbicides (Fourth Biennial Update.4-dichlorophenoxyacetic acid in man.nap. Arnold EK. Quantification of selected pesticide metabolites in human urine using isotope dilution high-performance liquid chromatography/ tandem mass spectrometry. 2005). Biomonitoring of herbicides in Ontario farm applicators. 2005). Baker S. Xenobiotica 1974.4:427-435. Reynolds SJ.4:97-100. geometric mean urinary levels of 2.niehs. Kolmodin-Hedman B. Baker BA. Holler JS.60(1):121-131.edu/catalog.4-D): exposure and urinary excretion. Forestry workers involved in aerial application of 2. Harris et al. 914. Beeson MD..nih. Available at URL: http://ntp.htm. Hill RH Jr.4-dichlorophenoxyacetic acid and its forms. Atlanta (GA). Hill RH Jr. Honeycutt R. Beasley VR.4-D in urine does not mean that the level of the 2.4:318-321.4-D and 2.4-D. cfm?objectid=06FF8DA6-E5A1-90CD-3F26562CEC5CDDE5. Vet Hum Toxicol 1989. et al. Chapman P.org/documents/jmpr/jmpmono/v96pr04. To T. 3/17/09 Institute of Medicine (IOM).5-T). Driskell WJ. Campbell RA. Harris SA. 2003. J Toxicol Environ Health 1992. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. References Arbuckle TE. Barr DB. Third National Report on Human Exposure to Environmental Chemicals. Finding a measurable amount of 2.php?record_id=10603. Biomonitoring studies of 2. et al. Smith SJ. The pharmacokinetics of chlorinated phenoxy acid herbicides: a literature. Toxicol Sci 2001. Kohli JD. Veterans and Agent Orange: update 2002. Cook BT. 3/17/09 Fourth National Report on Human Exposure to Environmental Chemicals 59 . Assessment of exposure to 2. Philbert MA.4-D).. 2005 Charles JM. Frank R.31 Suppl 1:90-97. Mandel JS. Crit Rev Toxicol 2002. et al. the amount of pesticide applied. Survival and Growth Curves from NTP Toxicity Studies. Sirons G J. Shealy DB.4-D) epidemiology and toxicology. Absorption and excretion of 2. Pesticides residues in food: 1996 evaluations Part II Toxicology. Arch Environ Contam Toxicol 1985. In farm families. Hein MJ. Tandon JS. Wilson RD. Garabrant DH.gov/index. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children.4.4-. Head SL.31 Suppl 1:98-104. Tables.4-dichlorophenoxyacetic acid (2. National Toxicology Program (NTP). Bus JS.4 dichlorophenoxyacetic acid (2. the number of acres to which it was applied (Curwin et al. 2006. Erne K.32(4):233-257. Khanna RN. Acquavella JF. J Environ Sci Health B 1992. Baker SE.4-D than levels found in the general population. Arch Environ Contam Toxicol 1989.. Available at URL: http:// www.Herbicides the time since application. Ripley BD. 3/17/09 Knopp D. Available at URL: http:// www.18(4):469-474. Cole DC. J Expo Anal Environ Epidemiol 2005 Nov.31(2):121-125. Gregg M. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. Scand J Work Environ Health 2005. Review of 2.4-D will result in an adverse health effect. Needham LL. Dichlorophenoxyacetic acid. Ritter L. Estimation of occupational exposure to phenoxy acids (2. Scand J Work Environ Health 2005.inchem. Developmental toxicity studies in rats and rabbits on 2.

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

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

220) < LOD 1192 1346 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < 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 . population from the National Health and Nutrition Examination Survey. 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 .670 (<LOD-.S.S. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.Herbicides Urinary Metolachlor mercapturate Metabolite of Metolachlor Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. Urinary Metolachlor mercapturate (creatinine corrected) Metabolite of Metolachlor 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. Survey Geometric mean (95% conf. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.200 (<LOD-. 62 Fourth National Report on Human Exposure to Environmental Chemicals .2. which may vary for some chemicals by year and by individual sample.740) 679 700 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. Survey Geometric mean (95% conf. population from the National Health and Nutrition Examination Survey. < LOD means less than the limit of detection.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 .200 (<LOD-.240) 679 701 957 Limit of detection (LOD.

Kolpin DW. Environ Health Perspect 2000. 2003. 1998. EPA). Davison KL. Available at URL: http://water.111(5):749-756.usgs. et al. California. Reynolds SJ.gov/nawqa/ pnsp/pubs/wrir984245/text. Curwin BD. imidazolinone.php. Finding minimal herbicide concentrations in ground water? Try looking for their degradates. Supplemental Technical Information (available on-line only).html. Dialkylquinonimines validated as in vivo metabolites of alachlor. Water-Resources Investigations Report: Distribution of Major Herbicides in Ground Water of the United States Water Resource Investigations Report No. Coleman S. Casida JE. Gilliom RJ).41:3409-3414.S.S. Available at URL: http://water.11(4):353359.pdf. 6/1/09 Whyatt RM.47(6):503-517.int/water_sanitation_health/dwq/chemicals/ metolachlor. usgs. 1992-2001. Background document for development of WHO Guidelines for Drinking-water Quality. Environ Health Perspect 2003.gov/nawqa/pnsp/pubs/files/051507. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay.15(6):500-508. Occurrence of sulfonylurea.gov/nawqa/pnsp/pubs/circ1291/ supporting_info. streams and groundwater. U. Kolpin DW. Metolachlor in Drinkingwater. Hodgson E. R. 2005. Hladik ML.S. J Expo Anal Environ Epidemiol 2005. Brown KK.248(2-3):115-122. Hsiao JJ. Environ Sci Technol 2005. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. Linderman R. Feil VJ. Hein MJ.39(17):6561-6574. Ann Occup Hyg 2003. Barr JR.24(10):1003-1012. Comparative metabolism of chloroacetamide herbicides and selected metabolites in human and rat liver microsomes. Shoemaker DA. 2007.pdf 3/30/09 Hines CJ. Wratten SJ. Alavanja MC. Reregistration Eligibility Decision (RED) Metolachlor. Rose RL. World Health Organization (WHO). Kinney PL. Barr DB. Geological Survey (USGS).ESTfeature_gilliom. March 2006. and metolachlor herbicides in rats. Barr DB. 3/27/09 Fourth National Report on Human Exposure to Environmental Chemicals 63 . Thelin GP. Sanderson WT. Third National Report on Human Exposure to Environmental Chemicals. 4/2/09 U. Sci Total Environ 2000. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. acetochlor. Quistad GB. Geological Survey (USGS). sulfonamide.gov/oppsrrd1/ REDs/0001. 1999. Sacramento. Xenobiotica 1994. Available at URL: http://www. Furlong ET.epa.37(4):10881093.248(2-3):123-133. EPA 738R-95-006. Available at URL: http://www. Environmental Protection Agency (U. and other herbicides in rivers. reservoirs and ground water in the Midwestern United States. Available at URL: http://water. Biagini RE.Herbicides References Battaglin WA. Gillion. et al. 98-4245 (by Barbash JE. Roberts AL. Larsen GL. Ward EM. Peter CJ. Comparative metabolism and elimination of acetanilide compounds by rat.108(12):1151-1157. Striley CA. Burkhardt MR. 3/26/09 U. Chem Res Toxicol 1998. Heederik D. April 1995. Andrews HF. Thurman EM. Camann DE.who. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. Atlanta (GA). The Quality of Our Nation’s Waters Pesticides in the Nation’s Streams and Ground Water. Sci Total Environ 2000. Feng PCC. Centers for Disease Control and Prevention (CDC). J Agri Food Chem 1989. Deddens JA. Pesticides in U. Jefferies PR.S.usgs. Linhart SM.S. Environ Sci Technol 2007. revised February 15. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. Circular 1291.pdf.

.g.4.4-D were used as defoliants in the Vietnam War (e.. 1986.. abdominal pain.4.4. Given the commercial unavailability of 2. 2. these herbicides can enhance plant growth. At low levels.5-Trichlorophenoxyacetic acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. it is not well absorbed through the skin.4. 2..Herbicides 2.4. 1992. Teratogenic and developmental effects have been reported in studies of multiple rodent strains treated with high doses of technical grade 2. with an elimination half-life of approximately 19 hours (Arnold et al.5-T in soil varies with conditions.4.5-trichlorophenol and other degradates. the general population is unlikely to be exposed to it.5-T (Holson et al. 93-76-5 General Information 2. with the exposure to chlorophenoxy herbicides as defoliants Urinary 2. hypotension. and concern about contamination with 2.4.2 and 0.7. 64 Fourth National Report on Human Exposure to Environmental Chemicals . which may vary for some chemicals by year and by individual sample.5-T was once applied as either an aqueous salt or as an oil-soluble ester. 2.5-T at low environmental doses or at biomonitored levels from low environmental exposures are unknown.5-Trichlorophenoxyacetic Acid CAS No.5-Trichlorophenoxyacetic acid (2.4. Intentional overdoses and unintentional high dose occupational exposures to chlorophenoxy acid herbicides have resulted in weakness.4. but higher levels are herbicidal. renal and hepatic injury.4. Once absorbed into the body. Ester forms of 2. Human health effects from 2.5-T has been rarely detected in ground waters (USGS. Mohammad and St.4..S. 2. Agent Orange).3. 2007).5-T use as a herbicide in 1985.5-T) is a chlorophenoxy acid herbicide that is no longer registered for use in the United States.1. see Data Analysis section) for Survey years 99-00 and 01-02 are 1.4. 1989. Chlorophenoxy herbicides act as plant growth hormones. 1974). 2004). Omer. headache. ranging from several weeks to many months. 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.4. nausea.. Survey Geometric mean (95% conf.5-T and 2. 1992). and delayed neuropathy (Bradberry et al.5T is rapidly absorbed via oral and inhalation routes.8-tetrachlorodibenzo-p-dioxin (TCDD) led to the discontinuation of 2. Kohli et al.4. population from the National Health and Nutrition Examination Survey.4.5-T is eliminated mostly unchanged in the urine. < LOD means less than the limit of detection. myotonia. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. dizziness. Although 2. Nelson et al. The half-life of 2.5-T. Epidemiological studies have reported associations of several types of cancer.5-T degrades to 2.4. such as soft tissue sarcoma and non-Hodgkin’s lymphoma.

S.EPA. or to contaminants in the herbicide formulations (specifically 2. 1992).5-T does not mean that the level will result in an adverse health effect. Additional information is available from U.4. IOM. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 2. Fourth National Report on Human Exposure to Environmental Chemicals 65 . 1980).5-T in urine also provide physicians and public health officials with reference values so that they can determine whether other people have been exposed to higher levels of 2. IARC considers the chlorophenoxyacetic acids group of chemicals as possibly carcinogenic to humans.S.5-T reflect recent exposure. 2002.4. In the NHANES 1999-2000 and 2001-2002 subsamples (CDC. in which urinary levels of 2. It is unclear whether these associations are related to the chlorophenoxy herbicides. 2005).7.8-tetrachlorodibenzop-dioxin) (Garabrant and Philbert.000 times higher than the detection limit for the NHANES 2001-2002 data (Kolmodin-Hedman and Erne. IPCS. 2003. 1996.3.5-T itself is not mutagenic.5-Trichlorophenoxyacetic acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.epa. urinary levels of 2.4.4. similar to results of NHANES II (19761980).5-T than levels found in the general population.5-T were generally below the limit of detection.4.4. Finding a measurable amount of 2. Pearce and McLean. U. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 2004).5-T also were below the limit of detection (Kutz et al.4. Mean urinary levels of 2.4. 2005.4.gov/pesticides/.S. other exposures.Herbicides or contaminated herbicides. Survey Geometric mean (95% conf.5-T measured after a day of exposure in a few asymptomatic herbicide applicators were 35.. population from the National Health and Nutrition Examination Survey.EPA at: http://www. Biomonitoring Information Urinary levels of 2. Biomonitoring studies on 2. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1814 2537 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 430 580 618 830 766 1127 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 891 1192 923 1345 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 652 679 483 700 531 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. Urinary 2.

Proudfoot AT. Nelson CJ. Kutz FW. Washington (DC): National Academies Press. Gaylor DW. Holson JF. Absorption and excretion of 2. Centers for Disease Control and Prevention (CDC).4. Available at URL: http:// www. Gaines TB. Washington (DC): U. Developmental toxicity of 2. 914. Board on Health Promotion and Disease Prevention.5-t mixture.EPA. 3/17/09 66 Fourth National Report on Human Exposure to Environmental Chemicals . Third National Report on Human Exposure to Environmental Chemicals.31(2):121-125.pdf.32(4):233-257. Dichlorophenoxyacetic acid. Carter-Pokras OD.5-T). Arch Int Pharmacodyn Ther 1974. Review of 2.S. Fundam Appl Toxicol 1992. May. Pesticides residues in food: 1996 evaluations Part II Toxicology. II. Beasley VR.4. LaBorde JB.4-dichlorophenoxyacetic acid (2. LaBorde JB.edu/catalog.8(5):551-60. Developmental toxicity of 2.php?record_id=10603.2000 and 2001 market estimates.4.4. Estimation of occupational exposure to phenoxy acids (2. 2.23(2):65-73. Available at URL: http://www.31 Suppl 1:1825.4-. Toxicol Rev 2004. Vet Hum Toxicol 1989. Multireplicated dose-response studies in four inbred strains and one outbred stock of mice. Tandon JS.4. Crit Rev Toxicol 2002.4-D and 2. Philbert MA. 210:250-255. St Omer VE.4. Nelson CJ. Agricultural exposures and non-Hodgkin’s lymphoma. Pesticide industry sales and usage .nap. Available at URL: http:// www.4:318-21. et al. Erne K. Scand J Work Environ Health 2005. Dhar MM. Arch Toxicol Suppl 1980. 2004.EPA). Vale JA.19(2):286-297.epa. U. Khanna RN. Committee to Review the Health Effects in Vietnam Veterans of Exposure to Herbicides (Fourth Biennial Update. gov/oppbead1/pestsales/01pestsales/market_estimates2001.S.4-D/2.inchem.4-D) epidemiology and toxicology. 2003. Mohammad FK. I.37(2):277-91.4.5-trichlorophenoxy acetic acid in man.19(2):298-306. McLean D.Herbicides References Arnold EK. Bradberry SM. Gaines TB. S. discussion 5-7. International Programme on Chemical Safety-INCHEM (IPCS).5-trichlorophenoxyacetic acid (2. Sheehan DM. Atlanta (GA).5-trichlorophenoxyacetic acid (2. Kolmodin-Hedman B. Veterans and Agent Orange: update 2002. McCallum WF. Office of Prevention Pesticides and Toxic Substances.4. Murphy RS. Selected pesticide residues and metabolites in urine from a survey of the U.org/documents/jmpr/jmpmono/v96pr04. Multireplicated dose-response studies with technical and analytical grades of 2. Gupta BN. J Toxicol Environ Health 1992. Behavioral and developmental effects in rats following in utero exposure to 2.5-T). Fundam Appl Toxicol 1992. Environmental Protection Agency (U.5-T). 2005. et al. Sircar KP. The pharmacokinetics of chlorinated phenoxy acid herbicides: a literature.5-T in four-way outcross mice. Poisoning due to chlorophenoxy herbicides. Neurobehav Toxicol Teratol 1986. Garabrant DH. general population. Cook BT. 3/17/09 Kohli JD.htm. Holson JF. Brody D. Wolff GL.S. 3/17/09 Institute of Medicine (IOM). Pearce N.

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

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

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

160 (.0) 21.4) 19.60-10.053 (<LOD-.120-.5-17.6 (15.138 (.0-25.8-17.1) < LOD 9.130) .058) < LOD .0 (10.054-.8-24. Survey years 01-02 03-04 Geometric mean (95% conf.8-25.098 (.120 (.177) Sample size 2159 1952 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD .1-18. see Data Analysis section) for survey years 01-02 and 03-04 are 10.4-17.150 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.086-.50) 15.063-.109 (.070) .5 and 7.160 (.2) 11.5 (<LOD-11.102 (. which may vary for some chemicals by year and by individual sample.140) .1-19.064) 90th .30 (8.9 (14.110-.8) 14.049-.9-22. interval) Selected percentiles ( 95% confidence interval) Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * * 50th < LOD < LOD 75th < LOD 9.3 (18.00-14.0 (10.084-.1 (13.059 (.090-.S.80 (<LOD-10.180) .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 .6 (14.4) 95th 20.109-.069) < LOD < LOD .8) < LOD 8.054-.158) .139 (.080-.3 (19.090 (<LOD-.093) .130-.9-38.9 (13.139 (.117) < LOD .1-16. Survey years 01-02 03-04 Geometric mean (95% conf.120 (.113 (.6) 9.070-.6) 16.110 (.120 (.101) .062 (.5 (16.4 (12.70 (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 8.0) 19.1-24.3 (13.075) < LOD .112) 95th .80-9.100-.077 (.112-.120) .190) .1) 10.116) .4) 539 456 484 487 980 885 Limits of detection (LOD.100) . 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.150 (.077-.1 (18.2) 12. Fourth National Report on Human Exposure to Environmental Chemicals 79 .160) .202) 539 456 484 487 980 885 < LOD means less than the limit of detection for the lipid adjusted serum level.4) 20.100-.083-.060) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.180) .8 (18.130) .090-.9 (13.6-24.7) 15.130-.110) .140 (.130) .0) < LOD 9.096-.3-21.7 (14.1) 13.073-.4 (12.190) .9 (12.5-17.1) 14.6-33.109-.149) .3 (18.8. population from the National Health and Nutrition Examination Survey.103 (.8-19.090-.124) .5) 21.2) 15.182) 716 587 1443 1365 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD .2) 14.110 (.5) 19. 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 .1) 15.1) 15. < LOD means less than the limit of detection.40-10.S.4-18.7 (15.8 (9.8 (11.7-19.088-.4) 14.3 (14.0-21.064 (.6) 19.130-.8) 15.054-.062-.2-15.40-9.090 (.8-17.147 (.089 (.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. which may vary for some chemicals by year and by individual sample.00 (8.80-10.130 (.5) 15.100-.080) .110) .108-.103 (. population from the National Health and Nutrition Examination Survey.242) .4) 21.6-24.2) Sample size 2159 1952 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD 10.070 (<LOD-.7 (<LOD-15.140-.50 (8.90) 90th 15.30 (8.9 (12.4) < LOD < LOD 16.9-23.6 (15.100 (.5-15.080 (.100) .10 (<LOD-16.048 (<LOD-.062 (.056-.170) .7) 716 587 1443 1365 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD 9.0 (11.110 (.055 (.0 (15.7-22.1) 20.138) .

No:429-436. Hartvig HB.gov/toxprofiles/ tp1. Vol. Environ Health Perspect 2001. and epidemiology in the United States. Grandjean P. Brock JW. Chung KL. Basit A. Andersen A. Stehr-Green. Tully DB.14:95-102. Teta MJ.html. Serum organochlorine levels and breast cancer: a nested case-control study of Norwegian women.91(1):122-126. International Programme on Chemical Safety (IPCS). Int Arch Occup Environ Health 1994. Mink PJ. plasma dieldrin. PA. Corrigan FM. Reprod Toxicol 2000. Sodium and GABA-activated channels as the targets of pyrethroids and cyclodienes. Sanchez-Ramos J.59:229-234. and lymphocyte sister chromatid exchange. Kitzazwa M. Organochlorine exposure and risk of breast cancer. Exposure to low doses of the environmental chemical dieldrin causes behavioral deficits in animals prevented from coping with stress. Available at URL: http://www. New York. 1991.26:701-719. August 2008. Serrano FO. Ellis H. 80 Fourth National Report on Human Exposure to Environmental Chemicals . Part A 2000. Cox. Schulte P.66(4):229-234.usgs. 2007 [online]. Jr and Laws ER.352:1816-1820. 2 Classes of Pesticides. David VL.atsdr. The E-SCREEN assay as a tool to identify estrogens: an update on estrogenic environmental pollutants. Anantharam V. Carlson JN. Jr.Organochlorine Pesticides in the NHANES 2001-2002 and 2003-2004 subsamples (Edwards and Priestly 1994).html. 1992-2001. Dieldrin-induced neurotoxicity: relevance to Parkinson’s disease pathogenesis. VT. Patterson DG Jr.fda. Revised Feb. J Toxicol Environ Health 1989. Priestly BG. Environmental Health Criteria 91. McIntosh LJ. Sonnenschein C. Toxicity of dieldrin for dopaminergic neurons in mesencephalic cultures. In Hayes WJ. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. Needham LL. Wienburg CL.cfsan. Shore RF. 1989. Cancer Epidemiol Biomarkers Prev 2000. 15. Organochlorine insecticides in substantia nigra in Parkinson’s disease.htm. Patterson DG Jr. Narahashi T. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. References Agency for Toxic Substances and Disease Registry (ATSDR).gov/~dms/ pesrpts. pp. Exp Neurol 1998. 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. 6/1/09 Ward EM. Roy ML.27:405-421. Smith AG.103(Suppl 7):113-122. Psychopharmacology (Berl) 1987. Inc. Six high-priority organochlorine pesticides. Environ Health Perspect 1995. 4/21/09 Jorgenson JL.inchem. et al. Aldrin and Dieldrin [online]. Turner W. Academic Press. Food and Drug Administration (FDA). Jorgensen T. Handbook of Pesticide Toxicology.org/documents/ehc/ ehc/ehc91. J Toxicol Environ Health. Olea N. Available at URL: http://www. Toxicological profile for aldrin/dieldrin [online]. Mumtaz MM. Fernandez MG. Toxicol Lett 1992. toxicology. United States Geological Survey (USGS). 731-915. Available at URL: http://pubs. Rosellini RA. Kanthasamy AG.47:1059-1087.150:263-271. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Finley B. Soto AM.54:1431-1443. Chapin RE.gov/ circ/2005/1291/. Chemosphere 2004.cdc. Li AA. Neurotoxicol 2005. either singly or in combination. Lancet 1998. 4/21/09 Hoyer AP. Demographic and seasonal influences on human serum pesticide residue levels. Buckland SJ. Kanthasamy A. Effect of occupational exposure to aldrin on urinary D-glucaric acid. Evaluation of epidemiologic and animal data associating pesticides with Parkinson’s disease.9:1357-1367. Aldrin and dieldrin: A review of research on their production environmental deposition and fate. Pesticides in the Nation’s Stream and Ground Water. Frey JM. et al. bioaccumulation. September 2002. Grajewski B. J Occup Environ Med 2005. Song S. Ginsburg KS. Edwards JW. 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. 4/21/09 Bates MN. Facca A. Garrett N. Chlorinated Hydrocarbon Insecticides. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Available at URL: http://www. are nonestrogenic in transfected HeLa cells. Daniel SE.109(Supp1):113-139. Eds.64-65 Spec. Mann D.

8-32. which may vary for some chemicals by year and by individual sample.7-56. Both pesticides are persistent in soils and sediments and have been detected in water from agricultural run-off and near production and disposal facilities (ATSDR.8 (18.7-25.1) 30.6) 39.S.8-61.9) 47.1-51.7) 9.5 (31.6) 48.9 (29.9 (36.5-38.8) 52.10-11.6-24.5) 9.9 (15.3-43.4-21. Heptachlor was used as a soil and seed treatment and for termite control in and around buildings until 1988.3-49. Both of these chemicals and their metabolites can cross the placenta and are excreted into breast milk.3 (27.2-49.1-25.1 (<LOD-12.10-18.7) 28.0 (<LOD-12.2 (9.1 (16.5) < LOD < LOD 9.5) 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 * * * * 11.0 (16. 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.9 (15.0-13.1-19.2) < LOD 11. Consequently.3) 10.8) 27. fish.5.2) 37.7) 19.4 (<LOD-12. see Data Analysis section) for Survey years 99-00.8 (10.1 (20.2 (36.8) 18.0) 27.1) 30.7 (43.8-23.3) 10.9) 10.9-21.2) 22.1 (15.4) 22..Organochlorine Pesticides Chlordane CAS No.6) < LOD 11.20 (<LOD-11.9 (21.8 (17.9) 31.89-10.7 (42.1) < LOD < LOD < LOD < LOD < LOD 8.5.1) 22.7-12.8-43.6-18.5) 37.1-25.9 (11. As a result of the manufacturing process.0-61.7) 35.2-28.1 (17.3 (11.4 (35.4-40. 57-74-9 Heptachlor CAS No.9) 36.70 (<LOD-10. and 03-04 are 14.6) 49.9-40. population from the National Health and Nutrition Examination Survey.8-33.9 (31.9 (26.8-42.6 (9.1-50.1) * 11.1 (27.0) 31.6) 11.8 (17.5-65.6-45.82-11.5-42.S.0) 75th 20.3 (25.0-33.4 (30.1-15.5 (<LOD-12.1) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * 12.8) 53.4 (31.3-45.5) 38.4) < LOD < LOD < LOD 23.1 (44. Fourth National Report on Human Exposure to Environmental Chemicals 81 . and in soil.37 (8.4-45.6) 9.4 (22.36-11.S. buildings. 2007).8) 44.1 (11.5) 10.5 (8. respectively. foods high in fat such as meat. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.20-11.2 (37.9) 39.4-51.6) 9.7) 19.4) 18. heptachlor use has been limited to treatment of fire ants near power transformers.5-43.0 (32.90 (8.3-32.74 (<LOD-10.3) 37.9 (17.3-45.4-14.8 (42.6 (43.3 (28.5) 44.1 (25.6) 8.2 (21.5) 56.7 (19.5-41.7 (<LOD-13.0) 20.2) < LOD 11.5 (41.1 (<LOD-12. and 7.7 (34.3 (20.4) 29.9 (26.2) 36.2) 33.1-65.4) 39.5-47.2-26.3 (26.2 (28.9 (18.9 (11.3 (9.7 (<LOD-32.7) 31.6 (25.4) < LOD 11. 2007).7) 42.9-38.0) 41.8.6) 48. chlordane was used to kill termites and other insects on agricultural crops.5-13.9) 17.5) 628 557 462 350 501 493 559 1031 898 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. Technical grade chlordane had contained 7% trans-nonachlor.4) 37. Since 1992.8-31.2) 34.30-11.9-21.7-39.8) size 1661 2249 1978 Total years 99-00 01-02 03-04 50th < LOD 11.0) 21. and dairy products are the usual sources of exposure to these chemicals in the general population.8) 52.6-24.10 (8.5 (34.2 (41.0 (26.63 (8.6) 36.0-12. Heptachlor and chlordane and their metabolites bioaccumulate in fatty animal tissues. lawns.9) 13.1) * 11.69-10.0) 37.8-33.7-70.4) 12.6-53.3 (21.7 (34.7 (32.5-32.2-56.2) 46.9) 23.0 (37.3) 18.8-20.5) < LOD < LOD < LOD < LOD 13.5) 21.8 (40.0 (20.8 (10.9) 11.3 (<LOD-19. 1994.0-25.6) 23. Until 1988.0-18.7 (17. 10.2-49.9) 11.7-14.1 (<LOD-12.2 (10. the technical grade product of each chemical contains 10%-20% of the other chemical. Survey Geometric mean (95% conf.2-21.1 (40. 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.6 (16. Chlordane is not currently produced or used in the U.3) 18.5-40.1) 16.6-12.9) 23. < LOD means less than the limit of detection.2) * 12.0-67.4 (30.5 (33. 1994). in addition to trace amounts of numerous other related compounds (ATSDR.5-44.6) 20.1) 90th 34.3) 41.8-73.9) 37.8) 663 752 595 998 1497 1383 20 years and older Gender Males 99-00 01-02 03-04 * 11. 76-44-8 General Information Chlordane and heptachlor are structurally related organochlorine pesticides and were used in the U. from the early 1950’s until the mid-1980’s.7 (10.6 (9.9-42.20-10.2 (39.3-24.4 (10. interval) Selected percentiles ( 95% confidence interval) Sample 95th 44. 01-02.

270 (.320) .310-.126 (.100 (<LOD-.146) .287) .128 (.120-.258 (.070 (<LOD-.373) .140 (. 1977b. 1977a.190-.315 (.091) .290-.065-.280) .330 (.066-.083) .133) 90th .200-.242-.220-.077) .. Chlordane is metabolized primarily to oxychlordane and to a lesser extent.208 (. 82 Fourth National Report on Human Exposure to Environmental Chemicals .190-.200 (.069 (<LOD-. Chronic feeding studies with either chlordane or heptachlor have demonstrated reduced fertility.168-. which may vary for some chemicals by year and by individual sample.170) . EPA has established environmental criteria for chlordane and heptachlor.160) .310) .260 (.140 (.170) .400) . Shindell and Ulrich.140-.450) . interval) Selected percentiles ( 95% confidence interval) Sample 95th .066 (<LOD-. 2001. No clear evidence of excessive cancer rates was demonstrated in human epidemiologic studies (ATSDR.291) size 1661 2249 1978 Total years 99-00 01-02 03-04 50th < LOD .148-.056 (.204 (.165-.074-.058-.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 * * * * . which is also persistent in the body (ATSDR.050 (<LOD-.070) < LOD < LOD < LOD < LOD < LOD .070-.223) . Human health effects from either chlordane or heptachlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown.350 (.253-.280 (. both chlordane and heptachlor induced hepatic cytochrome P450 enzymes and increased the incidence of liver tumors (NTP. Subtle neurodevelopmental effects have been observed rodents after prenatal exposure to heptachlor (IPCS.070 (.320 (.108-.300) .082 (.068) .077) .073 (.210 (.049 (<LOD-. 1986).160 (.210 (.340) .068-. heptachlor.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. 1986).231) .286 (.130) .430) .115-.100-.053-.340) .400) .290-. and heptachlor epoxide in foods and bottled water. and NIOSH and ACGIH have recommended workplace exposure levels for each pesticide.063 (.258-. The major metabolite of heptachlor is heptachlor epoxide.120-..064) < LOD . IARC.230 (.320 (. dermal.270 (.150 (.560) .070-.075 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 1991.062) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * .300) . neonatal mortality.510) .269 (.240) . Survey Geometric mean (95% conf.320) . Takahashi et al.087-.083 (.180) .150 (.080 (.310) .290 (.280-. Epidemiologic studies have not demonstrated teratogenic or developmental effects (Baker et al.245-.250-.062) < LOD .060 (<LOD-.S.068) 75th .130 (.180) .250 (.140 (.216-.070 (<LOD-.180-.320 (.302) .100-.149 (.210-.130-.450) .300) .070) .130-.150 (.058 (.136) .130) .203-.110 (<LOD-.150-.380) .230-. The U.280 (.S. and breast milk is a major excretion route in lactating women.150) .220 (.100 (.140 (.230-.300) .350 (.090) .130-.070 (<LOD-.189-.170) .189 (.370 (.S.115 (.286 (. FDA established allowable residues of chlordane. Elimination of all these chemicals from the body occurs over months to years.112 (.070 (<LOD-. 1981).080) .130-.130 (.260 (.160) .063-.140-.410) .170) .104-.066 (.240 (. high doses of either chlordane or heptachlor block inhibitory neurotransmitters and result in central nervous system toxicity.063) * . 2002.270 (.047 (<LOD-.104) .063 (.280-.199-.170) . chronic doses of heptachlor have produced liver enlargement and injury.080) .048-.077) .230 (. and alterations in immune function of offspring.080) .090) .250 (. 2006).230-.220-.053-.120 (..057-.290) .180-. 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. to heptachlor. Chlordane and heptachlor are absorbed after oral.063 (.079) . characterized by seizures and paralysis.348) .146) < LOD < LOD .440) .350) .090-.230) .300 (.200-.300-. 2007).310 (. 2007.066-.160) .140) .240-.130-.073) < LOD < LOD < LOD < LOD .207) .106-. population from the National Health and Nutrition Examination Survey.225 (.057 (.227) < LOD .430) .126) . In laboratory animal studies. OSHA has established occupational exposure criteria.092) .050-.290) .080 (. Acute. Le Marchand et al.320 (. 1991).120-. Rogan.067 (.240-.119 (.290-. IARC considers chlordane and heptachlor as possibly carcinogenic to humans.063) .370 (.213) * .260-.260 (.071 (.246-.057) * .370 (. 1996. and the U.320) 663 752 595 998 1497 1383 20 years and older Gender Males 99-00 01-02 03-04 * .271 (.076) < LOD .148) .Organochlorine Pesticides (Dallaire et al.310) .063 (.110-..070-.360) . Smith.061-.200-.170-.055-.079) < LOD < LOD < LOD .207 (.077) .280-.130 (.190-.058-. and inhalation exposure.

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

9 (12.8-46.6 (8.2) 20.5 (<LOD-32.8-24.2-27.8) 21.9-23.4) 21.2-16.6. respectively.8) 14.8 (<LOD-23.9) * * * 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 8.7-25.Organochlorine Pesticides Serum Heptachlor epoxide (lipid adjusted) Metabolite of Heptachlor Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U.6) 22.8) 19.0-19.5) 598 553 460 336 503 490 539 1041 888 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.6 (12.8-24.8 (13.9-29.2) 15.3 (<LOD-25.8-24.1) 23.3-18.3) 27. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.4) 18.0-17. see Data Analysis section) for Survey years 99-00.2 (18.1) 13.0 (11.8 (15.9) 15.8) 15. and 03-04 are 14.2-17.0-16.90 (<LOD-9.3) 23.1-38.0) 13.8) 19. 84 Fourth National Report on Human Exposure to Environmental Chemicals . which may vary for some chemicals by year and by individual sample.3) 18.6-21.6 (16.8) 13.1 (16.7 (13.1-15.6 (14.8 (13.4 (11. 10.9-25.3) 22.5) 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 7.3) 18.1-29.5 (18.0 (15.50) < LOD < LOD < LOD 17. < LOD means less than the limit of detection.4 (11.2) 26.9-16.5.5 (<LOD-21.7 (16.7 (10.10-13.7-19.7-18.8) 20.0) size 1589 2259 1963 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th 90th 15.4 (15. population from the National Health and Nutrition Examination Survey.5 (11.6) 13. interval) Selected percentiles ( 95% confidence interval) Sample 95th 24.S.6 (11.4 (<LOD-19.8) 16.8-23.5 (11.5) < LOD 14.5 (10.8) 13.3) 16.6) 14.0-17.1 (19.9-29.1-16.9 (15.3 (13.20 (<LOD-9.0) 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 13.40) 15.2) 13.6 (<LOD-27.5) 19.8.2 (<LOD-16.0-54.3) 18.2 (<LOD-62.4 (<LOD-54.6-17.6 (16.3) 10.2-27.8) 14.6 (13.2 (<LOD-25. and 7.1) 20.8 (18. Survey Geometric mean (95% conf.8 (18.6) < LOD < LOD < LOD 27. 01-02.

100 (.150 (.090-.190) .170 (.111-.113) .111) .130-.170 (.190 (.140) .120 (<LOD-.108) * * * Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .090-.150 (.077-.090-.100 (<LOD-.106-.140-.097) < LOD .120-.100-.130-.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 .090-.180) 598 553 460 336 503 490 539 1041 888 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the lipid adjusted serum level.130) .090-.200) .071-.110 (.190) .200 (.126 (.110 (<LOD-.069 (.096 (.100-.120 (<LOD-.063) .180 (<LOD-.110 (.130 (<LOD-. which may vary for some chemicals by year and by individual sample.108) .113-.100 (.310) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.190) .090 (.130-.130 (.150 (<LOD-.120 (.S.130-.082-.100 (.135 (.170) .108-.107-.087 (.110) .161) size 1589 2259 1963 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th 90th .104) .090 (<LOD-.170) .380) .149) .094 (.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.076-.170 (.070-.130) .133 (.053-.170 (<LOD-.180) .270) .180) .110 (<LOD-.170) .074-.128 (.098 (.135 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th .200) .140) .310) .157) .116) < LOD < LOD < LOD .110-.067-.101 (.180) .120) .101 (.055 (<LOD-. Survey Geometric mean (95% conf.063) < LOD < LOD < LOD .110) .180) . population from the National Health and Nutrition Examination Survey.117) .120) .240) .180 (.100 (.057 (<LOD-.094 (.090-. Fourth National Report on Human Exposure to Environmental Chemicals 85 .110-.077-.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 .220) .

8-19.8-79.1 (10.1) 17.1) 18.9-65.7) 17.4-35.3) 32.5-36.7) 14.10 (<LOD-11.1) 16. population from the National Health and Nutrition Examination Survey.0) 19.6 (52.3) 18.8-16.7) 59.8-77.6 (56.1) 17. interval) 18.2-21.6 (16.7) 56.9) < LOD < LOD < LOD 20.9-89.2 (64.5) 36.8-41.9-58.7-22.5) 90th 55.8 (12.0) 33.2 (27.1-126) 67.7-38.4 (12.3-32.8 (26.7 (74.8 (28.3-50.9 (66.7-20.4) 19.4 (11.1 (41.1-34.0) < LOD < LOD 8.0) 75th 31.9 (51.4-52.8 (15.7-77.8 (13.0-38.2 (7.4 (16.6) 82.2) 59.9 (15.9 (51.9 (28.6-19.2) 30.9 (16.5) 14.8 (28. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.7-21.4) 55.7 (13.1 (48.6 (32.0-123) 74.3) 30.0 (16.1) 17.2 (15.9-35.0-23.7) 52.0-93.3-58.7) 78.8) 51.1) 31.5-87.9 (36.3-74.9) 14.3 (16.3-39.9 (19.4) 20.8 (28.0) 49.5) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * 20.2) 19.5) 19.3) 15.2-88.9-22.0-22.7) 78.6) 10.5-20.7-17.1-16.3) 16.0-143) 112 (68.1-51.4) 107 (84.8-110) 59.1) 17.4 (30.3-30.9 (<LOD-14.2 (19.8 (49.3 (58.6 (57.3) 30. 01-02.6-22.1-28. 10.0-37.9-45.5) 30.9) 922 1062 955 1011 1224 1000 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 * 11.0 (15.0 (48.7-160) 86.9-65.8-129) 74.0-68.5 (13.0-59.8 (19.2) 39.2-18.4 (67.1-22.3) 36.7) 15.2) 20.9-20.6) 56.0-20.1) 30.4-18.5) 77.4) 48.6) 60.4-67.1-55.7 (11.0-93.8-19.7-35. and 03-04 are 14.0-113) 68.0-23.86-13.6 (12.3 (49. respectively.7 (16.1 (65.4) 59.5 (45.3-57.5.8 (30.3-86.7 (30.5) 14.8-16.5-95.9-69.1) 17.0 (13. < LOD means less than the limit of detection.8) 19.7-32. and 7.1-20.2 (60.0 (62.3-21.8-67.2 (59.1) 14.8 (11.5-111) 68.5) 20.0 (29.9 (29.0) 18.3 (45.1) 17.4-23.0-24.5) 35.7-18.3) 25.3 (56.2 (14.9 (15.5-19.8 (16.5 (25.7-113) 68.5 (44.2 (25.1-16.6-20.7) 35.8 (17.6-54.6) 34.2) 34.7-34.0 (15.6-88.5) 26.7 (59.9) 51. Survey Geometric mean (95% conf.7) 28.0) 664 758 589 1269 1528 1366 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 17.0 (60.0) Selected percentiles ( 95% confidence interval) Sample 95th 79.6) 54.5.4-22.2 (26.3 (14.7-29.6 (50.0) 40.2-23.4 (45.9-40.8 (42.4 (28.6 (<LOD-14.8 (26.9) 51.8 (71.3 (17.0 (16.0) 13.6) 25.9) 14.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 (28.5-69.5) 78.2) < LOD 10.8-90.2-16.8 (<LOD-20.9 (47.1) 62.0 (14.5) 22.4) 16.6) 84.3) 32.8 (45.6-66.7 (35.5) 9.8.6-82.5-17.0 (42.4-36.2 (14.0 (13.4-62.3 (14.1) 18.6 (56.0 (19.5 (15.7 (18.0 (42.3) size 1933 2286 1955 Total years 99-00 01-02 03-04 50th 17.S.9-36.8 (26.6 (15.9-64. see Data Analysis section) for Survey years 99-00.3) 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.1) 78.8 (13.1) 17.8) 47.1) 32. 86 Fourth National Report on Human Exposure to Environmental Chemicals .7 (59.1-34.2 (36. which may vary for some chemicals by year and by individual sample.3) 19.3) 18.1 (22.1-18.7) 73.5) 48.1 (47.2) 17.2-18.1 (17.2-17.7-23.1) 78.6) 56.5 (15.6) 13.2-37.8-21.8) 80.70 (<LOD-12.8-90.

120 (.580 (.099-.286-.120 (.343 (.054-.191 (.069) .510-.230 (.210 (.131) .470-.110 (.260) .130) .414 (.098 (.460) .100-.092 (.060 (<LOD-.240) .128 (.327 (.405) .550 (.395-.640 (.096-.470 (.145-.170 (.240) .310-.330-.684) .300) .270-.130) .130) .120) .430-.105 (.079-.109 (.250) .440) .840) .110 (.370 (.180-.080-.450) .091-.186 (.220) .210) .108 (.100) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * .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.090-.220 (.390-. which may vary for some chemicals by year and by individual sample.240 (.112 (.070 (.360-.237) .520 (.134) .409-.760 (.220 (.190-.470-.310 (.490) .085-.397-.160-.400-.090-.350 (.112 (.100-.220 (.590 (. interval) .084-.098-.260) .130 (.580 (.180-.320-.630) .565) .120-.158-.250) .130) .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.202 (.080-.210-.119) < LOD < LOD < LOD .350-.310) .171-.085-.580 (.520) .161) .680 (.090 (<LOD-.119) Selected percentiles ( 95% confidence interval) Sample 95th .130) .183 (.120 (.400 (.417 (.690) .100 (.190-.288 (.090-.330 (.068-.480) .390) .290-.370 (.130) .242) .470 (.390 (.367) .310-.150) .093-.141) .060) .830) .390 (.190-.490 (.110 (.410-1.124) .099-.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 .093) . population from the National Health and Nutrition Examination Survey.210 (.095-.458 (.080-.080 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.085-.062 (.109 (.110) .380 (.090-.135 (.090-.127) < LOD < LOD .130 (.186-.160 (.395) .410-.300-.500) .430-.430-.340-.590) .20) .122) .080) .565) 922 1062 955 1011 1224 1000 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 * .690) .111 (.558) size 1933 2286 1955 Total years 99-00 01-02 03-04 50th .470 (.055 (<LOD-.240) .108) .093-.082) .310-.108) 75th .079-.081 (.110 (.220 (.317 (.830) .078-.930) .340) .061-.301-.100 (.559) . Survey Geometric mean (95% conf.210-.510 (.120-.285-.S.090) .210) .240-.104-.310-.400-.600 (.110 (.220 (.540) .800) .594) .234) .092 (.573 (.390 (.103 (.960) .173-.041 (<LOD-.116 (.210) .103 (.440-.093-.232) .490 (.106 (.060-.324 (.120) .460-.080-.126) .110-.114) .330-.106 (.096-.630) .490-.104 (.280) .461 (.190-.177-.130) .071 (<LOD-.111-.069-. Fourth National Report on Human Exposure to Environmental Chemicals 87 .125 (.117) .078 (.091) .272-.100-.220 (.400 (.190-.161-.098) .190-.089 (.320-.279-.590 (.113) < LOD .400) .094 (.680) .081-.140) .220 (.390 (.371) .520 (.141) .600) .129) .180-.390) .630) .120) .090 (.125) .100-.106 (.205 (.122) .460) .420 (.237) .497-.420) .097) .150) .220 (.110 (.096) .288-.360-.355 (.651) .210 (.090-.120) .340-.047-.116-.116) .120-.087 (.098 (.250) .113) .211) 90th .

Natl Cancer Inst Carcinog Tech Rep Ser 1977a.pdf.niehs. Available at URL: http://ntp. 2001. 1986. Tartter P. 1963-1967. organochlorine pesticides and polybrominated diphenyl ethers in human umbilical cord serum. Takahashi W.html. Bjerselius R. A Report to the Hawaii Heptachlor Research and Education Foundation. Organochloride pesticide residues in human milk in Hawaii.111:349355. Jr and Laws ER. 4/21/09 Baker DB. 1994-1997 organochlorine compounds. Environ Health Perspect 2002. Siegel BZ. 1991 pp. Concise International Chemical Assessment Document 70 Heptachlor [online]. Handbook of Pesticide Toxicology.nih.gov/toxprofiles/tp31. Evaluation of human exposure to the heptachlor epoxide contamination of milk in Hawaii. Determinants of serum polychlorinated biphenyls and organochlorine pesticides measured in women from the child health and development study cohort. KalubaSkotarczak A. Vol. Aune M.atsdr. Natl Cancer Inst Carcinog Tech Rep Ser 1977b. Organochlorines in Swedish women: determinants of serum concentrations.330:55-70. Toxicological profile for heptachlor and heptachlor epoxide [online].htm. Mortality of workers employed in the manufacture of chlordane: an update. New York.html. Hawaii Med J 1991. Voorspoels S. Ayotte P. J Occup Med 1986. 88 Fourth National Report on Human Exposure to Environmental Chemicals . Darnerud PO. An evaluation of serum pesticide residue levels and liver function in persons exposed to dairy products contaminated with heptachlor. Senie R.372:20-31.150:981-990. Gilman A. Estimation of Human Exposure to Heptachlor Epoxide and Related Pesticides in Hawaii. Available at URL: http://ntp. Smith AG. Eds. et al.28:497501. Atuma S. Baker DB. Van Oostdam JC. Pollutants in breast milk. Dewailly E. 6/1/09 National Toxicology Program (NTP). Berkowitz GS. Glynn AW. Trends in birth defects for a Hawaiian population exposed to heptachlor and for the United States. Drews K. et al.html. Takei G.gov/ntp/ htdocs/LT_rpts/tr009.Summaries & Evaluations. Circumpolar maternal blood contaminant survey.nih.8:1-123. LeMarchand L. Chlordane and heptachlor [online]. Lulek J.org/ documents/cicads/cicads/cicad70. Arch Pediatr Adolesc Med 1996. Academic Press. Kolonel LN. Toxicological profile for chlordane [online]. 1993. JAMA 1988. Hansen JC. Lawrence River (Quebec.inchem.cdc. Environ Res 2000. Jaraczewska K. Distribution of polychlorinated biphenyls. Arch Environ Health.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Bleiweiss IJ. 6/1/09 Rogan WJ. Organochlorine exposures and breast cancer risk in New York City women. Saidein D. Charles MJ.heptachlor. Granath F. Wohlleb JC. Hertz-Picciotto I. 1979-1980. Keller JA.84:151-161. Jr. 731-915. May 1994. Stehr-Green P. Bioassay of heptachlor for possible carcinogenicity. Inc. Canada).gov/ntp/ htdocs/LT_rpts/tr008. 2006.110(8):835-838.cdc. Sci Total Environ 2004.pdf. International Agency for Research on Cancer (IARC). National Toxicology Program (NTP). Available at URL: http://www. Available at URL: http://www. maternal serum and milk from Wielkopolska region. Loo S. Available at URL: http://www. Shindell S and Ulrich S. Bull Environ Contam Toxicol 1981:27:506-511. August 2007. Royce W. Head SL. Brower S. Dewailly E. Wong L. Covaci A. Sci Tot Environ 2006. 4/21/09 Dallaire F. Environ Health Perspect 2003.9:1-109. 79. Chlorinated Hydrocarbon Insecticides. 2 Classes of Pesticides.inchem.org/site/foundation/ research/projects2. 4/21/09 Agency for Toxic Substances and Disease Registry (ATSDR).htm.110:617-624. Environ Health Perspect 2002.259(3):374-377. Bioassay of chlordane for possible carcinogenicity.50(3):108-118. Temporal trends of organochlorine concentrations in umbilical cord blood of newborns from the lower north shore of the St. Vol.atsdr. et al. et al.org/documents/iarc/ vol79/79-12.41:145–148. 4/21/09 James RA. Laliberte C.niehs. Poland. 9/25/07 International Programme in Chemical Safety (IPCS). In Hayes WJ. Available at URL: http://www. Chashchin V. Wolff MS. gov/toxprofiles/tp12. Odland JO. Muckle G. Dendle WH. Willman E. Available at URL: http://www. Barker J. International Agency for Research on Cancer (IARC) .

2) 30. 17. inhalation. fish.6 (22.8-23. sediments.5 (14.9) 17.S.7 (19.6 (31.7) 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. DDT was used at one time as a treatment for head and body lice.p’-DDT (65%-80%).8-26.3) 21.1 (<LOD-39.0-53.2 (11.2 (<LOD-40.70 (8.7) < LOD 18. 2002. population.3) 28. and water.6-33.0) 19. In the general U. 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.3 (<LOD-31.5 (23.9-34.5) < LOD < LOD 9. resulting in fetal exposure. 1988).9 (<LOD-20.1) 31.0-35. which is a mixture containing p.1’-(2.10 (<LOD-12. continues to be the primary source of DDT exposure. Smith.4.3) 22.9 (10. particularly for endemic vector and malaria control.5 (15.8) 36. Food imported from countries that still use DDT may contain the chemical or its residues. and 03-04 are 20.90 (<LOD-12.10-13.2-65. 1991).3-590) 293 (104-541) 48.0-155) 83. Fourth National Report on Human Exposure to Environmental Chemicals 89 .0-15.0) 26.0-27.8-17. and trace amounts of several related compounds. DDT and DDE can cross the placenta.0 (10.1) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 12. These chemicals are highly persistent in soil.9) < LOD < LOD 9. population from the National Health and Nutrition Examination Survey.5) 25.3-16. interval) Selected percentiles ( 95% confidence interval) Sample 95th 28.2) 155 (59.7) 12. DDT and DDE are distributed to all body tissues with the highest concentrations found in adipose tissues (ATSDR.S. o.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 8.8-39. It is still used in some countries. DDT usually refers to the technical product. It was produced and used in the U.1’-dichloro-(2.9 (10.9 (10.0 (21.Organochlorine Pesticides Dichlorodiphenyltrichloroethane (DDT) CAS No.2-dichloroethenylidene)-bis[4-chlorobenzene] (DDE) and 1. 2008. food.1-71. when virtually all use of it was banned. air.2) < LOD < LOD 9.0 (18.7. p.9-28. see Data Analysis section) for Survey years 99-00. Both Serum p.S. including 1.9) 29.1 (23.5 (23.0) 40. respectively.50-11. 01-02.3 (27. and dairy products.9 (21.4) < LOD 17. < LOD means less than the limit of detection.9) 14. The biodegradation half-life of DDT in soil varies from 2 to 15 years.7 (15.5-54. after World War II until 1972. DDT is converted to DDE and several other metabolites. as well as in plant and animal tissues. depending on conditions.8. or dermal exposure.4 (23. In the body.5) size 1679 2305 1965 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * * 11.0) 20.7-16. 1991).8) 30. which may vary for some chemicals by year and by individual sample.3-236) 24.p’-DDD (4% or less).0-37. particularly meat.00 (<LOD-10.p’-DDT (15%-21%).0 (18.3 (<LOD-21.6 (<LOD-25. DDT can be absorbed after ingestion. DDT is converted in the environment to other more stable chemical forms. and 7.6 (25.1 (33.5) 23. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.8) 15. although DDT and DDE intakes have decreased over time (FDA.1-27.5-36.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) 635 566 461 356 514 490 564 1061 890 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. Survey Geometric mean (95% conf.2-95.6 (9. Gunderson.2-bis(p-chlorophenyl) ethane (DDD).4) < LOD < LOD < LOD 61.3) 21. Only a small proportion of DDT is metabolized and excreted (Smith.

2001). 2001).170-. 2006).201 (.627) .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 . both DDT and DDE may induce specific cytochrome P450 isozymes (Nims et al. 2006.065-. 1997). and leukemia have also been inconclusive (ADSDR. polychlorinated biphenyls. 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. fertility. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.26) 1.075) 1.Organochlorine Pesticides chemicals are excreted in breast milk. reproductive organ abnormalities. Human health effects from DDT at low environmental doses or at biomonitored levels from low environmental exposures are unknown.343) < LOD . Hayes et al.530) .01) .150-.071-.. 2002.230) .170) .150 (<LOD-.142 (..180) .. population from the National Health and Nutrition Examination Survey.190 (.. although the risk for preterm delivery may be related to maternal DDE levels (Longnecker et al.054-.150) .130-.069) .180-. other organochlorines.074-.S.130 (<LOD-. Jusko et al. interval) Selected percentiles ( 95% confidence interval) Sample 95th .p’-DDD and p..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.051 (<LOD-. A workplace standard for DDT has been established by Serum p. tremor.250-1. and altered behavior after neonatal exposure (Eriksson and Talts.098-.106) < LOD < LOD . Longnecker et al. 2002. 1995. 1998).063 (<LOD-. 2002. accidental exposures.079) < LOD < LOD .220) ..120-.048 (<LOD-.330-4. Survey Geometric mean (95% conf.260) . dioxins and furans).180 (. 2001).128 (. Gladen and Rogan. Mariussen and Fonnum.140-.061) < LOD < LOD < LOD .g. In laboratory animals.420) .068-..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 . In high dose.087 (. 1956).146 (. lung cancer. resulting in exposure to nursing infants (Rogan. 2004. It is difficult to attribute outcomes in human studies solely to DDT because of potential co-exposure to other persistent organohalogen chemicals (e. 2000. 1996). premature delivery.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.400 (. Calle et al.078 (.064 (. DDT may bind to estrogen receptors (Chen et al.120 (<LOD-. Animal studies reported reduced fertility..240 (. and duration of lactation. 2001)..200 (.290) .220) . Snedeker.167) size 1679 2305 1965 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * * . Beard.132-.250 (..059-.400) . Studies of DDT exposure and pancreatic cancer. Reproductive effects in humans affecting birth weight.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 ..130 (<LOD-.071 (. and o.105-. Gray et al. Jusko et al.189-.180 (. 90 Fourth National Report on Human Exposure to Environmental Chemicals .240) .180) .146 (.570-4. Epidemiologic studies of children with environmental exposure to DDT and DDE have not demonstrated neurologic or developmental abnormalities (Gladen et al.00) ..313 (.34) .086 (. 2006.170 (.150-.112 (.160-. 2006). Several reviews of cancer epidemiologic studies have concluded that a link between DDT and breast cancer is inconclusive (Beard. 2002. 2006.140) .p’-DDE can produce anti-androgenic effects (Gray et al.00 (. have not been consistently demonstrated (Beard.143) < LOD < LOD .080-.190-1.095) < LOD .130 (<LOD-.114-.530 (.190 (.108 (. which may vary for some chemicals by year and by individual sample.150 (<LOD-.106) .203) .106-.084 (.230) . overt signs of acute human toxicity include vomiting.078-.62 (. and seizures. 2006).

1998..html.S. IARC classifies DDT (p. see Data Analysis section) for Survey years 99-00. EPA at: http://www. so serum DDE levels may be an indicator of historic exposure and may be higher than DDT levels in the same person. 2003). environmental levels) and health effects is available from the U. mean DDE levels were about fivefold higher among women of southern Spain exposed by virtue of Serum p. 1989). More information about external exposure (i.Organochlorine Pesticides OSHA and a guidance established by ACGIH.3.. 2004). Stehr-Green. NTP considers DDT as being reasonably anticipated to be a human carcinogen. In general.. population declined by about fivefold to tenfold. Heudorf et al.e. and 03-04 are 18. population from the National Health and Nutrition Examination Survey. Smith. respectively.cdc. 2002. In a population-based sample of men and women from eastern Slovakia. and the most recent median levels for German adults and children are similar to levels in this Report (Becker et al. Biomonitoring Information DDE persists in the body longer than DDT.. 1991).. compared to levels observed in this Report (Anderson et al. 8. 2005).6 (81.p'-Dichlorodiphenyldichloroethene (DDE) (lipid adjusted) Metabolite of Dichlorodiphenyltrichloroethane Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U. Compared to females in the NHANES 1999-2000 subsample. mean serum levels of DDT and DDE in the U.atsdr.7-129) 297 (256-344) 338 (303-376) 268 (217-332) 108 (97.S.gov/ toxpro2. the lipid-adjusted geometric mean levels of DDT and DDE were each fivefold to tenfold higher than the 95th percentile and geometric mean levels.p’-DDT) as a possible human carcinogen. Link et al. 01-02.gov/ pestcides/ and from ATSDR at: http://www. and 7.S.. 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 (84.0-114) 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..8. levels of DDT and DDE increase as a person ages as a result of cumulative exposure (ATSDR. Declining DDE levels over time have also been observed in the German population.. Since the 1970’s. 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. 2002. Survey Geometric mean (95% conf. respectively. 2003.7-119) 113 (100-140) 93. 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. for males and females in the NHANES 19992000 subsample (Pavuk et al.epa. 2004).6. Fourth National Report on Human Exposure to Environmental Chemicals 91 .

29 (1.71 (6.9-38.25) 8.23 (7.81 (7. 2001-2002 and 2003-2004 subsamples.39-1.14) 2.55-9.58) 1.56-3.80) 1.68-4.63-15.76) 1.6) 9.66) 4.4) 14.32-1.36 (3.9 (26. Survey Geometric mean (95% conf.13-2.9) 5.21) 3.01-15.00) 7.44) 1.34) 2. o.820-1.12-1.14) 2.726) .6) 9.26-2.54 (1.72) 1.01-5.58) 75th 3. 1971).12 (.6 (9.63 (1.26) 3.36-2.30 (1.54-7.99) 1.1) 7.3) 16.40-8.77 (1.66-17..51-15.2 (9.p’-DDT.71) 12.85-4. 309 versus 268 ng/g lipid.18) 1.2 (6.40 (3.0) size 1964 2298 1956 Total years 99-00 01-02 03-04 50th 1.1) 40.5) 5.7) 13. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.963-1. serum levels of o.02 (2.26 (1.57 (1.63 (6.69 (.18-1. Finding a measurable amount of p.25-16.17 (3. 2004).17-3.10-1.37-16.34 (7.430-.91-3.96) 1.2-32.890-1.69 (2.0 (9.07 (5.57 (3.24) 1.41 (1.69 (1.557) 1.31-12.1) 12.57 (1.75) 6.39-2.2) 19.12 (6. or p.30-1.Organochlorine Pesticides nearby agriculture (Botella et al.5) 10.79) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 .06) 3.88 (2.37-1.488-.75 (4.43-8.19-14.57) 2.52 (3.51) 1.3 (9.69) 4.52 (1. 1991).31-2.2 (19.90) 22.10) 2.37-4.60-13.34) 6.9-17.16-1.71 (5.18-4.97-4.19) 4.84 (3. Serum p.18-1.456 (.01-11.28) 1.51-49.500-.13) 4.87-16.14-1.51-8.p’-DDT.70-3.8 (13.43-4.32-1.490 ng/L) were found many years ago in a study of pesticide workers in Argentina (Radomski et al.80) 3.6 (7.66) 1.81-18.01-1.1 (8.78 (4.56-6.3) 10.05) 1.p’-DDE in serum does not mean that the level of the chemical causes an adverse health effect.24-17.76 (2.6 (17.600) .6) 9.59 (1.01) 1..796 (.40-4.75) 2.01) 1.66) 3.91 (6.24 (1.26-10.69) 8.8-90.635) 1.38 (1.00 (.4) 13.88-35.50 (2.22-1.02) 1.7-48.2) 26.25 (1.14 (1.4 (8.21) 90th 7.46-2.p’-DDT (Stehr-Green.34-11.36-1.561 (.45 (1.71) 32.53) 7.93 (7.04-1.646) .80) 1. which is similar to the overall geometric mean of 260 ng/g lipid in the NHANES 1999-2000 subsample (Bloom et al.32 (1.S.20 (.32-9.84-3.54) 8.01-11.49 (6.68 (2.64-2.3) 13.50-17.35) 1.6) 11..85 (1.47 (1.66-4.00-1.590 (.7 (8.32) 1.65) 1.75) 1.05 (3.37-10.79) 4.57-3.49 (1.07) 1.22 (7. 2004).13 (1.81) 11.76) 1.61 (1.85-10.48 (6.730) .55 (2.70) 1.75 (8.6) 12.36-11.25-14.7-19.49 (1.623 (.40-4.43-4.18 (6.61-2.3 (8.51) 3.11 (2.870 (.34-3.31 (1. considerably higher than levels in this Report (Smith. High mean levels of whole blood DDT (about 3.9) 7.15-4.58) 1.91) 3.79) Selected percentiles ( 95% confidence interval) Sample 95th 11.9 (15.65 (1.57-13.97 (3.3-43.11-1.39) 1.83 (1.51 (1.385-.4 (12.611-1.8 (14. population from the National Health and Nutrition Examination Survey.6) 8.5) 22.7-20.8 (13.77 (1.46 (1.p’-DDT were below the limits of detection.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 .92) 1.860 ng/L) and DDE (about 14.57-2.68) 2.09-1.81-5.53 (2.32 (1.8) 15.91-2.14-9.82) 1. Workers involved in production or application of DDT developed neurologic abnormalities associated with blood levels around 100-300 mg/L.680-1.07) 1.27) 3.6) 9.96) .64) 3.59) 6.7) 9.39 (3.10-5.1 (9.00 (6.4-19. interval) 1.0 (12.965-1. 1989).63 (1.03-4. 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.92 (3.41-12.516 (. In the NHANES 1999-2000.25 (. 2005).72) 1.76-3.8 (9.82 (1.53-15. Consumers of Great Lakes sport fish had mean serum DDE levels that were only slightly higher than nonconsumers.6) 13.5) 7.06) 1.56-2.59) 3.80 (2.66) 1.59 (1.43 (5.3) 937 1069 955 1027 1229 1001 Females 99-00 01-02 03-04 Race/ethnicity Mexican Americans 99-00 01-02 03-04 3.92 (3.6 (8.2 (9.90-8.0) 2.52-6.49) 8.45 (1.04 (6. less than one percent had detectable serum levels of o.16 (2.38 (1.59 (4.994-2.47) 3.25) 1.56) 2. In a subsample of NHANES II (19761980) participants.22) .534-.5) 16.87 (5.10) .36) 3..520 (.30 (1.37 (1.48-4.62-6.30-1.02-8. 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.46 (1.419-.81 (1.p'-Dichlorodiphenyldichloroethene (DDE) (whole weight) Metabolite of Dichlorodiphenyltrichloroethane Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U.03-1.33-1.18-3.27-1.8) 686 758 588 1278 1540 1368 20 years and older Gender Males 99-00 01-02 03-04 1.7) 16.4) 9.01-1.53) 1.66-2.

01-02.7. 17. 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. Fourth National Report on Human Exposure to Environmental Chemicals 93 .S. population from the National Health and Nutrition Examination Survey. Survey Geometric mean (95% conf. which may vary for some chemicals by year and by individual sample.Organochlorine Pesticides Serum o.p'-Dichlorodiphenyltrichloroethane (lipid adjusted) Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U. see Data Analysis section) for Survey years 99-00. and 7. and 03-04 are 20. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. < LOD means less than the limit of detection.4.8. respectively.

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

html. Parks L. Darnerud PO. et al. Int J Hyg Environ Health 2003. Willman EJ. dichlorodiphenyldichloroethylene. Saiyed HN. Vorojeikina DP. Maternal DDT exposures in relation to fetal and 5-year growth. and dichloro(diphenyl)ethylene (DDE).html. Gray KA. Jr. Association between maternal serum concentration of the DDT metabolite DDE and preterm and small-for-gestational-age babies at birth. Buckland SJ. DDT and human health. Biomonitoring of persistent organochlorine pesticides. Greenfield TA. Rogan WJ. Biochem Pharmacol 1997. Beard J. et al. et al. Angerer J. Durham WF. Calle EE.52:301-309. 4/21/09 Gladen BC.21(1-2)37-48. and Mirex among male Lake Ontario sportfish consumers: the New York State Angler cohort study. Maternal serum level of 1. Kulkarni PK. Koepsell TD. selected elements. Environ Res 2005. Food and Drug Administration (FDA). Hurd C. Available at URL: http://www. India.58:1185-1201. DDE and shortened duration of lactation in a northern Mexican town. Environ Health Perspect 2004. Barr DB.162:890-897. Davis MD. Schulz C. Paepke O. Bates MN. Furr J. Neonatal exposure to neurotoxic pesticides increases adult susceptibility: a review of current findings.17(6):692-700. Bhatnagar VK. et al. JAMA 1956. Zhou H. Frumkin H. Kaus S. et al. Ellis H. Needham LL. Arnold SF. Organochlorines and breast cancer risk.atsdr. Exposure of women to organochlorine pesticides in Southern Spain. Olson JR. Longnecker MP.1-dichloro2.72:261265. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. hypospadias.71(6):1200-1209. Piechotowski I. Seiwert M. Prenatal DDT exposure in relation to anthropometric and pubertal measures in adolescent males. August 2008. Becker K. Cueto C. Herrman T. Granath F. Effects of environmental antiandrogens on reproductive development in experimental animals. Zaidi SS. Transcriptional activation of the human estrogen receptor by DDT isomers and metabolites in yeast and MCF-7 cells.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR).cfsan.111:349355. FDA total diet study. Link B. Longnecker MP. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003.358:110-114. Current internal exposure to pesticides in children and adolescents in Germany: blood plasma levels of pentachlorophenol (PCP). Baker RJ. Moysich KB. Chemosphere 2005. Gabrio T. September 2002. Needham LL. Gray LE Jr. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Am J Public Health 1995. and other chemicals. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. and polythelia among male offspring. Vena JE.fda. Hediger ML. Rivas A. Lepom P. Brock JW. Neurotoxicol 2000. 4/21/09 Anderson HA. et al. Charles MJ. et al. Am J Epidemiol 2002. The Great Lakes Consortium. Profiles of ortho-polychlorinated biphenyl congeners. Burse VW. Int J Hyg Environ Health 2002. Jr. Environ Res 2004.355:7889. Needham LL. and HCB residues in human blood in Ahmedabad.155(4):313-322. HCH. Chemosphere 2004.. Hum Reprod Updat 2001. Fourth National Report on Human Exposure to Environmental Chemicals 95 . Patterson DG Jr. Hayes WJ.106(5):279-289. Organochlorines in Swedish women: determinants of serum concentrations. Notides AC. Chen CW. Brock JW. Eriksson P. Levels of DDT.205:297-308. Environ Health Perspect 2003. Drexler H. Cerrillo I. Glynn AW. Henley SJ. Lambright C. J Assoc Off Anal Chem 1988. et al.54:1431-1443.96:34-40. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. Bull Environ Contam Toxicol 2004.112(17):1761-1767. lindane (g-HCH). Lancet 2001. Bloom MS. Katz SH. April 1982 to 1984. Garrett N. Falk C. Sci Tot Environ 2006. Kashyap R. Klebanoff MA. Klebanoff MA. Zhou H. Olea-Serrano MF. Toxicological profile for DDT. Ostby J. Available at URL: http://www. Zoellner I. Savitz DA. Atuma S. Wolf CJ. Talts U.85:504508. DDE. Bjerselius R.206:485-491. Heudorf U. Aune M. Epidemiology 2006.gov/~dms/ pesrpts. et al.gov/ toxprofiles/tp35. The effect of known repeated oral doses of chlorophenothane (DDT) in man. Hanrahan L. hexachlorobenzene. Thun MJ. Krause C. Olson J. Gladen BC. Gunderson EL.53(8):1161-1172.97(2):178192. Botella B. Klebanoff MA. Jusko TA.2-bi(p-chlorophenyl)ethylene and risk of cryptorchidism. Olea N. a biostable metabolite of dichloro(diphenyl)trichloroethane (DDT). Crespo J. and DDD [online]. Swanson MK. CA Cancer J Clin 2002. Environ Health Perspect 1998. dietary intakes of pesticides.7(3):248-264.cdc.

Pesticides and breast cancer risk: a review of DDT. PA. Lubet R. 96 Fourth National Report on Human Exposure to Environmental Chemicals . Blood levels of organochlorine pesticides in Argentina: occupationally and nonoccupationally exposed adults. In Hayes WJ. Arch Pediatr Adolesc Med 1996. and dieldrin. Demographic and seasonal influences on human serum pesticide residue levels. DDE. Handbook of Pesticide Toxicology. Nims R. Pollutants in breast milk. 1991 pp. Fox S. Pavuk M. Chemosphere 2004.150:981-990. and DDD in male rat liver and cultured rat hepatocytes. Environmental exposure to PCBs and cancer incidence in eastern Slovakia. Rey AA. Schecter A. Vol.20(2):186-193. Astolfi E. Neurochemical targets and behavioral effects of organohalogen compounds: an update. Chlorinated Hydrocarbon Insecticides. Rogan WJ. Jr. Fonnum F.109:35-47. DDE. 731-915. et al.27:405-421. Lynch CF.54:1509-520. Smith AG. Chovancova J. Eds. Toxicol Appl Pharmacol 1971. Jones CR. New York. Radomski JL. Academic Press.Organochlorine Pesticides Mariussen E.36:253-589. Petrik J. Crit Rev Toxicol 2006. Environ Health Perspect 2001. Thomas PE. Comparative pharmacodynamics of CYP2B induction by DDT. Inc. J Toxicol Environ Health 1989. Deichmann WB. Cerhan JR. Reddy AB. Jr and Laws ER. Snedeker SM.53:455-477. et al. Stehr-Green. 2 Classes of Pesticides. children and newborn infants. J Toxicol Environ Health Part A 1998.

30 (<LOD-6. inhalation or dermal exposure routes.S. which may vary for some chemicals by year and by individual sample.40-5.20 (<LOD-5.40 (<LOD-6.40) < LOD 547 433 487 446 1000 831 Limit of detection (LOD. Hepatic effects of endrin exposure have included necrosis. fatty infiltration. Skeletal abnormalities and cleft palate in the offspring were associated with endrin when it was fed to pregnant laboratory rodents (Chernoff et al.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. largely the result of historical agricultural application or run off from contaminated soils (ATSDR. a stereoisomer of dieldrin. population from the National Health and Nutrition Examination Survey. Survey Geometric mean (95% conf. At high doses.50) < LOD < LOD < LOD 5. anti-12hydroxyendrin. IPCS. EPA. have been cancelled by the U. Further conversion occurs to 12-ketoendrin and various conjugated metabolites which are excreted in urine and feces. All uses of the pesticide in the U.S. Endrin was not widely used as a termiticide.. unlike aldrin and dieldrin. rodenticide and avicide. endrin usually is not detected in serum of exposed individuals.8. 1981). Over time. Ketoendrin is a major photodegradation product (IPCS. manufactured. 1992). 1992). or from contact with contaminated soils and sediments in areas where endrin was applied.. 1979. Depending on soil conditions. < LOD means less than the limit of detection. High doses produced renal tubular necrosis and diffuse kidney degeneration in animals. interval) Selected percentiles ( 95% confidence interval) Sample 95th 5. and inflammation (Smith. Endrin was used as an insecticide.10 (<LOD-5.S.. Serum Endrin (lipid adjusted) Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U. endrin blocks inhibitory neurotransmitters in the central nervous system resulting in excitation and seizures (Narahashi et al. endrin can persist for years.Organochlorine Pesticides Endrin CAS No. 2008). see Data Analysis section) for Survey years 01-02 and 03-04 are 5. endrin is converted rapidly to its major metabolite. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.09 and 7. or discarded. unless the dose is high and the exposure is very recent.S.40) < LOD size 2187 1825 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 03-04 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 5. An epidemic of acute endrin poisoning. total diet surveys (FDA.50) < LOD 5. General population exposure can occur after ingestion of endrin residues on food items imported from countries where endrin is still used. is no longer manufactured in the U.30) < LOD 5. endrin has been detected with declining frequency in U.S.60 (5. 1991).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. Because it is metabolized so rapidly. Fourth National Report on Human Exposure to Environmental Chemicals 97 . 1992). Human health effects from endrin at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 1992. Kavlock et al. Endrin does not accumulate in body tissues (IPCS. Endrin has been detected in soils.. characterized by generalized seizures in previously healthy persons occurred in Pakistan when sugar contaminated with endrin was ingested (Rowley et al.10 (<LOD-5. 72-20-8 General Information Endrin. 1996.20 (<LOD-5. In the body. Endrin is absorbed rapidly after ingestion. and occasionally at low levels in sediment and surface waters. 1991). 1987). Smith.

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

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

9-20.2 (14.S. see Data Analysis section) for Survey years 99-00.6-33.0-16.6-19. Urinary metabolites include pentachlorophenol (PCP).1 (14. particularly by consuming fish.2 (14.7-29.9) < LOD < LOD 16.5-15.5-14.S.5-trichlorophenol (2. wildfowl.4. Hexachlorobenzene has entered the environment as a result of industrial activities and pesticide applications. 2002).4. EPA cancelled its use in 1984.7-26.9 (25.1-20. primarily as a fungicide and seed treatment until the U.8.9 (25. and accumulates in fatty tissues where it persists for years.6-32.4) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * 13. Gunderson.3 (12.4 (18.1 (13.9-30. Therefore.0.6) < LOD < LOD 14. water. and has been detected in soil.7) < LOD < LOD 75th < LOD < LOD 90th * * 15. < LOD means less than the limit of detection.3 (22. HCB may be created as either a byproduct or an impurity in the manufacturing process for certain chemicals and pesticides. or game taken from areas with HCB contamination.6) < LOD < LOD 26.. 2008.9) < LOD < LOD 28. 01-02.1 (14.4 (18.8 (26. 1988).7 (19.3) 24.7-21.7 (15. 100 Fourth National Report on Human Exposure to Environmental Chemicals .2 (17.2) < LOD < LOD 13.2 (24. 31. distributes widely throughout the body. breast milk is an additional route of elimination in nursing women. air.1) < LOD < LOD 15.3) * * 15.0 (25.8 (15.5-15.0 (18. 2.3 (14.4.4-15.7 (27. Survey Geometric mean (95% conf.9-17.5-14.S. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD 28.0) < LOD < LOD 24.0) * * 15.1) * * 15.3) < LOD < LOD 29.6 (23.5) < LOD < LOD 18.4) < LOD < LOD 22.6) < LOD < LOD 26.0-28.3-20. and elimination occurs by renal and fecal routes. The FDA dietary surveys have shown that over time.3-22.8) size 1702 2277 1961 Total years 99-00 01-02 03-04 50th < LOD < LOD 14. 1976). 118-74-1 General Information Hexachlorobenzene (HCB) was used from the 1930’s to the 1970’s in the U.Organochlorine Pesticides Hexachlorobenzene CAS No.7) < LOD < LOD 24. 2005).4-16. HCB is slowly metabolized.5 (13.5-33.7-22.8) 583 554 460 350 511 488 636 1052 888 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.4) < LOD < LOD 18.9) < LOD < LOD 20.5-18. these metabolites can also be produced after exposure to other chlorinated compounds (Kohli et al.2-15. HCB has been detected in fewer foods since the 1980s (FDA.9-32.2-15..0 (14.3) < LOD < LOD 20.9) < LOD < LOD 19.7) * * 14. and 03-04 are 118. It is a persistent chemical and bioaccumulates in both aquatic and terrestrial food chains (ATSDR.9-15.8 (22.6-26.8-15. Workers in chemical manufacturing industries may be exposed to HCB via inhalation or dermal pathways. 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. HCB is well absorbed after oral administration.0-25. and foods with a high fat content.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 * * 14.7) 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 * * 16.3 (22. 1997).5-TCP) and 2.. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.1 (17.9) < LOD < LOD 15.4) < LOD < LOD 19.9 (23.4) < LOD < LOD 33.0) < LOD < LOD 15. The general population may be exposed to HCB through diet.8) < LOD < LOD 27.7-16.4 (11.2) < LOD < LOD 29.6) < LOD < LOD 24. respectively.9) 19.3-26.5 (13.4.2 (13.4.0) < LOD < LOD 15.7-30. population from the National Health and Nutrition Examination Survey.9 (14.9-24.3 (16.9) < LOD < LOD 20.6-TCP) (To-Figueras et al.S.3 (20.6) < LOD < LOD 25. and 7.7-16. which may vary for some chemicals by year and by individual sample.6-trichlorophenol (2.4) < LOD < LOD 14.4 (22.4) < LOD < LOD 23.7 (15.7-15.5 (14..1-16. Although it is not manufactured as an end-product in the U.0 (18.6 (24.2-31.0-19. and sediment (Barber et al.6 (21.6-44.

169-.118-.155) < LOD < LOD .086-.090 (.109) * * .081-.081 (. very high.176) < LOD < LOD . and many died before 2 years of age (Peters et al.173) < LOD < LOD .095-. 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.069) * * .156 (.gov/pesticides/ and from ATSDR at: http://www.118) < LOD < LOD ..078 (.147 (.157-.123 (. which may vary for some chemicals by year and by individual sample.087 (.140 (.212) size 1702 2277 1961 Total years 99-00 01-02 03-04 50th < LOD < LOD .S.115 (. were seen in an epidemic of poisoning in Turkey that occurred from 1955 to 1959 when HCB-treated seed grain was diverted for bread production.epa.097 (.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 * * . The U. as well as hypertrichosis.088-.094 (. 1960). acute doses produce central nervous system depression and seizures. Survey Geometric mean (95% conf.086-. Human health effects from HCB at low environmental doses or at biomonitored levels from low environmental exposures are unknown. which is manifested by increased deltaaminolevulinic acid synthase activity and decreased uroporphyrinogen decarboxylase activity. 1982. reproductive and developmental toxicities.104 (.163-.107-.118-. thyromegaly.cdc.196) < LOD < LOD . and liver and thyroid cancers (ATSDR.088-.086) < LOD < LOD .258) < LOD < LOD .102 (. environmental levels) and health effects is available from the U.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.179 (.098 (.163 (.111) < LOD < LOD .191 (. ACGIH has developed workplace exposure limits for HCB.182 (.082-.143-.gov/toxpro2.095 (.094) < LOD < LOD .145-. In humans.135-.069) < LOD < LOD .122) < LOD < LOD . EPA has established a drinking water standard.107) < LOD < LOD .092 (.203) < LOD < LOD . EPA at: http://www.097) < LOD < LOD .123 (..064 (. immunologic abnormalities. IARC classifies hexachlorobenzene as possibly carcinogenic to humans.095 (.065 (.167) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * .089-.159-.062-.175) < LOD < LOD .095) < LOD < LOD 75th < LOD < LOD 90th * * .072-. 2002).225 (.102) < LOD < LOD .090-. a consequence of these heme abnormalities is a condition known as acquired porphyria cutanea tarda.atsdr. and the FDA has established a bottled water standard for HCB.092-. More information about external exposure (i.130) < LOD < LOD .073-. * 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 .S. HCB interferes with normal heme synthesis.090 (.099) < LOD < LOD .148-.160 (.088-.121 (.099) < LOD < LOD .145-.190 (.html.114-.e.079 (.125 (.178-.163) < LOD < LOD .060-.132) < LOD < LOD .186 (. population from the National Health and Nutrition Examination Survey.176-.114-.097) .077-.095) * * .174-.141) < LOD < LOD .129) < LOD < LOD .092 (. arthritis.203) < LOD < LOD .123 (.099) < LOD < LOD .091-. and weakness.090 (.S.152) < LOD < LOD .111-.120 (.171 (.147-.100) < LOD < LOD .157 (.092 (. This condition.083) < LOD < LOD . Fourth National Report on Human Exposure to Environmental Chemicals 101 . and NTP classifies hexachlorobenzene as reasonably anticipated to be a human carcinogen.167 (.Organochlorine Pesticides chemical. Chronic feeding studies in animals have demonstrated kidney injury. anorexia.126) .113-.127-.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 * * .085) * * . Biomonitoring Information Serum concentrations reflect the body burden of HCB. Infants were exposed transplacentally and through breast milk. Schmid.085-. With chronic exposure.089-.

Bertram HP.81(2):82-85. Int J Hyg Environ Health 2002. HCB detection in serum also was proportional to age. Safe A. Herrero C. et al. Link et al. As a result of the lower limit of detection in NHANES 2003-2004. Bradman et al. Factors predicting organochlorine pesticide levels in pregnant Latina women living in a United States agricultural area.. Sci Tot Environ 2005. 2002.135(4):400404. Residency near industrial or agricultural areas has been associated with higher serum HCB levels (Barber et al. 2002). IARC Sci Publ 1986. Ozalla D. only 4. factory workers chronically exposed to HCB and residents near the factory had serum HCB levels that were 150 to 50 times higher. 1986. J Assoc Off Anal Chem 1988. Bryan GT. more HCB levels were quantified.fda. Organochlorines in Swedish women: determinants of serum concentrations. J Exp Sci Environ Epidemiol 2007. 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.110(8):835-838. declines in background HCB levels ranging from around 50%90% have been documented in studies using cord blood (Dallaire et al. Toxicological profile for hexachlorobenzene update [online]. Sala M..gov/~dms/ pesrpts. 1989).349:144. trends and processes. 4/21/09 Barber JL.gov/ toxprofiles/tp90. Temporal trends of organochlorine concentrations in umbilical cord blood of newborns from the lower north shore of the St. April 1982 to 1984. Gunderson EL. dietary intakes of pesticides. Chemosphere 2005.. Granath F. Available at URL: http://www. Seiwert M. 1999). Jones D.71(6):1200-1209. Schwartz JM. Hexachlorobenzene content in human whole blood and adipose tissue: experiences in environmental specimen banking. Biol Neonate 2002.html. Cripps DJ. Zoellner I. Sweetman AJ. Kohli J. 2002.Organochlorine Pesticides in the NHANES 1999-2000 and 2001-2002 subsamples. Ayotte P. Polychlorinated biphenyls and hexachlorobenzene in full-term neonates. The metabolism of higher chlorinated benzene isomers. respectively. Holland NT. but approximately five times higher than the overall geometric mean level in 2003-2004 (Becker et al. 2002. Lawrence River (Quebec. 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. Atuma S.. Biomonitoring of persistent organochlorine pesticides... 2005. Environ Health Perspect 2003.. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Lackmann. than the limits of detection (on a whole weight basis) in NHANES 19992000 and 2001-2002 (Herrero et al. Environ Health Perspect 2002. selected elements. Gocmen A. Canada). Piechotowski I. and the geometric mean concentration of HCB in whole blood was 0. In a representative sample of the 1998 German adult population. Reference values updated.atsdr. Food and Drug Administration (FDA). Becker K. Link B. Lackman. Peters HA. August 2008. Arch Dermatol 1999. 2005). van Wijk D. September 2002. Available at URL: http://www. 4/21/09 Glynn AW. Kemper FH. but overall. Schulz C. Hexachlorobenzene in the global environment: emissions. Urinary porphyrin excretion in a human population highly exposed to hexachlorobenzene. Bertram et al. et al. Epidemiology of hexachlorobenzene-induced porphyria in Turkey: clinical and laboratory follow-up after 25 years. Dallaire F. Arch Neurol 1982. 102 Fourth National Report on Human Exposure to Environmental Chemicals . Lackmann GM. Jones KC. 2006).cfsan. Kaus S. Herrman T. Dewailly E. Gabrio T. References Agency for Toxic Substances and Disease Registry (ATSDR). 2003). 2005)... Darnerud PO. distribution. Agerelated increases of HCB in body fat and serum have been consistently noted in general population studies (Becker et al. levels.. Krause C. Glynn et al. Barr DB. Lecha M. In Spain. Otero R.39(12):744-749. and other chemicals. Dogramaci I. however. Aune M.58:1185-1201. 2002. Bjerselius R. lower than the limit of detection (on a lipid adjusted basis) in NHANES 1999-2000 and 20012002.44 mg/L. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.111:349355. FDA total diet study. Muller C. et al. Lepom P. Finding a measurable amount of hexachlorobenzene in serum does not mean that the level of the hexachlorobenzene causes an adverse health effect. HCB levels were directly related to age. et al. Paepke O. Over the past two decades. Fenster L. Laliberte C.9% of participants had quantifiable levels (Stehr-Green.. FDA Pesticide Program Residue Monitoring 1993-2006 [online].205:297-308. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. In the 1976-1980 NHANES subsample. Santiago-Silva M.html.54(3):203-208.77:173182. Eskenazi B. 2002) and among children (Link et al.17:388–399. Muckle G. Can J Biochem 1976.cdc. Bradman A.

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

**In survey period 2001-2002.1 (12.9-21.8-16.2-52.4 (52. The other isomers can be formed during the synthesis of lindane.9-56.6) 16.8) 39.8.7-96. the U.80 (<LOD-14. and have been used either as fungicides or to synthesize other chemicals.9 (11.3 (26.8 (10.4-111) 84.46-11.89 (<LOD-9.7-166) 70.4-45. beta.2 (18.2 (50. and 03-04 are 9. interval) 9.8 (21. gamma.70-12. 319-85-7 gamma-Hexachlorocyclohexane CAS No.9 (40.2-67.0-23.7-69. Lindane (1%) lotion and shampoo are available by prescription for singleuse application to treat human scabies and head lice.1) 71.0 (37.0) 8.1 (18.45) < LOD Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 99-00 01-02** 03-04 16.20-16. exists in several isomeric forms.09) < LOD Gender Males 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD 14.36.70 (8.8 (33.4-50.8-199) 134 (85.7 (35.4-73.4) < LOD 9. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.8-68.9 (9.7 (25.0 (<LOD-12.66-12. commonly known as lindane.3) 14. particularly alpha and gamma have been detected widely in air.6) 35.3) 25.7-20.6) 47.6 (22.6 (10.9-51.8) 27.3 (42.1-27. 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. It is no longer produced or sold in the U.0) 41.5) 11.4) 10.2 (34.7) 23.9) 45.0) 17.9) 81.43 (<LOD-9.9 (62.9 (50.0-20.90) 7.1-15.4) 21.5) 14.7) 10.6 (33.9 (32. containing about 64% alpha and 10%-15% gamma isomers.3) 34.3-38.1) 31. Survey years 99-00 01-02** 03-04 Geometric mean (95% conf.6-89.2) 13.6-20.4) 11.04-10.7 (53. which may vary for some chemicals by year and by individual sample.90-8.Organochlorine Pesticides Hexachlorocyclohexane CAS No.6) 653 758 589 1240 1533 1370 20 years and older 10.2-42.2-22.0-70.5) 40.6) 50.9-178) 48. 608-73-1 beta-Hexachlorocyclohexane CAS No.2) 9.0 (33.50) 8. population from the National Health and Nutrition Examination Survey. < LOD means less than the limit of detection.70 (6. Technical grade HCH is a mixture of all four isomers.6-14.9-24. and sediment as a result of historic production and use.2 (48. 2005).1-32. EPA cancelled agricultural uses of lindane (ATSDR.60-13.8) 95th 68.5528.5 (16.1-16.3 (13.4) Sample size 1893 2291 1959 Age group 12-19 years 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD 21.1 (9.S.1) 12.90-8.2) 62.5) 29.5) 632 563 460 403 513 487 702 1051 887 Non-Hispanic blacks Non-Hispanic whites Limits of detection (LOD. The gamma isomer.0) 7.1 (21.9 (30.2-98.0) 35.S.8 (64.6) 18.0) 71. HCH isomers are lipophilic.8-54.0-111) 70.8) 12.0 (14.5) 16.S.6) 36. and 7. see Data Analysis section) for survey years 99-00.5 (43.1 (11.4) 27.6-18.2-87. including alpha.4 (16.61-12.1-49.6 (40.4 (12. Lindane has a half-life of about two weeks in soils and water.3 (62. 01-02.7) 56.6 (17.2-46.9) Selected percentiles ( 95% confidence interval) Total * * 50th < LOD < LOD < LOD 75th 19.4 (11.8 (17.4) 901 1067 952 992 1224 1007 Females 11.7 (62.4) 44.6-42.8) * * * * * * 15.7 (29. 6. formerly referred to as benzene hexachloride.5) 67.7-96.1 (27. respectively.56-12.7 (13.2 (29.9-14. water.7) 32.3-56.76.8-19.8) 7.70-19.1 (16.5 (24.7) 97.5 (14.8) 52.9 (26.7 (<LOD-16.2) 142 (99.0-34.5) 22.3) 51.30-11.1-32.9) 17.4) 51.87 (9.3) 37.6-37.2 (31.7) 10. 2005).6 (16.68 (<LOD-10.4 (50.4 (8.80 (6.3-85.7) 73. See the section “What’s New” at the beginning of this Report for details.9-81.5-123) 49.2) 36. environmental levels declined. As pesticide applications of HCH were increasingly restricted or eliminated. 58-89-9 General Information Hexachlorocyclohexane (HCH). soil. HCH does not bioaccumulate to an appreciable extent in plants (ATSDR. HCH isomers.2 (9.6-47.3 (42.5) 90th 42.0 (8.2-55.7-69.4) < LOD < LOD < LOD 46.1) 12.7) 27.6-135) 69.1) 13.1-36.5 (8.7-26.7) < LOD < LOD < LOD < LOD < LOD < LOD 37.7) 18.0-70.8) < LOD 10. 104 Fourth National Report on Human Exposure to Environmental Chemicals .6-62. can be used as an insecticide and has been used to kill soil-dwelling and plant-eating insects. In 2006.0-21.5 (37. so they can accumulate in fatty tissues of animals.7 (30.8 (9.5 (11.8 (32.9) 15.1 (30.8-87.5-29.8 (23.2-20. and delta. each result has been multiplied by 1. However.1 (9.0 (35.2-17.1-37.0 (19.

290) .050-.297-. Saxena et al.260) .290) .174) . respectively.120 (. which may vary for some chemicals by year and by individual sample.160) .234 (.118-.216 (.370-.390 (.073-.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 .560 (.37) 1.080) * * * * * * .372 (.250 (.131-. and nephropathy developed (IPCS. OSHA and ACGIH have established workplace standards and guidelines.661) 901 1067 952 992 1224 1007 Females .051 (<LOD-.220-.480 (.057 (<LOD-.078 (.050 (.254) 95th . **In survey period 2001-2002. 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.170-.190) .310) .300-. FDA pesticide monitoring program has shown a temporal decline in the detection of lindane.190) .062 (.310 (.059-.382-.110) .222 (.410 (.190-1.305) .221-.083 (.814) .066) Selected percentiles ( 95% confidence interval) Total * * 50th < LOD < LOD < LOD 75th .350) .081-.150) .210) .330 (.139 (.191-.051-.064 (.191-. Acute high dose toxicity in rodents affects the central nervous system producing decreased activity.160-.125) < LOD < LOD < LOD .250 (.32) .077) < LOD .150-.. 1977).Organochlorine Pesticides exposure to HCH is through the diet.350 (.150) .100-. Workers who directly handled HCH have complained of headache.089) .200 (.050 (<LOD-. After dermal application of lindane 1% lotion.220-.040-.124-.119) . Rogan.501) . hepatic enzyme induction.210 (. 1981). The beta isomer accumulates in fatty tissues and is metabolized more slowly.200-. interval) .470) .067) .450) .580 (.067 (.070-. and memory loss (Nigam et al. U.120) .587) 653 758 589 1240 1533 1370 20 years and older .150 (. HCH isomers are metabolized to chlorophenol metabolites that are excreted in the urine (Angerer et al.070 (. The U.092 (.410-.700) . each result has been multiplied by 1.270 (.103 (. Fourth National Report on Human Exposure to Environmental Chemicals 105 .331 (.690) ..250-. Pesticide applicators or agricultural workers could be exposed to HCH by inhalation and dermal pathways.120-.080-.058 (<LOD-.058) < LOD Gender Males 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD .110) . 1986).480 (. Gunderson 1988).340) .190-.319) .103-.048 (<LOD-.680) .090 (. population from the National Health and Nutrition Examination Survey.360 (.047-.240 (.220) .S.570 (.089-.140) .360-.210 (.090-.580-1.077) < LOD .310) . HCH crosses the placenta and is also excreted in breast milk (Radomski et al.146-.090 (.070) .360) .100) .260-. HCH isomers are absorbed after inhalation.098 (.069) .01 (. probably by blocking inhibitory neurotransmitters in the central nervous system.840) .S.. and FDA has established a bottled water standard and food residue tolerances for lindane. resulting in a half-life of about seven years.056-.100 (.140 (. 2008. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.521 (.050) .280-.200-.120 (.290 (.460) .100 (. ataxia.600) .070-.050-.710) .100) .130 (.167 (.140) .230-.250 (.260) . and seizures.130-.050-.560) .144 (.057-.280-.100-.320 (.080-. 1983).065 (.080-. 2002).210-.118 (. enlarged livers. Distribution is mainly to fatty tissues.S.120) .450 (.294-. Acute high doses of lindane after ingestion or excessive skin application of the 1% lotion have produced seizures in humans.173-. ingestion. from 6% of samples in 1982-1984 to 2% in 1994 (FDA.410) .100-.244-.086) < LOD < LOD < LOD < LOD < LOD < LOD .060) .910 (.057-. Human health effects from HCH isomers at low environmental doses or at biomonitored levels from low environmental exposures are unknown.420-. 1971.070-.290 (.062 (.410) .120 (.056-.400) .390-.050 (.281 (.080) .083) .05) .340-.096) .250) .450-.065 (.064) . See the section “What’s New” at the beginning of this Report for details.072 (.214) .460 (..057) < LOD Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 99-00 01-02** 03-04 .620) .400) .110-.290 (. tremors.090 (..180-. or dermal exposure.240-.120-.5528.170-.330-.068-.080 (. paresthesias.175 (.510) .140) .480) . When animals were chronically fed lindane at high doses. the serum half-life was about 20 hours among children (Ginsburg et al.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.130) . EPA has established a drinking water standard.110) .442 (. 1996. for lindane.287 (.160 (.308-.404) .412 (.103) 90th .470 (.091) .080 (.050 (<LOD-.050-.120-.620-1.380 (. Survey years 99-00 01-02** 03-04 Geometric mean (95% conf.250-.220 (.070 (.

Studies of general populations have shown declining beta-HCH levels since the 1970s (ATSDR. Sturgeon et al.. EPA at: http://www. studies in populations with environmental exposure have reported lindane levels below the limit of detection in most persons (Anderson et al. 1971. 2002. respectively. respectively. which were considerably lower (as much as twentyfold) than mean levels reported in small studies of adults in Spain (Botella et al. Becker et al. 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.. the maximum and 95th percentile beta-HCH values. 2001-2002.. 1998.. Stehr-Green. Kutz et al. 2005. and 03-04 are 14. 2005. beta-HCH may be detected in a higher percentage of the general population than are the other HCH isomers. and 7. male sex. < LOD means less than the limit of detection..Organochlorine Pesticides hexachlorocyclohexane isomers as possibly carcinogenic to humans. 2002).. which may vary for some chemicals by year and by individual sample. 1989. 1989). Additional factors associated with higher beta-HCH levels include rural residence.e. Kutz et al. 1991.S. aged 9-11 years. and 2003-2004.. 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. serum levels of lindane were generally below the limits of detection. Bates et al. and a diet that includes meat (Becker et al.. older age. Biomonitoring Information Because of its longer half-life. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. In populationbased studies of New Zealand adults and German adults and children. Stehr-Green. 2004) and India (Bhatnagar et al. 01-02. 2004. In recent years.. 106 Fourth National Report on Human Exposure to Environmental Chemicals .. 2004).cdc. 10. Survey Geometric mean (95% conf. Link et al. were similar to the 95th percentiles in this Report.8. environmental levels) and health effects is available from the U. 1991.. In NHANES 1999-2000. see Data Analysis section) for Survey years 99-00.epa. population from the National Health and Nutrition Examination Survey.atsdr.. More information about external exposure (i.gov/toxpro2. Radomski et al.5.5. 1998).gov/pesticides/ and from ATSDR at: http:// www. In an earlier (1996-1997) sample of German children.html. and NTP classifies hexachlorocyclohexane isomers as reasonably anticipated to be human carcinogens.S.

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

et al. FDA total diet study.150:981-990. VI. Lepom P.cfsan. Kashyap R. Needham LL. Garrett N. Exposure of women to organochlorine pesticides in Southern Spain. Ellis H. et al. et al. Needham LL. Occupational exposure to hexachlorocyclohexane.96:34-4Food and Drug Administration (FDA). Piechotowski I. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. Maass R. Rey AA. Bull Environ Contam Toxicol 2004. The Great Lakes Consortium.htm. Toxicol Appl Pharmacol 1971. FDA Pesticide Program Residue Monitoring 1993-2006 [online].48:127-134. Crespo J. Chemosphere 2004.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Int Arch Occup Environ Health 1986. dietary intakes of pesticides. Olson J.atsdr. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. selected elements. Biomonitoring of persistent organochlorine pesticides. Saiyed HN. Saxena MC. Toxicological profile for hexachlorocyclohexanes update [online]. Absorption of lindane (g benzene hexachloride) in infants and children. Glynn AW. Zoellner I. 4/21/09 Ginsburg CM. Environ Health Perspect 1998. Raju GS. Darnerud PO. Krishna Murti CR.91:998-1000.20(2):186-193. org/documents/jmpr/jmpmono/2002pr08. 2002. J Toxicol Environ Health 1989.52(1):59-67. Available at URL: http://www. Reisch JS. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. Organochlorine pesticides and polychlorinated biphenyls in human adipose tissue. Rivas A. Environ Health Perspect 2003. children and newborn infants. Bottimore DP. Chemosphere 2005. Becker K. Falk C. Gabrio T.fda. Arch Pediatr Adolesc Med 1996. Herrman T. Wood PH. HCH. Siddiqui MKJ. Rev Environ Contam Toxicol 1991. Kulkarni PK. available at URL: http://www. Angerer J. Cancer Causes and Control 1998. Karnik AB. Int J Hyg Environ Health 2002. Seiwert M. PA. Nigam SK. and HCB residues in human blood in Ahmedabad. Serum concentrations of organochlorine compounds and endometrial cancer risk (United States). Lindane. Bhatnagar VK.html. Deichmann WB. Paepke O. Arch Toxicol 1981. Granath F.gov/~dms/pesrpts. Lowry W.cdc. Patterson DG Jr. Demographic and seasonal influences on human serum pesticide residue levels. Schulz C. 4/21/09 Anderson HA. Needham LL. Atuma S. Bjerselius R. April 1982 to 1984.57(4):315-320. J Assoc Off Anal Chem 1988. Bhargava AK. Olea-Serrano MF. Burse VW. Link B. Rogan WJ. Levels of DDT. Metabolism of gammahexachlorocyclohexane in man. Serum hexachlorocyclohexane residues in workers engaged at a HCH manufacturing plant. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Astolfi E. 4/21/09 Kutz FW. Environ Res 2004. Stehr-Green. 108 Fourth National Report on Human Exposure to Environmental Chemicals . Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. Bates MN. Pollutants in breast milk. Majumder SK. Pesticide residues in food-2002-Joint FAO/WHO meeting on pesticide residues. Gunderson EL. Olea N.58:1185-1201. Botella B. Brock JW. Krause C. Radomski JL. Potischman N.72:261265.27:405-421.205:297-308. Brinton LA. et al. et al. Rothman N. Buckland SJ.106(5):279-289. et al.120:1-82. August 2008.111:349355. Heinrich R. Bai KM. Hanrahan L. Int Arch Occup Environ Health 1983.71(6):1200-1209.inchem. India. Cerrillo I. August 2005. Kutty D. Zaidi SS. Organochlorines in Swedish women: determinants of serum concentrations.54:1431-1443. J Pediatr 1977. Aune M. and other chemicals. et al. gov/toxprofiles/tp43. Kaus S. Blood levels of organochlorine pesticides in Argentina: occupationally and nonoccupationally exposed adults.9(4):417-424. International Programme on Chemical Safety (IPCS). Visweswariah K.html. Available at URL: http://www. Placental transfer of pesticides in humans. Sturgeon SR.

4) 617 548 459 398 500 484 688 1049 884 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.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 13.0 (<LOD-108) < LOD < LOD 50. and 03-04 are 14. Formerly.5 (<LOD-42. 10. EPA have issued public health advisories or warnings that fish from contaminated lakes and rivers may contain mirex. mirex was detected in human adipose samples. In studies conducted in the 1970’s and 1980’s.3-225) 15.8. Survey Geometric mean (95% conf.70 (<LOD-15. Mirex has been detected in air. which may vary for some chemicals by year and by individual sample. Fourth National Report on Human Exposure to Environmental Chemicals 109 .0-374) 11. resulting in exposure to newborns and nursing infants.1 (8.70-24.1 (<LOD-104) < LOD < LOD < LOD < LOD 39.6) < LOD < LOD < LOD < LOD 71.0 (14. Ingested mirex that is not absorbed is eliminated in the feces within about 48 hours. it is a highly persistent chemical in the environment. disposal.3 (15.0 (12.2) 51.S. Mirex can cross the placenta and be excreted in breast milk.3) < LOD < LOD < LOD < LOD < LOD < LOD < LOD 15. or pesticide application. after which it is widely distributed in the body and stored in fat.6. Mirex is absorbed through the skin and from the gastrointestinal tract.S. where it was applied directly to soil and by aerial spraying.. Some states and the U. animals.7 (<LOD-47.5-82.40 (<LOD-13. aquatic organisms.10-37.5.6 (<LOD-108) 9. Occupational exposure is limited to workers at sites where mirex contamination is present. sediments.6 (<LOD-31.Organochlorine Pesticides Mirex CAS No. especially those from persons living in the southeastern U.3 (15.S. Human health effects from mirex at low environmental doses or at biomonitored levels from low environmental Serum Mirex (lipid adjusted) Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U.4) < LOD 63.8) < LOD 15.4) < LOD 15.6 (<LOD-23.10 (<LOD-15. 1985.5 (<LOD-115) 153 (30..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 66. < LOD means less than the limit of detection.S.S.8 (<LOD-73. 2385-85-5 General Information Mirex has not been produced or used in the U. 1991). interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 57. and 7.1 (<LOD-65.7) 8. Mirex contamination of Lake Ontario and adjacent waterways has been well documented (ATSDR. where it has a half-life of 12 years.5-291) 11.6) 9.8 (12. respectively. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.90-29. since 1977.7 (12. and foods.6-305) 15.5 (9.6) size 1853 2257 1951 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th 15.2-230) 13.4 (8. 01-02. 1995).4-230) 18.1 (13.2 (7.70-40. Mirex binds strongly to soil. (Kutz et al. population from the National Health and Nutrition Examination Survey. Mirex is not metabolized in the body. see Data Analysis section) for Survey years 99-00. soil.5-425) 40. 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. water.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. its major uses were as a flame retardant additive and as a pesticide to kill fire ants and yellow jackets in the southeastern U.

450 (.. 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. 110 Fourth National Report on Human Exposure to Environmental Chemicals . 1991).37) .79) . as well as in a subsample of NHANES II (1976-1980) participants.053-.090 (<LOD-.73) .html.92) .370 (. and NTP classifies mirex as reasonably anticipated to be a human carcinogen.470) .170-3.S. which is approximately twofold to threefold lower than the 90th percentile for females in the NHANES 20012002 subsample but similar to 95th percentile for females in the NHANES 2003-2004 subsample (Van Oostdam et al.080-1.170) size 1853 2257 1951 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .8.79) .635) < LOD .110 (<LOD-.310 (..100 (<LOD-.090 (<LOD-. and 2003-2004 subsamples.430 (.108 (. More information about external exposure (i.690) .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 ..510) < LOD < LOD .052-. environmental levels) and health effects is available from the ATSDR at: http://www.090-1.100 (<LOD-.7 ng/g of lipid.090-1.610) < LOD < LOD < LOD < LOD .090 (<LOD-. serum mirex levels were generally below the limits of detection (Stehr-Green.090-1.268) < LOD . Finding a measurable amount of mirex in serum does not mean that the level of mirex causes an adverse health Serum Mirex (whole weight) Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U.170) < LOD .240) < LOD < LOD < LOD < LOD < LOD < LOD < LOD .054 (<LOD-.170) 887 1052 949 966 1205 1002 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .450) 1. 2004).02) .S. 2005).070-1.079 (<LOD-. which may vary for some chemicals by year and by individual sample.08 (.470) . Biomonitoring Information In the NHANES 1999-2000. In addition.106) < LOD .140 (<LOD-.220) .256 (. and the FDA monitors foods for pesticide residue and has established an action level for mirex in fish tissue.41) . The U. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.410 (.080-1. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD . Laboratory animals fed high doses developed liver enlargement and liver tumors. and 4.gov/toxpro2.220 (<LOD-.106 (. EPA has established environmental standards for mirex. reproductive toxicity included decreased fertility and testicular damage.Organochlorine Pesticides exposures are unknown. In samples obtained between 1994 and 1997. developmental abnormalities including cataracts and edema in the offspring have been reported (ATSDR. 1995. IARC classifies mirex as possibly carcinogenic to humans. 2001-2002.470 (.059 (<LOD-. 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.cdc.112 (. Smith.064 (<LOD-.atsdr.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.055-.093 (.102) < LOD < LOD < LOD < LOD . 7.084) * * * 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 . 1989). population from the National Health and Nutrition Examination Survey. Survey Geometric mean (95% conf.089-.062-.077 (<LOD-. The geometric mean mirex levels of the Inuit mothers were 8.e.

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

4. 1976).0) < LOD 973 1178 1021 1319 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * . < LOD means less than the limit of detection.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 1.00 (3. which may vary for some chemicals by year and by individual sample.90-33.0) < LOD 21.19 (<LOD-6.40 (2.920-3.4.0) 2.0) 14.40) < LOD 4.31 (<LOD-9. and polychlorinated benzenes (Kohil et al.5-Trichlorophenol Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. 2.0) 2.50-16.80 (2.4.40) < LOD 1.0 (4. but they may be produced as by-products during manufacturing of other chlorinated aromatic compounds. surface water.9 and 0. however.0) 2.0) < LOD 5.40 (. including hexachlorobenzene and hexachlorocyclohexanes.S.9.980-3.30-40.03) 9.980-3.63) 18.4.40 (2.72) < LOD 1.00-3. Formation of 2.6-TCP in any of the samples (U.27) 482 570 681 815 831 1112 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD 1.40 (2.40 (.20) < LOD 5.60-18.42 (<LOD-12.0) 2. hexachlorobenzene. Survey Geometric mean (95% conf.80) < LOD 1.40 (1.20-36.50 (.4.60) < LOD 8.4. 88-06-2 Metabolites of Organochlorine Pesticides and Other Environmental Chemicals General Information The chlorophenols.30) < LOD < LOD < LOD < LOD < LOD 1.0) 5.4.40 (1.0) < LOD 5.0 (4.30) < LOD 4.60 (2.7.5-Trichlorophenol CAS No.4.5-TCP) and 2. may occur by inhalation or dermal routes.7) 24.10-3.0 (3.71 (<LOD-8.0) < LOD 11.20) < LOD 1. Small amounts of trichlorophenols also can be produced during combustion of natural materials and the chlorination of drinking water or waste water that contains phenols.6-TCP was also used as a wood preservative and may still be used in production of some fungicides (ATSDR.8) 21. usually at herbicide production or waste incineration facilities.6-TCP were used as intermediates in the production of certain pesticides.80-41.4.00-8. and sediments.6-Trichlorophenol CAS No.50-63.S. Both chemicals have been detected in air. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.80 (1.3. Trichlorophenols are no longer manufactured commercially.5-trichlorophenol (2. 1999). interval) Selected percentiles ( 95% confidence interval) Sample 95th 16.4. 2.6-trichlorophenol (2. other organochlorines.42 (<LOD-8. recent sampling of U. Exposure to trichlorophenols also may result from metabolism of lindane.50) < LOD 1.8-tetrachlorodibenzo-p-dioxin occurs during the synthesis of 2.40) < LOD 6. Trichlorophenols have been detected in fish taken from waters near waste water treatment and industrial discharges (ATSDR.27) 696 661 521 696 603 939 Limit of detection (LOD.40 (2.30-27.5-trichlorophenol.30-44.0) 2.4. public drinking water systems did not detect 2.50 (1.Organochlorine Pesticides 2.0) 2.0) < LOD 11.30-11.. are metabolites of several organochlorine chemicals. 2. 2006). population from the National Health and Nutrition Examination Survey. 95-95-4 2.30-3.60 (4.71 (<LOD-8. EPA.30 (.0 (5.30-27.20-71.20 (4.S.0 (3.50-25.0) < LOD 5.00 (2.00-3.40-18.30-27.0 (8. 1999).57 (<LOD-15.950 (<LOD-1.5TCP and 2. Environmental sources of these compounds include industrial discharges or run off from pesticide facilities or disposal sites. 112 Fourth National Report on Human Exposure to Environmental Chemicals .50 (2.60-8.4. Occupational exposures.6-TCP).0 (4.60 (. General population exposure may occur by ingesting contaminated food or water and by inhaling contaminated air. soils. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.0) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 1. Such workers would probably Urinary 2.900-2.940-3.20) < LOD 90th 5.40-11.9 (<LOD-121) 9. Historically.

3) < LOD 973 1178 1021 1318 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * ..78 (3.4.75 (<LOD-6. was similar to the corresponding percentile for 6-11 year olds in NHANES 1999-2000 (Hill et al. environmental levels) and health effects is available from ATSDR at: http://www.e.78-19.62-20.57 (<LOD-7.43) < LOD 12.6) 4.. Human health effects from 2. NTP classifies 2..5-Trichlorophenol (creatinine corrected) Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. 2003.57 (3.6-TCP levels at the 95th percentile were up to eight times higher than 3.15) < LOD 2..81 (<LOD-9.79-4.. which includes trichlorophenols.8 (5. In the same 2-6 year old children. 1995) were similar.32) < LOD 4. 2004).2) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 2. 1989). but almost twenty times higher than 95th percentile values reported in German adults aged 18-69 years (Becker et al.0 mg/L. * 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 11.33) < LOD < LOD < LOD < LOD < LOD 2. Survey Geometric mean (95% conf.88-16. and other chlorinated compounds. More information about external exposure (i.00-29.05-8. Neither 2.2) 2.37) 16. Radon et al.5) < LOD 12.gov/toxpro2.6) 4. animals showed hepatocellular abnormalities.1) 2.S.3 mg/L in a nonrandom subsample from NHANES III (Hill et al.html.9) 12.27-17.11) 482 570 681 814 831 1112 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD 1.82 (<LOD-32.980 (<LOD-1.43 (2.67 (1. Among 6-11 year old children in NHANES 1999-2000.49 (1.cdc.4.13-13.69-18.78) < LOD 1.36 (1.6-TCP were developmental or reproductive toxicants in animals (ATSDR 1999).60-3.5) 11.4.53-3.5-TCP.17) 9. At lower doses. Biomonitoring Information In the NHANES 1999-2000 and 2001-2002 subsamples.4.44 (1.4. IARC considers the experimental evidence for animal carcinogenicity inadequate for 2.24-11.4) < LOD 3.4.83-12.atsdr.50) < LOD 2.6-TCP at low environmental doses or at biomonitored levels from low environmental exposures are unknown. Fourth National Report on Human Exposure to Environmental Chemicals 113 .90 (4.4.6-TCP level was approximately eight times higher than the corresponding percentile in a small group of 2-6 year old children living near an herbicide manufacturing facility: 33 versus 4 mg/L (Hill et al.4) < LOD 3.6-TCP as reasonably anticipated to be a human carcinogen.29 (1.4.5-TCP and limited for 2.64 (4.02) < LOD 7.68-4.31) < LOD 2.05-17.24) < LOD 5. 2003). in addition to dioxins.53-3. The 95th percentiles for 2.16) < LOD 90th 5.73 (<LOD-8.5-TCP among adults in this Report and in a nonrandom subsample from NHANES III (Hill et al.44 (.00) < LOD 4. the 95th percentile urinary 2. 2003). and lymphomas.920-2.4.8) 4.Organochlorine Pesticides be exposed to mixtures of chlorophenols.3 mg/L reported in German adults aged 18-69 years (Becker et al.820-2.24 (3. recent small studies have not demonstrated increased exposure to trichlorophenols in workers who dredged contaminated soils or incinerated waste materials (Agramunt et al. urinary 2..37) 696 661 521 695 603 939 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. Laboratory animals chronically fed high doses of 2. 7.68 (<LOD-8.16 (..4.6-TCP had increased rates of hepatic tumors.74) 11.28-25.4.47-8.67 (1. population from the National Health and Nutrition Examination Survey.24) < LOD 1.80 (1.4.7 (4...4 (6.6-TCP.4. However.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. Urinary 2.20-6. the 95th percentile urinary 2. furans.93-11.4) 5. leukemias.37-11.69 (2. as being possibly carcinogenic to humans.5-TCP or 2. 1989).46 (1.02-3.9 (5.5-TCP nor 2.19-12.95 (3. IARC classifies combined exposures to polychlorophenols.86 (3.75 (3. 1995) and up to 19 times higher than the 95th percentile value of 1.0) 7.6) 4.1 (<LOD-58.2 (2.8) < LOD 9.55 (4.24) < LOD 6.2) < LOD 5.00-19.57 (<LOD-7.19-4.3 (5.

0 (12.60-37. 1998).67-12.70) 3.30-2.32) 3.14 (2.85) * 3.60) 6.63) 90th 15.30-11.50 (2.36 (1.78 (2. 2003).75 (8.65) 15.1 (10.0-38.4. 0.26 (2. Biomonitoring studies on levels of 2.0 (20.30-33. 114 Fourth National Report on Human Exposure to Environmental Chemicals .45) < LOD 11. Urinary 2.48-26.0) 14.0) 10.6) 970 1178 1019 1325 99-00 01-02 99-00 01-02 99-00 01-02 2.4.6 (12.0) 15.44) 75th 4.9) 694 677 519 696 602 931 Limit of detection (LOD.4.7 (9.0 (15.59) 4.4.10) 2.0 (4.0 (14. Survey Geometric mean (95% conf.60-21.0-44.60 (2.59-6.4.0-50.72-10.2) 25. Mean values of 2.78 (2.2) 12.76) 3.8-15.0-41.79 (5.0 (7.49 (6.28) 24.55-3.7 mg/L.0) 17.30-2.65 (5.4.09) 15.23) 3.52-3.3) 37. population from the National Health and Nutrition Examination Survey.04) 2.87-14.8) 32.95 (4.02) 2. Urinary 2.70-6.6-TCP exposure and health effects.09-7.54) 6.5-TCP and 2.32) * 3.40-32.0) 13.36-5.6-TCP level.40-14.0 (16.31 (3.99) 6.23-2.4 (9.0 (6.0-68. which may vary for some chemicals by year and by individual sample.0 (20.40-7.0) 6.7) 21.40-2.6-Trichlorophenol Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.0) 19.0 (14.0) 17.90) 2.0 (14..45-9.53) 2.5-TCP level of 0.0) 13.4.40 (2.4.45 (5.00 (2.70 (2.36 mg/g creatinine.0 and 1. 2004).20-6.60 (3.0 (9.7-16.40) 4.40 (2.85 (2.80-6.6-TCP (0.10-2.01-6.4.60) < LOD 5.8 (9.0) 19.24 (2..7-3.S. < LOD means less than the limit of detection.73-9.80-25.0 (11.6) 21.00 (1.20) 4.23) 2..4 (8.5-TCP or 2.0) 9.92 (2. was about six times lower than the median urinary levels for males in this Report (Radon et al.1) 16.95) 3. Biomonitoring data will also help scientists plan and conduct research about 2. similar to the limit of detection for this Report (Anderson et al.10-3.08 (2.52 (2. see Data Analysis section) for Survey years 99-00 and 01-02 are 1.20-23.0-54.4.80 (2.5-TCP or 2.0) 12.8-13.31) * 2.69 (3.40) 3.70) 5.4.40) 2.4.33-4.6 mg/g creatinine) and 2.9) 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 2.98-11.07 (<LOD-3.68 (<LOD-2.84) 2.4.6-TCP than are found in the general population.1 (8.0) 13.18) Selected percentiles ( 95% confidence interval) Sample 95th 25.0 (6.6) 26.47 (3.25-11.7) 33.4.28) * 2.6-TCP levels that were as much as 450 times higher than the median level among adults in the NHANES 1999-2000 subsample (Pekari et al.56 (3.2) 481 574 678 820 830 1109 99-00 01-02 99-00 01-02 2.6 (11.6-22.0 (8.0) 7.5-46.18-3.50-5.51-12.90-8.0 (15.90 (4.10) 6.3-17.0 (6.89 (3.98-7.6-TCP in urine does not mean that the level of 2.5-TCP or 2.74 (2.90 (3.40) 2.3 (11.0-43.40-2.32-4.53) 4.Organochlorine Pesticides A small study of adults who ate Great Lakes sport fish reported a mean urine 2.46-3.6TCP causes an adverse health effect.00-4.3 (11.4.70 (2.80-7.70) 1.58 (1.5-TCP (0.0) 7.00 (4.0) 11.0-18.3) 20.91-4.89-6..12) 2. the median urinary 2. Sawmill workers exposed to chlorophenol wood preservatives had urinary 2.3.6-TCP were monitored in a group of hazardous waste incinerator workers from 19992002.4.6-TCP provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of 2.6-19.7 (13.4 (10.35-3.20 (3.0 (13.80) 1.0) 9.2-0.7) * 99-00 01-02 99-00 01-02 99-00 01-02 4.3-26.6TCP values. 1991). * Not calculated: proportion of results below limit of detection was too high to provide a valid result.2 (14.4-17.6-17.40-4.66 (8.60 (3.80 (3.9 (13.10 (5. In harbor workers exposed to chlorophenol-contaminated river silt.10-3.06) * 2.8) 18.0-38.80 (2.0) 11.8-24.5 mg/g creatinine) were similar to the limit of detection for 2.9) 13.45 (2.0-37.3) 23. Finding a measurable amount of 2.9 (11.57 (<LOD-2.0) 10. interval) 2.5-TCP or 2.74-3.0) 14.4.4. respectively.70) 5.20 (3.00-21.60-3.5-TCP and to the median 2.0) 13. for males in NHANES 19992002 (Agramunt et al.70-6.1-25.95-6.4 (17.58-3.80-20.0 (8.20-3.4.4.70-3.67) 4.30) 4.5-TCP and 2.

88 (2.9) 8. Survey Geometric mean (95% conf.6 (6.72-16.5) 12.09-3.90) 2.9 (9.27-9.10-9.52 (5.81) 2.17) 13.62-15.87 (3.56) < LOD 11.65) 2.98 (1.65-21.53) 4.00) 4.50-8.1 (8.88) 1.88) 4.90 (1.2 (13.70-9.50 (2.88) 4.33) * 2.71 (3.41-6.6) 8.3-23.8 (8.43 (2.00 (3.76-8.75) 75th 4.79-17.6-Trichlorophenol (creatinine corrected) Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.33 (7.87) * 2.56 (7.49-3.11) 10.82) 2.95-2.78 (2.87-6.78) 2.63 (<LOD-2.14-13.89) 10.81-9.83-6.43 (<LOD-2.2 (12.68) 2.05 (6.51-21.35 (3.0) 10.91 (7.10) 4.0 (9.14-2.73) 5.5 (10.55-2.32 (2.6-31.59 (2.89-2.2 (7. population from the National Health and Nutrition Examination Survey.82-2.28-4.8) 21.9-29.4 (11.25 (3.54 (2.77-4.18-4.1) 694 677 519 695 602 931 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.47-5.76) 4.49) 4.5) 11.33-2.04-16.41 (3.76) 2.77) 2. interval) 2.98) 10.63-13.63 (2.30-2.53) * 2.2) 19.6 (10.6) 970 1178 1019 1324 99-00 01-02 99-00 01-02 99-00 01-02 2.65) 18.92) 4.42) 2.40 (7.29-4.6 (9.82 (3.1 (13.91-2.52) 2.22 (<LOD-2.76) 1.4) 8.96) < LOD 4.63-15.91 (3.87-7.72) 32.7) 25.33 (1.26-13.02) 3.63) 4.00 (2.58 (4.8) 11.22 (3.73-22.88-7.9 (9.81) Selected percentiles ( 95% confidence interval) Sample 95th 21.25 (3.6 (9.05 (3.6 (22.26) * 99-00 01-02 99-00 01-02 99-00 01-02 4.38-5.65-2.32-19.22-9.38 (4.7 (14.4.0 (6.52) 2.01 (3.6) size 1989 2502 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.08-2.16-10.5 (8.2 (8.42 (2.13 (1.51 (2.5) 11.02 (1.78) 90th 12.9-64.82 (8.8 (7.60 (4.1) 11.3 (9.24 (1.9) 8.46-14.23) 4.6) 13.1-21.6) 12.7) 6.44 (3.22 (1.48-2.67-17.S.20-2.04-2.0 (11.66-4.5) 9.06) 11.17) 2.38) 22.23 (1.43-7.5 (7.15 (6.25-2.Organochlorine Pesticides Urinary 2.4) 4.52 (3.29 (6.60-2.6 (5.9) 7.8) 12.7-36.22-2.06) 4.53-11.38 (2.68) 2.3) 8.18-2.17-4.3-37.83-6.25-17.40 (2.94-13.00) 4.10 (6.21-11.9-34.88) * 2.0) 8.83 (3.87) 2.63) * 4.83-5.1-32.06-2. Fourth National Report on Human Exposure to Environmental Chemicals 115 .56-5.53 (3.25-15.88) 5.99-2.26 (6.9) 19.9-32.4) 9.13-6.19-5.29-4.5) 8.9) 481 574 678 819 830 1109 99-00 01-02 99-00 01-02 2.15 (1.1) 14.5-28.4 (12.6 (12.8) 19.51) 18.

Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine.pdf. To T. Needham LL.EPA). Radon K. Int Arch Occup Environ Health 1991.gov/safewater/ccl/pdfs/reg_determine2/report_ ccl2-reg2_ucmr1_occurrencereport.146:83-91.S. Environ Res 1995. Szadkowski D. Fast DM. Lindroos L. 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]. 5/19/09 116 Fourth National Report on Human Exposure to Environmental Chemicals . html.18(4):469-474. Safe A. The Great Lakes Consortium. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children. Schulz C.106(5):279-289. Luotamo M. Holler JS. Pekari K. Available at URL: http://www. et al. Smith SJ. Hill RH Jr. Seiwert M. Chlorophenol exposure in harbor workers exposed to river silt aerosols. Seifert B. The metabolism of higher chlorinated benzene isomers. Environmental Protection Agency (U. Monitoring internal exposure to metals and organic substances in workers at a hazardous waste incinerator after 3 years of operation.atsdr. Falk C.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). 206:15-24. Am J Ind Med 2004. December 2006 Draft.63:57-62. Kohli J. 4/21/09 Agramunt MC. Urinary excretion of chlorinated phenols in saw-mill workers. Int J Hyg Environ Health 2003. Bailey SL. Corbella J. Burse VW. Heinrich-Ramm R. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Wegner R. Shealy DB.45:440-445. Head SL. Aitio A. Baur X. Kaus S. July 1999.54(3):203-208. Toxicol Lett 2003. Gregg M. U. Jones D.gov/toxprofiles/tp107.epa. Jarvisalo J. S. et al. Hill RH Jr.71:99108. Available at URL: http://www. Poschadel B. Becker K. Needham LL.cdc. Domingo JL. Arch Environ Contam Toxicol 1989. Domingo A. Toxicological profile for chlorophenols [online]. Olson J. Environ Health Perspect 1998. Pesticide residues in urine of adults living in the United States: reference range concentrations. Anderson HA. Can J Biochem 1976. Baker S. Hanrahan L. et al.

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

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

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

20-7.33 (5.79-7.08-2.20 (.58 (5.0) 5.8-32.0) 6.9 (8.2 (14.490-2.94) 3.70-19. which may vary for some chemicals by year and by individual sample.3) 14.91) 4.290 (<LOD-.599-1.1) 13.5-17.37 (3.21 (.2.8) 19.52) * * 1.80) 2.50 (4.82-12.30-6.00-27.94) * * .42) .1 (9.9-18.830 (<LOD-3.60-25.13-2.83 (5.1) 10.61 (3.4 (7.20 (. and 0.2) 16.954 (.72) 5.0 (7.0) 5.02-5. see Data Analysis section) for Survey years 99-00.890 (<LOD-2.11 (.0) 15.0) 10.45 (2.2.0) 11.03 (.81) 11.23-5.97) 90th 7.8) 11.15) 14.50 (.50 (2.60 (1.2 (9.80 (2.0) 11.60-11.13 (2.70-14.8) 7.8 (8.0) 20.32 (.4 (7.40-16.47) * * 1.4 (9.2) 16.00-12.98-5.9) 14.S.4 (9.22 (.5 (11.0) 12.70) .68-7.90-4.52) 6.40-14.0 (12.00-27.44-3.1-17.0 (7.70) < LOD < LOD 1.5) 20.860-2.21) 9.98-12.1 (10.00-12.71 (2.36-4.2 (7.0) 10.10-7.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.7 (14.0 (7.70 (2.35-16.5-16.93 (4.2 (14.26-8.8 (14. population from the National Health and Nutrition Examination Survey.20-4.80) 3.2) 672 678 473 509 696 578 595 948 752 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.0) 10.4) 18.40-5.30 (2.56 (1.93-24.58 (2. interval) 1.2-20.80) 2.32) 1.76 (2.80) .17-3.73) * * .30 (4.0-28.0-27.0 (6.10 (2.6) 7.80) 11.07-10.80) 2.51) 2.81) 1.90 (1.70 (4.5 (8.19) 9.0) 10.56-13.95) 5.50-5.47) 5.40-11.30 (2. 0.40 (.0 (9.00 (5.04) < LOD 1.90) 3.620-1.00) 3.08-15.60-18.56 (6.16) 4.20 (.2 (7.2 (9.50) 2.0 (8.2) 14.86-15.26 (5.48-7.0) 11.758-1.74 (8.80-24.10 (2.0) 5.750-1.9) 8.00 (4.86 (1.80) 4.82) 10.97) 8.12-19.38-5.66) * * 1.44 (2.7) 11.34-7.27-3.4) 17.670-1.0 (4.10) < LOD .28) 1.00-19.55-6.20 (.35-11.80-4.39 (3.63) 1.40-1.54 (3.20-30. 01-02.05-7.27-15.10) < LOD < LOD 4.55-8.8 (12.79 (5.3-15.15-12.0) 10.1-23.0) 9.9) 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 1.0) 6.43-12. < LOD means less than the limit of detection.44-38.01) * * 1.2 (7.46) 10.780) < LOD 3.623-1.26-6.74 (8.90) 2.10 (.81) 11.58) Selected percentiles ( 95% confidence interval) Total * * 50th 1.5) 15.2) 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 1.90-5.70) < LOD < LOD 75th 3.61) 4. and 03-04 are 0.0 (5.10 (.4) 20.89) 9.52-11.0) 7.757-2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.290 (<LOD-1.16 (2.840-1.13 (2.810-1.981 (.1) 95th 13.60 (5.70-11. 120 Fourth National Report on Human Exposure to Environmental Chemicals .6) 18.7 (12.57-7.970-2.00 (1.53) 4. respectively.34-3.14) * * .3) 17.56 (4.42-3.8) 7.80 (4.70-23.00-7.00) 3.80) .0) 11.99 (5.0) 6. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.33-18.35-12.579-1.58 (3.96-3.2 (11.67) 3.12) 4.60) .717-1.0 (6.71-9.60) < LOD < LOD 4.29) * * 1.0 (8.0 (8.530 (<LOD-2.8 (9.3) 16.0 (7.740-2.700-1.39 (8.2) 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 1.08 (<LOD-2.30-4.600 (<LOD-1.955 (.20 (2.80-22.02) 4.1.50-36.40-19.0 (9.85 (3.

996 (.80 (7.820 (.7 (9.570-1.28 (5.6) 13.40-12.8) 16.56) .510-1.75 (7.9-28.3) 15.94-10.94 (2.620-1.77 (6.00 (4.81-5.82-14.93-9.2) 7.574-1.37 (5.7) 12.87-5.1-15.533-1.07 (.5) 12.98-22.06-2.95 (3.75 (3.72) 11.818 (.04 (1.5) 11.7) 5.920 (.47 (1.88-15.960 (<LOD-2.02 (2.21-23.98) .30) 2.98) .29) * * .540-1.47) 2.34) < LOD < LOD .93) 9.3) 16.2) 5.24-3.650-1.54-15.2 (8.29 (2.82-26.15-10.2 (6.03 (2.40) 4.94 (4.0) 7.54-11.75) 14.35) < LOD < LOD 3.5 (4.62) .78 (2.67) 1.02 (7.93-5.37-5.44 (2.75-7.88 (5.500-1.40-28.92-5. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.7 (10.7) 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.38) .45-5.37-3.3) 12.890 (<LOD-1.56-13.32-12.87 (1.13) 4.38 (1.76-4.81 (1.1 (11.45-11.40-14.19 (4.71-2.633-1.8) 12.69) 2.84 (5.7) 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 .57-10.66-15.7 (8.25) < LOD .66 (1.69) 4.87 (3.52) 4.1 (10.05) .60-9.4) 4.64-5.71) 10.430-1.75) 2.56) 4.94-23.54-2.830-1.94-9.870-2.62-5.90-8.03) 2.02-2.89-3.1 (8.54-4.855 (.20-8.9 (9.45-5.566-1.0 (8. population from the National Health and Nutrition Examination Survey.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 1.40 (3.85 (6.54) .36) * * 1.98 (3.549-1.95) 2.82-14.5) 8.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.780 (<LOD-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.09) 2.4) 13.28 (2.68-4.9 (5.6) 9.98) 9.2) 95th 12.57 (6.34 (6.27) < LOD 2. interval) .924 (.18 (.61-13.932 (.1 (6.2) 9.6) 11.60) 2.79-9.01-2.80 (2.710 (<LOD-1.50) 7.5-20.1) 4.4) 4.00-19.31-14.80 (6.34) * * .608-1.5) 7.883 (.83 (7.6) 8.79-3.4 (9.9) 11.5-16.00-13.84) 7.8) 6.68) < LOD < LOD 3.2) 13.773-1.2) 5.42 (3.43 (3.92-2.6 (10.30 (1.02-14.40-5.14 (3.41) Selected percentiles ( 95% confidence interval) Total * * 50th .2) 8.57 (4.57) 4.9) 16.8) 7.900 (.66 (2.05 (1.23 (4.37) 9.960 (.43) 2.46) 2.03-6.37 (4.42) 12.47 (3.34 (6.790 (.0) 6.5) 7.10-13.28 (4.40-3.46-5.03 (7.88) 2.73 (1.40) < LOD < LOD 75th 2.4 (4.560-1.94-22.860 (.00 (4.31 (3.8 (10.00) 8.750 (<LOD-1.66 (5.82-6.41-12.41) .9 (9.28) 10.00-17.26) * * .11-6.5-32.10 (3.80) 9.05 (.35 (1.7) 18.61 (1.03) 2.76) < LOD .67) 4.88-10.09 (.66-34.1 (7.47) * * .61 (1.56) 7.28-9.89) * * 1.58) * * 1.60) * * .53 (6.3) 5.55-20.98-5. Fourth National Report on Human Exposure to Environmental Chemicals 121 .74) 90th 7.53) 9.69 (4.04-6.9) 12.5-13.69-10.83) 8.67-19.2 (10.51-5.1 (9.90-5.8) 8.85) 2.74) 4.43 (.09-11.53-11.6 (9.1) 4.39 (2.S.25) 6.61-29.47 (3.23) 4.440 (<LOD-2.3) 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 1.890 (<LOD-1.

34 (6.6) 952 1187 946 997 1332 1019 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * 1.30) < LOD < LOD 4.3) 10.66) 4.67) 3.40 (2.70-8.7-21.0 (14.50) 3.790 (<LOD-1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.40) < LOD < LOD 75th 2.95 (5.29) < LOD < LOD < LOD < LOD 3.5.6) 18.1 (10.89 (2.0 (8.9-17.5) 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 * * * * * * .70 (1.0-33.8-17.80) 5.62-17.31-7.90 (6.96) 90th 7.0 (9.3) 8.24-5.63-14.11-6.88) 10.00-16.16-1.0 (10.27) .90 (6.22 (6.90-15.74) * * * * * 1.4) 672 678 498 509 695 579 595 948 757 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.20-18.50) 5.0) 19.72) 2.90-15.8-20.1 (10.90 (2. population from the National Health and Nutrition Examination Survey.20) .3) 14.3 (9.00-18.4-17.51) < LOD 1.41-5.00) < LOD .24 (2.90) 4.9) 10.7 (10.30) 3.29-4.46-28.7) 16. and 0.680 (<LOD-1.80-3.95 (2.6-41.0) 13.27) 4.99 (3.18 (3.86-10.00-9.00) 7.0) 9.5.37) 2.0 (9.3 (11.4 (10.00-4.4 (10.0) 13.0-29.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.35-3.35 (6.5) 21.7) 22.0) 6.6 (10.47-6.00) 3.60) < LOD < LOD 2.9-15.60 (2.34-3.2 (7.60 (6.39-13.52 (6.20) 3.9-14.64) 10.4) 7.10-4.20) 3.70-9.670 (<LOD-1.77-3.15-2.1) 11. and 03-04 are 0.0) 18.70 (8.0 (13.80 (2.30) < LOD < LOD .80-6.80-4.78) 5.14 (6.70) 2.2 (9.80 (2.4) 11.7-19.84-4. see Data Analysis section) for Survey years 99-00.27 (7.89) 2.73) 7.90 (2.70-9. which may vary for some chemicals by year and by individual sample.00) 3.740 (<LOD-1.6) 14.0) 14.60 (5. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.0) 12.27 (3.20-8.670 (<LOD-1. 01-02.9) 95th 14.0) 14.82) 8.00) 8.7 (11.92) 9.8 (12.18) * * * * * * * * 1.98-9.42 (1.8-21.30) 8.0) 23.25 (2. 0.35) 4.3 (12.61 (3.58.7) 15.0 (15.0-24.5-26.8 (12.31-12.22) 8.0-24.8) 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) 10.45 (3.3 (9.10 (.9) 9.8) 9.9 (12.61-32.80-8. < LOD means less than the limit of detection.10) 6.3 (7.0 (7.59-3.39 (5.0-19.70-5.910 (<LOD-2.37 (3.3) 22.0) 7. 122 Fourth National Report on Human Exposure to Environmental Chemicals .28 (7.90-31.04 (3.95-9.96) 3.92-17.97-4.66-13.5 (8.8) 8.00-18.S.0) 11.00-4.49-4.6) 14.0) 12.670 (<LOD-1.30) 3.80) .31) 1.80 (5.27) 9.0) 11.9) 16.970 (<LOD-2.33-11.80-21.53 (3.10 (<LOD-1.77-14.0) 12.9 (7.34-10.46-4.17 (7.50) .22-12.40 (2.10-10.00 (.90 (6.58 (1.34-5.1-23.5 (9.3) 20.67-10.50-5.10-15.6) 11.50-4.90) 8.90 (5.75 (3.0) 9.4 (14.6-19.0 (10.580-2.90 (2.8-20.01 (2.06 (2.67) 4.41) 3.20 (<LOD-2.88) 3.2) 14.80) .20-4. respectively.650-1. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th .80-12.0 (5.3 (6.15-6.22 (6.90 (6.90-9.12 (4.80-14.6 (10.81-6.7) 14.75 (2.670 (<LOD-1.5 (8.90 (1.

38 (.530-1.75-3.1 (13.00 (<LOD-1.18) 2.72-4.09-11.74-19.86) 9.5) 13.96-11.86-3.23-3.9-25.88-7.3) 12.2) 10.87 (3.61 (2.0 (10.2) 16.2) 15.89) 5.5 (8.27) < LOD .25 (4.52-3.68-19.6 (12.32) 2.38 (1.780-1.27) 1.32-8.9) 19.96-10.81 (7.20-3.59-3.19) 3.77 (2.75-3.00 (3.70-35.85-8.71 (1.74-4.4) 15.4-18.77 (2.89 (3.03 (6.9 (9.4-16.44-6.2) 12.8 (8.1) 10.2) 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.70-2.30) 8.79-9.34-18.6) 12.950) .3-17.25-9.4) 7.6) 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 * * * * * * .2 (9.8 (10.00) 8.67 (7.99) 2.760 (<LOD-1.37-5.00 (5.54) 9.33-10.2) 12.28) 6.0-19.07) 2.51-10.45) 3.3-34.4) 7.12 (7.6) 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 (15.973 (.55) .77) 3.73 (5.85-17.21) * * * * * 1.92 (5.6) 13.29 (5.29 (2.28-12.50 (6.0) 14.83 (7.00) 2.590 (<LOD-.54-5.36 (2.4) 7.68-4.5-17.9) 16.5) 8.3-17.8) 11.99 (4.29) 3.38) 1.3) 8.4) 16.3) 6.7 (10.93 (2.30-5.37) 3.690 (.93 (<LOD-2.51-7.27) * * * * * * * * 1.39-17.27-13.6) 7.3-21.03) 3.1 (8.78 (4.5 (10.43 (2.6 (10.93 (6.41 (7.02-4.7) 9.16 (3.79-6.5) 22.7) 14.30) 2.82-11.9-17.5) 10.8) 14.95) 90th 8.0-21.9 (9.620 (<LOD-.7 (11.71) < LOD < LOD 2.940) < LOD < LOD 1.97-4.27) 5.5 (9.91) 3.67 (1.890-2.92) 3.7 (10.88 (1.95) 3.38-13.38 (2.72) 4.3) 9.7-19.S.89 (2.15) < LOD < LOD 75th 2.5 (11.03 (2.07-3.68) .07 (5. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th .00 (<LOD-1.01-5.78-10.00 (2.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Dimethylphosphate (DMP) (creatinine corrected) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.6-19.11 (5.80) 3.6) 6.3-15.2) 8.89-3.34) < LOD < LOD < LOD < LOD 3.14 (2.1) 13.42) 8.2) 12.0 (8.6) 14.16-14.63 (2.78) 4.0 (13.95 (2.83 (6.94 (5.920 (<LOD-1.0 (11.3 (7.00 (7.89-13.93-10.12) < LOD < LOD 4.4-16.54 (7.89-10. population from the National Health and Nutrition Examination Survey.9 (9.21-21.30) 7.42-19.33) 3.6 (11.06 (<LOD-1.2) 19.86 (3.28 (1.4) 6.64-11.6 (11.91-9.68-10. Fourth National Report on Human Exposure to Environmental Chemicals 123 .58 (4.78 (6.45) 6.05-3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.29-2.6 (13.7-23.55 (2.69-11.8) 16.2 (9.7) 12.15 (1.53-8.04) 9.6) 95th 16.09-11.48 (2.810 (<LOD-1.4 (11.94-14.06) .50-17.910 (<LOD-1.47-9. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.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 1.1) 20.11-3.2-15.850 (<LOD-1.97) < LOD .6 (13.55) 16.4-15.07) 2.63 (6.42) 7.82-8.4) 9.2-30.7) 14.1 (19.7 (8.89-3.7) 15.

50 (1.780) .50-2.800 (. interval) Selected percentiles ( 95% confidence interval) Total * .30-3.50-2.850) < LOD .970) 1.550 (.549 (.58 (1.19-1.48 (1.550 (.597) * .70-7.86 (1.22-3.10) 1.34) 2.45-4.54-2. 01-02.49) 2.690) .340-.740 (.96-5.453 (.590-.32 (1.587) * * .760 (.08 (2.749 (.570 (.10) 1.00 (1.810) .240 (<LOD-.08 (2.31-3.560-.585) * * .54 (2. 124 Fourth National Report on Human Exposure to Environmental Chemicals .343 (.90 (1.17-4.83 (2.680-1.570 (<LOD-.620-1.22-8.27 (3.930) 1.10-1.960) .280-.580-1.80 (1.70-2.390-.570 (.20) 1.13) 2.49) .76-6.50 (1.500 (<LOD-.740-1.690 (.700) .600-1.76 (1.57 (2.36-4.820 (.467 (.450 (<LOD-.260 (<LOD-.570) * .95-5.16) 1.14-1.00-4.20) 2.910) 1.00) 1.710 (.60) 2.730) .98-3.720-1.20-1.90) 2.17) 1.26 (2.510 (.460-.74) 3.01-3.60 (2.32) 3.303-.01) .580-.46 (2.01-1.759) * .30) 1.46-3.80 (2.59-6.47) 2. see Data Analysis section) for Survey years 99-00.26) .592) * .380-.400) .89-6.70 (1.90) 2.201-.31) 2.31-3.570-1.382-.700) .30) 2.68-5.63 (1. and 03-04 are 0.960) .83 (2.80) 5.94 (2.680-1.720 (.80) 3.30-3.11-3.160 (<LOD-.880 (.73-5.390-.29) 1.94 (3.11-3.34) 2.47 (1.35) 1.780 (.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Diethylthiophosphate (DETP) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.96-3.09 (.09.540 (.780 (.980) 1.27 (2.31) 95th 2.30 (. and 0.22 (1.80) 3.359-.33-2.388-.75 (2.30 (1.90) 3.710 (.10) 1.618) * .91) 2.79) .710) .83) 2.80) 2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.70 (1.87-3.930-1. 0.750) 1.740-.03) 1.600 (<LOD-.650-.910 (.10-1.29-2.380-.1.670) .930) < LOD .690-.45 (1.20) 2.940) < LOD .30 (.15) 2.89) 672 678 478 509 695 553 595 948 745 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.80) 3.50) 1.950) 90th 1.15) 2.00) 2.83) .46) 1.46 (1.30 (.57 (1.457 (.790 (.86) 3.80) 2.50 (1.840 (.449 (.32-1.75-2.00-2.740 (.18 (.73 (1.960-1.880) < LOD 75th .65 (2.41-5.970) .20 (1.860) < LOD < LOD .97 (2.69-4.22-3.830 (.45 (2.990-1.18 (1.720-1.37-2.910-1.74-5.30) 4.73 (2.16-3.20) 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 * .05-3.50 (1.21) 3.455 (.490 (<LOD-.48 (2.20 (2.20-2.95 (2.98 (2.336-.960) 1.77-2.77 (1.350-.S.98) .40 (1. respectively.353-.960 (.16) 2.04) .210 (<LOD-.20 (1.750-1.54) .42-2. which may vary for some chemicals by year and by individual sample.94) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.690-1.38) 1.398-.20) 3.83) 1.570 (<LOD-. population from the National Health and Nutrition Examination Survey.79) .22-2.45 (1.89) 471 575 296 664 822 690 814 1122 919 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * .78) .90-4.440-.61 (1.70 (1.2.10) 3.820 (.50 (1.39) 2.20-2.17) 1.20 (1.88) 1.584) .60-4. < LOD means less than the limit of detection.20-3.592-.59-2.505 (.30-1.425 (.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 * .23-3.510 (<LOD-.592) * 50th .14 (1.25-1.64 (1.04) 1.657) * * .949) .600-.880) < LOD .13) .930 (.05-2.95) 2.20) 3.30) 4.380) .55 (3.89) 1.350-.459 (.41 (2.40 (1.60) 3.89) .

20-7.390-1.43 (1.08-3.70 (2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.740) .530 (.540-.88 (1.380-1.07-2.830 (.07) 1.42) .00 (3.22) .11 (.44) 2.81) 2.58-6.89 (1.73 (2.710 (.350) .09) .60) .73-3. interval) Selected percentiles ( 95% confidence interval) Total * .253-.470) .38 (2.72 (2.19 (1.368) * .820) .23) 3.460 (.91 (1.60) 1.377-.305 (.72-4.05 (1.67-3.580 (.88) .07) 5.05) 1.270-.700 (.830) 90th 1.16) 1.645) .67) 1.05) < LOD .70 (3.47-4.22-3.08) 2.50) 1.57-2.22) 1.590-1.11-2.552 (.22) 4.08-2.08-3.66 (2.509 (.28 (1.39 (1.16-1.520 (.66) .136-. population from the National Health and Nutrition Examination Survey.17) 2.90) 2.900) 1.57 (1.590) * 50th .50 (1.33) .38 (1.800) < LOD .08-3.29-4.32 (.640 (.39) 2.760) .64 (2.980-1.79) 1.591 (.370-.535 (.447 (.840) 1.920) .930-1.80) 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 * .44-2.330 (<LOD-.34 (1.99) 1.640 (.17-2.32) 5.560-.42 (.870) .330-.80) 2.22 (2.60 (1.380) .870 (.71 (1.590 (.720-1.69 (3.910) < LOD .33 (1.280 (<LOD-.92 (1.97 (1.560-.87 (2.690) < LOD < LOD .640 (.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 * .24) 4.67) .285-.32) 2.23 (.31-1.230 (<LOD-.730) .61-3.412-.00-3.444-.880) 1.43) 2.950-2.84 (2.23) 2.840) .742) * * .550-.393 (.403) .61 (3.700 (.480-1.471-.550-1.17) 2.30-2.65) 2.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.05-2.60 (2.688) * .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 * .72 (1.05-4.270 (<LOD-.720 (.S.57 (3.72) 1.71) 2.597) * .470 (<LOD-.800-1.97) 1.58) 3.460) .49-4.08) 1.02-3.180 (<LOD-.64 (2.660-.42-6.32) 1.440-1.750 (.13 (1.990-1.760) < LOD 75th .38-3.43) 1.335-.08 (2.61) 2.300 (<LOD-.61-3.560 (.04-5.02-3.300-.84-6.740) < LOD 1.08 (.92) 3.400) .63 (1.62 (1.20-2.22-2.77 (3.790) .680 (.510 (.47 (1.98) 1.75) 6.18-2.07) 1.03-2.10) 2.07 (.67 (1.41 (.739) * .97 (1.52 (1.92-8.318-.06-2.460-1.940-1.23) 2.76) 1.25-3.43) 2.79 (1.71) .52) 3.04-1.45 (1.320-.820) 1.07-3.250 (<LOD-.99) 2.710 (.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.448 (.380-.04) 95th 2.515) * * .07) 1.630) * .62 (2.390) .42-8.850) 1.49 (1.550-.02-6.453 (.47 (1.77-4.710 (.08-2.53) .580-.250 (<LOD-.11) 1.510 (.580) .480) .22-3.30) 3.36) 3.310-.69 (1.00-1.03-1.14 (2.55 (1.78) 3.790 (.77-3.75-3.08-3.840) 1.400-1.08-2.270-.95) 1.89-3.75 (2.82) 2.310 (<LOD-.550) .97) 2.750 (.45 (2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.57-4.510-.06) 4.348-.372 (.320-.310 (<LOD-.23) 1.485) * * .670 (.94) .75 (1.700 (.32-1. Fourth National Report on Human Exposure to Environmental Chemicals 125 .67 (1.520-.490 (.82 (2.16-2.58 (1.55-3.20) 1.234 (.500-.

19) 2.60) < LOD 1.690-3.92) * 2.83 (1.40-4.8) 671 678 498 509 695 579 595 947 757 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.5-20.470 (<LOD-1.610 (<LOD-1.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.3 (14.10 (1.77) 38.18.44-7.04 (<LOD-2.4-76.3) 33.3 (12.0 (38.0) 4.72 (1.9) 18.16) * 1.0) 19.0 (24.0 (33.5) 30.2) 31.13 (1.0 (6.0 (26.26) 75th 11.70) 5.64-8.04-8.30) 11.95 (5.35-6.3 (24.0) 471 575 310 664 822 717 813 1121 938 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 2.0 (8.00-24.1-46.45) 2.2-27.0-39.0) 28.0-41.88) 1.23-2.0) 3.8-21.71-2.70-17.40) 50th 2.0) 3.48) 5.0) 32.05-3.70) 1.8-24.70 (7.6-45.2) 16.25-3.43-7.8) 39.0 (38.20 (2.0) 15.58) 16.87-7.11) 2.0 (8.0 (11.97) 6.41) 1.0-62.32 (2.00 (.5-74.88) 3.33 (5.40-16.50-20.5-40.6-22.0 (38.5) 69.0-92.4 (15.23-2. interval) 1.20-4.0 (25.0-69.1 (25.93-3.0-62.96) 5.14) 5.30) 4.0 (8.41) 5.0) 3.10) 39.1-25.1) 38.0-41.2-27.6 (11.48-2.8 (22.66-5.86-3.5 (24.9) 38.80) .7-22.41 (1.0 (19.3 (10.06) * 2.00 (.4 (10.80) < LOD 1.69) 2.12) 1.80-2.0) 31.81-3.3) 28.40) < LOD 2.0-110) 34.50-5.70 (.10-4.99 (2.3 (12.1-20.46-6.79 (2.18) 20.05) 1.46-2.76 (2.1) 140 (46.59 (1.9 (10.0 (40.0 (37.54 (3.65 (4.0) 4.44) 2.29-4.6 (26.44) 3.7) 47.16) 2.50-7.90-8.27-6.5-27.2 (19. 0.6 (15.53) * 2.7) 20.60 (2. and 03-04 are 0.5-45.0-43.8 (12.5.76 (2.0) 33.0-58.52 (4.1 (25.0 (38.58-2.0) 30.1 (11.7-41.82 (1.02 (2.23) 9.29) 2.98) * 2.10-13.54 (1.0-53.49-2.20) 1.0-110) 42.04) 3.50-2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.1 (26.57-2.0) 3.29-9.2 (12.8 (12.67 (1.18) 6.830-4.2-39.4) 38.90 (1.48-2.830-3.0) 20.0 (17.0-29.0 (7.71) 5.9-51.0 (32.2-62.0-50.10 (7.90) 11.61-2.10 (1.1-47.17-2.0-41.3) 31.80) 1.11 (4.50-17.7 (12.21 (4.64-3.70 (1.61 (1.71 (4.79 (1.06 (1.53) 1.2-47.36-2.80) 90th 38.31-6.26 (.0) 4.92-5.6) 52.0-49.1) 38.0) 17.0) 28. < LOD means less than the limit of detection.0) 8.85 (1.70 (1.30 (.21 (1.0-53.0 (20.0-260) 34.530-4.1) 95th 48.8) 41.0) 17.660-2.8) 62.07-5. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.4 (19.3) 38.0) 16.41-4.70-6.21 (3.0 (20.0) 5.0-47. 126 Fourth National Report on Human Exposure to Environmental Chemicals . see Data Analysis section) for Survey years 99-00.90 (1.9 (19.8) 32.10) .9) 48.0 (38.8 (26.63-6.86 (1.98 (1.83-2.91 (4.83 (3.0) 15.3) 26.78) 9.9) 17.9-21.0 (21.0-58.6 (9.50 (2. population from the National Health and Nutrition Examination Survey.0-230) 35.10 (1.1 (22.41) 1.0) Sample size 1948 2518 1965 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 2.70) 1.0) 20.2-80.1 (10.77 (1.45) 2. which may vary for some chemicals by year and by individual sample.57-2.4.2-26.7 (28.78 (1.74-2.40) < LOD 1.0) 16.0 (13.6-27.4) 19.0 (38.0) 18.9 (27.1-19.30-14.9 (23.75-14.05) * 2.53) 40.2-33. respectively.10 (1.19-2.9 (19.13) 12.12 (3.1-40.79-2. and 0.4-22.S.0-31.81-2.600-2. 01-02.8) 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 1.44) Selected percentiles ( 95% confidence interval) Total * 2.3 (23.13 (1.0) 6.80-18.42) 1.0) 13.85) * 2.18) 14.09 (4.94 (1.59 (1.0) 45.0) 42.0-52.46 (.53 (1.0-39.0 (38.7 (12.6-54.1) 18.83-2.

66 (1.5-43.06) 1.4) 14.00) 6.2) 4.2) 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 2.3) 28.680-4.6) 11.70 (1.1) 52.46-6.1) 27.32-3.9-52.1) 25.750 (<LOD-1.46-5.70-4.36) 10.6-38.57) 4.06-1.69-5.27) 50th 2.83) .9) 24.55 (2.6) 3.50-5.68) 47.9) 3.62) 4.0 (23.4 (12.26-2.8) 3.38-1.18-1.7) 15.23-1.22-3.58-17.59-2.870-3.53) 1.4 (25.6) 23.88 (1.S.4-21.14 (.3 (10.3-19.38) 5.4-67.6) 7.7) 26.38 (3.94-20.45 (1.69-18.79 (2.95 (2.00-16.1 (33.7-43.17-3.9-18.7 (11.57 (6.1) 27.75 (1.0-70.0 (39.3-27.7 (24.1 (34.95) 90th 32.1-22.9 (39.4 (21.1 (50.33) 1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.7-37.34) * 1.3 (20.19) 5.51) .0) 47.64 (1.46) 1.3) 13.9-37.4-34.1) 17.71-2.1 (25.4 (19.19-6.7) 23.51) < LOD 1.95-16.5 (41.7 (18.43-2.72) 2.4 (25.6 (27.00) 1.28) 1. population from the National Health and Nutrition Examination Survey.1) 15.7-109) 22.52-4.2) 13.47 (3.3-22.62 (2.2 (21.88 (1.0 (17.60 (.5 (15.38-5.80-8.06) 1.9-41.63-5.45-1.4) 12.8) 31.12 (1.27-3.59-2.71 (1.2-47.30) 28.7-19.0-118) 29.58-2.60) 4.56) 1.3-42.2 (9.0) 25.5-36.36-13.7-47.2-38.24 (1.00 (4.3 (8.6-32.28 (1.0) 30.03-2.16-2.1 (39.5) 70.88 (4.61 (1.80 (1.11) < LOD 1.59-15.23) < LOD 2.7 (18.6 (24.47 (1.02) * 1.5 (34.47-17.35 (2.94) 1.90 (.08) 1.40 (5.82 (2.7) 61.670-1.4 (5.4) 3.84-13.75-6.6) 19.7 (10.82) 1.4 (11.0) 13.29-5.1-63.71) 8.61-22.9 (13.56 (2.07-2.44) 9.86) * 2.3 (10.5 (6.67-3.0 (14.4 (9.32 (3. interval) 1.99-4.07-2.8-26.43) * 2.76-2.18) 3.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Dimethylthiophosphate (DMTP) (creatinine corrected) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.9) 12.2 (8.5 (17.9 (19.54-2.37 (1.2-70.11-2.7) 34.890-4.61-2.46-22.21 (4.68 (1.08 (1.93) 5.26-4.40-7.18) * 2.19) 5.48) 1.899-2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.7) 95th 51.33) 2.20-5.40-4.9-36.9-95.888-1.7-20.5-190) 30.2) 41.8) 23.0 (32.2 (15.02 (.2-28.2) 13.6-49.39 (1.2 (16.0-71.9) 54.9) 3.0) 48.0 (25.8-34.8-43.03) 1.7) 66.0) 10.0) 3.33-5.48 (4.27) 10.4-71.35) 1.35) .25-3.2) 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 1.8-37.1-60.33) < LOD 1.9 (7.6 (7.96-16.0 (23.40 (2.37-2.9 (26.870-3.16 (1.2 (22.7) 30.09 (5.1) 13.930 (<LOD-1.7-38.4) 12.66) 8.31) 2.0-40.6-51.23) 37.8) 15.22-2.27 (6.5 (8.1) 25.0 (19.20) Selected percentiles ( 95% confidence interval) Total * 1.6) 3.8-45.75) * 1.3 (9.50 (2.8 (7.1 (12.52 (1.97 (1.9) 24.54-15.2) 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.75 (1.5) 27.8) 32.43-12.4-39.860 (<LOD-1.67-16.67 (1.19-14.67 (1.96) 2.16 (1.83 (.02) 1.2) 36.95-16.14-8.22 (.8) 11.91 (6.17) 2.41 (2.5-97.86) * 3.9 (10.91-2. Fourth National Report on Human Exposure to Environmental Chemicals 127 .1) 36.6 (11.2-34.15 (.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 1.01 (.88 (4.94) 19.870-3.07) 9.6) 112 (40.79-17.06) 75th 9.0 (6.2) 33.36 (4.22 (2.12) 3.19 (1.66 (1.16 (1.5 (15.5 (13.1) 13.

640 (.270 (.090 (<LOD-.160) . and 0.940 (.360-.140-.140) .05.210 (.660 (.100 (.280) < LOD < LOD < LOD < LOD .650-1.700-1.840) .830) .13) .10) .860-1.1.380-.620 (.300-1.430 (.770) < LOD 95th .40) .610 (. respectively.310 (.00) .20) .090 (<LOD-.540) .540) .120 (<LOD-.720-1.42) .650 (.430-.150) .870 (.420-.080 (<LOD-.370-.190 (.990 (.640-1.380-.310) < LOD < LOD < LOD < LOD .540) 672 678 498 509 694 579 595 947 757 Non-Hispanic blacks .530-.10) .410-1.630 (.680) .150 (<LOD-. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th 75th .130) .084-.60) 1.770 (.870 (.490 (.560 (.130-.410) < LOD < LOD < LOD < LOD .700-1.130-.32) .690-1.930 (.160-. 0.S.820 (.740) < LOD .870 (.680-1.1.36) .560 (.190 (.720 (.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 * * * * * * . see Data Analysis section) for Survey years 99-00.350) .470 (.390) < LOD < LOD .400-.510-1.30) .300-.610-.470-1.830) < LOD .120-.640) .160) .190 (.220 (. and 03-04 are 0.990) .310 (.650) .090 (<LOD-.540 (<LOD-.230) .720) .090 (<LOD-.760) < LOD . population from the National Health and Nutrition Examination Survey.550) .310) < LOD < LOD < LOD < LOD .360-.099-.460 (.12 (.680-1.171) * * .130-.610 (.140-.830 (.700-1.380-.850 (.080 (<LOD-.10) .110-. which may vary for some chemicals by year and by individual sample.600 (.200) < LOD < LOD .870 (.10 (.850 (.700-1.117 (.210 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.30) .450 (.320-.650-1.30) .860) .370-.220 (<LOD-.090 (<LOD-.900 (.050-.570) .290) < LOD < LOD < LOD < LOD Non-Hispanic whites Limit of detection (LOD.15) .820 (. 128 Fourth National Report on Human Exposure to Environmental Chemicals .990) .320 (.830 (.42) .870) < LOD .730) .460-.180) .290 (<LOD-.870 (.290) < LOD < LOD < LOD < LOD 90th .350) < LOD < LOD < LOD < LOD .120-.130) .162) * * * * * .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 * * * * * * * * * .330-.440-1.610-1.630 (.310-.450 (.03) .240 (<LOD-.090 (<LOD-.840) .58) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.170-.780) < LOD 1.410-. < LOD means less than the limit of detection.850) < LOD .260 (.230-.410-.650) .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.450 (.290) < LOD < LOD < LOD < LOD .640) .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 . 01-02.730-.390 (.130 (.680 (.140-.

02-1.190 (.470 (<LOD-.03) .880-1.330-.116 (.380 (.070 (<LOD-.20) 1.550 (.300 (.01 (.050 (<LOD-.43) .150-.610-1.330 (.650) < LOD .084-.730) .140) .110) .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.580) . Fourth National Report on Human Exposure to Environmental Chemicals 129 .960) .400) .090 (<LOD-.890 (.100-.140-.330-.710-1.02) .360) < LOD < LOD < LOD < LOD . population from the National Health and Nutrition Examination Survey.140-.730) .600-1.520-.860 (.410) .62) 1.410 (.940) .300-.86) .550 (.410-.500) .78) . interval) Selected percentiles ( 95% confidence interval) Total * * * 50th 75th .580 (.970) .860-2.12) < LOD .380-.640) 952 1187 945 997 1328 1017 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .330-.380-1.120) .60) .070 (<LOD-.780) < LOD 1.490-1.390-.03 (.09) .66) 1.340-.110-.58) 1.570-.86) .161) * * .03 (.170 (.230 (<LOD-.360-.450 (.29 (.380-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.370 (<LOD-.410-.500-1.700 (.440-1.260-.24) .080) .19 (.650-1.940) .450) .100 (<LOD-.220 (.380-.230) < LOD < LOD < LOD < LOD .860 (.730) .38) 1.270 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.00) < LOD .240-.560 (.14) 1.200 (.111) * * * * * .120) .260) .580 (.140-.760) .870) .190-.300-.410) < LOD < LOD .170) < LOD < LOD .460 (.230-.220) < LOD < LOD < LOD < LOD .990) .740 (.570-1.440 (.990) .500 (<LOD-.090 (.310) < LOD < LOD < LOD < LOD Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.190 (.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 * * * * * * * * * .670 (.750) < LOD 95th .810 (.080 (<LOD-.670-1.800-1.540) 471 576 310 664 821 715 814 1118 937 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * .070 (<LOD-.057-.330 (.540 (.730 (.270) < LOD < LOD < LOD < LOD .110) .060-.400 (<LOD-.540) .390-.200 (.580-1.310) < LOD < LOD < LOD < LOD .67) .S.670 (.280) < LOD < LOD < LOD < LOD .700) .720 (.880 (.570 (.660-1.36 (1.540 (.250-.640-1.700 (.080 (.320 (<LOD-.520) 672 678 497 509 693 578 595 947 756 Non-Hispanic blacks .03 (.700-1.140-.600) .24 (.210 (.850 (.360-.720 (.290) < LOD < LOD < LOD < LOD 90th .740) < LOD 1.110) .360 (.510-.070 (<LOD-.180-.410 (.580) < LOD .170 (.780 (.140-.110) .

05 (2.70) 2.30-6.10-9.37) .50) .10-3.0) 4.88-3. and 0.90-9.0 (3.840 (<LOD-1.14) 2.80) < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 4.07 (1.0) 4.30 (1.40 (1.0 (17.210-1. < LOD means less than the limit of detection.31-10.40) 2.40 (1.380-. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th 2.87) 12.87) 5.70-50.00 (1.94-3.0 (4.0) 3. respectively.07) 1.0 (16.70-7.800) 90th 13.63) 32.0 (17.0 (5.0-40.0) 2.07 (3.21) 3.0 (7.61 (1.32-9.28) .82-4.00-17.62-8.45 (2.16) Sample size 1949 2518 1930 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .425-1.0 (5.60) 1.610 (.800-4.0) 4.610) < LOD < LOD < LOD < LOD < LOD 2.99) 19.11 (1.800) 17.600 (.080-1.35) 5.20-4.0) 5.83-3.11) 13.10 (.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.360-1.00-17.90-37.53-7.36-3.76 (1.52) 5.590 (.6) 5.99) 11.29-10.28) 1.0 (17.90) .0) 4.0 (5.67) .0) 2.94 (1.6) 672 678 498 509 695 552 595 947 752 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.0) 2.0-44.12-1.260-.07 (3.35) 11.90-28.900 (.48 (2.15) 14.99 (1.40-8.370-.770) 2.21-3.11) .580 (.00) .S.00) .0 (5.65) 1.40-7.49 (1.30 (1.83) 2.59-5.1.42) 2.30 (1.90) .32 (1.70-3.110 (<LOD-. 130 Fourth National Report on Human Exposure to Environmental Chemicals .0) 2.83-3.86) 4.35-10.14-5.730 (.720) 2.50) 2.750-2.70-17.910) 2.53) 20.30) 95th 19.0 (17.36-3. see Data Analysis section) for Survey years 99-00.39 (2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.90 (2.38-3.67 (1. 01-02.0 (4.74 (3.640 (.51-8.350-.170-1.691 (.60) .0-40.0 (5.0-38.97) 20.830 (.14) .400-1.49) 17.74) 5.850) 16.39) .90-20.20 (1.42) .0-38.750-1.250 (<LOD-.960 (.20) < LOD < LOD < LOD < LOD < LOD 1.48) 13.480-.07-3.00 (.52 (1.740 (.840-3. which may vary for some chemicals by year and by individual sample.26 (2.28-9.53 (2.510-.55-8.67 (2.0 (17. population from the National Health and Nutrition Examination Survey.0) 7.46 (1.31) .30-3.0) 2.20-17.08.10 (3.10 (3.05 (3.20-4.0-39.30) .13 (3.890 (.01) 5.0) 2.960 (<LOD-1.0-38. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.07-3.10-3.94-8.03 (.70-30.90) .190-1.55-4.0) 5.63 (3.30 (2.97) 20.96 (1.05-3. and 03-04 are 0.33 (4.15) 19.0) 2.1.80 (4.18) 1.40) 1.640 (.40-4. 0.870) < LOD < LOD .620-1.20 (1.30-7.40-20.30 (.00) 1.0) 5.24-7.330 (<LOD-1.840 (.49 (1.0 (13.350-.51 (2.770 (<LOD-1.880) 5.3) 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 * * * * * * * * * .68) 2.690 (.52 (1.23-6.47 (3.43-4.90 (1.0 (6.0) 5.66) 4.12) * * * * * * * * .85-3.62) 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 * * * * * * .

560 (.960 (.07 (2.150 (<LOD-.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.21-3.5 (8.430) 1.56) .04-16.88) 17.0 (4.890 (.50) 11.45 (1.32) 9.310-.71 (.83-11.80) 3.630-1.53) .1 (7.748 (.85-3.25-38.57-40.2 (8.64) 30.28-6.14 (1.83 (4.69) 2.800-2.88 (.10-3.74 (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 .67) 2.930) .25 (1.13 (2.820) .7 (6.5) 7.240-.830-3.5 (9.370-1.600 (<LOD-1.330-1.370) < LOD < LOD < LOD < LOD < LOD 1.00-19.32-6.660) < LOD < LOD .S.8-33.55 (3.40-2.25-9.91) 2.580-1.650) 90th 10.71 (2.02-4.82-11.940-4.51-4.7) 4.17 (1.11) .820 (.18) * * * * * * * * .88-3.2-38.89 (2.41) 18.4 (4.57) 1.35 (.4-34.88 (2.740-1.64-4.580) 16.0 (9.22) 2.670 (.98 (4.67-6.500 (.5) 2.340-.09-3.260-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.700) < LOD < LOD < LOD < LOD < LOD 1.84) 9.55) 21.36 (.580 (.49-2.18) 1.10 (2.690-5.03) 16.650 (.31-18.11-5.02) .91-4.40-12.33 (3.02 (1.970-3. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.39) 20. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th 1.67 (2.62-17.97) .12 (4.580) 1.370 (.47-10.08) .15) 9.69-7.33-4.7) 6.22-27.85 (1.52 (.47) 5.60 (1.00) .340 (.53) 27.67) 1.700) 6.9 (11.92 (2. Fourth National Report on Human Exposure to Environmental Chemicals 131 .65 (2.37) 4.40) 1. population from the National Health and Nutrition Examination Survey.340-.3) 3.14-6.62 (1.30 (4.474-1.48-42.780-4.250 (<LOD-.270 (<LOD-.96) 2.73 (4.75) 5.1) 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 * * * * * * .31) .90-6.33-3.8) 4.38 (2.540 (.40 (.790) 11.44) .31) .55) 21.590) 2.7) 5.8 (20.8) 1.24) 3.8) 2.1 (5.9) 5.48 (4.29 (4.5 (11.4) 2.23-7.8) 7.6) 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 * * * * * * * * * .620-3.06 (.86) .3) 2.43) .340-.56) 2.51-44.850-3.860-2.360 (.47-10.0) 4.56 (1.1) 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.47) .540-1.470 (.18) 95th 21.33-5.7) 3.59 (1.5) 2.790 (.320-1.17) 5.80 (.190-1.03) 2.01 (1.27 (2.10) 2.770) .12-4.04 (1.1) 2.8) 2.79 (.57) 8.66-47.830 (.31-7.7 (12.60) < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 4.48-7.07-21.86 (3.96-25.41 (4.29-4.50) .450 (.260-.02 (.81-17.5-40.710 (<LOD-1.430 (<LOD-.05) .96-8.44-11.33 (1.390-.9) 6.57 (.730-3.8) 7.50 (2.50 (4.840-3.77 (.270-.

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Rohlman D. Sci Total Environ 2004. Russo J. Washington (DC). Masala G. metabolite clearance. EPA). Rothlein J. Saieva C. Tumino R.26(2):199-209. Buchanan D. Schenker M. McConnell R. Occupational exposure to organophosphate pesticides: a neurobehavioral study. Association between in utero organophosphate pesticide exposure and abnormal reflexes in neonates. 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. Gladstone EA. Lasarev M.38(4):546-563. 2004. Muniz J. Frasca G. Claypoole K.2000 and 2001 market estimates. Pedersen L. National Academy of Sciences. Available at URL: http://books. Lu C. The presence of dialkylphosphates in fresh fruit juices: implication for organophosphorus pesticide exposure and risk assessments. Narang A. McCauley L. Chrislip D. Hore P. Prendergast MA. Barr DB. Weisskopf C. vibration sense and tremor among South African farm workers. Lancet 1995. Aprea C. Pilkington A. Neurotoxicology 2005. Robson MG.52(2):190-195. Variation in organophosphate pesticide metabolites in urine of children living in agricultural communities.S.S. Keefe TJ. Environ Health Perspect 2006. Effects of occupational exposure to organophosphate pesticides on nerve and neuromuscular function. Wickremasinghe AR. Jenkins B.43(1):38-45. Petchuay C. J Toxicol Environ Health A 2005. Bradman A. Occup Environ Med 1995. Buccafusco JJ. Stark A.68(3):209-227 Maizlish N. Kidd M. Bravo R. O’Malley M. National Research Council (NRC). Am J Ind Med 1987. Occup Environ Med 2001. Effects of chronic. Biological monitoring of organophosphate pesticides in preschool children in an agricultural community in Thailand. 1/12/09 Peiris-John RJ. EPA. Rosenstock L. Neuropsychological effects of long-term exposure to organophosphates in sheep dip.30(2):98-103. and spatial learning in monkeys and rats. Savage EP. Neurotoxicity among pesticide applicators exposed to organophosphates. Vitayavirasak B. Scherer J. Mounce LM. Salvini S. Office of Prevention Pesticides and Toxic Substances. van der Hoek W. Jamal GA. Phillips J.24(1):18-29. Burcar PJ. Caltabiano LM. Heaton RK. low-level exposure to the organophosphate diazinon.epa. Environ Health Perspect 2005. Daniell WE. Terry AV Jr. 1991. Rodnitzky RL. Twenty-four-hour urinary excretion of ten pesticide metabolites in healthy adults in two different areas of Italy (Florence and Ragusa).338(8761):223-227. Samuels S. Lasarev M. Available at URL: http://www. Scand J Work Environ Health 1998. Ruberu DK. Lancet. Effects of long-term organophosphate exposures on neurological symptoms. Smit LA. Stokes L.52(10):648-653. 1993 [online].332(1-3):71-80. Johnson C.44(4):352-357.edu/ openbook.20(2):115-22. Weerasekera G. Arch Environ Health 1975. Levy LS. Ames RG. Chronic central nervous system effects of acute organophosphate pesticide intoxication. Washington (DC): U. Malathion deposition.113(4):504-508. The Pesticide Health Effects Study Group. Chronic neurological sequelae to organophosphate pesticide poisoning.114(5):691-696.12(2):153-172. Visuthismajarn P. Lewis JA. U. Steenland K. Nell V. Gillham R. Am J Public Health 1994. Santana J. Fourth National Report on Human Exposure to Environmental Chemicals 133 . Organophosphate pesticide exposure and neurobehavioral performance in agricultural and non-agricultural Hispanic workers. Pesticide industry sales and usage . A behavioral evaluation of pest control workers with short-term.nap. Eskenazi B. Berry H. Stephens R. Thompson ML. et al.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Krieger RI. S.345(8958):11351139. Int J Occup Environ Health 2006. Marshall E. Hansen S. low-level organophosphate exposure on delayed recall.php?record_id=2126&page=1.12(2):134-141. Lambert WE. Seiber J. et al. 4/7/09 Young JG. Bull Environ Contam Toxicol 1994. et al.84(5):731-736. Environmental Protection Agency (U. and cholinesterase status of date dusters and harvesters in California. Pesticides in the Diets of Infants and Children. gov/oppbead1/pestsales/01pestsales/market_estimates2001. Beach J. Monitoring of urinary alkyl phosphates in pestcontrol operators exposed to various organophosphorus insecticides. Arch Environ Contam Toxicol 2000. et al. Muniz J. Arch Environ Health 1988. Spurgeon A. Takamiya K. Irish RM. et al. discrimination. Neurotoxicol Teratol 1998. Myers JE. May.58(11):702710. London L. Rothlein J.pdf. Chronic neurological sequelae of acute organophosphate pesticide poisoning. Keifer M. Dinoff TM. J Occup Environ Med 2002. Calvert IA.

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

0 (7.09 (2. 2002).70-17.30-12.20-4.50-2.4 (9.0) 12. and inhalation routes.9 (10.0) 8.44-5.0) 6.22) 2.27 (7.97) 2.3 (8.53 (1.28-3.7) 8. air.35) 1.10) 2.80) 2.10 (3.0) 12.5-24.5.09 (3.0) 15.44-2.29) 90th 7. and is infrequently detected in ground water (IPCS. Chlorpyrifos is degraded in agricultural soils with a half-life of several months.43-2.04-10.39-2.9 (7.77) 1.45 (1. and sprayed to kill mosquitoes.90-2. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. Survey Geometric mean (95% conf.80) 12.89 (2.91 (1.71 (6.47 (4.63 (2.71 (2.20) 2.97) 2.1) 5.8) 10.03) 99-00 01-02 99-00 01-02 99-00 01-02 2.6-Trichloro-2-pyridinol Metabolite of Chlorpyrifos and Chlorpyrifos-methyl Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.66-15. 2007).50 (1.34) 1.0 (7. chlorpyrifos and TCPy were detected in all indoor air and dust samples (Morgan et al.77-6.36 (4. and dust.43-2.30-9. Chlorpyrifos is Urinary 3.7) 13. Chlorpyrifos is not well absorbed through the skin but dermal exposure can be significant when other routes of exposure are low. population from the National Health and Nutrition Examination Survey.86) 4.50-8.90) 3.30 (2.47-9.57 (2. applied to structures to kill termites.0) 12.95 (4.90 (3.97-7.30-5.0 (13.10 (1.0) 8. 2002).00) 1.80 (1. Estimated intakes from diet and water have not exceeded recommended intake limits. Approximately 21-24 million pounds per year were used domestically from 1987-1998. After 2001.50 (2.90-8.02 (1.77-15.90 (1. 2005).80) 4.0) 12.81-2.60-3.99-4.0 (7.20-11.70 (1.31-2.2 (10.97) 7.50-4. It also has been applied directly on animals to kill mites. 2921-88-2 Chlorpyrifos-methyl CAS No.51) 1.5.64) 3.98-15.1-16.22 (1.37) 5.00) 3.74-9.01) 1.20-2. For instance.0) 10.000 pounds are used per year.61) 75th 3.26) 7.61 (1.72-4.90-4.30 (4.60 (4.40-13.30 (2.70-11.60-4.4-15.61-7.0 (9.63 (8.24-1.04-10.10 (5.20) 4.70) 1.89-2.68 (7. 1999.91) 16.79-2.90-7.28) 2.87-6.4 and 0.0) 18.9 (9.70-15. staying bound to soil particles.8-15. dermal.6-trichloro-2-pyridinol (TCPy) is a metabolite of chlorpyrifos and chlorpyrifos-methyl.0 (10.0) 10.EPA.90 (2.62-2.30) 4.29-1. It has low leachability.50 (2.52-12.20-3.40 (5.0) 9.50 (2.21) 3.7-23.20) 2.40-2.5) 7.40 (5. Chlorpyrifos is very toxic to fish and aquatic invertebrates and shows modest degrees of bioconcentration.0) 10.32-1.3) 8.0) 12.60) 5.92 (1.60-3.97) 4.46-2.6) 7.02 (7.83) 1. Chlorpyrifos is a broad spectrum organophosphorus insecticide that has been widely used to control insects on food crops such as corn.20-16.50-14.20-14.02) 1.63 (1.44 (3. 5598-13-0 General Information The chemical 3.35) 2.60 (5.0 (7.4 (8.13 (1.66-4.S.32) 2.25) 1.51-2.90) 7.60-2.84) 1.20 (2.S.10-17.96) 3.74 (1.70-16.76 (1.59) 2.05-5.60 (2.17 (1.80-8. and on plants for days to several weeks.2) 972 1183 1022 1326 99-00 01-02 99-00 01-02 99-00 01-02 1.70-5.4) 481 573 681 823 832 1113 99-00 01-02 99-00 01-02 1. Inhalational and dermal routes of exposure are important in pesticide formulators and applicators.30) 5.40) 2.77 (1.67 (2.71 (1.72) 2.05) 1.20 (4.40 (6.37 (1.S.24-3.94 (4.and post-construction structural applications for termite control were to be phased out by 2005 (U.14) Selected percentiles ( 95% confidence interval) Sample 95th 10. The general population may be exposed to chlorpyrifos via oral.EPA. chlorpyrifos was no longer registered for indoor residential uses in the United States.30) 4.30-2.19 (1.3) size 1994 2509 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th 1.55-5.38 (3.3 (10.50-2.30-11. USGS. Chlorpyrifos-methyl is an organophosphorus insecticide also used in agriculture and not registered for residential use.9) 697 660 521 701 602 947 Limit of detection (LOD.5 (8.20) 10.37 (4.4.59-2.52-2.19-3. but can be detected in streams receiving runoff from application sites.67 (1. Approximately 80.00) 2.8) 9.03) 1. pre.40-10.0) 11. Exposure can also result from contact with contaminated surfaces.10) 6.10 (4.67 (2.76 (1.16) 2. 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. Fourth National Report on Human Exposure to Environmental Chemicals 135 .9-18.50-4.95) 7.50 (1.47) 1.4 (10.30-1.80) 1.9) 11.25) 3. interval) 1.90 (1.80 (7.47-13.Organophosphorus Insecticides: Specific Metabolites Chlorpyrifos CAS No.68-2.0) 7.7) 9.78 (7.50-5.47-11..88 (1.13-3. in 142 urban homes and preschools in North Carolina.0-28.0) 14.15 (1.51 (1.70 (1.3 (11.90 (6.40-26.00-8.39) 4.31-2.00-24.80-10.0 (7.40) 9.

Metabolic hydrolysis leads to the formation of TCPy.63-2.71 (1.72-2.55 (4. Urinary 3.9 (12.02 (5. Betancourt et al.72) 1..37 (1.11 (2. Chlorpyrifos is eliminated from the body primarily in the urine with a half-life of approximately 27 hours (Nolan et al.57-2.62-7.8) 9.60-3.39 (2.43-10.05) 3.01) 1.EPA.Organophosphorus Insecticides: Specific Metabolites rapidly absorbed following ingestion.65-15.49-2.2 (7. chronic exposure to chlorpyrifos may be associated with slight alterations in some components of neurophysiologic testing (Steenland et al.22 (6.19) 6. 2005.86 (3.44 (6.64-7.82) 8.93 (1.94-14.93 (4.0) 6.49 (1.39-1.44 (1.97) 3.49-2.83) 1.56 (1.92) 3.58-5.47 (1. 2002).19-1.86 (1.0) 16.S.88-10.68) 6.75) 6.26-14.20 (2.63 (5.27-1.06 (5. weakness.. Survey Geometric mean (95% conf. Human health effects from chlorpyrifos or chlorpyrifosmethyl at low environmental doses or at biomonitored levels from low environmental exposures are unknown.97-3.44-6.88-8.31-4.85-4. Two observational studies of pregnant women and their offspring exposed to chlorpyrifos at environmental levels have found inconsistent relationships with birth outcomes of weight and length (Eskenazi et al.85 (2.24) 75th 2.30-4.4) 4.53 (2.90-9.1 (7.66) 1.91) 2.63 (4.48 (2.91-13.35) 1.39 (4.74) 1.29 (3. 2006b).09 (1.66-11.23) 14.00-13. 2006.31-1.91) 1.0) 10.91 (3.45 (1. Thus. Based on animal data and human cholinesterase monitoring during occupational exposure.98 (6.80-11.33-7.07) 1.69 (1.36) 1.87-3.25-11.35-1.33 (5.40) 1.23-1.00 (7.3 (7.88 (1.00-8.32) 1. the detection of TCPy in a person’s urine may reflect exposure to the environmental degradates.11-9.94-12.7) 7.28) 2.44 (5.940-1. and behavior may occur at systemically nontoxic doses or at doses of chlorpyrifos that do not result in cholinergic signs (Aldridge et al.12) 1.84-6.71) 3.46 (2.33) 2.79-13.5) 5.93) 5.6) 10.42 (5.24) 5.05-4.25-12.3) 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 1.19-2. The metabolite TCPy does not inhibit acetylcholinesterase enzymes.12-3. Overt cholinergic toxicity from chlorpyrifos has been described following suicidal ingestion and unintentional high level occupational exposure.45-1. population from the National Health and Nutrition Examination Survey.91) 10.17-4.1-21.68) 1.0) 12.96) 3.8) 972 1183 1022 1325 99-00 01-02 99-00 01-02 99-00 01-02 1.09-2. neurotransmission. phosphorothioates such as chlorpyrifos are metabolically activated to the “oxon” form which has greater toxicity than the parent insecticide.58) 5. In addition to being a metabolite of chlorpyrifos and chlorpyrifos-methyl in the body.5 (6.01) 3. Howard et al.14-8.64 (1.3) 8.97) 3.98 (7.83-11.89) 4. Roy et al.62) 1.95 (3.82 (3.64-2.05-8.99-8.72) 2.24-24.97 (3..07) 5.42-2. Chlorpyrifos and chlorpyrifos-methyl both demonstrate moderate acute toxicity in animal studies. cholinergic effects.83-2.21-6.34-1. and producing acute symptoms such as nausea.24 (1. vomiting.1 (10.50 (4.05-3.09-1.08) 6.82-4.22) 1.14) 1.86 (1.56-2.06 (1.52 (5.54) 5.16 (4. Once absorbed. 2006a. Ricceri et al.01) 3.12-1.59-2.24-4.42 (6.81 (3.46 (1. 2006.62) 90th 5.95 (1..51 (1.05-1. 2000).58 (4. Recent in vitro and in vivo animal studies suggest that effects on neuronal morphogenesis.16) 6.11) 7.28) 2. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”).2) 6.93) 2.99) 1.54 (2.22 (4.88 (1.92-2.38) 3.6-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.47 (1.44 (5.24-1.80) 3..33 (1.03) 1. resulting in excess acetylcholine at nerve terminals.80-6. 1984).06-4.24-5.88-9.22-6.20-1.47 (5.0) 481 573 681 822 832 1113 99-00 01-02 99-00 01-02 1.75 (1..78 (1.82 (2.56 (4.01) 99-00 01-02 99-00 01-02 99-00 01-02 3..6) 9.92 (1.02) 7.44 (1.91 (4. TCPy can also occur in the environment from the breakdown of the parent compounds..55 (1. 2005.97 (2.76 (2.88-8.09-3. In pesticide applicators.39) 6.47-2.15 (4.17-4.19) 3.31) 1.3) 9.1-38.57) 9.58 (1. and other metabolites.21-1.55) 1.76 (3.5.66 (1.58) 1.70-4.93 (2.53-5.57) 2.59) 3.85) Selected percentiles ( 95% confidence interval) Sample 95th 8.91) 1.3) 8.S.49-2.73 (1.30-1.58 (1.80-4.77) 1.85) 1.33 (. These organophosphorus insecticides share a mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system.. paralysis.43 (4.65-11.85) 4.27-7. TCPy is more persistent in the environment than chlorpyrifos itself (U.11 (2. and seizures.81) 2. Slotkin et al.35) 2.48 (1.91-4.25-1. interval) 1.60 (1. ubiquitous lowlevel environmental exposures in humans would not be expected to result in inhibition of cholinesterase activity.88) 6.00) 1.57-2.85 (3.7) 697 660 521 700 602 947 136 Fourth National Report on Human Exposure to Environmental Chemicals .56) 5.41 (1.56) 2. 2005.

2002). 2005.113(8):1027-1031. Lioy PJ.6-trichloro-2-pyridinol in the Italian population—validation of analytical method and preliminary results (multicentric study).. 2005).gov/pesticides/. Environ Health Perspect 2005.gov/toxpro2.S.cdc. In Iowa farm families using several different pesticides. Meyer A. 2005). 2006) and episodically many times higher for pesticide applicators than median levels from NHANES 1999-2000 (CDC. Barisano A. the weighted population mean of TCPy measurements was approximately three times higher (Adgate.S. Barr DB. suggesting changing low-level exposure and variance in collection timing with respect to exposure (Meeker et al. 2005. Eberly LE. et al. 2000). 2004). CDC. In Minnesota and South Carolina farmers who used chlorpyrifos. 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. 2005). Magnaghi S. J AOAC Int 1999. EPA at: http://www. 76% had detectable levels of TCPy and levels were similar to those reported for NHANES 1999-2000 (Eskenazi et al. Following crack-and-crevice application of chlorpyrifos in their homes.. Chlorpyrifos is not considered to be mutagenic or carcinogenic (NTP. et al. the geometric mean urinary TCPy levels were similar in parents and children. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample.S. Other small studies of environmentally-exposed persons have shown a high frequency of detecting low levels of TCPy. Finding a measurable amount of TCPy in urine does not mean that the level will result in an adverse health effect. Haidar S... Slotkin TA. Clayton CA. Chlorpyrifos exposure and biological monitoring among manufacturing workers. Levels of TCPy in the U. Betancourt AM. Burns CJ. subsamples of NHANES 1999-2000 and 2001-2002 (CDC. Measurements of urinary TCPy in single spot urine collections show variability over time in environmentally exposed individuals and are poorly correlated between collections.S.63(3):218220. 1999).EPA.atsdr. Additional information about external exposure (i. 2006). In a probability-based sample of 102 Minnesota children aged 3-13 years. 2005.. Seidler FJ. 1995) and were similar to levels reported in studies of healthy adults in Germany (Koch et al. Perera et al. 2005). Albers JW. MacIntosh et al. Berent S. (1999) reported mean urinary TCPy levels in a sample of Maryland adults that were about three times higher than adults in the U. Koch et al. Betta A. Aldridge JE. population (CDC. Curwin et al...109(6):583-590. 2001) and Italy (Aprea et al.5. 1992.S. Chlorpyrifos levels in house dust and hand rinses did not correlate with levels of TCPy in urine (Lioy et al. 2004). Occup Environ Med 2006.. 2001).. References Adgate JL. but levels were roughly four to six times higher than the geometric means in the U. Biomonitoring Information Urinary TCPy levels reflect recent exposure. representative subsample of NHANES 19992000 (CDC. Effect of developmental exposure to chlorpyrifos on the expression of neurotrophin growth factors and cell-specific markers in neonatal rat brain. 2005). Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.82(2):305-312.html and from U.Organophosphorus Insecticides: Specific Metabolites 2004... 2005) appear roughly similar to values reported for a nonrandom subsample of NHANES III (1988-1994) participants (Hill et al. urinary TCPy levels in children were reported not to have increased (Hore et al. Of 482 pregnant women living in an agricultural community.e. 2003. et al. Giordani B. Garabrant D.92(2):500-506. environmental levels) and health effects is available from ATSDR at: http://www.. 2001) than the corresponding values reported for the group aged 6-11 years from the NHANES 1999-2000 subsample (CDC. Whyatt et al. Estimation of dose or intake based on the urinary excretion of TCPy indicates that environmental doses are generally below recommended limits (Hore et al. Freeman NC. Aprea C. Alterations in central nervous system serotonergic and dopaminergic synaptic activity in adulthood after prenatal or neonatal chlorpyrifos exposure. median urinary levels on the conventional diet were several fold higher than those in the NHANES 1999-2000 subsample (Lu et al. Lotti A..epa. Burgess SC. U.. Fourth National Report on Human Exposure to Environmental Chemicals 137 .Reference values of urinary 3. Replacing conventional diets with organic diets in 23 children led to about a fourfold decrease in urinary levels of chlorpyrifos. Toxicol Sci 2006.. Carr RL. 2005). Environ Health Perspect 2001. Urinary levels of TCPy have been found to be hundredsfold higher for chlorpyrifos manufacturing workers (Burns et al.. urinary TCPy levels averaged about sixfold higher than those in the NHANES 1999-2000 subsample (Mandel et al. but not chlorpyrifos. Some reproductive and teratogenic effects in animal testing were only observed at high doses of chlorpyrifos that caused overt maternal toxicity. Catenacci G. 2007).

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Pesticide residues in urine of adults living in the United States: reference range concentrations.112(10):1116-1124. Mandel JS. Sheldon LS. Environmental Health Criteria 198. Sanderson WT. Hill RH Jr. Adgate JL. Howell RJ. Chlorpyrifos exerts opposing effects on axonal and dendritic growth in primary neuronal cultures. Slotkin TA. Jett DA. et al.S. MacIntosh DL. House dust levels of selected insecticides and a herbicide measured by the EL and LWW samplers and comparisons to hand rinses and urine metabolites. Robson M. Exposures of preschool children to chlorpyrifos and its degradation product 3. U. Tsai WY.114(2):260-263.93(1):105-113. 4/7/09 Perera FP.111(2):201-205. Gregg M.10(4):327-340. Head SL. Available at URL: http://www. Environ Health Perspect 2004. Rauh V. Nolan RJ. EPA). et al. Chrislip DW. Dick RB. Needham LL. Rick DL. Bucelli R. Barr DB. Scand J Work Environ Health 2005. Freshour NL.114(10):1542-1546. 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. Reid TM. Hammerstrom KA. Bravo R. Seidler FJ. Comparative developmental neurotoxicity of organophosphate insecticides: effects on brain development are separable from systemic toxicity. Weltzien E. Freeman N. Environ Health Perspect 2000. Croghan CW. A longitudinal investigation of selected pesticide metabolites in urine. Environ Health Perspect 2006. Bailey SL.6-trichloro-2-pyridinol. Quantitative morphological assessment reveals neuronal and glial deficits in hippocampus after a brief subtoxic exposure to chlorpyrifos in neonatal rats. Acquavella JF. Pellizzari E. Edwards RD. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population. Irish R.cfm?objectid=6F5E95EB-F1F6-975E7C20F4211536F46F. Developmental neurotoxicity of organophosphorous pesticides: fetal and neonatal exposure to chlorpyrifos alters sex specific behaviors at adulthood in mice. J Expo Anal Environ Epidemiol 2005. Chlorpyrifos: pharmacokinetics in human volunteers. Ryan L. Steenland K. Jewell NP. Saunders JH. Hardt J. et al. Yang D. National Toxicology Program (NTP). Toxicol Sci 2006. Hore P.5. Cometa MF. Harley K. Barr D.51(1):53-65. Gurunathan S. Baker S.73:8-15. Biomonitoring for farm families in the farm family exposure study. 2921-882. Effects of transplacental exposure to environmental pollution on birth outcomes in a multiethnic population. Slotkin TA. et al. Interim registration eligibility decision for chlorpyrifos. Freeman N. Hein MJ. J Expo Anal Environ Epidemiol 2000. Baker BA. Angerer J. Herrick RF. Bravo R.S. J Expo Anal Environ Epidemiol 1999.htm.9(5):494-501.108(4):293-300. Environ Res 1995.org/documents/jmpr/jmpmono/ v99pr03. Seidler FJ. Hines CJ. mothers and fathers living in farm and non-farm households in Iowa. Environ Health Perspect 2006a. Howard AS. Bruun D. et al. Venerosi A. Kromhout H. Heederik D. Lu C.155(1):71-80. Neurologic function among termiticide applicators exposed to chlorpyrifos.15(4):297-309. EPA 738-R- 138 Fourth National Report on Human Exposure to Environmental Chemicals . Chapman P.5. 4/7/09 Koch HM. Environ Health Perspect 2006b. Ryan PB. Tate CA. Environ Health Perspect 2005. Bennett DH. Robertson GL. Brain Res Dev Brain Res 2005. Seidler FJ. Environmental Protection Agency (U. Zhang J. Barr DB. Chlorpyrifos. Honeycutt R. et al. gov/ntpweb/index.113(2):211-219. Executive summary of safety and toxicity information. Atlanta (GA). Roy TS. Lioy PJ. Alexander BH. 2005. Morgan MK. Third National Report on Human Exposure to Environmental Chemicals.204(2-3):175-180.nih.niehs. Toxicol Appl Pharmacol 2005. Capone F.114(5):746-751.Organophosphorus Insecticides: Specific Metabolites Centers for Disease Control and Prevention (CDC). et al. Chlorpyrifos accumulation patterns for child-accessible surfaces and objects and urinary metabolite excretion by children for 2 weeks after crack-and-crevice application.

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

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

see Data Analysis section) for Survey year 01-02 is 0. population from the National Health and Nutrition Examination Survey. Survey Geometric mean (95% conf. Urinary 3-Chloro-7-hydroxy-4-methyl-2H-chromen-2-one/ol (creatinine corrected) Metabolite of Coumaphos Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.27) < LOD < LOD 567 814 1099 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1169 1311 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . * 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.270) < LOD 659 701 920 Limit of detection (LOD.Organophosphorus Insecticides: Specific Metabolites Urinary 3-Chloro-7-hydroxy-4-methyl-2H-chromen-2-one/ol Metabolite of Coumaphos Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.380 (<LOD-. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2481 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .670 (<LOD-1.S.200 (<LOD-. population from the National Health and Nutrition Examination Survey. Survey Geometric mean (95% conf.2. which may vary for some chemicals by year and by individual sample. < LOD means less than the limit of detection.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 . 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 .560) < LOD 659 700 920 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.S. Fourth National Report on Human Exposure to Environmental Chemicals 141 .

Centers for Disease Control and Prevention (CDC). EPA 738-R-00-010. Reprod Toxicol 1998.12(6):619-645. Reregistration eligibility decision (RED) addendum and FPQA tolerance reassessment progress report: Coumaphos. Nguyen JV.376(6):808-815. Comparative organophosphate-induced effects observed in adult and neonatal Sprague-Dawley rats during the conduct of multigeneration toxicity studies. Olsson AO.gov/oppsrrd1/ REDs/0018tred. Third National Report on Human Exposure to Environmental Chemicals. Available at URL: http://www.pdf.Organophosphorus Insecticides: Specific Metabolites References Astroff AB. U. Anal Bioanal Chem 2003.epa.S. Freshwater KJ. Environmental Protection Agency (U. September 2000. EPA). 2005. Barr DB.S. 1/14/09 142 Fourth National Report on Human Exposure to Environmental Chemicals . Sadowski MA. Atlanta (GA). Eigenberg DA. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine.

dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”). and other metabolites. see Data Analysis section) for Survey years 99-00 and 01-02 are 7.49 (<LOD-2. Experimental diazinon exposure in people has demonstrated its rapid elimination into urine.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. It has been infrequently detected in general groundwater sampling but has been detected in streams receiving runoff from application sites (IPCS. diazinon produced wild bird kills before use restrictions were in place.45 (<LOD-3. Prior to 2000. 2007). fruits. 2004). which may vary for some chemicals by year and by individual sample.EPA. but is rapidly absorbed orally (IPCS. 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.Organophosphorus Insecticides: Specific Metabolites Diazinon CAS No. diazinon was widely used in residential and garden application. Survey Geometric mean (95% conf. < LOD means less than the limit of detection. but these uses have been phased out.EPA. diazinon cannot be sold for residential use. 1998.S. and forage crops. Diazinon is not well-absorbed through the skin. Metabolic hydrolysis leads to the formation of 2-isopropyl4-methyl-6-hydroxypyrimidine. about 13 million pounds of diazinon were used annually on agricultural sites in the United States. Once absorbed. since 2004. vegetable. in the past.05) < LOD < LOD 644 678 484 700 554 956 Limit of detection (LOD. Diazinon is biologically and chemically degraded in soils with a half-life of about a few weeks. seed and foliar applications are planned to be phased out (U.S. Inhalational and dermal routes of exposure can be significant for pesticide applicators. aerial. phosphorothioates such as diazinon are metabolically activated to the “oxon” form which has greater toxicity. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Fish and aquatic invertebrates show modest degrees of bioconcentration and are very sensitive to toxic effects. 2004).2 and 0.7. It is also used for cattle ear tag applications to control flies and ticks and. 333-41-5 General Information The chemical 2-isopropyl-4-methyl-6-hydroxypyrimidine is a metabolite of diazinon. 1998). population from the National Health and Nutrition Examination Survey.S. in some pest strips. and particularly when it was ingested in granular form. Most granular formulations. Estimated intakes from diet and water do not exceed recommended intake limits (U. an organophosphorus insecticide that is used to control insects on nuts. 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. USGS. Before these restrictions. 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. Fourth National Report on Human Exposure to Environmental Chemicals 143 . It is toxic to birds.

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. respectively (Baker et al. Biomonitoring Information Urinary levels of 2-isopropyl-4-methyl-6hydroxypyrimidine reflect recent exposure.atsdr. diazinon does not accumulate in tissues (IPCS. the detection of 2-isopropyl4-methyl-6-hydroxypyrimidine in a person’s urine may reflect exposure to the environmental degradate. The U. population from the National Health and Nutrition Examination Survey. agricultural.cdc.72 (<LOD-4.76 (<LOD-3. 2000. Seifert and Pewnim. 2002). and producing acute symptoms such as nausea. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Olsson et al. Diazinon has moderate acute toxicity in animal studies.EPA considers diazinon unlikely to be carcinogenic in humans.. environmental levels) and health effects is available from ATSDR at: http://www. EPA at: http://www.. although the 95th percentiles for children 6-11 years old and for non-Hispanic blacks were 1. 1992). 2003).S.epa.gov/toxpro2. respectively.49 μg/L. Additional information about external exposure (i. teratogen. Urinary 2-Isopropyl-4-methyl-6-hydroxypyrimidine (creatinine corrected) Metabolite of Diazinon Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.S. 1998). subsamples of NHANES 1999-2000 and 20012002. 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.html and from U. 2-isopropyl-4-methyl-6-hydroxypyrimidine can also occur in the environment from the breakdown of the parent compound. Intoxications in humans from intentional overdose.. and seizures. In addition to being a human metabolite of diazinon. In the U.. 1986 Rajendra et al. cholinergic effects.S. in the 2001-2002 subsample (CDC. 1998). In animals. most of the measurements of 2-isopropyl-4-methyl6-hydroxypyrimidine in urine were below the limit of detection. diazinon and other organophosphorus insecticides share a mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system. At high doses. 1986.e. Thus. paralysis. vomiting. 144 Fourth National Report on Human Exposure to Environmental Chemicals .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.gov/pesticides/. resulting in excess acetylcholine at nerve terminals.45 and 1. Survey Geometric mean (95% conf. and indoor applications have been documented.S. 2-isopropyl-4-methyl-6-hydroxypyrimidine was detectable in 57% and 43% of the 130 and 140 participants.Organophosphorus Insecticides: Specific Metabolites from dialkyl phosphate metabolite excretion (Garfitt et al. weakness. Diazinon is not considered to be a mutagen. animal carcinogen. Human health effects from diazinon at low environmental doses or at biomonitored levels from low environmental exposures are unknown.. There has been only limited study of diazinon at systemically non-toxic doses that do not result in cholinergic signs (Anthony et al.. or reproductive toxicant (IPCS.

Third National Report on Human Exposure to Environmental Chemicals. Available at URL: http://www. March 2006. Oloffs PC. Oloffs PC. Pesticides in the Nation’s Streams and Ground Water.S. EPA).114(2):260-263. J Expo Anal Environ Epidemiol 2000.htm. Environmental Health Criteria 198. Seifert J.S. The Quality of Our Nation’s Waters. Atlanta (GA). Available at URL: http://pubs. 2006).111(12):1478-1484. International Programme on Chemical Safety-INCHEM (IPCS). Diazinon. Environmental Protection Agency (U. Sadowski MA. Environ Health Perspect 2003. Alteration of mice L-tryptophan metabolism by the organophosphorous acid triester diazinon. Barr DB. Driskell WJ.inchem. Diazinon. 1992-2001.37(4):501-507. In 54 Canadian greenhouse workers. Nguyen JV. (2003) found that 2-isopropyl4-methyl-6-hydroxypyrimidine was detectable in 96% and 58% of the subjects. 6/1/09 Fourth National Report on Human Exposure to Environmental Chemicals 145 . Rajendra W.50(5):505-515.9(2):117-131.org/documents/ehc/ehc/ehc198. May 2004. Bouchard M. Cocker J.10(6 Pt 2):789-798. 2005. References Anthony J.gov/ oppsrrd1/REDs/diazinon_ired. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides.Organophosphorus Insecticides: Specific Metabolites 2005). Geological Survey (USGS). Semen quality in relation to biomarkers of pesticide exposure.. Toxicol Lett 2002. Interim reregistration eligibility decision (IRED. EPA 738-R-04-006. Toepel K. 2007 [online]. In a small number of men visiting fertility clinics in Missouri and Minnesota. urinary 2-isopropyl-4-methyl-6-hydroxypyrimidine levels were below the limit of detection (Bouchard et al. Bull Environ Contam Toxicol 1986. Swan SH. Bravo R. 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. 2006).376(6):808-815. Drobnis EZ.S. Effect of sublethal levels of diazinon: histopathology of liver. 1/14/09 U. Anal Bioanal Chem 2003. et al. 4/7/09 Lu C. Centers for Disease Control and Prevention (CDC). 1998. Exposure to the organophosphate diazinon: data from a human volunteer study with oral and dermal doses. Needham LL. Barr DB. Brunet RC.gov/circ/2005/1291/. Banister EW. 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. Barr DB.usgs. U. revised February 15.. Barr DB. Effects of chronic intake of diazinon on blood and brain monoamines and amino acids. Quantification of selected pesticide metabolites in human urine using isotope dilution high-performance liquid chromatography/ tandem mass spectrometry.134(1-3):105-113. Drug Chem Toxicol 1986. Beeson MD. Carrier G. Environ Health Perspect 2006. Mason HJ. Ann Occup Hyg 2006. Banister E. Noisel N. Dumas P. Redmon JB. Baker SE.pdf.44(11):2243-2250. Available at URL: http://www. In 23 children. Swan et al. Liu F. Kruse RL. Irish R. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine. Biological monitoring of exposure to organophosphorus insecticides in a group of horticultural greenhouse workers. Study for Future Families Research Group. Biochem Pharmacol 1992. urinary 2-isopropyl-4-methyl-6hydroxypyrimidine was detected in less than 14% of multiple samples collected during varied diets (Lu et al. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Jones K. Pewnim T. Garfitt SJ. Olsson AO. Fenske RA.epa.

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

Toxicity from unprotected bystander exposure during applications is rare (U. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 2006).S. Thomas et al..50) < LOD < LOD 453 660 807 99-00 99-00 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 937 983 99-00 99-00 99-00 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 680 498 580 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. IARC considers malathion not classifiable as a human carcinogen. Replacing conventional diets with organic diets in 23 children led to a tenfold decrease in urinary levels of malathion dicarboxylic acid. Survey Geometric mean (95% conf. Malathion itself has not been considered genotoxic (U.S. population from the National Health and Nutrition Examination Survey. 1999).atsdr. CDC. median urinary levels on the conventional diet were similar to the detection limit in the NHANES 1999-2000 subsample (CDC. Of 382 pregnant women living in an agricultural community.html and from U. A study of agricultural workers reported preshift urinary levels of malathion dicarboxylic acid that were twofold to eightfold higher than detection limits in the NHANES 1999-2000 subsample (Krieger and Dinoff. The 95th percentile urinary levels of malathion dicarboxylic acid in both urban and nonurban Minnesota children aged 3-13 years (adjusted for sociodemographic variables) in 1997 were several-fold higher than the analytical detection limits reported for children aged 6-11 years in the U.. Lu et al.0 mg/kg/day have shown no acetylcholinesterase inhibition or other short term effects (IPCS. Malathion dicarboxylic acid was infrequently detected in multiple samples from 80 Maryland residents in 1995-96 (MacIntosh et al. EPA at: http://www. 1996. some of the postshift urine levels in duster-applicators were thousandsfold higher than the detection limits in the NHANES 1999-2000 subsample. 2006).5 and 5. representative subsample from NHANES 19992000 (Adgate. 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.. Flessel et al.EPA.S. environmental levels) and health effects is available from ATSDR at: http://www. 1990). Additional information about external exposure (i.. 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. Fourth National Report on Human Exposure to Environmental Chemicals 147 .74 (<LOD-5.EPA. a malaoxon metabolite and a technical grade impurity tested positive in some chromosomal tests (Blasiak et al.cdc. 1999.S. Finding a measurable amount of malathion dicarboxylic acid in urine does not mean that the level will result in an adverse health effect. but isomalathion. but cholinesterase activity was not affected. Biomonitoring Information Levels of urinary malathion dicarboxylic acid reflect recent exposure. Giri et al.. 1987. 2004). 2001. 2005.. 2000).. 2003). 2005). 2002. 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. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 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.gov/pesticides/... 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..gov/toxpro2. 2006).. 1993. Pluth et al.epa.S. and it is not considered an animal teratogen or a reproductive toxicant. 2005). Malathion does not appear to produce human reproductive or teratogenic effects at environmental levels of exposure (Grether et al.e.Organophosphorus Insecticides: Specific Metabolites direct ingestion of agricultural strength solutions.

Bradman A. Flessel P. Jewell NP. Harris JA.pdf. 1992-2001. et al. Griffith W. Comparison of organophosphorus pesticide metabolite levels in single and multiple daily urine samples collected from preschool children in Washington State.Organophosphorus Insecticides: Specific Metabolites References Adgate JL.114(2):260-263. et al. Barr DB. Giri A. In vitro studies on the genotoxicity of the organophosphorus insecticide malathion and its two analogues. March 2006.15(2):164-171. et al. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. 2005. J Expo Anal Environ Epidemiol 2005. Barr DB. Ryan PB. Barr DB. Clayton CA. Quintana PJ. Environ Health Perspect 2004. Nicklas JA. 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.S. Genotoxic effects of malathion: an organophosphorus insecticide using three mammalian bioassays in vivo. Hertz-Picciotto I. Neutra R. 2007 [online]. Available at URL: http://pubs. Lu C. A longitudinal investigation of selected pesticide metabolites in urine. Reproductive outcome in women exposed to malathion. The Quality of Our Nation’s Waters. Am J Public Health 1987. 6/1/09 148 Fourth National Report on Human Exposure to Environmental Chemicals . Kizer KW: Exposure to aerial malathion application and the occurrence of congenital anomalies and low birthweight.445(2):275-283. Brunet RC. Geological Survey (USGS).112(10):1116-1124. Dinoff TM. U. Malathion deposition. Lu C. Toxicol Sci 2003 May.73(1):182-94. Hammerstrom KA. Lioy PJ. O’Neill JP. Carrier G. Rappaport E. 6/1/09 U. Centers for Disease Control and Prevention (CDC). Thomas D. Available at URL: http://www. Pluth JM. Erratum in: Toxicol Sci 2003 Aug. Krieger RI.132(4):794-795.56(10):2393-2399. MacIntosh DL. Eberly LE.epa. Gosselin NH. Weltzien E. Barr DB. Reregistration eligibility decision (RED) Malathion. and cholinesterase status of date dusters and harvesters in California. Petitti D. 4/7/09 Kissel JC.38(4):546-553. htm. EPA 738-R06-030. Samuel O. Bravo R. Third National Report on Human Exposure to Environmental Chemicals. Grether JK. Albertini RJ.inchem. Kedan G. Cancer Res 1996.514(1-2):223231. Mutat Res 1999. Genetic toxicity of malathion: a review. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population. Malathion (addendum). Environ Health Perspect 2001.109(6):583-590. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample. Prasad SB. J Expo Anal Environ Epidemiol 1999. metabolite clearance. Hooper K. Sharma GD.S. Jaloszynski P. Goldhaber M.org/documents/jmpr/jmpmono/v2003pr06. Szyfter K.gov/circ/2005/1291/. Mutat Res 2002. Am J Epidemiol 1990. Atlanta (GA). Fenske RA. Environmental Protection Agency (U. July 2006. Toepel K.usgs. Pesticides in the Nation’s Streams and Ground Water.22(1):7-17. Eskenazi B. Curl CL. Blasiak J.gov/oppsrrd1/REDs/ malathion_red. Needham LL. Arch Environ Contam Toxicol 2000. International Programme on Chemical Safety-INCHEM (IPCS). Trzeciak A. Bouchard M. Irish R. Environ Health Perspect 2006. Freeman NC. revised February 15. Giri S.S. Environ Mol Mutagen 1993. Swan SH. Harley K.9(5):494-501. Pesticides residues in food: 2003 FAO/WHO Meeting on Pesticide Residues. Dumoulin MJ.74(2):following table of contents. Available at URL: http://www.77:1009-1010. EPA).

11) 2.80 (2.50-14.28 (1. Given its limited use.74) 5.0) 3.0) 3.01) 695 660 518 679 603 941 Limit of detection (LOD.60) 1.02-6. Metabolism of ethyl or methyl parathion leads to the formation of paranitrophenol. 1977). and of the chemical nitrobenzene. It had been applied to cotton.700 (<LOD-.90-9. 2006).58) 3.40) 4.67 (1.70-6.41-4.S.92) 5.79) 4.27) 2. the potential for human exposure to either ethyl or methyl parathion through the diet or drinking water is low.50 (1. phosphorothioates such as methyl and ethyl parathion are metabolically activated to the “oxon” forms which have greater toxicity than the parent insecticides.0) 3.00 (2.60 (4. first registered in 1948.36-1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 5. was once a restricted-use insecticide with limited applications on certain agricultural crops.40-4.45) 5.37-2.28 (1.32-1.10-11.15-3. and oral routes can occur in pesticide and agricultural workers (Muttray et al.70) 2.70) 2.33 (1.44) 2. Both are toxic to birds. pulmonary.32-1. Ethyl parathion.EPA.37-4.S. fish.09-1. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.50) 3.60-36.30-3.50 (2.49 (1.37) 2. Many previous registered agricultural uses of methyl parathion have been cancelled (U. all registered uses were voluntarily cancelled (U.10) 22.71 (2.S.80 (2.Organophosphorus Insecticides: Specific Metabolites Methyl Parathion CAS No.32-3. ethyl parathion. population from the National Health and Nutrition Examination Survey. 56-38-2 General Information Para-nitrophenol is a metabolite of the insecticides methyl parathion. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.92-2.30 (2.22-3.21 (2. Estimated intakes from diet and drinking water have been below recommended limits.62 (1.01-4.730 (<LOD-. and Nitrobenzene Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. Methyl Parathion.70 (<LOD-3. Methyl parathion has low water solubility.33) 2. but by 2003.70-6.89 (2. 2007).57) 1.05) 4.20-5. Survey Geometric mean (95% conf.70 (2.10 (3.32 (1.12) < LOD < LOD 1.18-3. and eliminated rapidly from the body after absorption (Kramer et al. < LOD means less than the limit of detection.90 (1.13-1..860 (<LOD-1.61) < LOD 1.990-1.EPA. 2003).70 (3.50 (2.. Morgan et al.66 (2.28-4.0) 4.02) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .910) < LOD < LOD . peak domestic use was as high as 5-6 million pounds per year.50) 2.71 (3.1.70 (2.47) 2. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Urinary para-Nitrophenol Metabolite of Ethyl Parathion.71) 971 1164 1018 1313 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD ..60-19.40 (1.910) < LOD .91-3.70-3.30-5.50) 3. In the 1990s.300-.50 (1.72 (3.850) < LOD .60-24.37-4.45 (1.770 (.298-00-0 Ethyl Parathion CAS No.50) 1. methyl parathion was rapidly absorbed after ingestion.10) 4. In animal studies. and has a short half-life in soils and on plants. Increased risk of exposure via dermal.80) 2.46 (3.48) 90th 2. binds tightly to soils resulting in low leachability.20) 5. Fourth National Report on Human Exposure to Environmental Chemicals 149 .67) < LOD 1.69 (2.01) 4. and to a lesser extent.80 (1.50-9.40-4. on cereal grains.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 1.40) 1.20 (<LOD-2.16) < LOD 1.19 (.20 (2. O-ethyl-O-(4-nitrophenyl) phenylphosphonothioate.70) 2.30-16.40) 2.85 (2.70-6. with limited applications in agriculture.70 (2.50 (1.34 (3.10 (3. Ethyl and methyl parathion are infrequently detected in groundwater sampling (USGS.57-4.61) < LOD 1.0 (3. Methyl parathion is not registered for residential use in the United States. more slowly absorbed through the skin.69) 4.8 and 0.0) 3. Once absorbed.0) 3.10-1.50 (1.26 (1.70-3.30 (1. 2002.940 (<LOD-2. which may vary for some chemicals by year and by individual sample.40-3.10 (<LOD-6.00) 3.00 (2.910) < LOD < LOD < LOD 1.21-1.11-4. 2000).0) 2. and aquatic invertebrates.24) 479 565 680 813 830 1099 99-00 01-02 99-00 01-02 * * * * < LOD . Methyl parathion use is highly restricted.90-11.60-5.790 (<LOD-.

2004).41-2. 1990.html and from U. methyl parathion.7) 3.82 (2. Methyl parathion is not considered genotoxic. 1991).05) 4.78-2.94-47.44-3.86 (2. Jaga and Dharmani.2) 2.. U.07 (1.790-. At high animal doses of methyl parathion. environmental levels) and health effects is available from ATSDR at: http://www.83 (1. Methyl Parathion. In addition to being a metabolite of methyl and ethyl parathion.970 (. and unintentional acute or chronic high-level occupational exposure (Hill et al.84) 3.00 (1.90 (1.72-2. population from the National Health and Nutrition Examination Survey.15) 3.89 (2.2) 2.11) 1.S. Additional information about external exposure (i. resulting in excess acetylcholine at nerve terminals.01 (2.93 (2. Orsorio et al.67-2. Thus.04 (2.29) 1.10) 90th 2.9) 1. does not inhibit acetylcholinesterase enzymes. 2004). gov/pesticides/.56-2.14-3.790-1.21) 1.82) < LOD .73 (1. cholinergic effects.370 (<LOD-. weakness.55 (<LOD-3.97 (2.850-1. accidental exposure. the detection of para-nitrophenol in a person’s urine may also reflect exposure to the environmental degradate.23) 1. and other metabolites. and Nitrobenzene Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.26 (1.00 (1.11-4. In large doses.4 (3.60 (1.16-4.08-3.20) 3.60) 2. Slotkin et al.. 2003. interval) Selected percentiles ( 95% confidence interval) Sample 95th 4.17) .440 (<LOD-.38-3.29) 2.3) 2.55) 2.61) 4.67 (3. vomiting.e.15-10.35-3.96 (1. IARC does not consider ethyl parathion and methyl parathion classifiable as human carcinogens.S.48-4.33-6.01-3.20) .21-21.97 (<LOD-4.33-3.950) < LOD . teratogenic. 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..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 .39) 1.37-1. 1978.640) < LOD < LOD 1..500) < LOD < LOD .EPA considers methyl parathion unlikely to be carcinogenic to humans.57-7. 1995).44-3.88) 1.980 (. gov/toxpro2. 150 Fourth National Report on Human Exposure to Environmental Chemicals . Overt cholinergic toxicity and death from methyl and ethyl parathion have been described following suicidal ingestion.530) < LOD < LOD < LOD . Karanth and Pope et al.930 (. and other organophosphorus insecticides share a common mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system.830-1.08) < LOD .33-3. and seizures. paranitrophenol. 2005.25 (2.87 (1.31-3.80 (1.06) 971 1164 1018 1312 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD . or generally to have reproductive toxicity at doses below those causing acetylcholinesterase inhibition in most animal studies (IPCS.77-7. Lores et al.29 (2.970 (.430 (.33) 479 565 680 812 830 1099 99-00 01-02 99-00 01-02 * * * * < LOD . Urinary para-Nitrophenol (creatinine corrected) Metabolite of Ethyl Parathion.78) 2.13) 4.79) 1.400 (<LOD-.840 (.00) 2.78-2. retinal atrophy and sciatic nerve degeneration have also been observed (IPCS.1) 2.30) 3.09) 2.870) < LOD .31) < LOD .70) 3. 2006.03) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .45) 695 660 518 678 603 941 < LOD means less than the limit of detection for the urine levels not corrected for creatinine..17-4.940 (<LOD-1. Human health effects from parathion or ethyl parathion at low environmental doses or at biomonitored levels from low environmental exposures are unknown. The metabolite.680 (<LOD-1..57-2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.26) 17.13-12.08 (1.88 (1.91 (1.89 (2.60-2. para-nitrophenol can also occur in the environment from the breakdown of the parent these organophosphorus pesticides and from nitrobenzene.30-1.25) 1.310-.80 (1.Organophosphorus Insecticides: Specific Metabolites Metabolites”). 2006.57) 6. Survey Geometric mean (95% conf.880 (.91) 1.59 (1.atsdr.01 (.930 (. but lists ethyl parathion as a possible human carcinogen.79 (1.94-4. EPA at: http://www.20 (3.96 (1. ethyl parathion.04) 1. Zurich et al.S.730-1.epa.97-10. paralysis..690-1.78 (2.cdc. Parathion and methyl parathion have high acute toxicity in animal testing.71) 1.43) 4.76-14. and producing acute symptoms such as nausea..98-7.39 (1.95) 1.92 (2. 1995.720-1.71 (1.07) 2.800-1.540) < LOD .35-3. WHO.10 (1.720 (<LOD-.

Hill RH Jr. McCann et al. et al. 2002). Pope C. et al. Lu C. Curl CL.. Neurotoxicol Teratol 2003.inchem. Bailey SL. Eskenazi B. Guizzetti M. Rev Environ Health 2006. Third National Report on Human Exposure to Environmental Chemicals. oral or dermal administration. Environ Health Perspect 2002.14(4):213-216. Lores EM. Centers for Disease Control and Prevention (CDC).. Baker SE. 1999). Bradway DE.110 Suppl 6:1075-1078.71:99108.56(7):449553.215(3):182-190. general population (CDC. Atlanta (GA). References Barr DB. Kramer RE. Age-related effects of chlorpyrifos and parathion on acetylcholine synthesis in rat striatum. Environ Health Perspect 2002. Griffith W. Pesticide residues in urine of adults living in the United States: reference range concentrations. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Shealy DB.. Laboratory investigation of a poisoning epidemic in Sierra Leone. Bradman A. Rockhold RW. Parathion-Methyl (addendum). Ashley DL. Runkle KD. 2002. Turner WE. Toxicology 2005. Comparison of organophosphorus pesticide metabolite levels in single and multiple daily urine samples collected from preschool children in Washington State. Arch Environ Health 1978. Methyl parathion: an organophosphate insecticide not quite forgotten. Pharmacokinetics of methyl parathion: a comparison following single intravenous. Barr DB. ACGIH recommends a BEI of 0. Rubin et al. CDC. DiPietro E. Urinary excretion of paranitrophenol and alkyl phosphates following ingestion of methyl or ethyl parathion by human subjects. Environ Health Perspect 2004. Baker S. Barr DB. Slach EF. population (Olsson et al. Hill RH Jr. Wellman SE. Chicago area methyl parathion response. 2005. Kissel JC. Effect of organophosphorus insecticides and their metabolites on astroglial cell proliferation. Available at URL: http:// www. Pathak S.9:311-320. et al. Measurement of p-nitrophenol in the urine of residents whose homes were contaminated with methyl parathion. 2003) and in 482 pregnant females from an agricultural region of California (Eskenazi et al.. and levels were similar or slightly lower that those in a small convenience sample of the U.5 mg (500 µg)/g creatinine for workers at the end of shift. 2005). Barr JR. Lin LI. Hill et al.15(2):164-171. Head SL. Hetzler HL. McCann KG. et al. Fourth National Report on Human Exposure to Environmental Chemicals 151 . Needham LL. Clark JM.. Moomey CM.. Organophosphorus pesticide poisonings in humans: determination of residues and metabolites in tissues and urine. Alley CC. Morgan DP.Organophosphorus Insecticides: Specific Metabolites Biomonitoring Information Urinary levels of para-nitrophenol reflect recent exposure.. 2005. 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. 4/7/09 Jaga K. International Programme on Chemical Safety-INCHEM (IPCS). 1995. 2005). Moseman RF. Weltzien E. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population. Environ Res 1995. Pesticide workers may have much higher levels following pesticide applications. Kedan G. Dharmani C.33(5):270-276. 1995). Arch Environ Contam Toxicol 1977. Barr DB. Role of individual susceptibility in risk assessment of pesticides. Karanth S.org/documents/jmpr/jmpmono/v95pr14. Finding a measurable amount of para-nitrophenol in urine does not mean that the level will result in an adverse health effect. Jewell NP. 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. Occup Environ Med 1999. In a study of workers who handle parathion. Harley K. Gregg M. Costa LG. Hryhorczuk DO. et al. 2004).25(5):599-606.110 Suppl 6:1085-1091. end-of-shift urinary para-nitrophenol levels ranged from 190 to 410 µg/ gram of creatinine (Leng and Lewalter.S. J Biomed Sci 2002. Head SL. Leng G. 2002.21(1):5767. Lewalter J. J Expo Anal Environ Epidemiol 2005. 2005. Cline RE.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.6(2-3):159-173. and many residents were symptomatic (Barr et al. McClure PC. 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. Giordano G. Baker RC.112(10):1116-1124.htm. J Anal Toxicol 1990. a range of values several hundred times higher than levels found in the U.

Levin ED. pdf.04/106.S. 2004. Available at URL: http://www. EPA-738-FOO-009. 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. Olsson AO. Letzel S. Ethyl parathion. March 2006. Available at URL: http://www.epa. 1995-1996. Yacovac R. Sadowski MA. Case No. Backer G. Costa LG. Investigation of a fatality among parathion applicators in California. Environmental Protection Agency (U.114(10):1542-1546.pdf. Toxicol Appl Pharmacol 2004. Rubin C. Methyl parathion in drinking water.epa. Monnet-Tschudi F.gov/oppsrrd1/REDs/factsheets/0155fct. Ames RG.110 Suppl 6:1047-1051.who.S. External and internal exposure of wine growers spraying methyl parathion. 2007 [online].E. EPA). Rosenberg J. R. gov/oppsrrd1/REDs/methylparathion_ired. Jung D. Available at URL: http://www. Esteban E. 1992-2001.201(2):97-104. 6/1/09 World Health Organization (WHO). Environ Health Perspect 2006. Tate CA. Anal Bioanal Chem 2003. Environmental Protection Agency (U.20(4):533-546.S.S. Pesticides in the Nation’s Streams and Ground Water. U. Nguyen JV. 0153. The Quality of Our Nation’s Waters.D. Interim reregistration eligibility decision (IRED) for Methyl Parathion.gov/circ/2005/1291/. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine. Assessment of human exposure and human health effects after indoor application of methyl parathion in Lorain County. Ryde IT.Organophosphorus Insecticides: Specific Metabolites Muttray A. 1/12/07 U.162(2-3):219-224. et al. Barr DB. Available at URL: http://pubs. Schilter B. Dunlop B. EPA). 1/14/09 U. Mengle DC.int/water_sanitation_health/dwq/chemicals/ methylparathion. Ohio. Am J Ind Med 1991. Osorio AM. Involvement of glial cells in the neurotoxicity of parathion and chlorpyrifos. Hill RH Jr. Honegger P. Slotkin TA. September 2000. May 2003.376(6):808-815. Geological Survey (USGS). Environ Health Perspect 2002. WHO/SDE/WSH/03.usgs. Facts. Seidler FJ. 152 Fourth National Report on Human Exposure to Environmental Chemicals . Hill G. Toxicol Lett 2006.S. 5/19/09 Zurich MG. revised February 15. Kieszak S.pdf.

2005).S.S. Thus. and aquatic invertebrates. phosphorothioates such as pirimiphos-methyl are metabolically activated to the “oxon” form which has greater toxicity than the parent insecticide. weakness. which are mainly excreted in the urine (IPCS. Biomonitoring Information Urinary levels of 2-(diethylamino)-6-methylpyrimidin-4ol/one reflect recent exposure. subsample of NHANES 2001-2002.S. In a nonrandom sample of 140 urine specimens obtained from adults and children in the United States. (2003) detected 2-(diethylamino)6-methylpyrimidin-4-ol/one in 7. Human health effects from pirimiphos-methyl at low environmental doses or at biomonitored levels from low environmental exposures are unknown. In animal studies. pirimiphos-methyl and other organophosphorus insecticides share a mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system. EPA at: http://www. cholinergic effects. occurrence of such toxicity is mitigated by its rapid degradation and its use in closed storage systems. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”). 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. It has a lesser use as a cattle ear tag application to control flies. weevils.epa. vomiting. The metabolite 2-(diethylamino)-6-methylpyrimidin-4-ol/one does not inhibit acetylcholinesterase enzymes. sorghum. Additional information about pesticides is available from U. 2003). Fourth National Report on Human Exposure to Environmental Chemicals 153 .gov/pesticides/. Metabolic hydrolysis leads to the formation of 2-(diethylamino)-6methylpyrimidin-4-ol/one. In the general population. 2-(diethylamino)-6-methylpyrimidin-4-ol/one can also occur in the environment. Pirimiphos-methyl is not registered for residential use in the United States. 2006). and seed. Pirimiphosmethyl has low acute toxicity in animal studies.Organophosphorus Insecticides: Specific Metabolites Pirimiphos-methyl CAS No. and producing acute symptoms such as nausea. Once absorbed. U. 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.EPA. and it is not considered persistent. or known to cause delayed neurotoxicity. Though considered moderately-to-highly toxic in birds. the detection of 2-(diethylamino)-6-methylpyrimidin-4-ol/one may also reflect exposure to the environmental degradate.EPA. and seizures. Estimated intakes from diet and water have not exceeded recommended intake limits (U. which has limited applications for control of beetles. and other metabolites. It easily hydrolyzes in the environment to 2-(diethylamino)-6-methylpyrimidine and other breakdown products. 29232-93-7 General Information The chemical 2-(diethylamino)-6-methylpyrimidin-4-ol/ one is a metabolite of the organophosphorus insecticide pirimiphos-methyl. teratogenic.47 μg/L for the total population (CDC. although the 95th percentile was characterized at 0. and moths on stored grain products such as corn. or reproductive toxicity (IPCS. In the U. most of the urinary measurements of 2-(diethylamino)-6-methylpyrimidin-4-ol/one were below the limit of detection. 1992.1% of the sampled population. Pirimiphos-methyl is not considered mutagenic. fish. In addition to being a human metabolite of pirimiphos-methyl in the body. infrequent dietary exposure to pirimiphos-methyl residues may occur from ingestion of food products containing stored corn or other treated grain (FDA. resulting in excess acetylcholine at nerve terminals. Olsson et al. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. pirimiphos-methyl is rapidly absorbed and metabolized to 12 metabolites. 1992). At high doses. paralysis.S. 2006). Toxic effects below doses that cause inhibition of acetylcholinesterase are unknown.

700-.55) .680 (<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.820) < LOD < LOD . 154 Fourth National Report on Human Exposure to Environmental Chemicals .740 (.840) 669 687 929 Limit of detection (LOD. population from the National Health and Nutrition Examination Survey.210-. Survey Geometric mean (95% conf. which may vary for some chemicals by year and by individual sample.300-1.470 (. Survey Geometric mean (95% conf.64) . population from the National Health and Nutrition Examination Survey.200-.780 (<LOD-1.00) 669 687 929 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.S.31) . < LOD means less than the limit of detection.410 (<LOD-1. interval) Selected percentiles ( 95% confidence interval) Sample 95th .07) .210-1.780 (.500 (.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 .610 (<LOD-1.880) 567 810 1104 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD .430 (<LOD-.850 (.2. interval) Selected percentiles ( 95% confidence interval) Sample 95th . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.210 (<LOD-.950) < LOD < LOD 1.840 (. 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 .27) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.94) .S.760 (<LOD-.17 (.250 (<LOD-.Organophosphorus Insecticides: Specific Metabolites Urinary 2-(Diethylamino)-6-methylpyrimidin-4-ol/one Metabolite of Pirimiphos-methyl Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.580-1.670 (<LOD-1.780 (.460) 1165 1316 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .700-1.740-1.780 (<LOD-1.08) 1165 1316 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .670) 567 810 1104 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD .21) < LOD .15) < LOD .

4/7/09 International Programme on Chemical Safety-INCHEM (IPCS). Atlanta (GA). Case No.inchem. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine. 2535.fda. EPA).gov/~acrobat/tds1byps. Total Diet Study: Summary of Residues Found Ordered by Pesticide.S. Barr DB. June 2003.pdf.epa. U. org/documents/jmpr/jmpmono/v92pr16. Anal Bioanal Chem 2003. 1/14/09 Fourth National Report on Human Exposure to Environmental Chemicals 155 . Environmental Protection Agency (U. Available at URL: http://www. Food and Drug Administration (FDA). July 2006. gov/oppsrrd1/REDs/pirimiphos-methyl_ired. 2005.376(6):808-815. Pirimiphos-methyl. cfsan. Finalization of interim registration eligibility decision for pirimiphos-methyl. Nguyen JV. 4/7/09 Olsson AO. Sadowski MA.pdf.Organophosphorus Insecticides: Specific Metabolites References Centers for Disease Control and Prevention (CDC). Third National Report on Human Exposure to Environmental Chemicals. Market Baskets 91-3-01-4.S. 850.htm. Available at URL: http://www. Pesticides residues in food: 1992 evaluations Part II Toxicology. Available at URL: http://www.

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

gov/pesticides/ and from ATSDR at: http://www. Shafer. dopaminergic. and striatal dopamine levels in male and female rats. Agrawal AK.62:101-108.. et al. Okuno Y. 1998. 2002). Hu JY. Elwan et al. 2001. Estrogenic and antiprogestagenic activities of pyrethroid insecticides. choreoathetosis. Fredriksson A. 2006. IARC considers deltamethrin and permethrin as not classifiable as to their human carcinogenicity. EPA at: http://www. bioallethrin and deltamethrin. et al. fenvalerate. paresthesias) reported in agricultural workers from 1996 to 2002 (Spencer and O’Malley. The pyrethroids in general use are not considered teratogenic or to have significant reproductive toxicity (ATSDR. Leng G. Generally. Berger-Preiss E. Leng G. Int J Hyg Environ Health 2002. tremor. Kim HS. Effects of prenatal exposure to deltamethrin on forced swimming behavior. Song L.8(1):197-202. WHO. Lemonica IP. Bull Environ Contam Toxicol 1999. salivation. Kang IH. Shaw IC. Bernardi MM. Neurotoxicol Teratol 2005. et al. Idel H. hypersensitivity.8(1):18-21. J Environ Monit 2006. Assessing estrogenic activity of pyrethroid insecticides using in vitro combination assays. In California. Neurotoxic effects of two different pyrethroids. Human cases of systemic poisoning are rare and usually result from accidental exposure or intentional ingestion of pyrethroid insecticides. Available from URL: http://www. J Reprod Dev 2004. Elwan MA. Neurodevelopmental consequences of gestational exposure (GD14-GD20) to low dose deltamethrin in rats. 2003. Sunami O. Yamada T. Garey J. Concomitant exposure to organophosphorus insecticides may increase pyrethroid toxicity by slowing metabolic clearance of the pyrethroid. cdc. 2005). Soderlund et al. Neurosci Lett 2001.S. Adhami VM. Abell AD. Ranft U. Caudle WM. 2005). Kunimatsu et al. McCarthy AR. Shukla Y.1/15/09 Aziz MH. Toxicol Appl Pharmacol 1991. References Agency for Toxic Substances and Disease Registry (ATSDR). Eriksson and Fredriksson.. Richardson JR. Ose K. Toxicol Appl Pharmacol 2006. Leng A. 2004. Varoli FM. Wieseler B. Yang J. Shin JH. Neurotoxicol Teratol 2001.. Kim TS. Lazarini et al. et al. Thomson BM.107(3):173-177. and catecholaminergic pathways and behavioral changes have been demonstrated at subacute and subchronic doses for some pyrethroid pesticides (Aziz et al. September 2003. Kuhn K. Zhao RC. Lazarini CA. Hu et al.html. motor activity.. Transient dermal paresthesias have been reported among pesticide applicators after direct contact with certain types of pyrethroid pesticides.. Go V. Kamita Y. Cruz-Casallas PE. 2002).108(1):78-85. Lee SJ. Miller GW. cyfluthrin was the most frequent pyrethroid associated with symptomatic effects (irritant respiratory and dermal effects. Indoor pyrethroid exposure in homes with woollen textile floor coverings.251(3):855-859. Estrogenic potential of certain pyrethroid compounds in the MCF-7 human breast carcinoma cell line. Estrogenicity of pyrethroid insecticide metabolites. Go et al..35(2 Pt 1):227-237. Sugiri D. though a few pyrethroid pesticides and some metabolites have shown weak or inconsistent estrogenic effects on standardized assays (ATSDR. [Effects of fenvalerate on reproductive and endocrine systems of male rats] Zhonghua Nan Ke Xue 2002. Salzgeber SA. 2006).23(6):665-673.. Levsen K. Moniz et al. Environ Health Perspect 1999. 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. Pyrethroid pesticide-induced alterations in dopamine transporter function. Behavioral and endocrine changes induced by perinatal fenvalerate exposure in female rats.. on immature and adult mice: changes in behavioral and muscarinic receptor variables. and seizures (ATSDR. In developing rodents.. Kunimatsu T.. Toxicokinetics of pyrethroids in humans: consequences for biological monitoring. Wolff MS.. Garey and Wolff. Wolff MS. 2003. Leng G. Kuhn KH.27(4):609-614. neurochemical changes in cholinergic. Regul Toxicol Pharmacol 2002.. Human doseexcretion studies with the pyrethroid insecticide cyfluthrin: urinary metabolite profile following inhalation. Biochem Biophys Res Commun 1998. Pauluhn J.300(3):161-165. Bernardi MM. Garey J.cdc. Wang SL. 2006. Pogo BG. Signs and symptoms of acute pyrethroid poisoning after massive ingestions include agitation. Idel H. 2002. Ray et al. 2003. Xenobiotica 1997. Fourth National Report on Human Exposure to Environmental Chemicals 157 . Seth PK.205(6):459-472. Moniz AC.gov/toxpro2.gov/toxprofiles/ tp155. Additional information about pesticides is available from U. 2000. Eriksson P. Kim et al. Chen JH. 2003. epa. Lack of (anti-) androgenic or estrogenic effects of three pyrethroids (esfenvalerate. the pyrethroids are not considered genotoxic in in vitro testing or carcinogenic in animal testing (WHO.html.atsdr. 1999. and permethrin) in the Hershberger and uterotrophic assays. Kim IY.211(3):188-197. 1991.Pyrethroid Pesticides and other ion channels may also explain some pyrethroid effects. 2005).27(12):1273-1283. Guillot TS. Florio JC.50(2):245-255. Lewalter J. 2005). 2001.atsdr. McCarthy et al. Spinosa HS. Toxicological profile for pyrethrins and pyrethroids..

5/26/09 Woollen BH. Lesser JE.htm. Revised February 25.usgs. EPA). The metabolism of cypermethrin in man: differences in urinary metabolite profiles following oral and dermal administration. Pyrethroid insecticides: poisoning syndromes.S. Laird WJ. Forshaw PJ. Meyer DA.186:57-72. pdf. Mechanisms of pyrethroid neurotoxicity: implications for cumulative risk assessment. 2005. June 2006b. 5/26/09 U.S. Toxicology 2002.S.gov/pesticides/ health/mosquitoes/pyrethroids4mosquitoes.epa.10. Sargent D.Pyrethroid Pesticides Ray DE. Developmental neurotoxicity of pyrethroid insecticides: critical review and future research needs. Environ Health Perspect 2005.22(8):983-991.epa. April 2002. sumithrin synthetic pyrethroids for mosquito control. Clark JM. World Health Organization (WHO). Permethrin Facts (Reregistration Eligibility Decision Fact Sheet). June 2006a. and therapy. Pesticide and Evaluation Scheme. Environmental Protection Agency (U. EPA). Environmental Protection Agency (U. Pyrethroid illnesses in California. Safety of pyrethroids for public health use. Available at URL: http://www. Mullin LS.epa. O’Malley M. Reregistration Eligibility Decision for Cypermethrin. Rev Environ Contam Toxicol 2006. Xenobiotica 1992. J Toxicol Clin Toxicol 2000. 1992–2001.S. Pesticides in the Nation’s Streams and Ground Water.int/hq/2005/WHO_ CDS_WHOPES_GCDPP_2005.gov/oppsrrd1/REDs/ factsheets/permethrin_fs. Geological Survey (USGS). 5/26/09 U. Available at URL: http://pubs.S.38:95-101. Soderlund DM. EPA). Spencer J. Environmental Protection Agency (U. 5/26/09 158 Fourth National Report on Human Exposure to Environmental Chemicals . Crofton KM. 19962002. Shafer TJ.gov/oppsrrd1/REDs/cypermethrin_red.S. 2007.S. Marsh JR. Available at URL: http://www.pdf. Piccirillo VJ.gov/ circ/2005/1291/. resmethrin. U. March 2006. Permethrin.who.113(2):123-136.htm. Available at URL: http://www. et al.171:3-59. Available at URL: http://whqlibdoc. Sheets LP. 5/26/09 U. synergies.

Baker et al. Degradation of cyfluthrin to 4-fluoro-3-phenoxybenzoic acid occurs in the environment.S. 2001) showed that urinary levels of 4-fluoro-3-phenoxybenzoic acid at the 95th percentile ranged from either slightly higher or lower than the detection limit in the U. 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. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 2004). (2004) reported a geometric mean concentration of 4-fluoro3-phenoxybenzoic acid of 0.2 μg/L) in the U..95 µg/L. Following an indoor application exposure. Biomonitoring Information Urinary levels of 4-fluoro-3-phenoxybenzoic acid reflect recent exposure to cyfluthrin or its environmental degradate. representative 2001-2002 NHANES subsample (CDC. 2005.. most of which were dermal and respiratory irritations (Spencer and O’Malley... Cyfluthrin is rapidly metabolized and eliminated from the body.. Studies in Germany of 396 children and adolescents (Becker et al. Urinary levels for adults and children in these studies were similar (Heudorf et al. 2005). the presence of 4-fluoro-3-phenoxybenzoic acid in urine not only reflects the metabolic transformation of cyfluthrin. median urinary levels of 4-fluoro-3-phenoxybenzoic acid were slightly less than the limit of detection in the NHANES 2001-2002 subsample (CDC.Pyrethroid Pesticides Cyfluthrin CAS No.. 2005). Fourth National Report on Human Exposure to Environmental Chemicals 159 .68359-37-5 General Information The chemical 4-fluoro-3-phenoxybenzoic acid is a specific metabolite of the pyrethroid insecticide cyfluthrin. 2006) and estimated daily intakes based on urinary levels in children were considered to be below acceptable daily intakes (Heudorf et al. Leng et al. 2003). Seven individuals participating in floor exercises on cyfluthrin treated carpet demonstrated a rise in the urinary excretion of 4-fluoro-3-phenoxybenzoic acid in the 72 hours following the activity (Williams et al. Thus.S. Urinary levels of 4-fluoro-3-phenoxybenzoic acid were generally below the limit of detection (0. 2006) and 1177 urban adults and children (Heudorf et al. Biomonitoring studies of 4-fluoro3-phenoxybenzoic acid in urine provide physicians and public health officials with reference values so that they can determine whether other people have been exposed to higher levels of cyfluthrin than levels found in the general population. the mean elimination half-life of cyfluthrin from the plasma was 16 hours (Williams et al. In an analysis of 217 urine specimens from a nonrandom sample of United States residents. In 57 volunteers entering areas previously spot-sprayed with various pyrethroid pesticides (including cyfluthrin). 2003). Cyfluthrin accounted for one-third of pyrethroid-related worker illnesses reported in California from 1996-2002.. 2006). 2001. representative subsample in NHANES 2001-2002 (CDC. 2003). but it can also reflect direct exposure to 4-fluoro-3-phenoxybenzoic acid formed in the environment.

2.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.S. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. which may vary for some chemicals by year and by individual sample. population from the National Health and Nutrition Examination Survey. 160 Fourth National Report on Human Exposure to Environmental Chemicals .2 and 0. Survey Geometric mean (95% conf. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1949 2539 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 473 580 662 831 814 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 950 1193 999 1346 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 666 680 517 701 594 957 Limit of detection (LOD. < LOD means less than the limit of detection. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.

Fourth National Report on Human Exposure to Environmental Chemicals 161 . interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1949 2538 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 473 580 662 830 814 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 950 1193 999 1345 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 666 680 517 700 594 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. Survey Geometric mean (95% conf. population from the National Health and Nutrition Examination Survey.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. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.S.

Seiwert M. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides. Pyrethroid illnesses in California. Berger-Preiss E. Isotope dilution highperformance liquid chromatography-tandem mass spectrometry method for quantifying urinary metabolites of synthetic pyrethroid insecticides.Pyrethroid Pesticides References Baker SE. Butte W. Heudorf U. Schulz C. Environ Health Perspect 2001.209(3):293-299. Drexler H. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine. Arch Environ Contam Toxicol 2004.13(2):112-119.77(1):67-72. Williams RL. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides.46(3):281-288. Bernard CE. Idel H. Heudorf U. Centers for Disease Control and Prevention (CDC). Ball M. Human exposure to indoor residential cyfluthrin residues during a structured activity program. Barr DB. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. Third National Report on Human Exposure to Environmental Chemicals.186:57-72. 2005. et al. O’Malley M. Sugiri D. Angerer J. Atlanta (GA). Ranft U. Kolossa-Gehring M. Hoppe HW. Becker K. Int J Hyg Environ Health 2006. Heudorf U. Olsson AO. Rev Environ Contam Toxicol 2006. J Expo Anal Environ Epidemiol 2003. Int J Hyg Environ Health 2003.206(2):85-92. Angerer J. 162 Fourth National Report on Human Exposure to Environmental Chemicals .109(3):213-217. Angerer J. Krieger RI. Int Arch Occup Environ Health 2004. Int J Hyg Environ Health 2006. 19962002. Angerer J. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. Leng G. Spencer J. Hadnagy W.209(3):221-233.

330) .790 (.570-.770) .220) . and cis-Cypermethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.120-.420-.21) .220-.52645-53-1 General Information Several pyrethroid pesticides are formulated as a mixture of cis.570 (. but can also reflect exposure to trans-3(2.180 (. 1985. The presence of cis-3-(2.220-.740-2.250 (.210) 90th . trans-cypermethrin.350) .170 (. Kuhn et al.15) .460 (. cis-3-(2.200-.12 (.77 (..580) 1.210-.380-.200 (.2dichlorovinyl)-2.300 (.790-1. Biomonitoring Information Urinary levels of cis.43) .2-dichlorovinyl)-2.110 (<LOD-. Cyfluthrin.53) .262) * * * < LOD < LOD .610) . The chemical trans-3(2.880 (. population from the National Health and Nutrition Examination Survey.13 (.50) .890 (.740 (.650-1. 52315-07-8 CAS No.630-.730 (. which may vary for some chemicals by year and by individual sample.430-.2-Dichlorovinyl)-2. < LOD means less than the limit of detection.120-.220-.250-.520) .700) .850 (. more of the trans-metabolite than Urinary cis-3-(2.550) . Generally.610) .240) .2dichlorovinyl)-2.120-.54) .2-dichlorovinyl)-2.730 (.470 (.32) .490-.2dimethylcyclopropane carboxylic acid in urine not only reflects the metabolic transformation of any of the three pesticides. 1985.2-dichlorovinyl)2.200) < LOD < LOD < LOD .300 (.900 (. The cis-isomer of permethrin has more potent insecticidal activity than transpermethrin.790-1.960 (.140 (<LOD-.07 (.950-2. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.670 (.S. 1999).110-.380) . but it can also reflect exposure to cis-3-(2.370-.80) . Similarly.2-dichlorovinyl)- CAS No.330 (.690) . cis-cypermethrin.300-.280-.68) .140 (.2-dimethylcyclopropane carboxylic acid is a metabolite formed from cis-permethrin.380 (.630) .68359-37-5 Cypermethrin Permethrin CAS No.640 (.630 (.202 (.28) 671 680 518 701 591 957 Limit of detection (LOD.510 (.410) .670-1.600 (. Fourth National Report on Human Exposure to Environmental Chemicals 163 .670-2.380-.110-.Pyrethroid Pesticides Cyfluthrin the cis-metabolite is found in the urine.or trans-3-(2.11) . interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.310) .790) .2-dimethylcyclopropane carboxylic acid formed in the environment from the degradation of these pesticides (George.340) .680 (.2-dimethylcyclopropane carboxylic acid in urine not only reflects the metabolic transformation of any of the three pesticides.780) . transcypermethrin and trans-cyfluthrin.210) .160 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.630) .460-1.28) 468 580 667 831 816 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .410) .270 (.490-.400-.820 (.280 (.2-dichlorovinyl)-2.1.530 (.440 (.10) size 1951 2539 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD 75th .160 (.120-.770-1.300-.340) .710-1.44 (.200) .470-1.460-.490-1.47 (..150 (. ciscypermethrin and cis-cyfluthrin.260 (.160 (.35) 1.2-dimethylcyclopropane carboxylic acid Metabolite of cis-Permethrin.270-.340-.730 (.670-1.910-5.230) .580-1. and ciscyfluthrin.510 (.920) 1.155-.510 (.680) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .490-1.740-1.870) 1.220-.35) . Survey Geometric mean (95% conf.2-dimethylcyclopropane carboxylic acid that is formed in the environment from the degradation of these pesticides (George.600-1.2-dimethylcyclopropane carboxylic acid is a metabolite formed from trans-permethrin.180) .270 (.68) . 1999).68 (.200-.500 (.370 (.270 (.08) 947 1193 1004 1346 99-00 01-02 99-00 01-02 99-00 01-02 * * . trans-permethrin.740) 1.710) .200) .and trans-isomers.680-3.110-.08) . the presence of trans-3-(2.200-.890 (. In the body.600) . cis-permethrin.240) .380-.24) 1. and trans-cyfluthrin.1 and 0.500 (. Kuhn et al.

and trans-3-(2.59) .260 (.220 (. Studies in Germany of 396 children and adolescents (Becker et al.29 (. 2001..340-.2-dichlorovinyl)-2.130-.210-.31) .410) .2-dichlorovinyl)-2.230 (.430-.540 (.550) .170) < LOD < LOD < LOD . In these volunteers.780) 1.2-dimethylcyclopropane carboxylic acid levels at the 95th percentile were about one-third of the 95th percentile in the NHANES 20012002 subsample (CDC.12-2.80) .49) . 2003).710 (.300 (.590) .260) .540) .2dichlorovinyl)-2.890) .33) . These studies indicated that intake is mainly from the diet and that dermal absorption contributes little to intake (Heudorf et al.450-.and trans-3(2.280-.270) .350 (. post- Urinary cis-3-(2.S.290 (. 2005). Estimated daily pyrethroid intakes based on urinary levels in the German children were below the acceptable daily tolerances (Heudorf et al.380 (.640) 1.430 (. 2005). In the same residents.370-..24) ..640-.360-1. the levels at 24-72 hours were slightly less than the 95th percentile in the NHANES 2001-2002 subsample (CDC. median urinary levels of trans-3-(2.560) . 2002).2dimethylcyclopropane carboxylic acid at the 95th percentile were about half the 95th percentile in the NHANES 20012002 subsample (CDC.11) .810 (.200 (.59) .710-3.37) .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 . In a study of volunteers. 2002).300) .250-..230-.390-.440-. 2005).750-1.320-.290-.S.680-1..510-1.2-dichlorovinyl)-2.2-dimethylcyclopropane carboxylic acid did not increase.300-.250) .300 (.570) . representative NHANES 2001-2002 subsample (CDC.104-.370-.150-.2-dichlorovinyl)-2.200) . 2006).440 (.180-.470-1.14) 671 680 518 700 591 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.840 (.500 (.240 (<LOD-. though the 95th percentile levels increased several fold after exposure to nearby pest control operations (Leng et al. the median and 95th percentile of urinary levels of cis-3-(2.080-. 2006.250 (<LOD-. Survey Geometric mean (95% conf.270-.180 (.450 (.920 (.2dichlorovinyl)-2.550) .220 (. Urinary levels of the two chemicals in adults were similar to those in children in these studies (Heudorf et al.170 (.390 (.800 (.530 (.190) . 164 Fourth National Report on Human Exposure to Environmental Chemicals .11) 1.. 2005) In a small group of indoor pest-control operators.640-1.160 (<LOD-.. 2006). urinary levels of cis-3-(2.260 (.250-.150-.21) .380) .190) .2-Dichlorovinyl)-2.350) .300) .200-. urinary trans-3-(2.680-1.450-1.260 (.550-1. Schettgen et al.430-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.600 (.230-..200-.900 (.270) ..750 (. Lu et al.420 (. 2005).370-.250-. Cyfluthrin.700-2.390-.11) 947 1193 1004 1345 99-00 01-02 99-00 01-02 99-00 01-02 * * .320) .59 (1.890 (.290) .580-1.560) 1. the levels at 24-72 hours were slightly less than the 95th percentile in the NHANES 2001-2002 subsample (CDC.12 (.700) .840 (..2dimethylcyclopropane carboxylic acids at the 95th percentile that were similar or slightly less than the 95th percentiles in the U.140-..400-1.2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of cis-Permethrin.120 (.580) .03) 1.590 (.400 (.2-dimethylcyclopropane carboxylic acid reflect recent exposure to either their parent pyrethroid pesticides or their environmental degradates. 2006. In a study of urban residents in Germany (Berger-Preiss et al.260-.640-1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1. 2006) and 1177 urban adults and children (Heudorf et al.67) . population from the National Health and Nutrition Examination Survey.220) .170 (. 2004.380-.280 (.780 (.830) .520) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .2-dimethylcyclopropane carboxylic acid did not increase at 24-72 hours after exposure to nearby pest control operations (Leng et al.11) . Other studies have provided evidence that urinary levels of cis.150-.11 (.880) .250) .138 (. 2004).680 (.540 (.182) * * * < LOD < LOD . 2001) showed urinary levels of cis.270 (. and cis-Cypermethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.340) .640 (.230-.530 (.550 (.67 (.250) 90th .190 (.700) . 2003).Pyrethroid Pesticides 2.550-1.440 (.2-dimethylcyclopropane carboxylic acids in children were related to residential pesticide use and house dust levels (Becker et al.08) 468 580 667 830 816 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .290) .440-.690-1.340) .33 (.

43) 2.13) .800-1.16) 1.54) 4.68-3. interval) Selected percentiles ( 95% confidence interval) Sample 95th 3.940 (.or trans-3-(2.17 (.570) 90th 1.91 (1.39-5.7) 2.580 (.410 (<LOD-.49-5.550 (.2-Dichlorovinyl)-2.01 (1.12-6.66) 691 680 518 690 595 954 Limit of detection (LOD.and trans-3-(2. and trans-Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.11-2.19) 1. 2003) were similar to the 95th percentiles for adults in the NHANES 2001-2002 subsample (CDC.08) 1.01) 4.55-3.85) 4.810-1.89 (2.09 (.81) 2. Biomonitoring studies on urinary levels of cisor trans-3-(2.50 (1.500 (.68) 2.94 (1.69 (1.39 (1.19 (3.10) 2.19 (2.14) 1.76-4.62 (1.2-dichlorovinyl)-2.Pyrethroid Pesticides application median urinary levels of summed cis.830-1.680-1. population from the National Health and Nutrition Examination Survey.68) 1. 2005).54 (1.560 (.11-1.610) 1.60-4. Finding a measurable amount of cis.23) 2.40 (1.730) .66) .400 (<LOD-.41 (1.520) .77) 1.710 (.28 (2. Fourth National Report on Human Exposure to Environmental Chemicals 165 .2-dimethylcyclopropane carboxylic acid Metabolite of Cyfluthrin.49-3. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.500-.37 (1.66) 478 576 675 826 823 1123 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .23 (.68) 1. 2005).55-5.84 (1.77) 2.17-1.07 (1.20 (.35) 1.410 (<LOD-.920-1.69) 1.440 (<LOD-.490 (<LOD-.25 (1.S.76-3.41-14. were up to 27 times higher than the 95th percentile for adults in the NHANES 2001-2002 subsample (CDC.670) .420 (<LOD-.97-11.59 (1.670) .03-1.860) .460-.2dichlorovinyl)-2.20 (.480-.2-dimethylcyclopropane carboxylic acid in urine does not mean that the level causes an adverse health effect.4.48) 4.470 (.4 and 0. Urinary trans-3-(2.63) 1.820) .25-3.970 (.2-dimethylcyclopropane carboxylic acid (Hardt and Angerer.56) 2.03-1.620) < LOD 2. which may vary for some chemicals by year and by individual sample.26 (.520-.850-1.760) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.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 .910-1. trans-Cypermethrin. < LOD means less than the limit of detection.410-.87 (1.530) .68-2.780 (.49-3.500) .42) 1.56 (1.5) 2.56) 2.490-1.56 (1.560 (.07-3. Survey Geometric mean (95% conf.28 (1.42 (2.20 (.400-.27 (1.08-6.58) 961 1184 1015 1341 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .55-4.2-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.410-.750) .60) .14-6.08-4.64-4. The maximum post-application urinary levels.22 (1.840-1. however.2-dichlorovinyl)-2.77 (1.460-.470 (<LOD-.560 (.90) 1.63) 1.14-2.660) 1.60) 1.95) 3.700-1.17 (.700) .77) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD . see Data Analysis section) for Survey years 99-00 and 01-02 are 0.95) 2.910-1.

780) .65) 1.48-2.540) .42 (.2-Dichlorovinyl)-2.40-2. population from the National Health and Nutrition Examination Survey.700-.31 (.27-2.91) 1.740) .37 (1.26 (1. and trans-Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.470 (.00) 5.22) 1.31) 1.00 (1.3) 2.29) 1.880 (<LOD-1.61) 1.91 (1.900 (<LOD-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. trans-Cypermethrin.87-3.07) 2.41) 1.750) .28) 2.87) 1.74) .700 (.00) 1.31 (2.48 (1.780) 90th 1.30-6.11) 691 680 518 689 595 954 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.720 (<LOD-.15) 3.47-2.20-2.45 (1.19) 961 1184 1015 1340 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .19 (1.00) 1. Survey Geometric mean (95% conf.2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of Cyfluthrin.07) 2.20 (1.44) 2.56-2.35 (1.57) 3. 166 Fourth National Report on Human Exposure to Environmental Chemicals .08 (.55 (2.850) .87) 1.60) 2.660) . interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.800-1.39 (1.33-1.970 (.570-.770) < LOD 2.11) 478 576 675 825 823 1123 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .07-1.930-1.700 (.560 (.12-1.570 (<LOD-.47-2.56-5.68) 3.530 (.580 (.27-2.13) .81 (2.07-3.780 (<LOD-.730) .88) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 1.57 (1.530 (<LOD-.60) 2.440-.98 (1.Pyrethroid Pesticides Urinary trans-3-(2.22-2.87 (1.15-3.10) 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 .480-.65 (2.850-3.47 (1.42) 1.760 (.55 (2.610-.15-3.520 (<LOD-.74) 2.470-.670) .410-.33-2.880 (.12 (.34-3.89) 2.36 (1.39) 1.880-1.800-1.64 (1.60 (1.86 (2.720-1.33 (1.720-1.580) .640) .850) 1.19) .08 (.35) 1.07-2.55 (2.91-11.87-8.67 (2.820-2.36) 2.15 (1.15-3.22-1.45-2.16 (1.15) 2.02-1.570 (.00-5.11) .56 (1.30-3.80) 1.70 (.S.34-4.13) 1.75 (1.500-.

Third National Report on Human Exposure to Environmental Chemicals. Int Arch Occup Environ Health 2003. Idel H. Drexler H. Environ Health Perspect 2001. Indoor pyrethroid exposure in homes with woollen textile floor coverings. Hoppe HW.109(3):213-217. et al. Kuhn K. Heudorf U. Sugiri D. Bravo R. Idel H. Int J Hyg Environ Health 2006. Schulz C.68(6):1160-1163. Bull Environ Contam Toxicol 1999. Int J Hyg Environ Health 2002. Angerer J.Pyrethroid Pesticides References Becker K. Idel H. Berger-Preiss E. Angerer J. Angerer J. Heudorf U. 2005.114(9):14191423. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. Ball M.134(1-3):141-145. Kolossa-Gehring M. Int J Hyg Environ Health 2006.77(1):67-72. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides. Centers for Disease Control and Prevention (CDC). George DA. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine. Pyrethroid exposure of the general population-is this due to diet? Toxicol Lett 2002.209(3):293-299. A longitudinal approach to assessing urban and suburban children’s exposure to pyrethroid pesticides. Ranft U. Permethrin and its two metabolite residues in seven agricultural crops. Atlanta (GA). Sugiri D. Biological monitoring of workers after the application of insecticidal pyrethroids. Hardt J. Barr DB. Hadnagy W. Fourth National Report on Human Exposure to Environmental Chemicals 167 . Heudorf U. Butte W. Lu C. Angerer J. Drexler H. Toxicokinetics of pyrethroids in humans: consequences for biological monitoring. Ranft U. Environ Health Perspect 2006. Wieseler B. Heudorf U. Seiwert M. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation.209(3):221-233. Berger-Preiss E.62:101-108.206(2):85-92.205(6):459-472. Pearson M. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Angerer J. Leng G. Bartell S. Schettgen T. Int Arch Occup Environ Health 2004. Angerer J. Int J Hyg Environ Health 2003.76(7):492-498. J AOAC 1985. Levsen K. Leng G. Leng G.

2-dibromovinyl)-2.39 µg/L. 1990).S.. 2005). urinary levels of cis-3-(2. 2006) and estimated daily intakes based on urinary levels in children were considered to be below acceptable daily intakes (Heudorf et al.2-dimethylcyclopropane carboxylic acid at the 95th percentile ranged slightly higher (0.3-0.. 2001..2-dibromovinyl)-2. 2005). (2004) reported a geometric mean concentration of cis-3(2. Finding a measurable amount of cis-3-(2.2-dimethylcyclopropane carboxylic acid is a metabolite of the pyrethroid insecticide deltamethrin.2dimethylcyclopropane carboxylic acid reflect recent exposure to deltamethrin or its environmental degradate. 2005).2-dibromovinyl)-2.2-dimethylcyclopropane carboxylic acid of 0.2-dibromovinyl)2. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.5 μg/L) than the detection limit (0. Outside the U. Baker et al.2-dimethylcyclopropane carboxylic acid in the environment (IPCS. The peak mean levels in these children were more than 800-fold higher than the detection limit in the 2001-2002 NHANES subsample. Urinary levels for adults and children in these studies were similar (Heudorf et al.2-dibromovinyl)-2. In the NHANES 2001-2002 subsample. 168 Fourth National Report on Human Exposure to Environmental Chemicals .2-dibromovinyl)-2.2-dimethylcyclopropane carboxylic acid in children increased at least 450-fold relative to the non-detectable background levels for several days and mean levels remained slightly above background levels 45 days after the spraying (Ortiz-Perez et al.. Biomonitoring Information Urinary levels of cis-3-(2. mean peak urinary levels of cis-3-(2.2-dibromovinyl)-2.2-dimethylcyclopropane carboxylic acid in the urine may reflect exposure to deltamethrin or to cis-3-(2.2-dibromovinyl)-2.. Thus. In an analysis of 217 urine specimens from a nonrandom sample of United States residents..Pyrethroid Pesticides Deltamethrin CAS No. 52918-63-5 General Information Cis-3-(2. 2004).2-dibromovinyl)-2. Biomonitoring studies provide physicians and public health officials with reference values so that they can determine whether other people have been exposed to higher levels of deltamethrin than levels found in the general population.2-dibromovinyl)-2.1 μg/L) for the NHANES 2001-2002 subsample (CDC.2-dimethylcyclopropane carboxylic acid were below the limit of detection (CDC. 2001) showed that urinary levels of cis-3-(2. in some situations replacing the use of DDT. Deltamethrin can degrade to cis-3(2. in detection of cis-3-(2. Studies in Germany of 396 children and adolescents (Becker et al. 2006) and 1177 urban adults and children (Heudorf et al. deltamethrin has been used against mosquitoes that carry malaria. Following residential spraying with deltamethrin for malaria protection in Mexico.2-dimethylcyclopropane carboxylic acid in urine does not mean that the level will result in an adverse health effect.2dimethylcyclopropane carboxylic acid formed in the environment.

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

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

and genotoxicity in exposed children.209(3):293-299. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine. Int Arch Occup Environ Health 2004. Batres LE. et al. Heudorf U. Torres-Dosal A.org/documents/ehc/ehc/ ehc97. 5/26/09 Ortiz-Perez MD. Angerer J. Int J Hyg Environ Health 2006. Drexler H.209(3):221-233. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. Angerer J. Lopez-Guzman OD. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides. Third National Report on Human Exposure to Environmental Chemicals.htm. Fourth National Report on Human Exposure to Environmental Chemicals 171 . Deltamethrin. Heudorf U.109(3):213-217. Schulz C. [online] 1990. Ball M. Atlanta (GA). Butte W. Hoppe HW.77(1):67-72. Environmental Health Criteria 97.Pyrethroid Pesticides References Becker K. Carranza C. Angerer J. Environ Health Perspect 2001.113(6):782-786. et al. Centers for Disease Control and Prevention (CDC).inchem. Grimaldo M. Int J Hyg Environ Health 2006. 2005. Angerer J. Environ Health Perspect 2005. Available at URL: http://www. International Programme On Chemical Safety (IPCS). Kolossa-Gehring M. Seiwert M. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. toxicokinetics. Environmental health assessment of deltamethrin in a malarious area of Mexico: environmental persistence. Heudorf U.

Hardt and Angerer. the postapplication median urinary levels of 3-phenoxybenzoic acid were 24-fold higher than those for adults in the NHANES 2001-2002 subsample (CDC. CDC. mean peak urinary levels of 3-phenoxybenzoic acid in children increased at least sixtyfold over non-detectable background levels for several days and mean levels remained slightly above background levels 45 days after the spraying (OrtizPerez et al. In the New York City study. 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. Becker et al. In an analysis of 217 urine specimens from a nonrandom sample of United States residents. In one study of 145 urban residents in 80 private homes in Germany. 2003)..52315-07-8 CAS No. 2005). Biomonitoring studies of 3-phenoxybenzoic acid provide physicians and public health officials with reference values so that they can determine whether other people have been exposed to higher levels of pyrethroids than levels found in the general population. 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. 66841-25-6 General Information The chemical 3-phenoxybenzoic acid is a metabolite and an environmental degradate of the six pyrethroid pesticides listed above.. (2004) reported geometric mean levels of 3-phenoxybenzoic acid that were approximately sixfold higher than levels for adults in the NHANES 2001-2002 subsample (CDC. 2003.. CDC. 2006. 39515-41-8 CAS No. Fenpropathrin Permethrin CAS No. 52918-63-5 use and house dust levels (Lu et al. Baker et al. 2005). but can reflect direct exposure to 3-phenoxybenzoic acid formed in the environment from the degradation of these pesticides. 2002. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 2005). In a small group of indoor pest-control operators. 2005).. Finding a measurable amount in urine does not mean that the level will result in an adverse health effect. 2005. Urinary levels of 3-phenoxybenzoic acid in children were found to be related to residential pesticide 172 Fourth National Report on Human Exposure to Environmental Chemicals . The mean peak levels in these children were 83-fold higher than the geometric mean for children in the NHANES 2001-2002 subsample (CDC.. Thus. 2005. 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.Pyrethroid Pesticides Cyhalothrin CAS No.. A study of 396 German children (Becker et al.. Following residential spraying with deltamethrin for malaria protection in Mexico. a temporal variation in levels was observed and considered to correspond to seasonal spraying of pesticides. median urinary levels of 3-phenoxybenzoic acid were slightly less than median levels in the NHANES 2001-2002 subsample (Leng et al. 2005).. In 57 volunteers entering areas previously spot-sprayed with various pyrethroid pesticides. 2005). 2003. 68359-37-5 Cypermethrin Deltamethrin CAS No. A small sample of occupationally unexposed Italian residents had median levels of urinary 3-phenoxybenzoic acid that were about fourfold higher than for adults in the NHANES 2001-2002 subsample (CDC. 2004). Saieva et al. 52645-53-1 Tralomethrin CAS No. the presence of 3-phenoxybenzoic acid in urine not only reflects the metabolic transformation of any of the six pesticides listed above.S. 2006). representative NHANES 2001-2002 subsample (CDC. 2005). CDC. Biomonitoring Information Urinary levels of 3-phenoxybenzoic acid reflect recent exposure to the parent pyrethroid pesticides.

8) 3.46) .300 (.353 (.34 (2.16) 483 580 682 831 833 1128 99-00 01-02 99-00 01-02 .760 (.360) .315 (.320) .210-.05) .640 (.260-.190-.32 (2.490-.18 (2.36) 1.49 (1.26-2.25-7.610) .373) .160-.1 and 0.330) .01 (1.12) .520 (. population from the National Health and Nutrition Examination Survey.42-2.63-3.240 (.76 (1.810) 1.277-.250 (.250 (.710 (.53-3.750) .750-1.35 (2.560-.89-71.81 (1.02-6.64) 697 680 524 701 603 957 Limit of detection (LOD.870 (.350-. Deltamethrin.51-6.300 (.430-.34-6.470-.233-.620-1.25-1.820) .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 .288 (.52-5.30) 3.370) .740 (.78 (1.750) .29-1.1) 3.73) 1.38 (2.420) .311 (.320 (.48-2.250-.71 (1.35) 1.30 (1.78) 6.56-5.60) .271-.298 (.320) .69) 3.417 (.43) 3.590-. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.33 (1.270) .270 (.530-.21 (2.586) .630) .25 (2.246-.230-.53) 1.840-1.1) 3.321 (.990) .90) 1.530-.69 (1.250 (.78) 1.328 (.54) 1.340) 75th .16) 1.33 (2.300) .510-.50 (2.S.570-.490) .51-3.62-6.230 (.83-11.253-.41) 3.190-.39) 2.800) 1.210-.27-11.384) .297 (.427) .226-.273 (.340) 1.05) 1. interval) .65 (1.200-.450 (.26) 2.04-5.72 (1.800 (.160-.230-.345) Selected percentiles ( 95% confidence interval) Sample 95th 4.62) 5.45-5.406) .30 (.600 (.23 (2.850) .247-.12) 4.700 (.238-.14-6.13) .314) .25 (2.265-.440) .280 (.79) 3.35 (1.1.86 (1.230-.44) 5.27-2.730 (.190-.1) 3.362) .670 (.292-.352-.Pyrethroid Pesticides Urinary 3-Phenoxybenzoic acid Metabolite of Cypermethrin.41 (1.26) 2.48-2.560-1.454 (.28) 1.550-.830) 90th 1.200-.940) 1.260 (.04) .63 (3.276-.65-2.240 (.510-.220-.595) .227-.32 (1.190-.41-3.55 (1.560-.325 (.180-.601) .590 (.45 (2.49-2. Fourth National Report on Human Exposure to Environmental Chemicals 173 .12 (.960 (.850) .570-1.428-.336 (.295) .35) 2.374) 99-00 01-02 99-00 01-02 99-00 01-02 .18 (1.266-.52-4.32-21.260 (.710 (.33) .290 (.387) .03 (3.93 (1.650 (.230 (.260 (.27-2.35) 2.507 (.369) .292 (.300 (.330) .700-1.434) . Survey Geometric mean (95% conf.320) .16-1.680 (.430-.16) 974 1193 1024 1346 99-00 01-02 99-00 01-02 99-00 01-02 .200-.780) 4.13 (.41-2.62-8.46) 2.390) .75 (1.34) 8.314 (.320) .38 (2.25-4. and Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.364) .267 (.92-3.355) .49-2.830-2.340) .78) 1.820) .740 (.288-.49 (1.

230-.19 (2. interval) .40 (1.860-1.09) 3.160-.253) .227 (.280-.270) .930) .03-1.32 (2.362 (.311 (.13-1.55) 3.400-.290-.36 (1.390-.39) 1.49-2.0) 3.86 (1.530-.580 (.15-2.49) 1.650) .760) .83) 1.670) .52) 2.730) .81 (1.10 (2.92) 483 580 682 830 833 1128 99-00 01-02 99-00 01-02 .49) 3.200-.230-.380-.320) .09-2.270 (.460-.274 (.19) 974 1193 1024 1345 99-00 01-02 99-00 01-02 99-00 01-02 .44) 2.280) .S.290) .335-.550 (.590) .22 (1.350) .190 (.Pyrethroid Pesticides Urinary 3-Phenoxybenzoic acid (creatinine corrected) Metabolite of Cypermethrin.550 (.240 (.150-.72 (1.700-1. and Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.173-.40) 2.280 (.510 (.423 (.270 (.178-.330) .74) 3.35) 1. Deltamethrin.240-.240-.677) .43-64.316 (.60-4.229-.95) 1.274-.510 (.272 (.810) 1.06-3.11 (.94 (1.09-2.400) .25) 2.49 (1.750-1.720) 90th 1.210 (.13 (.41-4.275 (.670) 3.226-.35) .21 (1.04 (3.60) 1.224-.370 (.67 (1.73) 1.280 (.280) .278) .07) 2.730-1.261 (.190-.300-. Survey Geometric mean (95% conf.960-1.510 (.11 (.02-1.234 (.304) Selected percentiles ( 95% confidence interval) Sample 95th 3.02 (2.240-. population from the National Health and Nutrition Examination Survey.410) .490 (.48) 697 680 524 700 603 957 174 Fourth National Report on Human Exposure to Environmental Chemicals .67 (1.730) .43 (2.84 (1.25-5.75-8.330) 1.420-.590) .51-7.19-6.91 (2.387) .840-1.63) 1.460-.309 (.720 (.48 (1.400-.930) 1.290) .04 (.534) .250) .83 (1.329) .240 (.380 (.299-.54 (1.480 (.330) 75th .480-.312 (.272) .630) .350 (.52 (1.53 (1.80) 4.300-.370-.91-4.250 (.05-3.450 (.860-1.00) 5.63-3.200-.860 (.200-.310) .240-.240 (.190-.44 (1.330 (.640 (.261-.410-.440-.43) 1.09 (.440-.560 (.62) 1.202-.330) .329) .88-5.372) .740) .437) .500) .90) 3.35-3.21-4.271-.67) 1.03 (.309) .27) 1.220-.446) .580) .530-.61-2.35 (1.225-.200-.91) .610 (.490 (.490-.323 (.36-6.540 (.321-.17-1.378 (.238-.00) 1.00) 1.64-5.91) 9.62) .270) .264 (.590) .440-.210-.230) .25-2.41) 1.16-4.13-1.246 (.357) .07-5.210 (.590-1.328) .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 .216-.365) 99-00 01-02 99-00 01-02 99-00 01-02 .250 (.270-.550 (.17 (.37 (1.37) 1.570) .401) .220 (.43 (1.280 (.55 (1.640 (.19) 2.73-4.240 (.96 (1.

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

250-.190-.100-.530) .410) .320-.490) .280-.260 (.220-.137) .140) .130 (.120) .210 (.400) .120-.390 (.110) .230-.140) .220-.120-.170 (.350-.210-.360) .600) .250 (.160-.240 (.710) .350) .200 (.300-.570) .500) .560) .090 (.270 (.100-.180-.112-.280-.130 (.390-.070-.350 (.210) .250 (.130) .200 (.140) .160) .148-.220) .161) .200-.170-.145) Selected percentiles ( 95% confidence interval) 50th .470) .130 (.320-. 0.330) .180-. Two antimony compounds (sodium stibogluconate and antimony potassium tartrate) have been used as antiparasitic medications.190 (.240-.169 (.330 (.140 (.132 (.290-.330-.164-.146 (.300) .120-.260 (.123 (.220-.140 (.200) .126 (.170-.170-. storage batteries.207) .390) .126-.04.145 (.430 (.128 (.430 (.150) .280-.130-. to a lesser extent.190) .300) .143 (.120-.320-.130 (.510) . Workplace exposures can occur at smelters.310 (.07.220 (.200) .290 (.300-.270) .280) .190 (.230) .310 (.130-.330-.310-.154) .080) .230) .190 (.120 (.390) .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 . from air and drinking water.120-.090) 75th .280) . which may vary for some chemicals by year and by individual sample.117-. ceramics. The absorption.110-.197) .150) 90th .070 (<LOD-. water.090-.154-.100) .210-.119) . or other substances containing antimony is another means of exposure.330) .360) .220-.133) * .240 (.170) .130-.090-. Stibine is a metal hydride form of antimony used in the semiconductor industry. 01-02.180) .160) .190-.175 (.110-. solder.160 (.156-. respectively. sheet and pipe metal.220) .130-.260) . and glass.180 (.200-.240 (.04.160-. People are exposed to antimony primarily through food and.144) .Metals Antimony CAS No.120-.142 (. population from the National Health and Nutrition Examination Survey.310) .420) .087-.180 (.120 (.190) . 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. Antimony can exist in one of four valences in its various chemical and physical forms: -3.140 (. and 0. castings. see Data Analysis section) for Survey years 99-00.330 (.310 (.280-. Dermal contact with soil. and refuse incinerators that process or release antimony.400) .130) < LOD .400 (.125 (.230-.160) .460 (.190-.119-.180 (.120) .220) 95th .200 (.150) .140) .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 .430 (.400) .200 (.110 (.340) .300-.240 (.108-.310 (.190) .220-.210) .200 (.130 (.190 (.460) .180 (.093 (.099 (.122 (.390) .130-.350 (.130 (.095 (.170-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.390-.400 (.270) .210 (.178) .160 (.200) .130-.250 (. metal bearings.320) 787 683 618 554 667 723 768 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.160) .210) .270 (. 7440-36-0 General Information Antimony is found in ores or other minerals.370) .240-.120-.390-.120 (.115) .160) .350 (.150-.350-.130) .170 (.350 (.131-.120) .280-.460 (.160-.270-.250-.230-.098-.190-.180 (.130 (.300) . often combined with oxygen to form antimony trioxide or with sulfur to form stibnite.280) .470 (. and as a fire-retardant in textiles and plastics.180 (.150 (.180) .136) * .117-. It is also used in paints.340 (. It is used in metal alloys.160-. fireworks.390) .500) .280 (.220) .240) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.250) .114) .270 (.280 (.330 (.310) .200-.350 (.260 (.230 (. 176 Fourth National Report on Human Exposure to Environmental Chemicals .360-.240 (.230) .080 (<LOD-.360 (.260-.137) .200) .310-.270 (.150-.190) . Antimony enters the environment from natural sources and from its use in industry.158 (.320 (.180-. 0.080-.120 (.140) .330) .260) . and excretion of antimony vary depending on its oxidation state.320 (.190-.410) .300 (.134 (.280) .180-.157) .210) .210) .135) * .150 (.100 (.350) .360 (.260) .370-.400-.350) .190 (.110-.220-.410-.300 (.150-.170-.184) .440 (.260-.140-.141-.128 (.320) .220 (.110-.095-.120-.160) .150) .320-.490 (.130-. < LOD means less than the limit of detection. coal-fired plants.200 (.350) .136-.250-.176 (.190) .105 (.103) .108 (.460 (.470) .230-.109-. ammunition. and pewter.090 (<LOD-.350-.115-.200-.130 (. distribution. interval) .150-.290-.250-.140) . and 03-04 are 0.088-. and +5.150-. enamels.340 (.150 (.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 .080) .160 (.320) Total .230-.154) .120-.140 (.S.230 (.180-.120) .400 (.440) .100 (.130) .440) .134-.230 (.330) .120 (.079-.132 (. +3.070 (<LOD-.

152) .250-.119 (.140) .130) .228 (.148-. and kidney have been demonstrated in high dose animal studies depending on the dose.281-. Ming-Hsin et al.250 (.167-.343 (.135 (.163 (.204-.405) .135) .074 (. The toxicity of stibine after acute inhalational exposure is similar to that of arsine.105-. resulting in hemolysis with abdominal and back pain (Dernehl et al.129 (.138 (.194-.163 (.280 (.139 (.267) .107-.098) .195-.114 (.087) . 1973).352) .286 (. Inorganic antimony salts irritate the mucous membranes. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.417) .102-.185 (.333-1.146-.107-.199-.061-.208-.160 (.193) .295 (.112 (.170 (.130) .151) .269 (. 1988.265 (.112 (.385 (.211) .125-.208 (.153 (.104-.124) .068 (.192) . 1958) and occupational exposures (Briegner et al.196 (.30) .173 (.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 . diarrhea.086 (.S.400 (.122 (.118 (.120 (.333 (.108 (.176 (.078 (.109-.081) .098-.238 (.167 (.129) .185-.235-.425) . 1962). Dysrhythmias and T-wave changes on electrocardiogram have also been noted after both therapeutic (Berman.338) .313-.300 (.095-.115-.128-.256 (.117-.145) .429) .241-.119-.259 (.333-.320 (.113-.224 (.364 (.175 (.136) . 1986).086) 75th .153-.116 (.148-.122 (.080 (.250) .099-.191 (.159-.111-.079 (<LOD-.181) .444) .144-.310) .106-. species.206-.164) .429 (.233 (.250-. and eyes.147) .143) 90th .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.500) .133) .112-.159-.139 (.248-.138-.140) < LOD .338 (.228 (.278) .338 (.317) .391) . population from the National Health and Nutrition Examination Survey.203) .102-.278 (.192 (.417) . Acute antimony poisoning may cause a metallic taste.161) .253 (.244-.414) . An elimination half-life of approximately 95 hours has been estimated after occupational exposures (Kentner et al.318-.187) .164-.250-.373) .137 (.207) .124-.178 (.200) .092-.238) .188-.271-. Histopathologic inflammatory and degenerative changes in the lung.209) .127 (.364 (.164 (.233-.276 (.727) .172-.123 (.209-.217 (.183) .173) .096-.150-.124 (.230-.117-.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 .320) .114 (.127) . 1954).123) .146) .265-. Acute inhalation of antimony has been associated with irritation of the respiratory tract and impaired pulmonary function (Renes. Human health effects from antimony at low environmental doses or at biomonitored levels from low environmental exposures are unknown.268) .077) . Pulmonary edema may occur in severe cases of inhalation exposure (Cordasco et al.300) .471 (.138) * .317) .114 (.438) .148) * .310 (..318-.192-.352 (.103-.308-.131-.430) .092) .230) 95th .310) .380 (.225 (.138-.267 (.233) .214) .444) .178-.179-.159-.149-.333-.103-.099-.176 (.189 (.277 (.076-.130 (.126-.098-.421) . 1986).117-.118 (.075 (.161) .095-. 1953).245) .241-.320-. abdominal pain.228-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.143) .143 (.188) .121) .257) .121 (.255) .205-.200-.115 (.100 (.127) .250-.107-.320 (. liver.280-.108-.333 (. 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.143) Selected percentiles ( 95% confidence interval) 50th . 1995).321) .146-.485) .209) .741 (.255-.147-.156-.129) * .108-.317) .135) .116-.173 (.135 (.132 (.126) .120 (.250 (.300) .146-.261) .150-.131) .238) .229-.082) .129 (.247) .181) .198) .200-.068-.371 (.213 (.097-.248) .239-.106-. myocardium.Metals than for trivalent compounds (Elinder and Friberg.115 (.272) .125 (.162-.741) .080 (<LOD-.333) .220) .173-.167 (.069-.253-.082 (<LOD-.333-.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 ..203) .182 (.288 (.185 (. Fourth National Report on Human Exposure to Environmental Chemicals 177 .266 (.120 (.109 (.104-.320-.195 (.391) .085) .113) .127) .089) .209 (.084) .267-.120 (.132) .111 (.263-.480) .108-.127) .081 (<LOD-.121 (.315) .171) .333 (.471) .193 (. skin.222 (. and route of exposure (Elinder and Friberg. and ulcers (Werrin.115-.126 (.130) . 1944).242-..113-.156 (.115 (. and gastrointestinal symptoms such as vomiting.134) .075 (.119-.152) .135) .200-.069-.082) .149) ..181) .447 (.186) .195-.131 (.294) Total .115) .308) .225) .227-.226 (. interval) .071-.154-.357) .236 (.109 (.176-.357-.143) .076-.298 (.124-.167 (..263 (.

1990. Handbook on the toxicology of metals. Ju-Sun P.48:93-97. Information about external exposure (i. Stocks J. EPA. Delves HT.10(3):560-586. 1994) have reported values slightly higher than those in this Report. Stasney J. Antimony in blood and urine of infants. Review of elements in blood.51:238-240. Rev Infect Dis 1988.. Urinary antimony in infancy. 1998) or compiled reference ranges (Hamilton et al. Kentner M. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Carelli G. Biological assessment of exposure to antimony and lead in the glass-producing industry.. 1997).46:931-936. Schacke G.e. Luedersdorf R. even when exposure levels were below workplace air standards (Bailly et al. Roland H. Int Arch Occup Environ Health 1995. Piatnek DA. and 2003-2004. et al. Stead FM. Leinemann M. Cullen A. 26-42. Nau CA. Mayer P. Industrial Medicine 1944. Mechanism and treatment of cardiac arrhythmias in tartar emetic intoxication. Bolten C. Human biomonitoring of arsenic and antimony in case of an elevated geogenic exposure.521-523. Gebel TW.. Chest 1973.76(2):103-115. stibine. arsenic. and a drinking water standard has been established by the U. Br J Ind Med 1991. Semisch CW... Alimonti A... et al. Dernehl CU. Liao Y-H et al. population. and antimony in optoelectronic industry workers.. In: Friberg L. 2nd ed. Experimental and human studies on antimony metabolism: their relevance for the biological monitoring of workers exposed to inorganic antimony. Arch Dis Child 1997. Briegner H. Earlier measurements in general populations (Minoia et al. Apostoli P. Vouk VB. gov/toxpro2. Biomonitoring of a worker population exposed to low antimony trioxide levels. Antimony trioxide is rated by IARC as a possible human carcinogen. VI. Suchenwirth R.html.67:119-123. Stone FD. clinical efficacy. Costeloe K. respectively. Mayne P.16: 33-39. J Trace Elem Med Biol 2002. Pozzoli L. Iavicoli et al. Cordasco EM. Arsine. Gallorini M. New York: Elsevier. Dunkelberg. J Occup Environ Med 2004. Centers for Disease Control and Prevention (CDC). Elinder CG. 1998. Iavicoli I. Ming-Hsin H. Friberg L.64(2):182-185. Fuchs A. 1998). Biomonitoring studies on levels of urinary antimony can provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of antimony than are found in the general population. 1991. Minoia C. Konings J. Biomonitoring Information Levels of urinary antimony reflect recent exposure.S.. Nordberg GF. Lauwerys R. Finding a measurable amount of antimony in urine does not mean that the level of antimony causes an adverse health effect. Pilgrim L. Ho C-K. Biological monitoring of exposures to aluminum. or exposure differences.atsdr. Matthews T. 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. Industrial Medicine and Surgery (Dec. Wade A. which may be due to methodologic.158:165-190. Dezateux et al. 20012002. Third National Report on Human Exposure to Environmental Chemicals. External and internal antimony exposure in starter battery production. 2002. A study of 46 elements 178 Fourth National Report on Human Exposure to Environmental Chemicals . Delves HT. J Clin Pathol 1998. Shao-Chi C. Chia-Yu H. Caroli S. Ludersdorf et al. Environ Health Perspect 1998.Metals to antimony have been established by OSHA and ACGIH. 1986. Pulmonary edema of environmental origin. Sabbioni E. Int Arch Occup Environ Health 1987.. gallium. 1995. and hydrogen sulfide. Trace element reference values in tissues from inhabitants of the European community I. Element reference values in tissues from inhabitants of the European community. Antimony. Weltle D. Kentner et al. Skulsukai G. Dezateux C. indium.106:33-39. Bailly R. plasma and urine and a critical evaluation of reference values for the United Kingdom population. Van der Venne MT. Pietra R.)1954. eds. Chen J-R. Cheng-Wei L. Kiberd B..cdc. Petrucci F. et al. Chin Med J 1958. Liao Y-H. Hamilton EI.13:361-362. Chemotherapy for leishmaniasis: Biochemical mechanisms. Yang C-Y. Industrial antimony poisoning.. Sabbioni E. References Berman JD. Buchet JP.59:469-474. Schaller KH. pp. 1987). 2005. and future strategies. 2004. Yu H-S. Mahieu P. HH. Paschal et al. environmental levels) and health effects is available from ATSDR at: http://www. Wu M-T.76:432436. O’Regan M. Atlanta (GA). Sci Total Environ 1994. Kuo-Juie Y. Lenert G. Levels of urinary antimony in infants appeared to be similar to those reported by CDC (2005) for young children (Cullen et al.

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

8) 30. or rarely as elemental metalloids (yellow.5) 43. 2005).3-19.8) 17.6 (15.08 (5. In the last century.9-46.8 (48.41 (7.5) 41. it is found in over 200 crystalline or mineral forms. from coal burning.30 (6. a trivalent compound known as white arsenic) is a common natural and commercial form that can be released into the air during volcanic action.90) 16.90-8.5 (23.84) 8.0-60.4) 40.66-8.6 (13. 180 Fourth National Report on Human Exposure to Environmental Chemicals .0 (14.80 (5.5 (40.84) 8. black. gaseous hydride manufactured in small quantities for use in the semiconductor industry. Various arsenic compounds were used in paint pigments and for tanning animal hides.3-111) 78.4) 13.3) 10. CCA-treated wood has been restricted since 2003 and no longer can be used in residential applications such as decks.5 (14.8-61.0 (11. The United States no longer produces arsenic from mining but imports about 22. Before the 20th century. lead hydrogen arsenate.70) 8.5) 95th 65.4-65.97) 8. sodium arsenite.5-52. Arsenic trioxide is approved to treat acute promyelocytic leukemia. and monosodium methyl arsenate were used as pesticides but contemporary uses are restricted. In nature. pesticides.8) 29. alloys.12 (6.5 (36.2) 15.8) 33. referred to as inorganic arsenic compounds.6-141) 53.90 (7.9 (17.1) 1281 1276 03-04 03-04 03-04 9.6-35.70-9. and arsenates (oxidation states of -3. arsenic compounds.80-9. cacodylic acid. Arsine (AsH3) is a reactive.20 (8.2-61.9) 68.1 (32. population from the National Health and Nutrition Examination Survey.9 (8. Various forms of inorganic arsenic can occur in groundwater from natural sources or as a result of soil application or industrial waste.10-7.7 (11.7) 90th 37.74. particularly arsenic trioxide.2 (12.50 (8.50-14.4 (31.8) 7. Survey years 03-04 Geometric mean (95% conf. aluminum. interval) 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 7.34-9. Arsenic can also combine with organic substances in nature to form such organic arsenic compounds as arsenobetaine.000 metric tons annually.0 (15. Although it is still widely used in the United States.10 (6.9-62. Water sources contain mostly inorganic arsenate.1) 7.5-41.Metals Arsenic CAS No. +3 and +5).4 (48.10) 10.90-11. the smelting of copper.2-93. Arsenic and its compounds have had many uses in the past and present as medicines.5) 66. grain. and arsenosugars.70 (6.00-9.8-77. 7440-38-2 General Information Arsenic is an element that is widely distributed in the earth’s surface in small amounts. solders.3-15. Arsenic trioxide (As2O3.8) 7.9) 21.1-18.2 (13.0-19. Since the 1940s. to a lesser extent. cancers. and foods. psoriasis.90 (7. trimethylarsine oxide. and produce.1) 15. mostly for use in wood preservation (ATSDR. Also.5 (34. see Data Analysis section) for Survey year 03-04 is 0.6 (32.4 (7.2 (51. Roxarsone and other organic arsenicals are anticoccidial agents added to poultry feed.7) 24. arsenites.25-9.34-10. retaining walls.02-8.6-43.1) 290 725 1542 03-04 03-04 9. arsenocholine.27) 9.5-178) 46. lead.57) Selected percentiles ( 95% confidence interval) 50th 7. Arsenic is measurable in most soils.00 (6.80) 6.2) 46.S.7) 65.10-10.40) 7. and other metals.30) 17.0 (22. Groundwater Urinary Total Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.77) 6. Arsenic can combine with such non-carbon chemicals as sulfur and oxygen to form arsenides. were used as treatments for syphilis. mental disorders.30 (7.5-19. arsenic as elemental metalloids may be used in some ammunition.2-17.2-20.8) 34.4) 60. and as homicidal poisons. and indium arsenides are used in the semiconductor industry.1 (38.2 (41.1-40.90-8.13-8. though in some locations arsenite may be prevalent (WHO. chromated copper arsenate (CCA) has been used to treat outdoor timbers and pressure-treated woods to prevent wood rot. General population exposure to inorganic arsenic can occur through consumption of drinking water and.0 (43.4 (24.7-83. to a lesser extent.29 (8. and play sets. meats. such as arsenopyrite (FeAsS) and realgar (As4S4). ocean and fresh waters.6) 618 722 1074 Limit of detection (LOD.6 (9.9-34. and as a cosmetic to lighten complexion.12-10. 2001).90-14. Gallium.6) 11.7-95. and gray forms). semiconductors. copper arsenates.4 (26.55 (7. and.90 (5. as alloy in metal bearings.90) 75th 16.19-9.90-7. and in lead-acid storage battery grids.

2) 40.5-120) 40.0) 12.8-32. 2001).81-9. dust.7 (11. 2001).75) 13.4 (40. and contact with CCA-preserved wood structures.4 (24. shellfish.12-10...7-34. dose level. WHO. trimethylarsine oxide (TMAO).8) 27.. gallium arsenide and indium arsenide.59) Selected percentiles ( 95% confidence interval) 50th 7.20-9. and arsenosugars. Inorganic arsenic and its metabolites have elimination half-lives of approximately 2–4 days (Lauwerys and Hoet. The semiconductor dopants.1) 7.5 (9.47-6. Arsenate is reduced in the body to arsenite (oxidation state +3). so exposure to the general population is extremely limited.3) 6.88) 7.4 (42.1 (11.0) 26.1 (14. 1988).75 (5.0) 33.0 (31.7-188) 27. 2001). Ingestion of arsenosugars in kelp and algae can also lead to the excretion of DMA.01) 11. 2001).9 (45. 2007.5-17.30-9.7-17. Gamble et al. 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. Fish.9) 53. 2001). and some other seafood can contain organic forms of arsenic including arsenobetaine.51) 75th 14. selenium. Inorganic forms of arsenic demonstrate high acute toxicity.28-7. 2001.0-18.76 (6. inorganic arsenic is widely distributed within the body.96) 12.7) 28. 2001.9) 13.10-8.47 (7.11 (5.44) 6. NRC. are used in enclosed ultraclean operations within the semiconductor industry.00 (6.0) 42.66-8. U.6 (35.4) 54.6 (17.6) 45.86-17.Metals sources of drinking water often have measurable arsenic and several regions of the United States have naturally higher arsenic levels than the U.1) 58.4 (26.8 (12.93-8.45) 5. with trivalent inorganic arsenic (arsenite) being more toxic than pentavalent inorganic arsenic (arsenate) (NRC. Though modest bioconcentration occurs in some aquatic life.25 (6.g.66-8.9) 618 722 1074 Fourth National Report on Human Exposure to Environmental Chemicals 181 . Inorganic arsenic is well absorbed from the gastrointestinal tract and absorbed to a lesser degree through inhalation.4-64.3-64. arsenic does not show biomagnification in the food chain (WHO. Survey years 03-04 Geometric mean (95% conf. Direct exposure to DMA and MMA may result from use of the two pesticides. 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. Steinmaus et al.58-10.3-62.4 (11.5) 17. though some reduction may occur in the gut prior to absorption.32 (5.8 (27. as observed in Bangladesh where millions of people have been exposed.8-75.40) 8.8 (21. organic arsenic can be converted back to methylated and inorganic arsenic. interval) 8.33-10.7 (25. EPA.88 (5. population from the National Health and Nutrition Examination Survey.1) 6.2) 90th 30.S..04 (5.7) 95th 50.3-41.23-7.1-36.50 (6. Smoking tobacco is also a source of inorganic arsenic.8 (11.0-26. 2006...13) 8.0 (17.07-9.3 (27. mine tailings). TMAO is also formed in the environment from microbiological action and is a metabolite of arsenic in certain mammals.1) 24.7-35.3 (24. kelp.7-18.44-11. 2007.2 (12.8-62. Chowdhury et al. Arsenite is then oxidatively methylated to the monomethylarsonic acid (MMA) and dimethylarsinic acid (DMA) with subsequent excretion primarily in the urine (NRC.47 (6. but is poorly absorbed dermally (WHO. These organic forms of arsenic from seafood are absorbed and quickly excreted in the urine (WHO. In aquatic organisms. 2006.5) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites Sample size 2557 03-04 03-04 03-04 8.33 (6.0) 1281 1276 03-04 03-04 03-04 8. arsenocholine is converted to arsenobetaine and also to small amounts of TMAO (Christakopoulos et al.2-46. Tseng. 2001). After absorption. cacodylic acid and monosodium methyl arsenate.31 (6. have caused clinical arsenic poisoning. In aquatic sediments.38-10.0-69.93-9. WHO.S.2-15.8 (20.3) 9.66 (7.41) 6.35) 7.25-9. 2007. Extremely high groundwater arsenic levels.8) 22. 2001).61 (7.1) 8.4 (12.5) 290 725 1542 03-04 03-04 8.18 (5. arsenocholine. 2003.06 (4.3-53.24 (7. Children may have additional exposures from ingestion of contaminated soils (e.0-38.01) 7. Smelter workers can have significant inhalational exposures to airborne arsenic trioxide for which air standards have been established.S. and folate status (Chen et al.2) 15.6-17. 2001).99-9.04) 7.64 (7.4) 32.0) 14.6 (10.7 (9. age. EPA’s maximum contaminant level (Hughes.9-56.10-16.

50) 2568 95th 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1.20 (<LOD-1. hypertension.. NRC.10 (<LOD-1. Chronic elevated arsenic intakes have been associated with diabetes.EPA has established drinking water. renal failure. 182 Fourth National Report on Human Exposure to Environmental Chemicals . leading to a decrease in adenosine triphosphate energy production. and hyperpigmentation of the skin (NRC.S. NRC. 2004. Chronic arsenic exposure in humans is considered to be a cause of skin. 2004). 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. arsenic trioxide) includes hemorrhagic gastritis with nausea. 2001). which can lead to dehydration and shock. apoptosis.. hematocytopenias. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. gluconeogenesis. 2006) and newly discovered thioarsenic metabolites may also be as toxic (Naranmandura et al. 2006. 2007.30) 1. 2001)...10 (<LOD-1..S. and production of glutathione may be affected as well. Chile). Arsenic has many actions demonstrated in cellular studies.. and altered gene expression.80) 1. 2007. and childhood neurodevelopmental effects in observational human studies. vomiting. and peripheral neuropathy may also occur with large doses or after surviving an acute overdose. population from the National Health and Nutrition Examination Survey. 2001.50) 621 725 1078 Limit of detection (LOD.. 2001. which may vary for some chemicals by year and by individual sample. arsenite will inhibit cellular pyruvate dehydrogenase by binding to the sulfhydryl groups of dihydrolipoamide. including inhibition of numerous enzymes. hyperkeratosis. WHO.10 (<LOD-1. including drinking water sources with elevated arsenic levels (e. and bladder cancer (IARC. 2006. The U. fatty acid oxidation.EPA. Laboratory studies using inorganic arsenic have shown chromosomal aberrations.Metals +3) shows greater toxicity than arsenite itself (Aposhian et al. Studies of arsenic at levels typical of U. U. With chronic exposure.20 (<LOD-1. The risk of lung cancer appears more pronounced when large environmental exposures start in childhood (Smith et al. Chronic human intake of arsenic at less than acutely toxic doses.60) 1. 2001).60) 1. Survey years 03-04 Geometric mean (95% conf. The organic forms of arsenic occurring in seafood have little known toxicity. OSHA and ACGIH have established workplace standards and guidelines for arsenic exposure and monitoring. substitution in phosphate metabolism. it may have its own separate toxic action by substituting for phosphate in glycolysis and other pathways. Raml et al. 2006. WHO. Cardiac arrhythmias.10 (<LOD-1..g. and diarrhea.. Such actions may lead to decreased energy production. and it also will inhibit succinate dehydrogenase. 2001). 2004). some of these effects may take years to develop. noncirrhotic portal hypertension. peripheral vascular disease. food residue. Taiwan.S. Acute toxicity resulting from the ingestion of large amounts of trivalent arsenic (e. cytotoxicity. 2001). and environmental standards for arsenic and arsenic Urinary Arsenic (V) Acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. hepatotoxicity.. can cause peripheral sensorimotor neuropathies. Bangladesh.20 (<LOD-1.30) 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1. Acute unintentional inhalation of arsine gas can produce hemolysis of red blood cells. and DNA repair inhibition (Cohen et al. 2000. 2001). 1998. interference in signal transduction pathways. Acutely. increased oxidative stress. and endothelial injury (Kumagai and Sumi.g. drinking water have not been associated with increased cancer rates (Schoen et al. Although arsenate is reduced in the body to arsenite. Cellular glucose uptake. < LOD means less than the limit of detection. but additional or confirmatory research is needed (Kapaj et al.. lung. 2007).20 (<LOD-1. WHO. and by uncoupling oxidative phosphorylation (NRC. cell transformations. respectively. see Data Analysis section) for Survey year 03-04 is 1.. Bredfeldt et al.50) 1.S. WHO.0. Cohen et al.10 (<LOD-1. 2006) or when exposure occurs in smokers (Chen et al.50) 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD 1.

.e. 2006). Shalat et al. 2004. 2006). 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... 2006. 2001).. although urinary arsenic levels were not associated with CCA contact (Shalat et al. and were about two-fold lower than those for the U.Metals compounds. Valenzuela et al. 1999). * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 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.75 (<LOD-2. but generally only at maternally toxic doses (WHO. Meza et al.04 (<LOD-3. Pellizzari and Clayton. 1999. gov/toxpro2. 1992. In the German Environmental Survey III of 1998. 2000. Offergelt et al.. population from the National Health and Nutrition Examination Survey. the median total urinary arsenic in about 200 people was approximately four times higher than that of the U. Pellizzari and Clayton 2006). Daily variation in creatinine-corrected urinary arsenic is relatively small when intake is constant (Calderon et al.. 2008).. 1999. environmental levels) and health effects is available from ATSDR at: http://www. though air levels of arsenic fume and dust are correlated with urinary arsenic levels at higher occupational inhalational exposures (Jakubowski et al.S. 2005) and Urinary Arsenic (V) Acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U..50) 2568 95th 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2. Josyula et al. Pellizzari and Clayton.. In animal studies. 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. Caldwell et al. In a Nevada town where groundwater levels were naturally elevated. 2001).. higher mean or median total urinary arsenic levels have been reported among people living in specific western areas of North America (Calderon et al. arsenic has been fetotoxic and teratogenic.89) 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2. 2006). Consequently.html..S. IARC and NTP recognize inorganic arsenic and arsenic compounds as human carcinogens. 2006.95) 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.19) 3. Shalat et al.69 (<LOD-3.. 2008).. 2007. 1998..atsdr.18) 3. Additional information about external exposure (i..80 (<LOD-4. 2006). Vahter et al.41) 3..70) 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD 2. WHO.. 2003. DMA produced bladder cancer in some chronic rat studies (Cohen et al. urinary arsenic levels have been accepted as a good biomarker of dose (WHO. 1986). and the FDA has established a bottled drinking water standard. 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..00) 1. Caldwell et al. 2001). Survey years 03-04 Geometric mean (95% conf. 2004.61 (<LOD-3. 2000). hand washings from children playing on CCA-treated wood compared to children playing on non-CCA-treated wood playground equipment were slightly to fivefold higher (Kwon et al. population in NHANES 2003–2004 (Schulz et al. population (Rubin et al.S. Fourth National Report on Human Exposure to Environmental Chemicals 183 . 2008..cdc.S..75 (<LOD-2.33 (<LOD-3. Calderon et al. Levels of total urinary arsenic in the U. 2007..18 (<LOD-3. median urinary total arsenic levels in 4052 adults varied with seafood intake.33 (<LOD-3..50) 1. had decreased since the prior 1990– 1992 survey.. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th < LOD 90th < LOD Sample size 3. Though CCA-treated wood contains several thousand times more arsenic than untreated wood. 2006. Compared with this Report.

* Not calculated: proportion of results below limit of detection was too high to provide a valid result. Aposhian et al.74 (1.70-21.3 (21. 2008. 2003).70 (3.9-23.4) 31. see Data Analysis section) for Survey year 03-04 is 0... Total arsenic measured in the urine includes all species of inorganic and organic arsenic. 2005. 2008.80 (. 2005. arsenite. and arsenobetaine being the main contributors to the total urinary arsenic levels (Caldwell et al.g.40) 75th 5.. DMA has been the predominant metabolite composing the majority of measurable inorganic-related arsenic in the urine (i. In most human studies. 2008). Blom et al.28) 1. Caldwell et al.4 (16.6 (25.83) Selected percentiles ( 95% confidence interval) 50th 1.8) 35.66 (1.11-1. population (Sun et al.9) 13. 184 Fourth National Report on Human Exposure to Environmental Chemicals .70-21.7) 13.5 (26. MMA.50) . China.2-38.0) 4.20-25.4-35.00-1. Great Lakes region residents had median urinary DMA levels that were slightly less than median levels in NHANES 2003-2004 (Caldwell et al.10) 8.1-25.800-4... Individually measurable species resulting from inorganic arsenic exposure are arsenate. population (Ahsan et al.20 (2.00-6.3) 95th 35.e. and other factors such as nutrition.00 (. 1996. Caldwell et al.80 (4.20 (4..8 (17. dermal keratosis.2 (6.50) 90th 16. 2007) with higher levels of arsenic in the drinking water.80-5. 1990..6 (13..30 (1. 1985.3) 35.37 (1. respectively. Valenzuela et al.62) 2. In the residents of a Chilean town who consumed water with high levels of arsenic.40-7..20-3. geometric mean levels were about 70-fold higher than for the U. population from the National Health and Nutrition Examination Survey.90-29. < LOD means less than the limit of detection.90-7. 2007).6.45 (1.5) 621 725 1078 Limit of detection (LOD.. For residents of Inner Mongolia.0 (26. as evidenced by trace or nondetectable levels of arsenobetaine and arsenocholine in the urine.S. The higher percentiles of total urinary arsenic levels in the U. and urinary DMA represented about 67% of the total urinary arsenic (Hopenhayn-Rich et al.6-44.20 (.40-6. 2005. 2006). Levels of DMA and MMA increase in approximate proportion to the intake of inorganic arsenic.70) 6. Arsenate.50-6. 2000.10) 4. WHO.0) 29.8.Metals other areas of the world (Ahsan et al.1) 45. median levels of urinary DMA were about 40-fold higher than the adult median reported in NHANES 2003– 2004. population showed a higher contribution of arsenobetaine (Caldwell et al.20 (1.93) 1. 2008).871-1. 2008).3-39.55 (1. arsenobetaine.S. and TMAO.19 (..700-1.400-.3% of a representative sample of the U.29 (1.20-190) 31. population in the NHANES 2003–2004 subsample.900 (.7 (21.0-23. 2008). Caldwell et al. which may vary for some chemicals by year and by individual sample.. These associations are stronger at higher urinary levels. DMA and MMA.43-1. 4. 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.6. and 0.800-1.00-12. Urinary Arsenobetaine Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. 2001).. and duration of exposure are also considered important. 2000.5) 292 728 1548 03-04 03-04 1. 2001.9 (6.6) 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 * * 1.1-94. In the late 1980s. When seafood intake is avoided. methylation capacity.80) 1..5 (14..31-1. Tseng et al. After recent seafood ingestion.2-35.30 (2. a control population of 696 Tacoma residents had median urinary DMA levels similar to those for NHANES 2003–2004 (Kalman et al.50) .. when seafood organic arsenic is subtracted).6 (11. and peripheral neuropathy) have been associated with urinary levels as low as 50–100 μg/L in chronically exposed populations (ACGIH.7-22. and two methylated metabolic products.68) .60-3.00) 3. arsenobetaine and arsenocholine will greatly increase the level of total urinary arsenic and comprise the highest percentage of the total urinary arsenic level. vasospasm..700-1.900-1.500-1. Survey years 03-04 Geometric mean (95% conf.7) 15.1-51.20) 3. with DMA.5) 32. DMA and MMA compose most (about 75%) of the total arsenic species measured in urine.60) 1.8-40. Measurable organic arsenic species in this Report are three biologically generated environmental forms. arsenite. in NHEXAS 1995–1996.. arsenocholine.0 (27.20) 7.17-1.. arsenocholine.80 (3.40) 5.3) 1284 1284 03-04 03-04 03-04 1.48-2. Chowdhury et al.600 (. Also.00-4.30) 10. Detectable levels of MMA reported in NHANES 2003–2004 were found only at the upper percentiles and.8 (12.05) < LOD .70 (5.9 (7. Some noncancer effects of arsenic (e. 2000. interval) 1.4.20) 18. Pellizzari and Clayton. 1.7 (13.S.3 (9.10 (4.30) 2.800) 1. Sun et al.5) 29.8-50. and TMAO were detected in only 7.800 (.S.S.1) 18.4) 23.00 (1..800 (. Caceres et al.

0) 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.88) 2.18-1.15-4.16 (.36) 2.50-15.51) 5.79 (1. interval) 1.9) 32.3) 95th 29. The 95th percentile of the U. 1998.2 (13.15-1. Vahter et al.531 (.43) 14.9 μg/L.1-18.5) 26. Sun et al.4) 32.62-6.83) 2.6-29. 1992.82) Selected percentiles ( 95% confidence interval) 50th 1.1 (26.4) 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 * * 1.58 (3.28) 1.05 (... not to imply a safety level for general population exposure.9 (13.4) 13.14 (1.44 (1.39-3.43) 75th 5..15-1.47 (2. these levels were much lower than those found in other studies where environmental exposures were highly elevated (Chowdhury et al.73-6.. which is below the ACGIH BEI (Caldwell et al.6 (6.65 (1.11 (.68 (1.88 (5. Information about the biological exposure indices is provided here for comparison. population for the sum of inorganic related species was 18. Fourth National Report on Human Exposure to Environmental Chemicals 185 .25 (.40) 1.80-153) 17.4-21.Metals as with DMA.91 (4. 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.29 (4.21) 5.00 (1. Offergelt et al.25-7.4 (11.70) 5.50-7. 2008).6-46.0-36.901-2.72) 12. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.612-1.5-20.54 (1.5 (18.32-7.30) 1. 2003.55) 1.6 (9..3-24. Caldwell et al.81 (4.13-39.3 (10. 2001).78 (3..3 (10. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.7) 9.959-1.4-82.S. In recent years.76-27.93 (1. occupational monitoring and research studies have focused on the sum of inorganic-related species (arsenate + arsenite + DMA + MMA) as a measure of inorganic arsenic intake.4-28. 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.400-.4 (24..10 (.83) 8.2 (4. WHO.1) 26. population from the National Health and Nutrition Examination Survey.909-1.82) 4. Survey years 03-04 Geometric mean (95% conf.3) 1284 1284 03-04 03-04 03-04 1.40 (1.8) 29.00 (3.67) 1.12) < LOD .67) 4. Urinary Arsenobetaine (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.877 (.1-36. 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.19-2.37-2.S.0 (9.91) 90th 16.05) 1.7) 17.45) 1.29-14.2 (12.2 (12.7) 30.9-18.4) 292 728 1548 03-04 03-04 1.47 (1. 2001).64-29.5 (18. 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.80) . 2007).61-6..6-32. 1986.5) 17.9 (25.938-1.78-5.786-1.30-1.53 (.638) 1. Finding a measurable amount of arsenic in urine does not mean that the level of arsenic causes an adverse health effect.6) 19.51-2. 2006. 2008).9) 14.833-1.

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

40 (<LOD-1.2. population from the National Health and Nutrition Examination Survey. which may vary for some chemicals by year and by individual sample.00 (<LOD-2.80) < LOD 621 725 1078 Limit of detection (LOD.20 (<LOD-1.76) < LOD 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 3.Metals Urinary Arsenous (III) Acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. < LOD means less than the limit of detection.29) < LOD 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.S.95 (<LOD-2. Urinary Arsenous (III) Acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.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.S. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th < LOD 90th < LOD 95th < LOD Sample size 2568 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1.08 (<LOD-4.00) 1. Survey years 03-04 Geometric mean (95% conf. population from the National Health and Nutrition Examination Survey. see Data Analysis section) for Survey year 03-04 is 1. Survey years 03-04 Geometric mean (95% conf.44) 2. * 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 1.00 (<LOD-3. Fourth National Report on Human Exposure to Environmental Chemicals 187 . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.

S.78 (4.85 (3.37 (3.27-2.69 (3.00-11.16 (2.31-4.6) 1284 1284 03-04 03-04 03-04 4.18 (6.73) 6.05) 5.Metals Urinary Dimethylarsinic Acid Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.32 (4.0-16. population from the National Health and Nutrition Examination Survey. Survey years 03-04 Geometric mean (95% conf.0 (12.00) 3.49) 10.59 (6. Urinary Dimethylarsinic Acid (creatinine corrected) Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.48 (2.92-12. interval) 3.57-5.3 (7. interval) 3.00-5.80-6.7 (10.7) 13.42) 3.77 (3.70-4.34 (3.25 (4.84-18.80-5.95-4.11) 4.00-4.0 (13.1-18.6-18.0-12.20-4.00) 6.00 (6.82-9.94-3.9 (11.0-17.69-6.00) 12.69 (3.60-7.19) Selected percentiles ( 95% confidence interval) 50th 3.97-3.0) 9.7-16.16-11.00-3.0 (11.82) 3.71-4.4 (7.27 (3.30) 3.52) 3.05) 10.0-17.00-4.6) 292 728 1548 03-04 03-04 3.00-11.31) 4.89 (3.20) 11.12 (3.62) 4.0) 10.57 (3.00 (3.00-4.80) 7.5) 95th 13.17-6.0) 14.00 (6.72 (4.4) 621 725 1078 188 Fourth National Report on Human Exposure to Environmental Chemicals .8) 7.0-18.00) 9.7) 1284 1284 03-04 03-04 03-04 4.12-4.50-5.03-6.00-15.00-13.00-7.44 (2.00 (5.0) 95th 16.00-12.00 (6.10) 3.00) 90th 11.90) 5.70) 5.80 (4.00) 7.1 (8.11 (3.00-11.71 (4.00-10.22) 4.0) 17.08 (2.00-22.34 (3.00-4.00-8.00) 4.0 (9.50 (4.00-15.0) 11.88 (4.17 (2.00-4.67) 8.0 (9.45 (8.71 (3.74 (2.0-19.32 (8.79 (3.00 (3.0 (8.0) 11.27-5.33-4.29-4.24) 3.0) 13.6 (9.80-3.61-11.00 (7.33) 3.32-10.48 (3.20-12.1-15. population from the National Health and Nutrition Examination Survey.00) 75th 6.0) 17.0 (14.00) 3.49-4.06) 5.55 (2.78) 4.7) 12.0) 621 725 1078 Limit of detection (LOD.65-6.05) 3.45) 8.94) 3.00-3.90) 2.0) 16.0-16.70 (3.9 (7.00 (5.60-6.0 (10.61-16.98) 4.60-4.46 (4.30 (7.0) 292 728 1548 03-04 03-04 4.8) 7.00-4.86-21.1-22.95-6.16 (4.70-3.00) 6.7.50-15.44) 5.00) 6.60-3.8) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites Sample size 2568 03-04 03-04 03-04 3.0 (10.73 (3.71) 3.0) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites Sample size 2568 03-04 03-04 03-04 4.00) 6.00-12.27 (2.0) 9.34-4.0 (12.9) 5.9) 11.00 (5.00 (7.0 (8.70-12.91) 75th 5.00 (3.0) 12.92) 3.38 (3.00 (3.34-4.0) 9.39-3.00) 5.3 (8.03 (3.00 (3.0-25.09 (7.0 (10.00-7.15) 4.67) 9.81 (5.00-15.00-7.74) 90th 9.34) 3.24-4.14) Selected percentiles ( 95% confidence interval) 50th 3.00) 4.84-8.0) 16.10) 6.9) 12.0 (13.95 (4.45) 3.00 (4.3 (8.5) 12.13-4.14) 3.28) 2.0 (9.00-7.0 (10.5 (11.00 (3.00 (5.69-3.90 (3.00-9.82-5. Survey years 03-04 Geometric mean (95% conf.95-3.00 (5.37 (2.86-7.17-4.65-8.S.2) 10.86 (2. see Data Analysis section) for Survey year 03-04 is 1.9) 13.80) 2.0) 13.

80 (1.60) 292 728 1547 03-04 03-04 * * < LOD < LOD 1.80) Sample size 2567 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.00) 1.00-2.40) 1.10-1.28 (1.10 (.88-2.20 (1.54) 90th 2.43-3.00) 1.86) 3.22 (1.16 (2.40 (2.20 (1.00-2.985) 1.60) 2.07) 2.80 (2. Survey years 03-04 Geometric mean (95% conf.31-3.30 (1.53-2.30-2.40) 2.20 (1.80 (1.35-3.70-3.36 (1.52 (2.58) 2.50 (1.50 (2.60) 1.30-1.853-1.33 (1.73-2. Survey years 03-04 Geometric mean (95% conf.80 (1.70-2.17) 2.70-2.10-1.80) 1.30) 90th 1. population from the National Health and Nutrition Examination Survey.40-2.84-3.14-1.50 (1.85) 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. Fourth National Report on Human Exposure to Environmental Chemicals 189 .86 (2.50-2.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 1.50 (<LOD-1.37 (1.34) 2.00 (2.60-2. which may vary for some chemicals by year and by individual sample.20-3.30 (2.60 (1.00-4.82-2.46 (1.60) 2.80-2.88 (1.40-3.93) .81) 1.70-2.40-2.50) 621 725 1077 Limit of detection (LOD.30 (1.40 (1.10 (1.31 (1.82-2.40-3.816 (<LOD-.20 (1.79) 2.90) 2.30 (1.61) 2.10 (<LOD-1.20 (1.53) 292 728 1547 03-04 03-04 * * < LOD < LOD 1.40) 1.00 (2.50) 1.28 (1.63 (<LOD-1.20-1. see Data Analysis section) for Survey year 03-04 is 0.90) 1.07 (1.75) 621 725 1077 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.18-1.05-1.23) 1.86 (2.00) 1.9.80-2.60) 1283 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.53 (1.45) 3.90 (1.00 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.15-1.00 (<LOD-1.60 (2.46-2.Metals Urinary Monomethylarsonic Acid Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.53) 1283 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1. population from the National Health and Nutrition Examination Survey.62) 2.30) 1.10) 2.80 (1.77) 1.00 (<LOD-1.20 (1.00) 2.10 (.900-1.71-2.53) Sample size 2567 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.96-2. < LOD means less than the limit of detection.00) 2.18-1.86) 2.85) 2.30-1.30) 2.00-1.36) 1.61-3.10) 95th 2.22) 3.90 (2.30) 1.57) 95th 2.70-2.S. Urinary Monomethylarsonic Acid (creatinine corrected) Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.70) 2.20) 2.00-1.33 (1.11-1.10-3.10 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.07-3.90) 2.80) 1.88 (1.

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

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72) 75th 3.24-1.34 (2.50-1.81-2. In single dose animal studies.24-1.60-3.76) 1.64 (1.86 (4.86-5.50) 4.96-2.73) 1.40) 3.20-8.50 (3.70) 4.67) 6.60-2. such as brazil nuts.20-1.20 (1.70-6.37 (4.54-1.53) 692 683 618 540 667 723 765 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.78-3.30-2.50-1.69 (1.63) 1.40-13.99-5.36 (4.60-10.27 (1. Ingested soluble barium General Information Elemental barium is a silver-white metal which comprises approximately 0.40 (4.00) 4.65 (5.25-1.10-4.85 (2.54-8.31.30 (1.41-1.39 (1.80 (1.22-1.01-7.44 (1.29-1.80 (5.46-1.07 (2.25 (1.29) 5.60 (1.00-3.54) 2. Urinary Barium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.19) 2.88) 7.11-1.78-2.46) 1.95 (4.56) 1.61 (2.63 (8.47) 4.35) 5.52 (4. respectively.54 (2.49 (1. water.18-1.61-8.64-3.35 (3. 7440-39-3 Medically. interval) 1.26) 2.20-5.52 (1.56 (1.37-8.90-2.20-6.71) 1.50 (4.33 (1.28-1.18 (6.30-5.85) 1.56 (2. and 03-04 are 0.37) 5. barium sulfate and barium carbonate).73-5. Some barium salts are freely soluble in water.12 (2.76 (3.15-1.80-5.60) 3.30) 5.10 (4.12-1.4) 7.26-7.30) 3.20 (3.70) 5.49) 4.65-8.15) 5.65-1. and food.42 (1.50 (1. 01-02.41-3.70-5.43) 297 368 290 621 762 725 1262 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 1.50 (1.39) 4.14-6.04-2.57-7.28) 90th 5.60) 4.20-8.30 (5.66 (4.50 (1.02 (7.61 (1.43 (5.48-4.15-11.70-2.8) 5.70-2.63) Total 1.81-3.82) 2.65) 1.26-1.71 (2.76-3.32-7.37) 1.49) 11.20 (4.31 (2.51 (1.50 (2.30) 2.50-6.72) 1.82) 1.00 (1.77-3.08-8.51) 2.90) 2.77 (3.50 (6. Barium salts have also been available as rodenticides.30-1.50) 1.49) 8. barium sulfate is used as a contrast medium for taking radiographs of the gastrointestinal tract. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.43) 6.55-7. Workers employed by industries that make or use barium compounds can be exposed to barium dust.14 (6.80) 7.60 (2.34 (1..11 (3.24 (4.16 (1.Metals Barium CAS No.10) 3.80-2.16) 5. bricks. glass.57 (5.4) 6.85) 1.80 (1.22) 6.36) 5.40) 7.60) 1.90) 2. Fourth National Report on Human Exposure to Environmental Chemicals 193 .20-1. 0.91) 6.19-1.87-3. 2001).30 (5.88 (5.31-2.8 (6.15 (1.70) 3.35-1.20-8.8) 9.00-8.11 (2.4) 9.35-1.59-11.20-1.48 (6.10 (2.54) 1.51) 7.80) 1.90 (6.63) 1.30 (2.00-76.30-3.34) 2.57) 3.30-2.60-6.93-8.93 (4.75-3.06-1.56 (6.35-4.10) 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 1.87-7.20-1.40 (5.72) 4. and ceramics.50) 2.70 (5.12) 7.80-3.g.43) 2.21 (1.48) 1.12 (2. it combines with other chemicals such as sulfur or carbon and oxygen.81-2.39) 1.25-11.64) Sample size 2180 2690 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 2.00) 1.74-2.27) 2.04-6.65) 3.45) 7.53) 1.01 (4. Small amounts of barium can be released into the air during mining and other industrial processes.51) 1.97 (1.49-1.03 (1.38 (1.43 (1.70-3.40 (1.80 (2.74-3.76-2.35 (2.40) 7.32) 8. soluble forms of barium.30) 5.55-3. see Data Analysis section) for Survey years 99-00.63 (2.50 (4.40 (1.90) 4.38) 2.56) 4.71) 2.84) 5. fireworks.48) 1.61 (5.47-1.73 (6.08 (6.94-6.73) 3.38) 8. rubber.62 (1.32-1. such as barium chloride.35 (1.27 (1.50 (5.26) 5.53) 2.49) 2.71-9.29-5.86-4.40 (5.S.09 (2.50 (4.73 (5.68 (1.87) 7.90-9.50-6.70-8.44-5.43 (1.54) 1.06-2.76-7.80-7.39 (1.87-14.98) 1.41) 1.40 (1.48-4.63 (5.45 (1.10-5.47-1.62) 1.90 (4.78) 1.21-2.50) 2.78) 1.87 (5. Certain foods.88) 1.30) 4.70) 1.14-1.1) 9.61 (3.60-6.15-1.62 (1.30) 8.87 (6. Barium compounds are used by the oil and gas industries to make drilling muds.86) 6. were relatively well absorbed following inhalation (60-80% of a dose) or ingestion (11-32 % of a dose).86 (4.21-8.30 (3. whereas others are practically insoluble (e.77) 1.63 (1.80 (1.39-1.00) 1.92) 2.62) 1. are high in barium (Genter.54 (6.87-9.80) 6.50 (1.99 (4.93-2.12.44-2.09 (1.88) 4.82-6.18) 3.05-2.75) 2.50 (1.46) 1.20) 2.36-1. and 0.00 (2.53-5.90) 1.05% of the earth’s crust.10 (3.56 (1. In nature. The general population can be exposed to low amounts of barium in air.70) 1. tiles.65) 1.90-13.36-1.21 (1.11 (3.65-5.61 (1. Barium compounds are also used commercially in paint.12) 6.40 (5.15 (6.59) 3. population from the National Health and Nutrition Examination Survey.74) 3.36 (1.30) 5.34 (1.70) 7.30-1.22-1.38 (1.70 (1. depilatories.17-1.91) 2.15 (2.95-6.80 (2.90 (1.71) 95th 6.60) 1.9) 5.91 (2.00) 6.49-9.54-1.2) 6.10) 5.66) Selected percentiles ( 95% confidence interval) 50th 1.12.37-1.

30 (1.37) 2.. vomiting.20-8.27) 7.65 (5.39 (2.68) 3.. Urinary Barium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.68-3.50 (4.82) 1.47) 4.921 (.13-3.62) 2.98 (2.74 (5. 1984. Wones et al.00 (3.34 (1.29-1.14-2.16 (1.83) 3.47-8.80-6.29-7.55 (1.0) 6.36 (1.57-10.38 (4.00-7. water solubility.31-1.32 (2.72 (2.77) 1.2 (3.48 (1.4 (5.79-5.53-21. hypertension.33) 1.02-5.18 (1.703-1.68 (3.51) 4.21 (1.61 (4.11) .06) .18 (1.47 (5.70) 1.16-1.10 (6.99 (2.75) 1.33-1.26) 4.00) 4.80) 3.37-2.24-1.22-2.24-1.832-1.38) 4.08-2.36-2.0) 5.76 (2.04) 5.13-2.49 (1.963 (.26-1.38-1.68 (2.34-1.11) .38-5.51) 4.36-1.41 (1.44-2.59) 1.86 (2.04) 1.75) 2. Barium is not rated for human carcinogenicity.59-7.24 (5.54 (1. in urine.60 (2.96 (4. paralysis.86-7.99) 1. 1986).25-11. Following intravenous injection in animals.01 (5.35-1.55-5.24-6.31-1.45-1.99 (4.73) 2.33-4.39 (2.56-3.55-6.62 (4.39-1..38 (1.41) 5.51 (1.40 (1.85-5.23-5.47) 10.48 (1.06) 2.62 (2.42 (4.53) .97 (4. Symptoms following acute high dose include perioral paresthesias.49-1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.28-6.12) 2. The health effects of exposure to barium compounds depend on the dose.891 (.74) 1.754-1.76) 2.77) 5.19-1.46) 1.75-22. such as those used in medical radiographic procedures.32) 2.10-2. Chronic high doses in animals resulted in kidney damage (McCauley et al.47) 1.70) 4.4) 5.57-5.29-4.24-6.27) 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 .96 (4.50) 1.45 (3.S.68-3. 1985.42) 1.77) Total 1.47 (2.30) 2.64 (1.44 (1.36 (3.56) 4.80) 4. 1989).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 1.41 (2.91-2.45-6.19-1.01) 1.35-3.51) 6.34-3. and route of exposure.51 (3.02) 4.27-3. Insoluble barium salts.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 1.70) 10.88 (2.28 (1.59 (1.64) 7.27 (2.22-4.97) 1.41) 4.65 (2.92 (4.22-1.03-1.20-1.10) 3.55 (1.00) 1.71 (5.42) 1.59 (1.03-1.00 (3.82) 1.05-1.51-3.51 (1.46 (2.24) 3.20 (1. 2001). Barium blocks cellular efflux of potassium resulting in profound hypokalemia.41 (1.10-1. a benign condition that may occur among barite ore miners.58-6.45) 1.49-1.39) 4.52-4.75-3.76) 1.905 (.26-4.29-4.49-1.43) 1.72) 4.75) 1.29) 1.58) 1.35-1.79) 1.38) 1.36 (1.40-1.68) 1.96-6.64 (1.74) 1.84-2.40 (1.69 (5.880-1.56 (1.76 (3.84) 2.63) 1.30 (1.50) 2.39-1.53 (2.0) 7.36 (5.777-1.24-3.76 (4.52 (3.81-7.48-1.31 (4.47) 1.25) 4.27-1.84-5.44-2.52) 7.37 (1.19-2.43-6.03) 2.96) 4.04 (2.29 (3.36-1. Perry et al.881 (.77) 1.00 (2. diarrhea.26-1.38-7.91) 2.64 (1.09) 6.91 (3. about 75 % of a dose of soluble barium was eliminated within 3 days (Reeves. Chronic accumulation of inhaled barium dust in the lung tissue may cause baritosis.48) 2.56 (1.28) 5.60 (1.36 (3.49 (1.40 (1.8) 4.77-5.11-2.38 (4.15-4.57 (6.32 (1.33 (5.45 (1.00) 6. 1990).52) 2.54 (2.3) 6.19-1.33 (1.2) 5.92) 2.60 (2.69-9.48 (1. Human health effects from barium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.2) 6.16) 11.90-2.915 (.26-1.32) 2.97 (5.87) 1.31 (1.97-3.31) 5.37-1.39 (3.96) 4.59) 1.33 (1.31-1.55 (5.96) 4.Metals was eliminated primarily in feces and to a lesser extent.26-1. NTP.68 (3.96) 7.54) 2.78 (2.84 (3. population from the National Health and Nutrition Examination Survey.63-4. weakness.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 2.72) 6.34) 1.39 (2.01 (4.38) 1.75) 2.45) 95th 6.88 (6.66 (1.73-4.91 (3.00) 4.60 (1.83) 2.52) 1.39-10.48-3.86) 5.81-6. interval) 1. and cardiac dysrhythmias.28-1.37 (1.00-1.54) 1.33) 6.58 (2.23-2.710-1.23-1.25 (1.58) 4.00 (5.89) 90th 4.58 (4. Toxicity from soluble barium salts is rare.81-6.58) 75th 2.61) 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.29 (1.38 (1.03) 3.10) 6.02 (3.55 (4.64 (1.34-5.76-3. but can occur after intentional or accidental ingestion of barium carbonate in rodenticides (Genter.3 (6.20) 4. chemical form. 1994.64) 7.32 (1.24 (3.28-7.89 (2.57-7.50) 1.03) 1.77) 1.48-5.67-6.39-5.22-1. are not absorbed when administered.76) 2.08-1.97-4.52-10.02) .46-22.24-11.59) 2.20-2.60 (5.45-1.55) .46) 3.46) 2.62 (1.57) 2.45-8.29-3.73-2.28-11.56) Selected percentiles ( 95% confidence interval) 50th 1.

PS. 5th ed.Metals Workplace standards for external air exposure to various barium salts have been established by OSHA.85:355-359.niehs.. Cohressen B. Third National Report on Human Exposure to Environmental Chemicals. p. Laurie RD. 2005. 1986.197210. et al. Handbook on the Toxicology of Metals. barium. New York: Elsevier. and a drinking water standard has been established by U.niehs. 1990. Howerton K. Pozzoli L. Environ Health Perspect 1990. Powell C. 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. ed. Investigations into the effect of drinking water barium on rats. Weltle D. Inc.S. 2005. Studies reporting urinary levels of barium in general populations have found values generally similar to those reported in NHANES 1999-2000.. p. Reeves AL. Gallorini M. Patty’s toxicology. Information about external exposure (i. Finding a measurable amount of barium in urine does not mean that the level of barium causes an adverse health effect. Schaller KH. 4/8/09 Paschal DC. Trace element reference values in tissues from inhabitants of the European community I. Princeton NJ: Princeton Scientific Publications. blood. et al. Apostoli P. et al. Biomonitoring Information Levels of urinary barium reflect recent exposure. 2000) to levels in NHANES 1999-2000 and 2001-2002. calcium. strontium. Calabrese EJ. 2001-2002.. Fourth National Report on Human Exposure to Environmental Chemicals 195 . and radium In: Bingham A.gov/toxpro2. Zschiesche W. the welders had no obvious adverse clinical effects (Zschiesche et al. Ting BG.. patient population and literature reference intervals for urinary trace elements. In: Calabrese EJ. 1992). Minoia C. Urinary concentrations in acute poisonings are often hundreds to thousands of times higher than in this Report. Wones RG. New York: John Wiley & Sons. Vol 2: Specific Metals.64(1):13-23. 84-94. Paschal et al.html?charset=iso-88591&url=http%3A//ntp. [online].pd f&qt=barium+chloride+dehydrate+1994&col=020rpt&n=3&la= en. Atlanta (GA). Barium. and serum of Italian subjects. Advances in modern toxicology. eds. National Toxicology Program (NTP). Nordberg GF.nih. A study of 46 elements in urine. et al. p. Jr. 2nd Ed. Pietra R. LA. Sampson EJ.nih.296(1-2):71-90. Kopp SJ. Princeton (NJ): Princeton Scientific Publications. Douglas BH. Sci Total Environ 1990. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. In: Inorganics in drinking water and cardiovascular disease. Comparison of representative ranges based on U. 10326-27-9) in F344/N rats and B6C3F1 mice (drinking water studies). Frohman. and 2003-2004 (CDC. Costa R. Minoia et al. NTP. Genter MB. Epidemiological study of barium in Illinois drinking water supplies. Pirkle JL.gov/ntp/htdocs/LT_rpts/tr432.atsdr.. In Friberg L.e. Vouk VB.28(3):373-388. Jackson RJ. EPA. 1984. Perry EF. Exposure to soluble barium compounds: an interventional study in arc welders. Clin Chim Acta 2000. Lack of effect of drinking water barium on cardiovascular risk factor. References Brenniman GR. eds. Magnesium.gov:8080/cs. J Toxicol Environ Health. Levy..95:89-105. 221-252 Komaromy-Hiller G. Centers for Disease Control and Prevention (CDC). 1989.cdc..html. ed.S. Available at URL: http://ntp. Sabbioni E. Trace metals in urine of United States residents: reference range concentrations. 1998). 1985. 231-249.76(1):53-59. Perry HM.. Stadler BL. Barium levels determined in clinically submitted specimens were broadly comparable (Komaromy-Hiller et al. Ash KO. McCauley PT. environmental levels) and health effects is available from ATSDR at: http://www. pp. 2001. Environ Res 1998. Morrow JC. Hypertension and associated cardiovascular abnormalities induced by chronic barium feeding. 1994. Welders of barium-containing electrodes had median urinary levels of barium that were 60 times higher than the median levels in this Report. Int Arch Occup Environ Health 1992. technical report on the toxicology and carcinogenesis studies of barium chloride dehydrate (CAS no..

soil. which may vary for some chemicals by year and by individual sample. Beryllium compounds are commercially mined. bertrandite and beryl. and machine-parts industries.130 (<LOD-.13. 01-02. inhaled insoluble beryllium sulfate was retained in the lungs and nearby lymph nodes. 0. are mined for commercial recovery of beryllium. and from breathing tobacco smoke. see Data Analysis section) for Survey years 99-00. nuclear. and volcanic dust. Beryllium is also used in the production of sports equipment such as golf clubs and bike frames. or drinking water containing the metal. In medicine. and 0.150) < LOD < LOD < LOD < LOD 1227 1335 1281 1238 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .Metals Beryllium CAS No. and refined beryllium is used in mirrors and special metal alloys for the automobile. 196 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.13. the lightest of all metals. coal.13. Exposure to beryllium occurs mostly in the workplace. near some hazardous waste sites. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.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. In studies of laboratory animals. 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.170) < LOD < LOD < LOD < LOD 340 368 290 719 762 725 1406 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . and dental bridges.140 (<LOD-. and 03-04 are 0. Low-level beryllium exposure in the general population can occur through breathing air. beryllium is used in instruments. respectively. and can be found in mineral rocks. electrical. population from the National Health and Nutrition Examination Survey.130 (<LOD-. eating food. A half-life of 450 Urinary Beryllium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. aircraft. Burning coal and oil can produce small amounts of beryllium dust that can be released into the air. less than one percent of the inhaled dose was slowly absorbed into the blood and eventually incorporated into the skeleton. x-ray machines. < LOD means less than the limit of detection. Two types of minerals. 7440-41-7 General Information Pure beryllium is a hard gray metal. computer.

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

Hamilton et al.inchem.23:827-839. 2000. Kriess K.76(1):53-59. it is likely that urinary beryllium levels in the U. References Apostoli P. Genetic and exposure risks for chronic beryllium disease. Ting BG.atsdr.95:89-105. population were generally undetectable in NHANES 1999-2000. 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.. HLA-DPB1 and chronic beryllium disease: a HuGE review. Paschal DC. Environ Res 1998. Trace metals in urine of United States residents: reference range concentrations. and 2003-2004. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Schaller KH.htm. VI.158:165-190.e. et al. Available at URL: http://www.html. patient population and literature reference intervals for urinary trace elements. 1990. Comparison of representative ranges based on U. Am J Epidemiol 2003. Levels of beryllium in urine for the U..gov/toxpro2.157:388-398. Apostoli and Schaller (2001) stated that detection limits in earlier studies were inadequate to estimate nonoccupational exposures. population are lower than levels in workers. 2001). Paschal et al. which approximate this Report’s limit of detection. blood.S.296(1-2):71-90. Sabbioni E. Environmental Health Criteria. A study of 46 elements in urine. International Programme on Chemical Safety (IPCS). In other studies. Sci Total Environ 1990.74:162-166. Morrow JC. Hamilton EI. Given these results.12 to 0. Pietra R.S. Weston A. 0.Metals (i. Urinary beryllium--a suitable tool for assessing occupational and environmental beryllium exposure. Minoia et al. less than 0. Atlanta (GA) 2005. Van der Venne MT. Finding a measurable amount of beryllium in urine does not mean that the level of beryllium causes an adverse health effect. 1990. Maier L. Review of elements in blood. 106. 3/27/08 Komaromy-Hiller G. Jackson RJ. Pirkle JL. Gallorini M. and serum of Italian subjects. McCanlies EC. 20012002. Trace element reference values in tissues from inhabitants of the European community I. Howerton K. urinary levels for general populations have been either undetectable or had different detection limits than in this Report (KomaromyHiller et al. Clin Chest Med 2002.e. Ash KO..S.13 μg/L. Apostoli P. environmental levels) and health effects is available from ATSDR at: http://www. They reported urinary beryllium levels ranging from 0. Pozzoli L. Clin Chim Acta 2000.1 μg/L). et al. Minoia C. 1998). Biomonitoring Information Urinary beryllium levels represent recent and accumulated exposure. Int Arch Occup Environ Health 2001. Andrew M. and the 95th percentile for males in NHANES 2001-2002. Sampson EJ. Beryllium [online]. Sabbioni E.15 μg/L in workers exposed at the recommended threshold limit value (Apostoli and Schaller. (1994) noted that analytical methods used in several general population studies appeared to have limits of detection that were insufficiently low (i. Sci Total Environ 1994. 198 Fourth National Report on Human Exposure to Environmental Chemicals . Costa R. plasma and urine and a critical evaluation of reference values for the United Kingdom population... and the fact that most NHANES participant levels were undetectable.org/documents/ehc/ehc/ ehc106.cdc. Centers for Disease Control and Prevention (CDC). Third National Report on Human Exposure to Environmental Chemicals. Element reference values in tissues from inhabitants of the European community.

50 (1.60 (1.00) .50-1.90) 1.400 (.400-.60) 1.40-1.30-1.400 (.333 (.00 (.50 (1.3. during refining of lead and copper from sulfide ore.700) 1.600) .304-.400-.400-.300-.500) .300 (<LOD-.337) .600 (.900 (.400 (.900 (.80) 1.700) .300) .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 .300-.20-1.400) .00 (.500 (.400) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.30-1. interval) .300-.14.500 (.500-. Fourth National Report on Human Exposure to Environmental Chemicals 199 .426-.600 (.60) 1.40 (1.20) 1.10) 1.S.700) .500-.400) .600 (.309-.500) .300-.400-.500-.400-. coatings and plating.300 (.800) .424) * .10) 1.600) .300 (<LOD-.60 (1.00-1.300 (.300) 75th . which may vary for some chemicals by year and by individual sample.200-.700 (.900-1.70) 1.10) 1.300-.300) .500-.00 (.70) 2742 2268 2085 1842 2219 2292 2716 3806 3478 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.800-1.362-.216-.300) .30) 1.30-1.50) 1.00 (.60 (1.30-1.20) 1. plastic stabilizers.50) 1.400 (.600 (.200) .00 (.304 (.366) * * .600 (.441) * .300) .255) . 01-02.300 (.10 (1.800 (.400) .460) .300-.500-.500) .600-. respectively.600) .400 (.400) .00-1. Important sources of airborne cadmium in the environment are burning fossil fuels such as coal or oil.200 (<LOD-.00 (.10 (1.452) .600 (.700-1.10) 1.266-.500-.500 (.800 (.900-1.20 (1.800) 1.300) .30 (1.20-1.700-1.400-.800-1.500-.40 (1.60 (1.600 (.20) 1.900-1.400 (.600) 1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.500 (.600) .400) .40 (1.326 (.00-1.40-1.300-.470) * .500 (.500-.900-1.320) Sample size 7970 8945 8372 Age group 1-5 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * .400 (.600 (.10) 1.20-1.00-1.900-1.300) .500-.300) .900-1.386-.400 (.300 (.421 (.300 (.900-1.70) 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 .412 (.20) 95th 1.600 (.449) Selected percentiles ( 95% confidence interval) 50th . see Data Analysis section) for Survey years 99-00.00 (. and incineration of municipal waste materials.200 (.60) Total * .00 (.800) .400 (.700) .00-1.10 (1.00 (.300 (<LOD-.300-.20) 1.200-.30) 1.30) 1.300) .300-.400 (.500-.500 (.300-.600-.600) 90th 1.00-1.300-. Other uses include pigment production.275-.400) < LOD < LOD < LOD . and 0.425 (.40 (1.3.368-.600 (.50 (1.344) .300-.393 (.400 (. Blood Cadmium Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U.20) .400-.378-.50 (1.300 (.300) . 0. or copper smelters (U.235 (.300) .300-.40 (1.10 (.70) 1.40) 1. as zinc sulfide) and to a lesser extent.500 (.376-.Metals Cadmium CAS No.10 (1.300-. cadmium use has declined in response to environmental concerns (http:// minerals.40) 1.313 (. < LOD means less than the limit of detection.20) 1.700) .20) 1.400 (. and nonferrous alloys.400 (.367-.700) . and 03-04 are 0.S.300 (.600) .20) .361-.20 (.60 (1.300-.400 (. lead.400 (.500) .400) .10 (1.900-1.300) 1.600) .50-1.500-.283 (.600 (. Since 2001.00-1. population from the National Health and Nutrition Examination Survey. The predominant commercial use of cadmium is in battery manufacturing.00 (1.300) .600 (.600-1.382 (.500-.300 (.50) 1.400-.00-1.700) .500) .300 (.60) 1. 7440-43-9 General Information Cadmium is a soft.S.10 (1.300 (<LOD-.300) .30-1.50-1.60-1.500) .200 (.00) .20-1.400) < LOD .300 (.400) .40 (1.200-.600) .30) .200 (<LOD-.600 (.40 (1.400) .500 (.403) .400) .700-1.468 (.300-.300-.300-.296-. bluish-white metal that is obtained chiefly as a by-product of processing zinccontaining ores (principally sphalerite.395 (.20-1.900-1.200-.300 (.10 (1.500 (.289-.300-.600) .50-1.400) .20-1.400 (.600) .400) < LOD .300) .400) < LOD .70) 1.200 (.20) 1.700) .427) * .300-.400-.10) 1.70) 1.300 (.500-.300-.400 (.500-.600 (.gov/minerals/pubs/commodity/cadmium).331) .00-1.200) .500-.398) < LOD < LOD < LOD < LOD < LOD < LOD .10) 1.00 (.10) 1.400) .00 (1.200-. EPA.400) .700) .300 (.500) .500-.300-.900-1.403 (.20-1.400-.600-.300 (.500-.304 (.359-. malleable.80) 1.420 (. Cadmium also may be emitted into the air from zinc.usgs.500-. U.80 (1.20) 1.378 (.400-.513) .400) .

226) Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 * .061 (<LOD-.078 (.195-.189-.090) .178-.180 (.977) . 2004a. **All results are corrected for molybdenum oxide interference in the ICP-MS method.177-.194-.858 (.806) .550 (.423-.890-1.475 (.200 (.918-1. drinking water is a source for cadmium intake.200 (.390 (.48 (1.462 (.519) .233) .230) 75th . For nonsmokers who are not exposed to cadmium in the workplace.167-.479) .238-.175 (.72) 1.282 (.733) .490) 1.713) .230 (.490) .520-.817 (.249) .963-1.080 (.445 (.22 (1.206) .257-.067-.219 (.20 (1.193 (.310) .57) 1.150-.226) .090) .313) .607) .705-.087-.179-.25 (1.255) .06-1.980 (.S.875) .390-.262) .281 (.13) .260-.855-1.160) .284) .440-.277 (.800 (.500) .700-.83) 1. The kidney is a critical target and shows the earliest sign of cadmium toxicity.17 (.25) 1.38) .476-.101) .17 (. including many food crops such as cereal grains.272-. whose body burdens of cadmium can be approximately twice that of nonsmokers.261-.240) .157-.241) .28-1.222) .135 (.260 (.067-..03) .198) .919) . copper) and protein.190-.580) .817 (.192-.450 (.235) .960 (. Cadmium absorption may be increased with iron deficiency (Berglund et al. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.249-.589 (.255) .210 (.790 (.120 (.326) . To a lesser extent.539) .960) 1. With chronic exposure.160) .140 (.17 (.892-1. Cadmium is absorbed via inhalation and ingestion.350 (.320) .210) .306 (.06-1.990) .400-.500) 90th .481) .189-.870) .238) .753-.436-.400-.187 (.092 (.717-.160-.452 (.285-.183-.061-.170 (.09-1.38) 1. Urinary Cadmium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.52 (1.839 (.191-.456-.300 (.818 (.34) 1.13-1.15 (.Metals 2000).130 (. 1994).15) .530 (. 01-02.253-.206 (.221 (.302 (.251) .748-1.243-.260-. The estimated half-life of cadmium in the kidney is from one to four decades (ATSDR.255) .20 (1. 0.733-.480) .47) 1.181 (.596) . potatoes.17) . and various seeds.110-.227 (.148-.150) .640) .875 (.980-1.173) .263) .836-1.265) .12 (.202-.972 (.189) .10 (1..492 (..257) .237-.216 (.211-.387) .430) .208-.20) 1.848 (.081) . ingestion through food is the largest source of exposure. calcium.06.843-1.36) 1.220-.192-.121 (.551) .989-1.233) .74) 1.41 (.175 (.310 (.06.362) .530) .171-.220) Selected percentiles ( 95% confidence interval) Sample 95th 1.510) . and 0. 2001).510-.813 (.170-.223 (.32 (1.30-1.209 (.170-.82) 1. Kikuchi et al.265 (.190-.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.700-.210 (.381-.191 (.092) .820-1.366-.** Survey Geometric mean (95% conf.730-.199 (.221) .151-.240-.289-.210 (.366) .440 (. wheat.100-.115-.329 (.229) .394-.107-. respectively.886) .498-.295) .610) .246) .211 (..559 (.51 (1. 1999.886-1.351-.519) .623) .507) . 2003.210 (.203) .820 (.28) 1.13 (.892 (.065-.308) .204 (.880) . an inducible metal binding protein.229) .126) .247) .01) .231) . 2003). Cadmium in soil is absorbed by plants.440 (. About one-third to one half of the total body burden accumulates in the kidney tissues (Nordberg and Nordberg.160 (.203 (.109 (.077 (.38) . however.169-.26) size 2257 2690 2543 Total years 99-00 01-02 03-04 50th .322 (. Horiguchi et al.714-1. 2003).940-1.800-.43) 1.234 (.426 (.210 (.077 (. cadmium accumulates in the liver and kidneys where it is bound to metallothionein.04 (.200-.232 (.219 (.38) 1.354) .316 (.447 (.430-.207-.141 (.445 (.810-1.482) .136) .273 (.261-.493-.330-.790 (.270 (.766 (.458 (.148) .279 (.165-. interval) . 200 Fourth National Report on Human Exposure to Environmental Chemicals .283 (.060-.07-1.455 (.393-.339) .372) .22 (.686-.114-.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 .196-.388-.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 .24) 1.545 (. individual values vary and are affected by factors such as dietary intake of essential nutrients (iron.20 (1.134) .28 (1.19) 1.01-1.230) ..270 (.193-.214-.700-.470-.336) .157) .466 (.360) .201 (.202 (.190-.412) . see Data Analysis section) for Survey years 99-00. Renal tubular and glomerular damage. The gastrointestinal absorption of dietary cadmium is about 5% in adult men and 10% or higher in women (Diamond et al.890 (. rice.763-.860) 1. Diamond et al.741-1.239 (.980-1.153-. Inhalation of cigarette smoke is a predominant source of exposure in smokers. a factor that may contribute to the higher absorption of cadmium by women (Diamond et al.232) .299) .633-1.980) .220-. and 03-04 are 0. population from the National Health and Nutrition Examination Survey.433-.12-1.551 (.820) 1.200-.980) .280 (.112-.06) . zinc.20-1.680 (.109-.540) .191-.128 (.04 (..450 (.06.210) .390-.633 (.135-.327 (.290-.366-.300) .220) .219 (.02-1.15) 1.184-.220 (.229-. 2003).01 (.

740 (.806-1.591 (.Metals manifested by irreversible proteinuria and progressive reduction in glomerular filtration rate.143-.757) .232) .184) . interval) .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 .10) 1.159 (.187-.177) . 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.097) .253 (.266-.614) .917) .161-.767) .074-. Horiguchi et al.941 (.950) ..280 (.S.388-.818) .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.795) 1.063-.168-.156-..423-.261-.562-.182) .255-.173 (.404) .075-.432 (.690-. a condition known as “itaiitai” (“ouch-ouch”) affected postmenopausal women living in a cadmium-polluted region of Japan.196 (.13) .826-1.440) .266) .241) .678-.304) .998) .077-.101) .873 (.253) .329 (.490 (.292) .444-.426-.686 (.239-.191 (.856 (.256-.143-.106) .234 (.297) .718 (.270 (.191) .668-.175 (.091 (.199 (.481 (.091) .470) . population from the National Health and Nutrition Examination Survey.078 (.962) .093 (.364) .150-.238-.113-.678 (.174-.712 (.533) .194-. 2003.202 (.421 (.688-.398-.874-1.545) .541) .07) . 2000.415) .221 (.884) .792 (.929) .687-.147-.268 (.700) .813-1.190 (.296 (.833-1.147 (.382-.223) .219 (..104) .131-.250) ..219 (.224 (.130-.218) .308 (.173-.263 (.321) .235) .850) .168-.191-.137-.094) .208 (. At lower environmental exposures.826-1.175 (.16) 1.343-.04) size 2257 2689 2543 Total years 99-00 01-02 03-04 50th .729 (.261 (.491-.696-.985 (.267 (..300-.225) .663 (.412 (.267 (.282 (. 2004).784) .381-..336-.479 (.940-1.17) .518) . 2004b).051-.158-.233 (.538) .08) .199-.078-.516-.197-.00 (. Noonan et al.404 (.136-.135) .216-.708-1.211 (.232) .687 (.261) .263-.906) .178) . 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.084 (.757 (.433-.207-.183 (.288 (.210 (.438-.325 (.691-.473 (.168 (.181 (.449) .154 (.091 (.140-.162 (.215 (.221-.827) .185) .176 (.783) .434 (.192) .472) . Staessen et al.171-. Jarup et al.531 (..170 (.647-.690-.181 (.143) .247-.201-.316 (. Fourth National Report on Human Exposure to Environmental Chemicals 201 .783 (. two studies in Japan did not find an association between cadmium in urine and renal biomarkers (Ezaki et al.02 (.631) .085-.653) .865 (.234) .382) .084-.273 (.377-.281) .281) .225) .163 (.00 (.219) Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 * .802 (.207) .238) .123-.288) .716-.536 (.278) .38) .650-.100 (.245 (. **All results are corrected for molybdenum oxide interference in the ICP-MS method.338 (.176 (.227-.16) .690 (.693 (..438) 90th .274) 1.423 (.813-.204-.187) . 1996.304-.184-.311) .06 (.283 (.09 (.** Survey Geometric mean (95% conf. 2002.123-.190 (.667) .086 (.200 (.154-.607) .148 (. During the 1950’s and 1960’s.850) .979 (.331 (.387 (.700 (.645-.12) 1.622 (.085 (.252 (.222-.144-.335 (.856) .083-.198) .391-.189-..560-. 2002.210 (.476) . 1999).136-.769 (.767 (.725-1.234-.112) .507-.293-.170-.183) .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 .206-.630-. 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.166 (.719 (.071 (.185 (.156) .318 (.181) .182) .931 (.441-.470) .828) .818) .289) .617 (.208-.163) .727-.096) ..830) .159 (.537-.909-1.209) .418) .501 (. 1999).126 (.414-.229) .666-.500-. most often a result of occupational exposure (Roels et al.927-1.340) .940 (.919 (.175-.431) . Olsson et al.209) Selected percentiles ( 95% confidence interval) Sample 95th .414 (.242) .157-.917 (.212 (.839) .104) .830-1.236-.316) . 2002.350) .182) .303) .446) .352) .487 (.288-.07 (.418-.107) .098) .551) .184-.067-.674-1.789 (.205 (.484 (.146-.876-1.247-. 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.181-.140-.05) 1.226) 75th . 1999).075 (<LOD-.289) .559-.228-. However.240) .210) . can result from high dose chronic exposure.178-. 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.240) .137 (.779 (.122 (.308) .157-.147-.716) .220 (.156 (.387-.440) .090 (.722-.754) .111-.247-.

2005. the risk of low bone mineral density increased by nearly three-fold when the blood cadmium exceeded 1.. 2000. Jin et al.. Finding a measurable amount of cadmium in blood or urine does not mean that the levels of cadmium cause an adverse health effect.. 2002). For NHANES 19992000. 2002. Zhang et al.S. Biomonitoring studies on levels of cadmium provide physicians and public health officials Fourth National Report on Human Exposure to Environmental Chemicals . 2002.. approached these values associated with subclinical changes in renal function and bone mineral density. Waalkes (2003) provides an overview and summarizes potential mechanisms for carcinogenicity... However. 2004).gov/ toxpro2. In this Report the urinary and blood cadmium levels at the 95th and 90th percentiles. Cadmium can produce lung.. respectively. Biomonitoring Information Blood cadmium reflects both recent and cumulative exposures. pituitary gland and kidney tumors in animals and has been associated with lung cancer in humans in occupational epidemiologic studies.. 2002).. 2003.. Komaromy-Hiller et al. 2004. Both IARC and NTP consider cadmium a human carcinogen.. 2006. Staessen et al. Olsson et al. intermediate in former smokers and lower in never-smokers (Becker et al.. as may occur from welding cadmium-alloyed metals.. Friedman et al.. 2003.. 2002. Horiguchi et al. Suwazono et al.. 2003. 2000.46 mg/gram of creatinine) (Ezaki et al. two studies of women in Japan with lower exposures found no correlation between renal tubular effect markers and blood or urine cadmium levels (geometric means were 1. Becker et al. Further research is needed to address the public health consequences of such exposure in the United States.. has resulted in severe. respectively.. Occupational standards are provided here for comparison only. 2004.. Jarup et al. 1999. Wennberg et al.. Information about external exposure (i. 1996. People who are occupationally exposed may have blood and urine cadmium levels that are higher than those of the general population. 2003. Small epidemiologic studies have noted an inverse relationship between cadmium in cord blood.html. The 95th percentiles for cadmium levels in this Report were less than the OSHA standards for both blood cadmium (5 mg/L) and urine cadmium (3 mg/gram of creatinine). 2005. 1999).. 2006). 2004b).. Noonan et al.. 1996). study subjects living near a former zinc smelter were similar to those from an unexposed community and to those in this Report (Noonan et al.. 2002. Moriguchi et al. 2002). 2004. Salpietro et al. 2002... Ezaki et al.Metals greater urine cadmium levels may have an increased risk for bone fracture and diminished bone mineral density (Alfven et al. maternal blood or maternal urine and birth weight (Nishijo et al. and drinking water and environmental standards have been established by U. Subtle increases in markers of renal tubular effects have been associated with urine cadmium levels as low as approximately 1 mg/gram of creatinine (Akesson et al. Wilhelm et al.e. Chronic inhalation exposure to cadmium particulates was associated with changes in pulmonary function and chest radiographs that were consistent with emphysema (Davidson et al.. Acute and heavy exposure to airborne dusts and fumes. decreased bone density was correlated with mean urinary cadmium levels of approximately 1 mg/gram of creatinine (Staessen et al.. Animal studies have demonstrated reproductive and teratogenic effects. 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.. Staessen et al. Jarup et al.. Blood cadmium levels are about twice as high in smokers compared to nonsmokers (Becker et al. data (CDC. 2005). Wennberg et al. urinary cadmium reflects both cumulative exposure and the concentration of cadmium in the kidney.. CDC. Olsson et al. 2000). Ezaki et al.. 2004. Surveys of populations not known to have increased cadmium exposure have reported similar urine and blood levels (Becker et al.1 mg/L (Alfven et al.26 and 3..atsdr. In postmenopausal women. environmental levels) and health effects is available from ATSDR at: http://www. Olsson et al. 2002). Becker et al. Mannino et al. 2006). 2003.S.. Horiguchi et al.. 1999). 2004b. Becker et al. 2003). potentially fatal pneumonitis (Fernandez et al. Women had higher blood and urine cadmium levels compared to men of similar ages... In the typical environmental exposure.. Staessen et al.. Workplace standards and guidelines for air exposure to cadmium have been established by OSHA and ACGIH. 2005.cdc. 2002) and length at birth (Nishijo et al. In adults aged 60 years and older. EPA. 2002). with peak values observed in the fifth to sixth decades (CDC. Workplace exposure to airborne cadmium particulates was associated with decreases in olfactory function (Mascagni et al.S. blood cadmium was also slightly higher in Mexican Americans and participants 20 years and older (CDC. Creatinine-corrected urine cadmium values in U. 2003. 2000. 2002. 2005. Blood and urine cadmium levels are typically higher 202 in cigarette smokers. 1988). not to imply a safety level for general population exposure.... 2006.

Ye T.46:372-374. Persson B. Moriguchi J. Nomiyama T. Ezaki T. Urinary cadmium levels predict lower lung function in current and former smokers: data from the Third National Health and Nutrition Examination Survey. Oguma E. possibly better than b2microglobulin. Ikeda Y. Zhu G. Stock AL. 206:15-24. Hellstrom L. Thorax 2004. Lauwerys R. 102:10581066. Thayer WC.Metals with reference values so they can determine whether people have been exposed to higher levels of cadmium than are found in the general population. Int J Hyg Environ Health 2003. Jones RL. Kaus S. et al. Comprehensive study of the effects of age. Mascagni P. Fukui Y. Fayers PM. Mannino DM.gov/toxprofiles/tp5. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Toxicological profile for cadmium update. Choudhury H. Clin Chim Acta 2000. Friedman LS. Cadmium fume inhalation and emphysema. Pickering CA.110:699-702. Lison D. et al.59:194-8. References Akesson A. Environ Health Perspect 2005.95:20–31. Greves HM. J Occup Health 2003. Renal effects of low-level environmental cadmium exposure: 5-year follow-up of a subcohort from the Cadmibel study. 4/8/09 Alfven T. Lidfeldt J. Buchet JP. Dekio F. et al.000 women in the Japanese general population: a nationwide large-scale survey. Osteoporosis and renal dysfunction in a general population exposed to cadmium in China.148(1-2):11-20. Komaromy-Hiller G. Grubb A. Chislovska NV. Gadea E. Elinder CG. Howerton K. Toxicol Lett 2004. Sanz P. Oguma E. et al. Lancet 1988. Palomar M. Savage-Brown A. Fatal chemical pneumonitis due to cadmium fumes. Environ Health Perspect 2002. Intestinal absorption of dietary cadmium in women depends on body iron stores and fiber intake. Comparison of representative ranges based on U. Sasaki S. 2005. et al. Lancet 1999. 1999 [online]. Third National Report on Human Exposure to Environmental Chemicals.24:717-724. Bregante G. Jin T. Machida M.cdc.102:83-89.354:1508– 1513. Environ Res 2004b. Tsukahara T. Schulz C. Jarup L. Taylor AJ. No clear-cut evidence for cadmium-induced renal tubular dysfunction among over 10. Kundiev YT. Atlanta (GA). Neurotoxicology 2003. Agency for Toxic Substances and Disease Registry (ATSDR). Toxicol Appl Pharmacol 2004a. Bellerup P. Hotz P. environmental.66(Pt A):2141-2164. et al.96:353-359. Vahter M. Environ Res 2004.html. Tsukahara T. Chiappino G. Machida M. Costa R. Seiwert M. Lundh T. Toffoletto F. Kikuchi Y. Seifert B. Jarup L. population. et al. Miyamoto K. Cadmium and lead in blood in relation to low bone mineral density and tubular proteinuria. Tubular and glomerular kidney effects in Swedish women with low environmental cadmium exposure. Occup Med 1996.45:43-52. Bo M. Krause C. Occup Environ Med 2000. Available at URL: http://www. Vahter M. Ezaki T.13(11):1627-1631.S. Darbyshire J. Int J Hyg Environ Health 2002. Diamond GL.S. Nermell B. et al. Wang H. and dietary predictors of elevated blood cadmium levels in Ukranian children: Ukraine ELSPAC group. Venables KM.59:497].atsdr. and cadmium burden on dietary cadmium absorption in cadmium-exposed female Japanese farmers. ShkiryakNizhnyk AZ. Nerbrand C. Lepom P. Consonni D. Fourth National Report on Human Exposure to Environmental Chemicals 203 . Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Pharmacokinetic/ pharmacodynamics (PK/PD) modeling of risks of kidney toxicity from exposure to cadmium: estimates of dietary risks in the U. Mucha A.57:668-672. Fukui Y. J Toxicol Environ Health 2003. Horiguchi H. Becker K. Environ Res 2006. Uptake of cadmium in meals from the digestive tract of young non-smoking Japanese female volunteers. et al. Uemura T. Takebayashi T. Lukyanova EM.296(1-2):71-90. patient population and literature reference intervals for urinary trace elements. Low level exposure to cadmium and early kidney damage: the OSCAR study [published erratum appears in Occup Environ Med 2002. Dietary exposure to cadmium at close to the current provisional tolerable weekly intake does not affect renal function among female Japanese farmers.1(8587):663-667. Berglund M. Miyamoto K. Furuki K. Schulz C. Environ Health Perspect 1994. Alfven T. Horiguchi H. Fernandez MA. Okamoto S. Holguin F. Seiwert M. Ukai H. Moriguchi J. Centers for Disease Control and Prevention (CDC). Furuki K. Nordberg G. et al.76:186-196. et al. Carlsson MD. Ash KO. Bernard A. Sasaki S. Kumagai N. 196:114-123. Ikeda Y. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. a1-Microglobulin as a promising marker of cadmium-induced tubular dysfunction.205:297-308. Serra J. diabetes mellitus. Kaus S. iron deficiency. Anthropometric. Becker K. Davison AG. Akesson A. Olfactory function in workers exposed to moderate airborne cadmium levels. Int Arch Occup Environ Health 2003.

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4 (10.33 (5.30 (6. scintillation counters.8) 9.61-6.24) 4.2-12.30) 5.00-8. diarrhea.90-12.70) 5. 2004). cesium hydroxide is corrosive and irritating at high concentrations.7 (8.70 (8.25 (3. Radioactive 137Cs has been used medically to treat cancer.00-8.2-13.77-8.01) 7.7 (11.02 (4.10 (8.08-5.94 (4.80 (4.37) 7.1-12.70 (4.84) 8. and 03-04 are 0.70-5.12 (4.3) 12.2-13. and cardiac arrhythmia (ATSDR.7 (10.49) 4.70 (6.99) 7.08 (6.8 (11.0-15.9) 8.5) 10.90 (6.55 (7.04 (4.20) 8.0) 11.14.07) 4.26) 7.7) 884 683 618 568 667 723 821 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.99) 9.98 (7.4) 9. However.10 (6.0 (10.9) 12. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.4) 95th 11.97) 4.70 (5. semiconductors.27-5.60) 5.05-5.50 (4.89) 4.91 (7.45-8.1) 9.10-7.05) 5.2 (9.40-5. photographic emulsions.2) 11.8) 12.83) 6.33 (6.6 (11.26-11.00-10.40-5.6 (9.34 (4.64) 5.81) 9.3) 10.82) 5.94) 4.30-5. 0.35 (4.53 (6.4) 10.52) 7.62 (5.40-7.71-8.5-13.40) 7.95 (3.00-4.3-13.87-7.34) 9.81) 4. 01-02. respectively.09) 5.94-4.7 (9.20-8.6 (9.03 (4.99-6.17 (6.6) 10.9 (11.1) 9.29 (4.64 (4.69-6.68) 9.68 (7.94 (4.50 (4.50) 9.80-11.0) 12. and high-power gas-ion devices.60-6.8 (10.76-6.7 (9.9) 11. and clay.90-10.70) 7.70 (6.49) 75th 7.00) 6.08 (7.4-13.36 (6. Workplace guidelines for cesium hydroxide are available from ACGIH and NIOSH.91-8.1) 10. and as polymerization catalysts.Metals Cesium CAS No.77 (4.20-4.43 (5.9 (11.0 (9.23) 9.56) 5.60-12.96 (6.27) 4.71-5.66 (7.7) 11. interval) 4.21) 90th 9.5) 9.80) 7.2-14.74-5.80-6.20) 7.05-5.59-5.50 (4.86 (7.01-8.92-13.8) 11. Whether cesium compounds are carcinogenic is unknown.89) 5.13 (7.20 (6.04) 7.62) 4.S.3 (8.0) 10.63 (4.42) 7.40-5. Human health effects from cesium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.16-6.74) Selected percentiles ( 95% confidence interval) 50th 4.54-11.59-5.05) 5. Fourth National Report on Human Exposure to Environmental Chemicals 205 .13 (5.61) 7.49 (4.52-9.17) 4. soil.14 (4.13-8.56 (4. Urinary Cesium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.17-6.00 (7.22-4. 7440-46-2 General Information Cesium is a silver-white metal that is found naturally in rock.5-14.0) 12.73-5.90 (4.56-11.40-11.40-5.22 (4.00-9.20) 5.27 (7.80-13.90-10.64-5.90-12.0) 11.46) 7.80 (8.1) 11.90) 4.87 (4.36) 3.30-10.3) 10.70 (9.1) 11.1 (9.15-8.60 (7.60-7. and 0. Inorganic cesium compounds are used in photomultiplier and vacuum tubes.40 (4.60) 7.2) 12.97 (7.2. the body half-life is estimated to be 70-109 days based on 137Cs exposures.89-5.1 (11.74 (4.50) 5.71 (4.6 (11.90-8.0) 12.9 (10.60-5.20-7.60-6.8 (10.3-13.47-8.6) 11.8) 12.90) 5.71-9.33-5.6 (9.49 (5.84 (4.5-14.5 (10.4) 11.80 (8.7 (10.8) 12.7 (10.14.44 (8. although cesium was generally of low toxicity when given to animals.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 (6.1-13.30 (6.45-5.00) 4.53-11.1 (10.5-16.62 (5.86-11.31-8.80 (4.35-5.7-14.5 (8.95) 5.60-7.26) 4.81-14.50 (7.90) 9.21 (4.10-5.71 (8.29) 4.8-13.84-5.40) 5.08) 7.71) 4.12-11. Most human exposure to cesium occurs through the diet.7) 10.09-5.39-4.0-13.99-11.55 (4.9) Total 4.7 (9.26 (3.20) 4.80-10.2-13.10-9.82-4.12-5. For absorbed cesium salts.60) 7.03 (4.16-6.13 (8.50 (6.3) 10.42-7.67 (4.88 (8.30) 7.64) 5. see Data Analysis section) for Survey years 99-00.4 (9.55-11.90) 7.56 (4.73-11.84-9.72-7.32 (3.72) 4.87 (4.5) 12.93 (4.9 (11.59) 7.81 (4.40) 5.8) 9. Case investigations of ingestions of large doses of cesium chloride have reported decreased appetite.87 (4.70) 5.50-7.0) 9.7) 11.70 (8.54) 4.59 (5.63-4.8) 11.77 (9.9 (11.63) 6.57-5.07-11.64) 4. infrared lamps.60 (8.00) 7.6 (9.9 (10.3) 10.37) 5.83-4.79 (4.23-4.4) 10.03-4.81) 4.3 (8.4 (9.40-11.2 (9.80 (4.97-7.80 (8.47-4.25) 4.64-10.38) 5.10-8.10 (8.77 (9.39) 7.80-10.3) 9.87) 5.08-5.95-4.25-5.20 (4.86-12. nausea.35 (4.4) 12.80-10.7) 10.42) 6.97) 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 4.3-15.84) 5.59-5.90-10.36 (3.12) 5.99-11.1-12.6) 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 4.01-6. population from the National Health and Nutrition Examination Survey.98 (7.32) 4.4) 12.32-5.70-8.90) 5. Little is known about the health effects of this metal.43-8.20-5.

06 (3.24-10.10 (5.24 (3.8) 10.11 (5.84-7.66 (5.78 (3.47 (7.03-6.0) Total 4.74 (5.22-11.54 (3.51 (4.31-6.71 (7.65 (6.17-4.85) 5.97-5.00 (8.60) 3.0 (7. Finding a measurable amount of cesium in the urine does not mean that the levels of cesium cause an adverse health effect.72) 4.27 (6.87) 5.68) 3.2 (8.44-9.81 (4.75 (7.06 (5. population.43-11.9 (9. 2005.35) 3.84-11.46-8.94) 7.98) 5.81 (4.08 (3.15-11.3) 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 3.97) 8.50 (6. Urinary Cesium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. 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.60-20.44 (8.60-10.6) 6.22 (3.56) 4.09) 4.53 (4.15 (7.21-4.88-10.64) 5.14-7.29) 4.84-9.12-6.00-5..5) 9.92) 3.11 (5.08-3.43 (4.77 (7.15-4.35-11.66 (5.39 (5.43) 8.54 (4.79) 4.95 (3.76-9.30 (4.84-7.30-4.67 (6.98 (6.29) 5.95) 10.47) 6.89-4.26 (3.90-8.36-10.36-6.15) 95th 8.78) 4.99 (3.61-3.55 (3.25) Selected percentiles ( 95% confidence interval) 50th 4.9 (10.92 (5. 2004).27 (8.97-4.43 (4.13 (3.91) 4.10-4.77) 4.51 (3.41) 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 3.90 (7.03) 6.16-8..47) 7.41 (5.95 (5.67) 5.29) 4.72 (4.91-7.46) 6.06) 4.58 (4.27-4.8 (9.91-9.19-6.13-9.6 (9.63 (7.90-8.96) 4.18-7..46 (7.71) 6.30) 10.62) 5.58 (6.21-5.85) 4.3) 11.31 (4.07-4.44-5.45-6.68) 6.66-6.25) 4.68 (4.68-11.S.14 (6.10 (3.87-4.70 (7.42-6.82) 7.08 (5.98 (7. Two small studies of European populations reported urinary cesium levels similar to U.7) 10.50 (5.79) 9.63-6.42-4.34 (5.72-5.73-4.42-4. 1990).5) 7.00-10.87) 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 5.64 (4.37) 4.14-6.07) 8.48) 90th 7.59-8.43-6.55-5.2) 11.35 (4.3 (9.74) 75th 5. population results shown in this Report (Alimonti et al.04) 5.03-5.03) 5.51 (4.95) 4.46-4.91) 5.29-3.40) 7.31 (4.3) 9.56) 3.06) 5.30 (7.57) 3.93-9.10 (3.48-6.40) 6.0) 7.27-6.60 (5.47) 6.05) 6.38 (3.44) 3.70) 7.86 (4.91 (5.20-4.27) 4. interval) 4.16-8. and were also roughly similar to those in this Report.08) 3.19-3.12 (3.58) 3.23 (7.8) 6.50) 8.94 (5.05) 3.66 (6. Komaromy-Hiller et al.38-7.05-3.42 (4.2 (8. population from the National Health and Nutrition Examination Survey.83) 8.91-6.02 (5.29-3.4) 10.00) 6.02-4.7-12.3-15. (2000) found urinary cesium levels that were slightly lower than those reported for the U.85-4.79-5.31-4.63-6.8) 5.63 (6.17) 9.56) 4.21-3. Urinary cesium levels were similar in a group of forest fire fighters and residents living near the fire area (Wolfe et al.14) 4.50 (7.00-5.41-7.05 (4.04-5.1) 11.68) 4.16-5.S.30 (3.99-9.56 (4.49) 3.51 (7.99) 4.52-5.83-6.44 (4.96-4.20-4.64 (8.08-7.01-8.47 (4.43 (8.28 (4.87 (5.20-8.37-3.50-5.33-3.38 (3.13-9.96) 4.41 (8.58) 8.99-4.04) 6.33 (5.67 (5.33 (5.98) 5.16) 5.18-6.08) 4.5 (9.38-12.55) 4.05-4.58-5.56-10.77-5.41 (4.13) 7.05-3.96 (4.93-7.00-9.22) 6.12) 3.41-4.70) 6.0) 884 682 618 568 667 723 821 1132 1074 Non-Hispanic blacks Non-Hispanic whites 206 Fourth National Report on Human Exposure to Environmental Chemicals .64-6.53) 3.08 (6.78) 4.7) 10.14-4.96-4.74) 3.28) 7.Metals Biomonitoring Information Urinary cesium levels reflect recent exposure.30-4.50) 4.80) 6.88-4.24-4.S.65-4.50) 4.46 (8. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.54 (4.26-6.20) 5.08) 4.5) 9.17 (6.61 (7.73 (3.07) 8.77 (4.76-6.43 (3.09 (4.53) 6.95-6.91) 5.95-12.30) 10.45 (4.74-11.51) 4.41) 4.27 (6.07 (5.77 (6. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.84-9.09) 8.95) 8.65-3.90-3.53 (6. Minoia et al.51 (3.17) 4.3 (10.60 (3.04-11.35-7.28) 8.54 (5.9) 10.00-4.47) 4.63) 6.99-9.78 (3.21 (2.38) 10.14) 4.59) 4.48) 7.64) 4.10) 7.26 (4.35 (3.91 (5.39) 8.74 (4.18 (7.83-7.3 (8.40-5.82-4.75 (6.50) 4.62-8.18) 8.79 (5.6 (9.63 (4.64) 9.20-4.39) 5.36-3.00-8.79) 6. Using clinically submitted specimens.75-11.28 (5.33-8.42 (5.

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

50) 1.81) 1.47 (1.01 (.21) 1.520 (.530) .418 (.22 (1.16 (1.05 (.870 (.375 (.850-1.580 (.39) 1.890-1.700) .515 (. and kitchenware.480 (.640) .355-.460-.390-.416) .46 (1. population from the National Health and Nutrition Examination Survey.37-1.73) 1. Cobalt compounds are used as catalysts in producing oil and gas.610 (.910-1.410 (.454 (.770) .520) . hard metal (alloys of cobalt and tungsten carbide).461 (.390 (.03 (.28 (1.16 (1.820 (.23-2.364-.590) .650 (.23) .540) 1.333-.343 (.32) 1.47) 1.890) .360-.270-.880 (.03-1. see Data Analysis section) for Survey years 99-00.56) 1.430 (.520) .17 (1.S.310-. steel-belted radial tires.405-.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 .12) 1.600) . 01-02.22-1.640) .610-.01-2.330) .386) . Cobalt is used as a drying agent in paints.450-.42) 1.670-.810) .690-.610) . hard metal or in combination with other elements.24 (.520 (.301 (.410 (.419) Selected percentiles ( 95% confidence interval) 50th .20 (1.16) 1.14) .05) 1.340) .67) 1.950-1.980) .760 (.630-.59 (1.520-.590 (.32 (1.379 (.17 (1.350-.680) .940 (.350-.81) 1.270-.350) 75th .379 (.543) .370-.431) .520-.01 (.07.360-.870-1.07 (.710) 1.16-1.350 (.499 (.04-1.440-.398 (.340) .294 (.05 (.08-1.590-.48) 1.398) .710 (.370-.26) Total .680 (.670 (.840) .374 (. blue-colored pigments.430 (.460 (.319) .640) .450-.430-.435 (.750-.790-.04-1.800-.980-1.373-.540-.92) 1.470) .520 (. Usual human exposure is from food sources.340-.359 (.950 (.380-.17 (.620) .496) .820 (.550) 90th . Cobalt occurs naturally in airborne dust.32 (1.29 (1.530-.03) .393-.371 (.850-1.670 (.690-.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 .64) 1.740-.610) .26) 1.740 (.45 (1.700) .25-1.900-1.09) .790) .313) .630 (.630 (.730) 1. Among its many uses are manufacturing superalloys used in gas turbines in aircraft engines.570 (.740-. varnishes.540-.530 (.19) .68 (1.452 (.900) .450) .370) . It is also a component of porcelain enamel applied to steel bathroom fixtures. Medical uses include joint and dental prostheses and radioactive cobalt in cancer chemotherapy.950) .581) . 7440-48-4 General Information Cobalt is a magnetic element that occurs in nature either as a steel-gray.460 (.520-. 208 Fourth National Report on Human Exposure to Environmental Chemicals .417) .750 (. and soil. and magnetic recording media.490-.26) 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.930 (.960-1.380-.07.810-.520 (. The cobalt used in U.404) .367 (.390 (.469-.280-.523) .850) 1.620-.420 (.32) 1.890-1.410-.920-1. Cobalt compounds are also used in manufacturing battery electrodes.420) .04 (.570) .410) .830-1.860 (.900) . 0.590-.420) .460) .305-. seawater.660) .26-2.388-.07-1.330-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.16 (.340 (.600 (.330 (.750 (.36) 1.348-.460) .07-1. and fertilizers.520-.53) 1.334) .04-1.09 (. shiny.08) .940-1.650 (.03 (.510) 1. It is emitted into the environment from burning coal and oil and car and truck exhaust.519 (.320 (.650-.26-1.06 (.434 (.290-.60 (1.410) .431) .16) 1.03) 1.270-.750 (.360-. respectively.550 (.427-. and 03-04 are 0.259-.487) .900) .660) .369 (.410 (. automobile airbags.S.352 (.930-1.583) .428-.370 (.373) .03) 1.560 (.870 (.570-.28 (1.600-.48) 1.820 (. and 0.47 (1.790 (.950 (.04) 1.338-.310 (.28-2.760) .480 (.308-.480-. Cobalt may be released into the systemic circulation of patients who receive joint prostheses that are Urinary Cobalt Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.670 (. and inks.00) .12) 1.580 (.17-1.291-.75 (1.327-.670-.410-.950-1.540-.14-1.15 (1.380 (.372) .47) 1.340-.99) 1.465) .28 (1.410 (.620-.424) .01-1.463-.348-.380 (. industry is imported or obtained by recycling scrap metal that contains cobalt.710) .564) .65) 1.44) 1.300-.930) .500) .32-2.316 (.690 (.399) .380 (.660-.Metals Cobalt CAS No.02-1.850) .390 (.331-.570) .680 (.377-.810) .430) .300 (.414) .890-1.940-1.620-.370-.540-.24 (1.502) .06-1.33 (1.394) .470 (. large appliances.339 (.500 (.33-1.350-.410 (.333-.316-.450) .900-1.450) .800-. diamond-polishing wheels.50 (1.460) .400-. interval) .570-.06 (.22) 1.430) .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 .336-.450) .16-1.580 (.410-.890) 95th 1.430 (.490-.15-1.880-1.680) .920) 1.800) .390) . and in synthesizing polyester and other materials.09 (.52 (1.13) 1.08.285 (.550-.

33) 1.55) .476-.417 (.508-.753) 1.838 (. 1972).879-1.786-.380-.402 (.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 (..280-.455 (.585) .259 (.848 (.296) .290 (.781-1. interval) .289) .00 (.343 (.83) 1.487-.27) 1.562) .857-1.804) 1.439) .691 (.250) .362) .302-.335 (.417) .963-1.349) .606 (.689 (.. A portion of cobalt retained for long periods is concentrated in the liver.16 (.404-.342-.344-.24) .17) .898 (.243-.757-1.428-.50) 1.468) .360) .917) .833-1.700 (.821 (.251-.408 (.737 (.04-1.673-.248-.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 .00 (.829) .626-.407 (. Human studies with 60Co administered as soluble cobalt chloride have reported oral absorption ranging from approximately 1 to 25 % (Smith et al.391) Selected percentiles ( 95% confidence interval) 50th .900-1. 1994.36) 1.304) .28) 1.609) .955) .15 (.861 (.215-.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 .513) .361-.471-.278 (.753-. cobalt is excreted predominantly in the urine.560-.10-1.. Cobalt is absorbed by oral and pulmonary routes.537 (.Metals fabricated from cobalt alloys (Lhotka et al.611) .911-1.329 (.938-1.495 (.554 (. Cobalt constitutes 4% by weight of vitamin B-12 (cobalamin).421) .273 (.785) .683-.361-.00 (.358 (.727 (.723 (.895-1.600-.281) .30 (1.279) .328 (.826-1.552 (.333-.331-.00-1.301) .328 (.547 (.369 (.638-1.534 (.872 (.842) .73) 1.463-.279 (.259-.386 (.669) .306 (. 1994).630-.11-1.239-.640) .591 (.905) .744) 1.313-.407) .277-.363) .396) .388 (.361 (.792-1.481) 90th . but with a minor fraction (10-15 %) exhibiting a half-life of several years (Mosconi et al.317 (.733-1.728 (.438) .435 (.50) 1. respectively.444 (.57) 1. Exposure in the workplace may come from electroplating.963) .376 (.387) .976 (.16 (.409) .324) .27) 1.234 (.963-1.442-.983) .259) .50 (1.343-.394) .316 (.372) .329-.378-.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 .60) 1.393-.503-.949) .851 (.821-3.286) .830 (.523 (.990-1.313-.542 (.824 (.19) .29 (1. Lung retention of relatively insoluble cobalt compounds such as cobalt oxide may be prolonged.297) .708) .750) .290 (.500 (.29) 1.750-.388 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.368 (.952 (.479) .310) .S.333-. 2003).00) .337) .23 (1.348) .582-.471 (.49) 1.272-. and to a lesser extent. Urinary Cobalt (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.425-.850-1.574-.513-. an essential human nutrient.333-.955) .237-.534-. 1972).703-.736-.16) .452-.467-.707) .515 (.550-.248-.429) 1.581) .632-.777-.275-.334) .362 (.378-.12 (.44 (.268 (.323) .25 (.382-.963) .479-.25 (.346 (.29 (1.328) .932-1.488) .738 (.54) 1. Smith et al.393 (.324-.362-.257-.29) .353-.635 (.449) .616-.847) .313 (.314 (.523 (.469-.505) .09) 1.630-.471-.861-1. with pulmonary clearance half-lives of from one to two years (Hedge et al.608 (.533 (.704-.522) . Once absorbed and distributed in the body.333 (.303-.400 (.679-.938) .361 (.301-.647) .339-.543) . refining or processing alloys.728) .282 (.12-1.378-.33) .983-1.662) .563-.352) .03-1.02 (.513 (.274-.16 (1.391 (.433) .667-1.257 (.04 (.35) .304-..449-.352 (.290 (.256-.327-. Elimination reflects a multi-compartmental model dominated by compartments with half-lives on the order of several hours to a week.00) .461) .326-.548 (.760-1.850 (.396) .611) ..738 (.300) .11-1.291 (. Workplace standards and guidelines for external air exposure to cobalt and several of its compounds have been established by OSHA and ACGIH.561) .247 (.595) .278-.457) .384) .475 (.368) .306) 75th .774 (.781) 95th 1. 1979).554 (.435-.313-.365) .593) .700 (.434-.895-1.975 (.00 (.660-.667-1.14 (.381) .500-.694) .35) 1.10) Total .29 (1.355) . using hard metal cutting tools.615) .644 (. or using diamond-polishing wheels that contain cobalt metal.10 (.378 (.275-.337 (.426 (.598 (.462) .296-.309) .313-.271 (.297-.756 (.844 (.313-.15) 1.327 (. A nutritional requirement for cobalt other than that contained within dietary cobalamin has not been established.282-.529 (.487-.392 (. population from the National Health and Nutrition Examination Survey.500-.294-.829-1.937 (.425) .594) .06 (.599) .368) .634-.419) ..353 (.293 (.457-.990) .960 (.10) .740-1.964 (.298 (. in the feces.319-.60) 1.929) .365-.352 (.562) .03 (.36) 1. Recent inhalation exposure to soluble cobalt compounds can be monitored by measuring cobalt in urine or blood (Lison et al.457 (.

A subclinical decrease in thyroid production was observed in a study of cobalt production workers (Swennen et al. 2003.gov/toxpro2. 1997). has been associated with exposure to dusts that contain cobalt.. 2003) and produced lung cancer in rats and mice after chronic inhalation (Bucher et al. Hailey JR. “Hard metal” disease. Lisi. Cugell DW. Blood and urinary concentrations as estimators of cobalt exposure. 1994).cdc. Perkins DG.. Iavicoli et al. Cobalt compounds are a recognized cause of allergic contact dermatitis (Dickel et al. 210 2006. Toxicol Sci 1999.43(4):299-303. 1998). Exposure to soluble cobalt salts will produce proportionately higher urinary levels because they are absorbed better... population results in this Report (Kristiansen et al.html. Occupational exposure to cobaltcontaining dusts has caused occupational asthma (Pisati and Zedda. Atlanta (GA). 1988). 1997.. Arch Environ Health 1988. An industry-wide study of hard metal workers in France observed an increased mortality from lung cancer (Moulin et al. IARC has classified cobalt metal with tungsten carbide and other soluble cobalt salts as possibly carcinogenic to humans. Daniel et al. Thomassen et al. 2001... 1999).S... The extent to which cobalt exposure alone causes interstitial lung disease is unknown (Linna et al. 1988). Morgan WKC. Rubin A. Smaller population surveys of European adults reported urinary cobalt levels that were roughly similar U. Alexandersson R. Grumbein SL.. 1985. Lison et al.. 1994. Roycroft JR.. Swennen et al. Inhalation toxicity and carcinogenicity studies of cobalt sulfate. and this caused outbreaks of cardiomyopathy among heavy drinkers in the mid-1960’s (Alexander 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.. For workers exposed to cobalt in the air. Persons with occupational exposure to cobalt often have urinary cobalt levels that are many times higher than those of the general population. 1994. 2001. Case reports have also suggested a link between occupational cobalt exposure and cardiomyopathy (Jarvis et al. MacDonald et al. Shirakawa et al.cdc.49:56-67.. Information about the BEI is provided here for comparison...e. Haseman JK. Third National Report on Human Exposure to Environmental Chemicals. 2006. population (CDC. Linnainmaa and Kiilunen. Pharmaceutical preparations of cobalt used in the past as hematinics were associated with the development of overt hypothyroidism (Kriss et al. Am J Med 1972. Centers for Disease Control and Prevention (CDC). Cobalt-beer cardiomyopathy. Finding a measurable amount of cobalt in the urine does not mean that the levels of cobalt cause an adverse health effect.. 2005 [online]. an interstitial lung disorder with findings that range from alveolitis to pulmonary fibrosis.53:395417. Urinary measurements mainly reflect recent exposure. The ACGIH biological exposure index (BEI) for inorganic forms of cobalt (except insoluble cobalt oxides) is 15 mg/L. 1993). 2005.. 1990). Krause et al.gov/ exposurereport/. 1993). 1992)... 1998). 2003).. Poulsen OM. Cobalt was once added as a foaming agent to beer.. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Biomonitoring Information Urinary levels of cobalt decline rapidly within 24 hours after exposure ceases (Alexandersson et al. Sills RC. Correlations between air exposure levels and urinary cobalt levels in hard metal fabricators are well documented (Ichikawa et al. although substantial occupational exposures have produced elevated urinary levels for many weeks. not to imply that the BEI is a safe level for general population exposure.. a distinction is made between soluble and insoluble (oxides and metallic) cobalt (Christensen and Poulsen. 2005. biological levels and health effects following exposure to soluble or insoluble cobalt compounds in cobalt blue dyes. Available at URL: http://www.50(13):95-104. 4/3/08 Christensen JM. 1955). Sci Total Environ 1994. Cobalt compounds elicited numerous genotoxic effects in both in vitro and in vivo assays (De Boeck et al. Information about external exposure (i. The respiratory Fourth National Report on Human Exposure to Environmental Chemicals . usually in combination with tungsten carbide (Cugell et al. et al.atsdr. Bucher JR. Cobalt compounds appear to stimulate erythropoietin production and were formerly used in the treatment of anemia (Goldberg et al. 2003. Small studies of patients with hip replacements using metal alloy prostheses reported increased urinary cobalt concentrations. 2001). Lauwerys and Hoet. 2001. White and Sabbioni.. A 1982-1992 surveillance programme on Danish pottery painters. Dunstan et al.Metals Toxic effects of cobalt have been encountered in workplace settings. References Alexander CS. A clinical and pathological study of twenty-eight cases.S. 1972).. environmental levels) and health effects is available from ATSDR at: http://www. 1989). with mean levels that were about 15-20 times higher than in the general U.

The effect of the diameter of metal-on-metal bearings on systemic exposure to cobalt and chromium. Cresti R.44:124-132. Zedda S.(1-3):133-139. X. Salama A. Sci Total Environ 1998. Absorption and retention of cobalt in man by whole-body counting. MacDonald SJ. Co-sensitivity between cobalt and other transition metals. Thomassen H. Hoher T.242:1412-1415. Salvatori S. Unwin P.533:135-152. Szekeres T. Romazini S. Linnainmaa M. Fourth National Report on Human Exposure to Environmental Chemicals 211 .204:147-160. Buchet JP. Stanescu D. Bunn HF. Lisi P. Blunn G. Zhuber K. Clin Orthop Relat Res 2003. Lung cancer risk in hard-metal workers. Mosconi G. Lison D. Laippala P. Alessandrelli M. Shirakawa T. Lauwerys R. et al. Am J Ind Med 2003. Buchet JP. Goldberg MA. Gross RT. Oksa P. salt. Roto P. Sabbioni E. and hard metal dust. Science 1988.150:177-183. Kiilunen M. 2001. Steffan I. Kuska Y.51(7):447450. Moulin JJ. Regulation of the erythropoietin gene: evidence that the oxygen sensor is a heme protein. HoffmannB. DeSantis V. Daniel J. Int Arch Occup Environ Health 1997. Cobalt and antimony: genotoxicity and carcinogenicity. Biological monitoring of workers exposed to cobalt metal. Kristiansen J. Thakker DM. Kirsch-Volders M. Swennen B. Sabbioni E. Sanghrajka AP. Outcome of occupational asthma due to cobalt hypersensitivity. cobalt salts. Dunstan E. Cannon SR. Contact Dermatitis 2003. et al. Toxic trace element reference levels in blood and urine: influence of gender and lifestyle factors. Peltier A. Meier R. The release of metals from metal-onmetal surface arthroplasty of the hip. Trace element reference values in tissues from inhabitants of the European Union. J Occup Med 1992. Urinary cobalt as a measure of exposure in the wet sharpening of hard metal and satellite blades. Int Arch Occup Environ Health.406:282-296. Occupationallyinduced “isolated cobalt sensitization. Lison D. Leghissa P. 3rd ed.” Contact Dermatitis 2001. White MA.22:359367. Lauwerys R. Hoet P. Lasfargues G. Am J Epidemiol 1998. Pradhan C. Diepgen TL. Iversen BS. Palmroos P. Barnaby CF. et al. et al. Edmonds CJ. Uitti J. Radulescu M. Br J Ind Med 1993. Cobalt excretion in urine: results of a study on workers producing diamond grinding tools and on a control group. Hedge AG. Chest 1989.21(2):189-195. Lauwerys RB. et al. Lison D. Lhotka C. Kato M. Metal-on-metal versus polyethylene in hip arthroplasty: a randomized clinical trial. Vitali MT. J Rheumatol 2001. Rorabeck CH. Metal ion levels after metal-on-metal proximal femoral replacements: a 30-year follow-up. and cobalt metals. Angerer J. Iavicoli I. Christensen JM. Four-year study of cobalt and chromium blood levels in patients managed with two different metal-on-metal total hip replacements. J Orthop Res 2003. Falcone G. Boca Raton (FL): Lewis Publishers.150. Mutat Res 2003.88(4):443448. Kriss JP.50(9):835-842.87(5):628-631. Sci Total Environ 1997.55(4):269-276. Goto S. A report of two cases from mineral assay laboratories and a review of the literature. Chess DG. 1985.36:732-734. Sci Total Environ 1994.216:253-270. Respiratory health of cobalt production workers. Dickel H.Metals effects of cobalt. J Trace Elem Med Biol 2006. Wild P. Weber A. Kraus T.148:241-248. Dunning SP. Industrial Chemical Exposure: Guidelines for Biological Monitoring.95:29-37.69(3):193-200. De Boeck M. Sabbioni E. Tilley S.28(5):1121-1128.58(10):631-634. Weyher I.150(1-3):167-171. McMinn DJ. Ghat IS. Carnes WH. Exposure assessment in the hard metal manufacturing industry with special regard to tungsten and its compounds. Kusaka Y. Cobalt-specific T lymphocytes in synovial tissue after an allergic reaction to cobalt alloy joint prosthesis. Heki S. Occup Environ Med 2001. Swennen B. J Bone Joint Surg Br 2005.34:620-626. Schramel P. Schaller KH. Ziaee H. Schank M. Occupational asthma from cobalt sensitivity in workers exposed to hard metal dust. Health Phys 1979. Arch Intern Med 1990. McCalden RW. Zweymuller K. Health Phys 1972. Long-term clearance of inhaled 60Co. a study of 13 elements in blood and urine of a United Kingdom population. Bozec C. Occup Environ Med 1994. J Bone Joint Surg Br 2006. Smith T. Jarvis JQ. Fujimura N. et al. Biological monitoring of cobalt exposure based on cobalt concentrations in blood and urine.20(1):25-31.48:172-173. Zobelein P. Hypothyroidism and thyroid hyperplasia in patients treated with cobalt JAMA 1955. Bacis M. Bourne RB. Meyer zum Buschenfelde K-H. Epidemiological survey of workers exposed to cobalt oxides. oxides. Linna A. Hammon E.157:117121. Pisati G.45:246-247. Cobalt cardiomyopathy. Sci Total Environ 1994. Goto S. Thabe H. Robinson C. Ichikawa Y. Cleland D. Molders J.

60) 4.50-3.60) 1.81) 1.52-1.10) 2.60 (2.30 (2.80-5.75-2.90 (1.50 (4.90) 2.20 (3.20-3.10-2.70-1.40-3.22 (1.39) 1.80) 2.78 (1.70-2.20-3.00) 1.70) 1.70 (2.80) 3.40-1.68-1.90 (3.60-2.90-4.50 (4.90 (3.50-2.87 (1.70-2.80) 1.40-3.00 (3.40 (5.75 (1.90 (3.80-3. Since lead has been eliminated from gasoline. 0.04-1.20) 90th 3.10 (2.899-.50 (2.60) 2.62) 1.60 (2.50 (2.20 (3.30-1.43) 1.00-4.20-2.83 (1.37 (1.40-1.10-2.32-1. dense.60 (2.20-4.90 (2.30 (1.30) 1.70-4.20 (2.51 (1.40 (4.80 (5.10) 1.10-4.90-2.50 (1.60) 3. 01-02.10-2.36-1.30-6.60 (2.90 (4.70) 1.40 (2.12-1.10-1.70 (1.80-4.50-3.60 (1.00-1.30 (4.80) 2.80-4.20-1.60 (3.20) 4.30 (2.80 (1.10 (1.40-6.30-2.50-2.40) 1.48) 1. and 0.36) 1.60-1.70) 1.36-1.28.40-2.00 (1.62-1.40) 1.80 (1. ammunition.20) 3.62 (1.40-3.40) 2.90-2.20) 4.50 (3.10-3.01 (1.60-3.00 (1.50) 4.00) 1.53) 1.43-1.60 (1.50-1.00) 4.10) 3.80 (4.96-2.10-4.60) 2.40) 5.942 (.900 (.60 (1.50-1.60) 2.55-1.60-6.70 (3.60 (1.70) 4.60) 5.50-1.20 (4.00) 2.20 (3.50) 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 2.50 (1.39-1.30-1.10) 4.30) 2.90) 1.60 (1.30-1.09) 1.40-1.30 (2.32-1.80 (1. see Data Analysis section) for Survey years 99-00. bronze).40) 2.80 (1.89) 1. antique-molded or cast ornaments.50-4.50-4.69 (1.80) 1.70) 3.60) 4.50) 4.90) 2. and for radiation shielding.50) 75th 2.25 (1.10) 1.00-1. Lead has a variety of uses in manufacturing: storage batteries.70 (5. 7439-92-1 General Information Elemental lead is a soft.70 (2.40) Total 1. 212 Fourth National Report on Human Exposure to Environmental Chemicals .50 (1.50) 2.60 (2.10) 3.70-6.10-6. brass.87) 1.80-3.65 (1.20-3.19 (1.10-3.20-1.10 (1.60-2.20 (3.70) 2.90-3.00 (4.37-1.17) . population from the National Health and Nutrition Examination Survey.70-3.80) 3913 4339 4132 4057 4606 4241 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.40) 4.20 (1.30) 5.02) 1.20 (3.60) 4.30 (1.10-8.60 (3.40) 3.50) 1.75-1.80 (1.60) 2.10-1. the main source of lead exposure for the general U.90 (1.30-4. Before the 1980’s.70) 3.90) 2.80) 1.30-2.60-4.00) 1.60 (3. respectively.30-2.50) 5.43 (1.50-5. ceramic glazes.Metals Lead CAS No.60 (1.10) 2.50-6.40-5.90) 2.70-1.60-4.00) 4.50-5.51) 1.90-2.10) 1.23 (1.45 (1.80 (1.80-3.40-2. adult lead exposures tend to be limited to Blood Lead Geometric mean and selected percentiles of blood concentrations (in µg/dL) for the U.00-2.S.90) 3.90-6.40) 2.30) 2742 2268 2085 1842 2219 2293 2716 3806 3478 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.20 (1.30 (1.50 (3. Lead is most often mined from ores or recycled from scrap metal or batteries.20) 2.80-2.80) 1.00) 6.00-6.00) .946 (.00) 2.14-1.95) 1.60) 1.90 (3. Aerosolized lead is either inhaled or ingested after it is deposited on surfaces and food crops.70-5. blue-gray metal that occurs naturally in soils and rocks.90 (3.40-1.40-6.20 (3.00) 1.60-1.70-2.00-4.20) 5.60 (4.00) 1.3.50) 3.77 (1.878-1.70) 3.80 (3.70) 1. Elemental lead can be combined with other elements to form inorganic and organic compounds.00) 3.55-1.50 (2.69) 1.72) Selected percentiles ( 95% confidence interval) 50th 1.00 (4.80-3.30 (4.30) 95th 5.30 (3.60 (1.00) 3.10-2.34-1.50) 1.20 (1.30 (2.80 (2.90) 5.50) 1.52-1.43) 1.00-4.00 (5.30-2. In the past.50) 2.40 (1.40-1.30) 2. leaded glass.20-6.10-1.86) 1.00 (2.60 (2.56 (1. Lead was used in plumbing for centuries and may still be present.50-2.80) 2. interval) 1.50-2.90-4.10) 5.60-1.10-6.90-4.S.800-1.60) 3.31) 1.14-1.70) 4.10-2.10 (2.43 (1.90) 1.80 (5. and 03-04 are 0.90-4.70) 1.70 (1.80 (4.20 (1.20) 1.30-1.20-3.66 (1.00 (6.10 (3.20 (3.75) 1.20 (1.10 (4.3.40-4.20) .30 (1.40 (3.60) 4.00-5.69 (1.50) 5.00) 5.g.00) 2.90-2.40 (2.30) 2.37 (1.80) 2.986) .60 (3.30-1.10-2. metal alloys (e.50) 7.50 (2.69) 1.40 (1.20) 3.66) 1.900 (.60) 1.60-1.90) 1.90 (2.80 (2.14-1.90) 3.10-3.60) 3.60) 723 898 911 905 1044 856 2135 2231 2081 4207 4772 4525 6-11 years 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 2.50-1.30 (4. plastics.70-1.10) 3.30 (2.20-2.60) 3.40 (1.55 (1.60) 1.40-1.70 (1.52 (1.70 (2.50-1.40 (1.20) 3. such as lead phosphate and tetraethyl lead.70 (3.60) 2.70) 4.93-2.80) 1.900-1.30-1.80-4.25 (1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.40) 1.46 (1.71-1.50 (2.10 (2.30 (2.25) 1.45-1.49-1.40-2.70) 4. lead was added to gasoline and residential paints and used in soldering the seams of food cans.60) 5.00) 2. malleable.90) 2.40) 2.50) 1.30 (2.70 (1.30-5.20 (2. solders.20) 3.10-3.80 (2. population was aerosolized lead emitted from combustion engines that used leaded gasoline.91) 1.50 (1.10 (1.60) 1.

50 (1.30) 2.960-1.00-1.80) 2..700 (. imported children’s trinkets and toys.535-.50-2.745-.00) 1.80 (2.1.570-.50-1.40 (1.40) 1.800) .90) 2.10 (. and 03-04 are 0.920 (.910-.900-1.30) .60) 2.g.Metals occupational (e.600) .70 (2.690) 75th 1.50) 3.800 (.923 (.10-1.04 (.31-3.674) 1.589-.78-2.82 (2. 1991).20 (1.40) 1.757-.66 (2.40) 1.00 (2.30) 1. Lead is absorbed into the body after fine lead particulates or fumes are inhaled.677 (.82 (1.833 (.20 (1.70 (2.10) 2.680) Sample size 2465 2690 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1. or water contaminated by mining or smelting operations. bullet fragments retained in human tissue.10 (.27 (1.30-5.40 (1.572-.22) 1.900) .75) 3.604 (.30-2.70) 1.828) Selected percentiles ( 95% confidence interval) 50th .700 (.700) 1.50) 2.595-.800) .708-.857) .900-1.27) 1.900) .90 (2.32 (1.00 (1.04) 2.30) 1. pewter utensils and drinking vessels.59-2.820-1.630 (.62) Total . 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.00 (1.710-1.70) 3.700-.10) .800-.800) . However.60-3.00-2.44-2.20) .600-.700-.600 (.17 (1. absorbed lead is bound to erythrocytes and then is distributed initially to multiple soft tissues and eventually into bone.40) 1. interval) .818) .960-1.60 (2.10-3.564 (.10-1.20-1.986) .24-1.86-2.40 (1.80) 1.526-.00-1.40) 2.66 (2. battery and radiator manufacturing) and recreational sources.691-.753 (.800 (.86) 1.80 (1. Children may also be exposed to lead brought into the home on the work clothes of adults whose work involves lead.14 (1.40-1.90 (2.50 (2.60-1.40) 1.14-1.900) .90-3.710-. population from the National Health and Nutrition Examination Survey.636 (.10 (1.49) 340 368 290 719 762 725 1406 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .40 (2.80) 2.70-2.738) .90-2.40 (2.00-2. see Data Analysis section) for Survey years 99-00.33-2.700 (.73 (1.700-.20-1.800-1.80-3.50) 1.729-.60 (1.00-2.10-1.600) .661-.800) .701) . 0.90-3.80) 2.11 (1.990) 2.822-1.30-1. older plumbing systems with leaded pipes or lead soldered connections.70-3.00-1.605) .900 (.970-1.70 (2.80) 1.640 (.60 (1.30-1.610 (.90) 1.920 (.773) .80 (1.613) .50-3.21 (2.641-.90-2.591 (.40-1.50 (2.915-1.840 (.40) 2.00 (.86 (1.848 (.23-4.60 (1.50-2.579-.20 (2.50-2.30) 2.80) 1.20 (2.815 (.700-1.540-.20-2.70) 3.900 (.60-3.40 (1..70 (1.60-2.00 (1.11) 2.10) .30-1.50) 1.1.500-.20 (3.30 (2.600-.20 (1.862) .900-1. lead-contaminated dust in indoor firing ranges.04) .556-.650) 1.18-1.30) 1.90) 2.52-1.07 (.20) .90) 2.590 (.900) .30) 1.600-.14 (1. and contact with soil.40) 3.695 (.35 (.616) .20-2.00 (1.60 (1.560-.955-1.785) .40 (1.70) 1.07-1.33.10-1.20) 1.700) .90-2.637-.23) .13-3.10 (1.19 (1.12) 90th 2.680-.00) .20 (2.766 (.41) 2.33 (2. In the blood.730 (.49 (1.688 (.10-5.51) 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.90 (2.40-2.700-.70) 2.00) 2. the primary source of exposure in children is from deteriorated lead-based paint and the resulting dust and soil contamination (Manton et al.06) .671-.800 (.72) 1.700-.30-3.70) 1. CDC.30 (1.80) 2.558 (.50) 1.960 (.90 (1.40-1.80) 2.75) 4.651) .810-1.50 (1.90 (1. lead-based painted surfaces undergoing renovation or demolition.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 1.03 (1.800-.80-2.80) 3.40-5.540 (. 2007.10-3.20) 1. Fourth National Report on Human Exposure to Environmental Chemicals 213 .10) 1.731 (. Small amounts of environmental lead also may result from burning fossil fuels (ATSDR.990) 1.900) .940 (.00) .00) .935) 1.80-2. stained glass framing. Approximately half of the absorbed lead may be incorporated into bone.752 (.52-1.20) . 2000).40 (2.625 (.628) 1.04 (.680) .600-.620 (. or after soluble lead compounds are ingested.64) 2. and 0.680-.30) 2.10-1.900) .89) 2.900 (.506-.20 (1.13) .70 (2.20 (1.941) .718) .40 (2.600-.40) 2.553-.10-3.20 (1.20) .660) .31 (1.900-1.91) 2. 01-02.90-4.40) 2.62-4.09) 1.90 (1.40-1.30) 1.29) 2.90-2.800 (.800-1. Less common sources of incidental or unique lead exposure are numerous: lead-glazed ceramic pottery.04-2.579-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.40-3.580-.97) 4.78-2.850 (.808 (.573 (.625-.59) 1.50) 2.50 (2. which is the site of approximately Urinary Lead Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.30 (3.10 (.700 (.20-1.78-2.700 (.29 (2.800) .642 (.10) 2.30-1.600 (.20) 1.S.10 (1.480-.833-1.80) 3.02) 1.03-2.10 (1.700 (.60-2.00) 2.00) . dust.52 (1.02 (.86) 95th 2.749) . lead-containing folk remedies and cosmetics.640-.659 (.790 (.931) .620) 1.795 (. respectively.

31 (1.721 (.50 (1.64 (1.04-3.375 (.914 (.08) .428) .88-2.667-.65 (1.638 (.71 (1.569 (. CDC.09) 1.671 (.56-2.83 (2.18) .88) 2.09-1.03) 2.639 (.979 (.06 (.644) .469 (.03-2.07) .790) .66 (1.85 (1.655) .01 (.601-.667) .659-.655) 75th 1.18) 1.50) 1.707 (.698) .Metals 90% of the body lead burden in most adults.604-.06) 1.75-2.64) 2.696 (.55 (1.583-. abdominal pain.607-.39-1.48 (1.08) .810 (.92) 2.S.34-1.20) .56 (1.579-.28-1.58) 1.962 (.933-1.10) 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 .946-1. 1996).19-5.22) 1.61) 1.644 (.718) .75 (2.. with lesser amounts eliminated via the feces. interval) .618 (.52 (1.72) .07 (.587-.44) 1. and approximately 40 to 70% of lead in blood comes from the skeleton in environmentally exposed adults (Smith et al.61) 1.43) 2.918 (.47 (1.870 (.645-. hair.03) .97 (1.03) 90th 1.63) 4.609 (.615 (.83) 1.758) .876-1.853-1.796-1.975-1.85-2.730) 1.43 (1.33 (1.586-. scant amounts are lost through sweat.18) 1.22) .22-1.03 (.645-.608 (.992-1.594-.677-.722 (.22) 1.862-.37-1.79 (1.606-.56) 3.36-2.938 (.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 . BLLs near 10 µg/dL can affect blood pressure in adults and neurodevelopment in children (Bellinger.654) .53-1.535) .404 (.635 (.62) 2.10 (.51) 1.26) Total .07-1.88) 1.63) 1.882-1.679) 1. The toxic effects of lead result from its interference with the physiologic actions of calcium.702) .72-2.731-.693 (.605-.709 (. Nash et al.559-.19) 1.00 (1.608-.47) 1.97) 1.623 (. 1991. 2004.703) .62-1.649 (.639) .681-.404 (. through the inhibition of certain enzymes.61) 1.655-. Schwartz.86 (1.682) .50-2.11-1.461) .918-1.755 (.06 (1.38 (2.44 (1.436) .722 (.677) .917-1.02-1.37-1.658 (. In 1991.85-2.603-.11) 1.561-.10) 1.41-1.15) 1.898) .51 (1.11 (1. with a half-life of years to decades.893) .492-.781-1.98 (1.40-1.25-1. seizures.679-.670) 1.96 (1.23 (1.15) 1. and paralysis. based on prospective population studies.11 (1.400) .35) 2.496 (. Staessen et al.44 (1.43) 1.64-2.541-.88) 2.09-1.33-1.623 (.79) 2.622 (.00) .828-1.753) .510-.712 (.15-3.31) 1. 2003.00 (.615 (.66) 2.652 (.78-4.838) .800-. 1995). Additional mechanisms include generating reactive oxygen species and altering gene expression (ATSDR.89-2.938-1.700-.18 (1.828) .686) .05-1.812-1.03 (1.725) .65-2.739) . Approximately 70% of lead excretion occurs via the urine.701 (.49 (1.920-1.67-4.03) 1.667-. 2007).588-.10 (1.29 (1.639 (.621 (.971 (.88 (1.89-5.746) .988-1.594-.31 (2.734) . BLLs and associated toxic effects differ in children and adults.50-1. and nails (Leggett.668-.78 (2.508) .97) 1.763) .720 (. encephalopathy.648 (.05-1.68 (1.73-2.02) 1.988 (.43 (2.592-..28) 2.742) .59-3.74 (1.593 (.588-.701) .25-1.24 (1.31) 1.03) 1.698) .98) 2.15-2.662) Sample size 2465 2689 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.851) .708 (.85) 1.688) .73) 2.66 (1.33) 2.342-.742) Selected percentiles ( 95% confidence interval) 50th .625 (.20-3.62-2.26) 2.00 (1.926 (.977) 1.01) .87) 1.914 (.00 (1.710) .603 (.793-1.70 (1. and through binding to ion channels and regulatory proteins.33) 1.15-2.380-.64) 95th 2.97-18. O’Flaherty.98-2.11 (. Lead is cleared from the blood and soft tissues with a half-life of 1 to 2 months and more slowly from the skeleton.990 (.38 (2.38 (2.05 (1.612-.774 (. Large amounts of lead in the body can cause anemia. kidney injury.45 (1.702) .571-.676) .08-2.681-.05 (.52) 1.720 (.981-1. The skeleton acts as a storage depot.17-1.957-1. 1995. and iron.963-1.14 (1.765) .55 (1.03 (.61) 1..841-1. Lead can cross the placenta and enter the developing fetal brain.383-.47 (2.03) .94 (1.41 (1.408-.603-.529-.992-1.404-.09-1. For instance. Equilibrated blood lead levels (BLLs) after chronic intake are associated with certain toxic effects.22-2.61) 3. 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.551-.933) .46 (2.77) 2. 1993).27 (1.14) 1.632 (.432 (.31 (1.43-1. zinc.71-2.94-2.28) .50-2.20) .11 (.718) 1.46 (1.940 (.617-.641 (. population from the National Health and Nutrition Examination Survey.657) 1.69 (1.72-2.56-3.571-.03) 2.62-3.725) .18) 2.50-2.17 (.633 (.53) 1.639 (.702-.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 .06) .11) .12-1.82) 1.997-1.460-.673) .03 (.41) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf. 1993.887 (.683-.04) 2.914-1.900 (.677 (.0) 3.79) 1.

. the prevalence rate has declined annually since 1994 (CDC. Telisman et al.S.. 2007). which is an 84% decline. 1996.6%) were lower than those from NHANES 1991-1994. 2003. Staessen et al. 2009). High dose occupational lead exposure. 1996.. NTP considers lead and its compounds reasonably anticipated to be human carcinogens. urban residence. However. Surveillance data reported by U. Temporal declines in children’s BLLs have been found in other developed countries (Wilhelm et al. adults in the 19992000 NHANES sample (Apostoli et al. usually with BLLs greater than 40 mg/dL. 2003. the geometric mean BLL was 3.html. and low family income (CDC. Borja-Aburto et al. and decrease fertility (Alexander et al..3 million children tested had BLLs of 10 mg/dL or higher (http://www. A general population survey of adults Germany in 1998 reported a geometric mean blood lead concentration of 3. Many animal studies have established the multiple neurotoxic effects of lead (ATSDR.cdc. lead in women may be associated with hypertension during pregnancy. premature delivery. 1995) and associations between increased bone lead concentrations and blood pressure (Hu et al. and peripheral neuropathy generally occurring at much higher levels (e. Data submitted through state public health programs from 2006 showed that 1.0 µg/dL in females (Soldin et al. Lanphear et al. Jones et al (2009) showed that the prevalence of BLLs of 10 µg/dL or greater decreased from 8.S. 2000). adults in the 1999-2000 NHANES sample. 2003). 2002a). A decrease in BLLs is evident also in adult NHANES results reported over past decades (CDC. and spontaneous abortion (Baghurst et al.gov/toxpro2.000 adults. respectively. 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. CDC. 2003.. approximately 11..e. residing in housing built before the 1950’s.. 2005a).. 2002. Fourth National Report on Human Exposure to Environmental Chemicals 215 . In NHANES 1999-2002 in children 1-5 years old. Results of studies of adults with either occupational or environmental lead exposure have shown consistent associations between increased BLLs and increased blood pressure (Nash et al. In occupationally exposed adults. 1998). Schwartz et al. 2002).2 µg/dL in males and 3. The U. the national prevalence rate for adults with BLLs 25 mg/dL or higher was 7. 2001).S. Bellinger 2005. may alter sperm morphology. A general population survey of adults in Italy tested in 2000 found BLLs slightly more than double those reported for U. IARC considers inorganic lead compounds probable human carcinogens. 1999). particularly in the skeleton.. both the geometric mean (1.75 µg/dL in U.. 2005b. 1994).. Biomonitoring Information Blood lead measurement is the preferred method of evaluating lead exposure and its human health effects.S.S. subtle or nonspecific neurocognitive effects have been reported at BLLs as low as 20-30 µg/dL (Mantere et al. Workplace standards and guidelines for lead exposure and monitoring have been established by OSHA and ACGIH. seizures.5 per 100.. 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. Information about external exposure (i. environmental levels) and health effects is available from ATSDR at: http://www. Low level environmental lead exposure may be associated with small decrements in renal function (Kim et al.. higher than 100-200 µg/dL). adult residents. 1991. Muntner et al.. 1999).gov/nceh/lead/surv/database/State_ Confirmed_byYear_1997_to_2006. state childhood lead programs also show a decline in the percentage of children younger than 6 years of age who had BLLs of 10 mg/dL or higher.Metals µg/dL or higher as the level of concern in children.7 µg/dL and 4.21% of approximately 3..07 µg/dL (Becker et al. Urine levels may reflect recently absorbed lead. Both drinking water and ambient air standards for lead have been established by the U.9 µg/dL) and percentage of children with BLLs greater than 10 µg/dL (1. Jones et al.g.. 2005b). EPA.xls). 1984.6% in NHANES 1988-1991 to 1. Recent studies have suggested that neurodevelopmental effects may occur at BLLs lower than 10 µg/dL (Canfield et al. Korrick et al. 1995. Payton et al..atsdr.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.S.. BLLs reflect both recent intake and equilibration with stored lead in other tissues.... BLLs greater than 10 µg/dL continue to be more prevalent among children with known risk factors.4% in NHANES 1999-2004. Schwartz. 2006).cdc. though there is greater individual variation in urine lead than in blood and greater potential for contamination. reduce sperm count. More recently. when the geometric mean BLL was 2. adult population has similar or slightly lower BLLs than adults in other developed nations (CDC.. 2000).4% of children had BLLs of 10µg/dL or higher (CDC. almost double the geometric mean of 1. including minority race or ethnicity. At low environmental exposures. 1996.. For example. and organic lead compounds not classifiable with respect to human carcinogenicity. 1987. Overall. 2006). Pirkle et al.

Environ Res 2000. Weiss ST.53:411-416.1542/peds:2007-3608. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 2003-2004. Caldwell KL. JAMA 1996. Muller CH. A longitudinal study of low-level lead exposure and impairment of renal function: the Normative Aging Study.htm.htm. 2002 [online]. N Engl J Med 2003. 4/14/09 Centers for Disease Control and Prevention (CDC). Pediatrics 2004. Environ Health Perspect 1993. Baj A. Kaus S. Jusko TA. Payton M. Rios C.115:521-529. Manton WI. Available from URL: http://www. et al. CDC. Hernberg S. Aro A. gov/mmwr/preview/mmwrhtml/mm5420a5.101(7):598-616.287:1-11. 1999-2002. Atlanta (GA). Canfield RL.cdc. Kuehnemann TJ. References Agency for Toxic Substances and Disease Registry (ATSDR). Checkoway H. 2005. et al. The Port Pirie cohort study: lead effects on pregnancy outcome and early childhood development. Scand J Work Environ Health 1984. Cognitive deficits with blood lead concentrations < 10 µg/dL in US children and adolescents. Muntner P. Blood lead levels—United States. Krause C. Hunter DJ. Speizer FE. Neurodevelopmental effects of postnatal lead exposure at very low levels.275(15):1171-1176. Vimpani FB. doi:10. Bellinger D. Recommendations from the Advisory Committee on Childhood Lead Poisoning Prevention. Chiodo LM.atsdr. Sci Total Environ 2002. Public Health Rep 2000. Semen quality of men employed at a lead smelter. Pirkle JL. Sparrow D.26:359-371. Angle CR. Blanco J. Pediatrics 2009. Homa DM. Seiwert M. Am J Epidemiol 1999.87:1-471. Hu H. Ganzi A. McMichael AJ. Stanek KL. Occup Environ Med 1996. IARC Monogr Eval Carcinog Risks Hum 2006. Roberts RR. Blood lead and chronic kidney disease in the general United States population: 216 Fourth National Report on Human Exposure to Environmental Chemicals . Jacobson SW. Adult blood lead epidemiology and surveillance—United States. Trends in blood lead levels and blood lead testing among US children aged 1 to 5 yeas. Schulz C. Hu H.10:43-50. Available at URL: http://www. Am J Public Health 1999. et al.55(32):876-879. Rotnitzky A. Korrick SA. Lead. Atlanta. MMWR Morb Mortal Wkly Rep 2005a. Aug 2007 [online]. Baghurst PA.82:60-80. Leggett RW. Wigg NR. Available at URL: http://www. 4/14/09 Centers for Disease Control and Prevention (CDC).123:e376-e385. Borja-Aburto VH. Korrick S. A prospective follow-up study on psychological effects in workers exposed to low levels of lead.150(6):590-597. et al. Mantere P. 4/14/09 Centers for Disease Control and Prevention (CDC). Reese YR. Vupputyuri S. Lead and hypertension in a sample of middle-aged women. Toxicological profile for lead. Lanphear BP.205:297-308.cdc.htm. Third National Report on Human Exposure to Environmental Chemicals. Acquisition and retention of lead by young children. Hertz-Picciotto I. Henderson CR. MMWR Morb Mortal Wkly Rep 2006. Preventing Lead Poisoning in Young Children. Weiss ST. Inorganic and Organic Lead Compounds. Birth Defects Research (Part A). Intellectual impairment in children with blood lead concentrations below 10 µg/dL. Available at URL: http://www. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Age-specific kinetic model of lead metal in humans. Ga. Jones RL. Cox C. Rojas LM. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Hänninen H. Jacobson JL.gov/nceh/lead/ CaseManagement/caseManage_main. Blood lead reference values: the results of an Italian polycentric study.gov/nceh/lead/publications/ books/plpyc/contents. Centers for Disease Control and Prevention (CDC).89:330-335. 2005b. Teratogen update: lead and pregnancy. Atlanta (GA). Lanphear BP. Sparrow D.54(20):513-516. JAMA 1996. Robertson EF. Kaufman JD.cdc.73:409-420. Kim R. Blood lead levels measured prospectively and risk of spontaneous abortion. Bavazzano P.htm. Lepom P. Int J Hyg Environ Health 2002. Available at URL: http://www. 1991 [online]. Cox C. Brody DJ. Ewers TG. The relationship of bone and blood lead to hypertension.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.gov/toxprofiles/tp13.html.cdc. 4/14/09 Alexander BH. Rotnitzky A.113(4):1016-1022. Luukkonen R. Farias P. Dietrich K. Neurotoxicol Teratol 2004. Apostoli P. van Netten C. Managing Elevated Blood Lead Levels Among Young Children.8(3):395-401.cdc.275:1177-1181. Neurotoxicol 1987. Hu H. Wager C.gov/mmwr/preview/mmwrhtml/ mm5532a2. 1988-2004. Auinger P. Bellinger D.348:15171526. et al. Meyer PA. Cory-Slechta DA. Coresh J. 4/14/09 Centers for Disease Control and Prevention (CDC). Batuman V. Ronchi L. Becker K. Neri A.

Environ Health Perspect 1996.63:1044-1050. Telisman S.S. Arch Environ Health 1995. Amery A. O’Flaherty EJ. Roels H.106:745-750. Flegal AR. Exposure of the U.140:821-829. Gavella M. Fourth National Report on Human Exposure to Environmental Chemicals 217 . Pirkle JL. Sherwin R. Kaufmann RB. Low-level lead exposure and blood pressure. Payton M. Hu H.289(12):1523-1531. Lee BK.209:301305. Hickman T. cadmium.153(5):453464. Environ Health Perspect 2000. dimercaptosuccinic acidchelatable lead. blood pressure. et al. Lauwerys RR. lead. Blood lead. Kidney Int 2003.118:16-29. Lead. Magder L. stable lead isotopes to determine release of lead from the skeleton. Am J Epidemiol 1994. Soldin OP. Staessen JA. et al. Paschal DC. IV. and copper in men. Osterloh JD. Toxicol Appl Pharmacol 1993. population to lead: 1991-1994. Stewar WF. Environ Health Perspect 1998. Hwang KY. Lee SS. blood pressure and cardiovascular disease in men.9:303-327.104(1):60-66. Physiologically based models for bone-seeking elements. Wilhelm M. Soldin SJ. and mercury in blood or urine of children: basis for validation of human biomonitoring data in environmental medicine. Pizent A. Blood lead concentrations in children: new ranges. Smith DR. Clin Chim Acta 2003.327:109-113. JAMA 2003. Int J Hyg Environ Health 2006. Jurasovic J.108(1):45-53. Schwartz BS. Hanak B. Schwartz J. Brody DJ. Weiss ST. Use of endogenous. J Hum Hypertens 1995. and hypertension in perimenopausal and postmenopausal women. Sparrow D. cadmium. Schulz D. Lee GS. 50:31-37.Metals results from NHANES III. Schwenk M. Kinetics of lead disposition in humans. Rubin R. zinc. Lustberg M. Low-level lead exposure and renal function in the Normative Aging Study. Revised and new reference values for arsenic. Association of blood lead. and tibia lead with neurobehavioral test scores in South Korean lead workers. Semen quality and reproductive endocrine function in relation to biomarkers of lead. Am J Epidemiol 2001. Nash D. Gunter EW. Rocic B. Cvitkovic P. Kaufmann R.

1999 .600) 1.500-.80 (3.655-.60 (1. 7439-97-6 General Information Mercury is a naturally occurring metal that has elemental (metallic).300 (. Survey years 03-04 Geometric mean (95% conf.90-3.00) 1.700) .400-. Metabolism of mercury by microorganisms in aquatic sediments creates methyl mercury.814 (.900) 1.60-6.70-2.10-3. synthetic organomercury compounds were once used in pharmaceutical applications.563 (. Woods et al. constitutes the main source of dietary mercury exposure in the general population.419 (. and is distributed to most tissues.10) . Inorganic mercury exists in two oxidative states (mercurous and mercuric) that combine with other elements.30-2.00-1.00 (2.80) 3. The kinetics of the different forms of mercury vary considerably. such as chlorine (e.40-1.300-.30 (2.797 (.800 (. see Data Analysis section) for Survey year 03-04 is 0. Elemental mercury is used to produce chlorine gas and caustic soda for industrial applications.50) 4.363-. elemental mercury is absorbed mainly by inhaling volatilized vapor.40-2. After elemental mercury is absorbed. thermostats and switches). merbromin).50) 2.800 (.. inorganic.70 (4.800-1.60) 2085 2293 3478 Limit of detection (LOD..700-. sphygmomanometers and barometers.80 (1.00 (.776 (. Imported folk and alternative medicines occasionally are contaminated with inorganic mercury.484) .90) 3.00 (2.800-1.700) . 2007).800-1.00-5.60 (1.40) 1.50) 1.500 (.60) 1. with the highest concentrations occurring in the kidneys (Barregard et al.40 (3. Kingman et al.70) 911 856 2081 4525 03-04 03-04 . and organic forms.30) 3. Accidental spills of elemental mercury.90 (1. and dental amalgam.800-1.00) 3..574) . have often required public health intervention (Zeitz et al.500-.40) 3. 2002). Inhalation of elemental mercury volatilized from dental amalgam is a major source of mercury exposure in the general population (Halbach.g. interval) .00 (2.372) . may contain inorganic mercury. Atmospheric elemental mercury can be deposited on land and water. or oxygen.20-4.30) 4132 4241 03-04 03-04 03-04 .600 (. sulfur.800 (.700 (.70 (3. In addition.40 (4.80 (1. to form inorganic mercury compounds or salts.90 (4.20 (2.877 (.00) 1.S.800-1. and mining and smelting.490 (.00) 4.60 (2.800 (.900 (.60-5.900) 75th 1.00 (.30) 1.50-2. Elemental mercury is a shiny. water can be contaminated by the direct release of elemental and inorganic mercury from industrial discharges.500) . electrical lamps..40-2.80) 4.30) 3.2.703-.700-. 1998.40 (3.70 (1.. and mercury compounds are still used as preservatives (e.919) .12) .781 (.. elemental mercury is used in rituals practiced in some Latin American and Caribbean communities. predominantly from fish and other seafood.500 (.50-3.30 (1.g. 1993).753-1. solid-waste incineration. IARC.927) . it is oxidized in Total Blood Mercury—2003-2004 Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U. Hursh et al.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 . 218 Fourth National Report on Human Exposure to Environmental Chemicals . thimerosal.50) 5. silver-white liquid (quicksilver) obtained predominantly from the refining of mercuric sulfide in cinnabar ore.400 (.80 (1. The ingestion of methyl mercury. Apart from methyl mercury.60-2.20-3.30-4.326 (..02) .60-3.300) .60) 1. which can bioaccumulate in aquatic and terrestrial food chains.903) Selected percentiles ( 95% confidence interval) 50th . Some cosmetic skin creams from countries other than the U.700-.00 (1.g.672) .30-6. Poorly absorbed from the gastrointestinal tract. Also.900) 1.S.40 (4.30-5. mercuric chloride). Inorganic mercury compounds such as mercuric oxide are used in producing batteries and pigments and in synthesizing many organic chemicals.60-6.886) .Metals Mercury CAS No. population from the National Health and Nutrition Examination Survey. 1994.900) 1.472-.90 (1..979 (.00) .40-3.700-.00 (.418-. phenylmercuric acetate) or topical antiseptics (e. thermometers.80) 1..900) .860-1.20) 2.70 (1.400-. 1980.40-1.90) 95th 4.20-4.30) 1.700-.90) 90th 3.30) 5. Elemental mercury is released into the air from the combustion of fossil fuels (primarily coal). which create an episodic potential for volatization and inhalation of mercury vapor. Other major uses include electrical equipment (e.689-.00 (.714-.285-.g. an organic form of mercury.50-1.

1996.90) 5.40-2.833 (.30-2.50-3.20) .70-6. Sandborgh-Englund et al.200 (.70) 4.919) .70-3.299-.00-2.. 2005).00 (2.90 (4. The slow-phase half-life may be several weeks longer in persons with chronic occupational exposure (Sallsten et al. and the newborn’s levels decline gradually over several weeks (Bjornberg et al..10-1. 1984.90 (4.200-.3) 4.10 (1.70 (1.800 (.30 (1. Excretion occurs by renal and fecal routes..10-3. Miettinen et al.500-.23) .329 (.06 (.300) .30-3.30) 1. with most elimination occurring through in the feces (Sherlock et al.00-1.10 (.30) 1.300 (.90) 2.73) 1. 1971).14.40-1.700) 2..500 (.00) 1.60 (1.00 (2.944 (.50) 3.317 (.900 (.70-5.600 (. Smith and Farris.374) .50) 95th 2.377) .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 .300) . Geometric mean Survey years (95% conf.269-. excretion of mercury occurs predominantly through the kidney (Sandborgh-Englund et al.700-.30-5. 1996). Less than 15% of inorganic mercury is absorbed from the human gastrointestinal tract (Rahola et al.800) 75th .377 (..60) 2.300) .900-1.27) .00-2..369) 1.500-1.700 (.20-2. 1994.800) 1.80) 1.90) 90th 1. Mercury levels in the cord blood are higher than in the mother’s blood (Stern and Smith.871-1. Jonsson et al. 1998).. 1993).01) .664-1. 1975...900 (.40) 5.200-.20 (.00) 4.00 (3.00) . 1993).10 (5. 1995.600) . Vahter et al. for both acute and chronic exposures..40-2.. population.30-4.50 (2. 1969.50-2.90) 3..407) .40 (1.307 (. The fraction of methyl mercury absorbed from the gastrointestinal tract is about 95% (Aberg et al.50 (1.10 (3.00) 6.60) 1.70-5. 1994) and then undergoes slow dealkylation to inorganic mercury.90 (3.268-.800-1.200 (. the transfer Total Blood Mercury−1999-2002 Geometric mean and selected percentiles of blood concentrations (in µg/L) for males and females aged 1 to 5 years and females aged 16 to 49 years in the U. 1992). The half-life of inorganic mercury in blood is similar to the slow-phase half-life of mercury after inhalation of elemental mercury.90) 2.. 1973).318 (.70 (1. 1990).80 (1..10 (.20-3.900 (..800 (. 1999).800-1.40) 1. thereafter. Methyl mercury enters the brain and other tissues (Vahter et al.29) .825-1.00-3.60 (3.60 (3. Transplacental transport of methyl mercury and elemental mercury has been demonstrated in animals (Kajiwara et al. and a useful marker of exposure in epidemiologic studies (Grandjean et al. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. a measure of accumulated dose (Cernichiari et al.80) 579 527 370 436 588 806 Limit of detection (LOD.500-. Human pharmacokinetic studies indicate that methyl mercury declines in blood and the whole body with a half-life of approximately 50 days.30-6.20-3.00 (1. National Health and Nutrition Examination Survey.265-.500-. McDowell et al..500 (.700-1. Myers et al.800 (..06-1. 2003).14 and 0.20-3.00-6.726-1.20) .90 (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.395) .667 (.700 (.80-3.80 (3. Fourth National Report on Human Exposure to Environmental Chemicals 219 . 1999-2002.S.02 (. 1991.30-4.541-.700-. Vimy et al.738-.7) 4.200-.30 (1.475) .00-2.256-.90 (1. 2004.400-.50) 2.40 (1.60 (1.60 (1..200-.700-1. Smith et al.300) . 1992 and 1999.70) 1.697-.300 (.30-11.20-11.30 (1.500-.30 (.500-. After exposure to elemental mercury.820 (.20 (2.10) .35 (1..70-3. 1992.200-.600) . Suzuki et al.0) 4. 1998).Metals the tissues to mercurous and mercuric inorganic forms. 2003).700 (.70) 4.00) 7.10) . Lesser penetration of inorganic mercury occurs through the bloodbrain barrier than occurs with either elemental or methyl mercury (Hattula and Rahola. and peak urine levels can lag behind peak blood levels by days to a few weeks (Barregard et al.800-1.940) Race/ethnicity (females.700 (.30-6.60) 3. interval) Selected percentiles (95% confidence interval) 50th .00 (2.50) 1.800) 1. 1994).60 (2.50) 1.50-12..10 (1.30) 3.10) 1.300) .30-6.10 (1.300 (. Inorganic mercury and methyl mercury are distributed into human breast milk in relatively low concentrations.00) 1.60) 1.824) 1.20) 1.900-1.00) 2..300) .800) .40) 2.70 (1.297-.. urinary mercury levels decline with a half-life of approximately 1-3 months (Roels et al.200-. 16-49 years) Mexican Americans Non-hispanic blacks Non-hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 . Methyl mercury is incorporated into growing hair.300 (.800) .343 (.

500 (. Large amounts may cause irritant or corrosive effects on the gastrointestinal tract (Sanchez-Sicilia et al. short-term memory loss. Once absorbed. maculopapular rash. Acute.600 (. the existence of a causal relation is unresolved (Chan and Egeland. At levels below those that cause acute lung injury. 2006.800) .600-. ataxia.Metals may be more efficient for inorganic mercury (Grandjean et al.600) .600 (.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 . 220 Fourth National Report on Human Exposure to Environmental Chemicals . Occupational exposure to elemental mercury vapor has been associated with subclinical effects on biomarkers of renal dysfunction (Cardenas et al. cerebellar ataxia. dysarthria.700-.. Stern 2005.500-..500) .S. < LOD means less than the limit of detection.500-.500-. 1998.800) 4015 4132 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD . Oskarsson et al..800) 792 842 2060 4453 03-04 03-04 * * < LOD < LOD < LOD < LOD . see Data Analysis section) for Survey year 03-04 is 0. typically after a latent period of weeks to months.. In recent epidemiologic studies.600) .700 (. dysarthria. gingivitis..700-. which may vary for some chemicals by year and by individual sample.600) . 1995. 2005).600 (.600 (. fatigue.. 1951. lower levels of prenatal exposure due to maternal seafood consumption have been associated with an increased risk for abnormal neurocognitive test results in children (NRC. Inorganic mercury exposure usually occurs by ingestion. and pinkish discoloration of the hands and feet (Tunnessen et al.700 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 2000. 2004. altered physical growth. Low-level exposure from dental amalgams has not been associated with neurologic effects in children or adults (Bates et al. 1996).500-. 2003).600-. Sakamoto et al. high-dose exposure to elemental mercury vapor may cause severe pneumonitis. hearing impairment.700-. Smith et al. Factor-Litvak et al. High-level prenatal exposure may result in a constellation of developmental deficits that includes mental retardation.. depression.600-.500-. 1993). insomnia. and neurocognitive and behavioral disturbances.600) .500 (<LOD-. Rice. and sleep disturbance (Bidstrup et al. overt signs and symptoms of chronic inhalation may include tremor. The constellation of findings may include anorexia...600 (. 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.. Drexler and Schaller. pain in the extremities. Smith et al. Bellinger et al. particularly irritability. hypertension. 2004.700 (.500 (<LOD-. and a drinking water Inorganic Blood Mercury Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U. Rissanen et al. and progressive constriction of the visual fields.600) . causing parasthesias.. 2000. sensory impairments. DeRouen et al. 2004). limb deformities. Sakamoto et al. population from the National Health and Nutrition Examination Survey.600) . 2006. irritability.600 (. 1987). Survey Geometric mean (95% conf. 2002. Vupputuri et al.700 (.600) .500 (.600-. 1970.700) . the most prominent effect is on the kidneys where mercury accumulates and may lead to renal tubular necrosis. 1963). Mercury levels in breast milk also decline in the weeks after birth (Bjornberg et al.500-.600) .700) 2007 2240 3406 Limit of detection (LOD. Acrodynia is a sporadic and predominantly pediatric syndrome historically associated with calomel (mercuric oxide) in teething powders and occasionally other inorganic forms of mercury. Although recent investigations have suggested a possible link between chronic ingestion of methyl mercury and an increased risk for cardiovascular disease. Overt poisoning from methyl mercury primarily affects the central nervous system..500-.600) . Workplace standards for inorganic mercury exposure have been established by OSHA and ACGIH..700 (..42.500-. 2000).600 (. 1983). Salonen et al. and cerebral palsy (NRC.700 (.600 (.600) * 03-04 03-04 03-04 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .800) . 1995..500-.. 2004)... interval) Selected percentiles ( 95% confidence interval) Sample 95th . anorexia. 2005.

However. Among the three racial/ethnic groups.78 µg/L for adults and 0.382-.890 (.55 µg/L. 2009). 2002). although non-Hispanic black females had higher levels than non-Hispanic white or Mexican American females. 758 children. Clinically observable signs of ataxia and paresthesias may occur when blood mercury levels increase to approximately 100 µg/L after methyl mercury poisoning.97) 2.60-2. Kingman et al. military veterans (mean age 52. Urine mercury levels increase as more occlusal surfaces of teeth are filled with mercury-containing amalgams (Becker et al. In NHANES 19992002..840-1.34-3.Metals standard for inorganic mercury has been established by U.700-1.60) 619 713 1066 Limit of detection (LOD.509) .54 (2.76-3. total blood mercury geometric mean levels in females aged 16-49 years did not change.495 (.447 (.cdc.S. 2009). 1997.480) 75th 1.405-.330-.13-2.99-6.S.360 (.14. Over the NHANES 1999-2006 survey periods. et al.492) Selected percentiles ( 95% confidence interval) 50th .05) 1. Mahaffey et al.358 (. Benes et al..460) . Schober et al.290-.. average age 9.90) 2. environmental levels) and health effects is available from the U.408) .330-.gov/toxprofiles.9 years).e.52) 2.930-1. and the age-related changes differed across the groups (Caldwell et al.08 (1. From 1996 through 1998.epa.570) .08 (1.413-..03-4.26 (1.330 (.09 (2.S.78-2.463) .. aged 18 to 69 years.440 (.89) 3.85-2..S.430 (.430) . 2001. 1998).360-.480 (.42) 95th 3.12 (. Grandjean et al.23) 2. the total blood mercury concentration is due mostly to the dietary intake of organic forms.530) .14-2. 1995.60 (1.160-.420 (.213-.19 (1. who participated in a 1998 representative population survey (Becker et al.. 2003).46) 3. Information about external exposure (i.65) 1.31) 1266 1272 03-04 03-04 03-04 .76-4.960 (. 2003).870-1.304) .39-3.07 (.840-1.530-. the developing fetus may be the most susceptible to the effects of ongoing methyl mercury exposure (NRC.8 years.gov/mercury and from ATSDR at: http:// www. A cohort of 1127 U.313-.96 (1.549) .555) . total blood mercury increased with age.67-2. Urinary mercury consists mostly of inorganic mercury (Cianciola et al.00 (.29) 1. population from the National Health and Nutrition Examination Survey. slightly higher total blood mercury levels were found in U..19 (2.68 (2.410-. Biomonitoring Information In the general population.S. IARC considers methylmercury to be a possible human carcinogen and elemental and inorganic mercury to be unclassifiable with regard to human carcinogenicity. During the same survey periods.520) .534) .24 (2.254 (.14) 90th 2.16 (1.61) 1.66) 3. total blood mercury levels declined slightly in non-Hispanic black and Mexican American children. and increased slightly in non-Hispanic white children (Caldwell.33 (2. adult women in several ethnic subgroups (Hightower et al.20 (1.250) .77-2. 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.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 .770-1.416 (.. the median concentration of blood mercury was 0. 1998).280-.433 (.28) 1.530) . Urinary Mercury—2003-2004 Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. In Germany the geometric mean for blood mercury was 0.441 (.23) .24) 1.360-.330-.610-1. EPA.580) . (2000) studied 1216 blood donors in the Czech Republic (896 men and 320 women. 2000).31) 2. 2004.460 (. EPA at: http://www. average age 33 years. range 40 years to 78 years) had an average total blood mercury concentration of 2.46 µg/L for children.58 µg/L for 4645 adults.00) 1. particularly methyl mercury. Fourth National Report on Human Exposure to Environmental Chemicals 221 . 2001. interval) .420 (..840) 1. These men had no occupational exposure to mercury but previously had received dental amalgams at military facilities (Kingman et al.93 (1.700 (. These distinctions can help interpret mercury blood levels in people.940 (. Survey years 03-04 Geometric mean (95% conf.442-.88 (1.200 (.76-3.88) 287 722 1529 03-04 03-04 .01 (.509) .88-3.430 (. Sanzo et al.370) . Total blood mercury levels increase with greater fish consumption (Dewailly et al.476 (..396-.67-3.870-1.340-.. see Data Analysis section) for Survey year 03-04 is 0.16 (.05) 3.96 (1.30) 3.atsdr.400 (.18) 2. 2006).63-2.350-.406-...

et al.476 (. 2009).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 .652) .969-1.54 (2.566) . Department of Health and Human Services noted that several studies have observed a modest. Finding a measurable amount of mercury in blood or urine does not mean that the level of mercury causes an adverse health effect.12-3. Information about the biological exposure indices is provided here for comparison.32 (1.46-2.11) 2.246-.485 (.784) 1.275) .455-.455) .365 (. 2002) adult population surveys were similar to those in a U.588) .537) . interval) .392-.443 (.1 µg/L for each surface with a dental amalgam (Kingman et al. et al.447 (.368) . population from the National Health and Nutrition Examination Survey. among workers with urinary mercury concentrations of 25-35 µg/L or greater (Barregard et al.696 (.00 (. 1988.365 (. Urinary mercury levels in recent German (Becker et al.79 (1. 2009)...616) . and on average. 2006).04-3. The ACGIH (2007) currently recommends that urinary inorganic mercury in workers not exceed 35 µg/g of creatinine. 2003).87 (1.35 (1.532 (.306 (.07) 1. 1998).S.376-.486) Selected percentiles ( 95% confidence interval) 50th .13 (1.587 (.343 (.472-.76 (1. 1992).11) 1.714-1.404-.909 (.88-2.391) .619-. not to imply a safety level for general population exposure.23-2. reversible increase in urinary N-acetyl-glucosaminidase. Urinary Mercury (creatinine corrected)—2003-2004 Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.964-1. Urine mercury and the number of dental amalgams were correlated.970 (.522-.78-4.400) .77 (2.358) .265-.875-1.289) .525 (.280-.347) .333-.255 (.301-.30) 2.400-.385-.464 (. Langworth et al. 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. Biomonitoring data will also help scientists plan and conduct research on exposure and health effects..225-.61) 1. 2002).196-.64-2.03) 2.362 (.67 (1.785-1.13-2.217 (. DeRouen et al.40 (1.40-1.620-.417) .447-.31 (1. military veterans with dental amalgams.687) .21) 1.208-.30) 1.86) 95th 2.79) 1.768 (.667-1.307-.16) 1.S. ACGIH recommends that the blood levels due to inorganic mercury exposure in workers not exceed 15 µg/L.800-1. Czech (Benes et al.Metals 2000).41-2.67 (1.87) 2.S.63) 1.11-2.09) 1.455-.391-.44) 1. a biomarker of perturbation in renal tubular function.56) 1266 1271 03-04 03-04 03-04 .28 (. An expert-panel report recently prepared for the U.00) 90th 1.1 µg/L.06 (.S.32-2.297 (. and Italian (Apostoli et al.599) .18-1.88 (1.90) 618 713 1066 222 Fourth National Report on Human Exposure to Environmental Chemicals .276 (.535) 1.630) .62 (1..498) 75th . Levels in U. the urine mercury increased by approximately 0.. representative sample of women aged 1649 years reported in NHANES 1999-2006 (Caldwell.00) 286 722 1529 03-04 03-04 ..480) .545 (.463 (. Survey years 03-04 Geometric mean (95% conf.990) .S. In the study of U.06 (.65 (1.25 (. Blood mercury levels of women and children in NHANES 19992006 were also below levels established as occupational exposure guidelines (Caldwell.508 (. women of childbearing age have generally been much lower than these levels (CDC. Recent studies in children with dental amalgams and urinary levels less than 5 µg/g of creatinine did not have changes in cognitive-behavioral testing when followed for 5-7 years (Bellinger et al. 2006. mean urinary mercury was 3..51-2.309-.. 2005).39) 1.88-2.01) 2..384 (..

24-1. 16-49 years) 99-00 01-02 . 16-49 years) 99-00 01-02 . Geometric mean Survey years (95% conf.909-1.41 (2.32-3.631-.76 (1.27 (1.25) 2.61) 1.62 (3.00 (3. interval) Selected percentiles (95% confidence interval) Survey years 50th .580-.03-2.14-1.620 (.650 (.624-.61-6.45-3.89 (2.98 (5.76-5.578-.636-. 1999-2002.596 (.04-1.686) .615 (.84 (2.35) .97 (1.610-.560 (.55) 90th 3.65) 1.670) 75th 1.50 (2.42) 90th 2.710 (. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.48 (2.79) 1.24) 6.70 (2. National Health and Nutrition Examination Survey.94) 1.56) 4.21 (1.S.502-.56 (1.44) 3.53-3.37 (1.06 (.35 (1.31 (1.03 (.809) .600 (.832-1. population.790) .76) 2.56) 3.616-.520-.831) .580 (.500-.10-4.07-5.03) 1.655 (.721 (.14 and 0.637) .91 (2.870) .744) 1.522 (.28 (1.51 (3.41 (1.709) 75th 1.85-3.15-1. 1999-2002.72) 1.685 (.99 (2.38) 4.87-4.46 (1.39) Sample size 1748 1960 Age group (females) 16-49 years Race/ethnicity (females.23-1.710) 1.23-1. interval) Selected percentiles (95% confidence interval) 50th .Metals Urinary Mercury−Females Aged 16-49 Years Old.806) .62 (4.50 (1.910) .S.42) 2.30-2. 1999-2002 Geometric mean and selected percentiles of urine concentrations (in µg/L) for females aged 16 to 49 years in the U.68) 3.69 (1.475-.53) 595 531 381 442 594 826 Fourth National Report on Human Exposure to Environmental Chemicals 223 .47) 1.51) .07-2.420-.79) 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.22-3.691) .13 (2.30 (2.799) .81-6.665) Mexican Americans Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .97) 2.664) .740 (.68 (3.03 (.719 (.27 (2.52) 3.592 (.43-1.664) Mexican Americans Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .00 (2.709) .41 (1.99 (3.45) 2.658 (.45-2.77) 2.639 (.00) 2.14.09-1.14) 3.565 (.92) 2.426-.65-4.55-3.3) 5.824) .656-.77) 1.85) 4.97) 2.57-4. National Health and Nutrition Examination Survey.32) 2.760 (.540-.39-3.21-3.32 (1.526-.27-1.13-4.92) 3.569-.46) 3.650) 1.46-4.892) .18 (3.553-.59-5.99) 1.387-.605-.50-4.42-3.706 (.810) .07) 1.17) 95th 5. Geometric mean (95% conf.650 (.508-.62 (1.850-1.84 (2.41-6.21 (2.723 (.606 (.16-5.632 (.724 (.63) Sample size 1748 1960 Age group (females) 16-49 years Race/ethnicity (females.68-3.742-1. population.966) .930) .45) 95th 3.30 (1.18) 3.657 (.665) .699) 1.516 (.83-3.47) 1.410-.91-7.557-.774) .69-3.450-.14-2.99-2.560-.95 (2.45 (1.15 (2.05 (2.16) 5.81 (3.22 (.45) 2.97) 2.501-.04-10.92) 4.772 (.622-.54) 595 531 381 442 594 826 Limit of detection (LOD.31-1. Urinary Mercury (creatinine corrected)−Females Aged 16-49 Years Old.831) .09-1.833) .710 (.10-2.30 (2.579-.582-.05 (3.520-.37) 1.846) .540 (.

113(10):1381-1385. White RF. Snihs JO.205:297-308. Bellinger DC. Drago I. Aposian HV. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Drexler H.S. Chronic mercury poisoning in men repairing direct-current meters. Tavares M. Sandborgh-englund B. population: 19992006. Environ Health Perspect 2003. Health effects of dental amalgam exposure: a retrospective cohort study. Budtz-Jorgensen E. Mercury derived from dental amalgams and neuropsychologic function. Brewer R. Methylmercury exposure biomarkers as indicators of neurotoxicity in children aged 7 years. Sallsten G.289:1324. Luis H. Weihe P.212:588-598.33:1-9. Gagliardi T. Hasselgren G.72:169-173.19:478-484. Becker K. Berglund B. The mercury concentration in breast milk resulting from amalgam fillings and dietary habits. Apostoli P. Leitão J.2:856-861. Niklasson B. Conradi N. Monitoring methylmercury during pregnancy: maternal hari predicts fetal brain exposure. Impact of maternal seafood diet on fetal exposure to mercury.50:17-27. selenium. Bidstrup PL. Int J Hyg Environ Health 2009. Videro T. Kinetics of mercury in blood and urine after brief occupational exposure. Vahter M. Martin MD. Sallsten G. Zn. et al. Mortensen ME. Krause C. Sallsten G. 2005. Mangili A. Clarkson T. Schaller KH. Seiwert M. Jacobs D. Woods JS. and Se in blood of the population in the Czech Republic. Schulz C. Myers GJ. and lead. Jones RL.56(4):350-357. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Debes F. Cent Eur J Public Health 2000. Exposure of the Inuit population of Nunavik (Arctic Quebec) to lead and mercury. Int J Epidemiol 2004. Locket S. Bonnell JA. Skerfving S. Persson G. Begg M. Caldwell KL. Am J Epidemiol 1999. Cernichiari E.8(2):117-119. Cernichiari E. Based on the Documentation of the Threshold Limit Values for Chemical Substances and Physical Agents and Biological Exposure Indices. Kaus S. and heart diseases. Cerna M. Ayotte P. Pb. Factor-Litvak P.Metals References Aberg B. Greitz U. Grandjean P. Arch Environ Health 1992. Ekman L. Centers for Disease Control and Prevention (CDC). Cutress T. Atlanta (GA). et al. Weihe P.61:65-69. Lancet 1951. Echeverria D. Int JHyg Environ Health 2002. Chan JM. Hultberg B. Schuzt A. Biennow M. Cincinnati (OH): Signature Publications. et al. Barregard L. 2007 TLVs and BEIs. Hg. Neurotoxicology 1995.62(2):68-72. Bernard AM. Neuropsychological and renal effects of dental amalgam in children: a randomized clinical trial. Garrett N. Martin MD. Cardenas A. Environ Res 1998. Enzymuria in workers exposed to inorganic mercury. Barregard L. Application to workers exposed to mercury vapour. Cortesi I. Smid J.149:301-305. Elia G.7(3):176-184. Harvey DG. J Toxicol Environ Health 1997. Bernardo M. Schutz A. Kjellstrom T. Osterloh JD. Levallois P. Attewell R. Buchet JP. Rosenbaum G. Schulz C. Barregard L. Arch Environ Health 1992. The concentration levels of Cd. Assessment of reference values for mercury in urine: the results of an Italian polycentric study. Trachtenberg F. Arch Environ Health 1969. et al.295(15):17841792. Cu. Sci Total Environ 2002. Lepom P. et al. Grandjean P. Spevackova V. Transport of methylmercury and inorganic mercury to the fetus and breast-fed infant. Cernichiari E. Marsh DO. Int J Hyg Environ Health 2003. Caudill SP. Bruneau S. 224 Fourth National Report on Human Exposure to Environmental Chemicals . Daniel D.295(15):1775-1783. Total blood mercury concentrations in the U. Arch Environ Health 2001. Geier J. Townes BD. Lebel G. McKinlay S. Lauwerys RR. Benes B. Br J Ind Med 1993. Becker K. JAMA 2006. Seiwert M. Egeland FM.. mercury exposure. Jorgensen PJ. 206:15-24. Bjornberg KA. Metabolism of methyl mercury (203Hg) compounds in man. Weber JP. et al. Cianciola ME. Barbon R. Martins IP.111:719-723. Jorgensen PJ. JAMA 2006. Fawcett J. Int Arch Occup Environ Health 1988. Roels H. I. Woods JS. Bates MN. Kaus S. Falk R. Seifert B. Third National Report on Human Exposure to Environmental Chemicals. et al. Barregard L. Lapham LW. Castro-Caldas A. Nutr Rev 2004. ACGIH. Dewailly E.77(2):124-129. Cejchanova M. Markers of early renal changes induced by industrial pollutants. Fish consumption. Epidemiologic assessment of measures used to indicate lowlevel exposure to mercury vapor (Hgo).16(4):705-710.47(3):185-195. Kline J. Tissue levels of mercury determined in a deceased worker after occupational exposure. Environ Health Perspect 2005. Int Arch Occup Environ Health 1999. 52:19-33. DeRouen TA. Leroux BG. Neurobehavioral effects of dental amalgam in children: a randomized clinical trial. Cox C. Jarvholm B. Subrt P.

Sundquist KG. Mercury in biological fluids after amalgam removal. Voutilainen S. and any death in eastern Finnish men. Toxicol Appl Pharmacol 1999.90:185-189. J Dent Res 1998. Brown LJ. Patterson DG Jr. Relation of a seafood diet to mercury. Native American.59(5):692-706. Arch Toxicol 1996. Amalgam tooth fillings and man’s mercury burden.214(3):520-527. Greenwood MR. Pacific Islander. et al. Hattula T. Ceulemans E. Adachi T. Elimination of 203Hg-methyl mercury in man.77(4):615-624. Hum Exp Toxicol 1994. Ohlin B. Fernando R. Decrease in mercury concentration in blood after long term exposure: a kinetic study of chloralkali workers. 2000. Barregard L. O’Hare A. Seto DS. Washington (DC). Environ Health Perspect 2006. children and women of childbearing age: reference range data from NHANES 1999-2000. cardiovascular. Cadmium. Skerfving S. Environ Res 1995. Boeckx M. Urinary excretion of mercury after occupational exposure to mercury vapor and influence of the chelating agent meso-2. J Pharmacol Exp Ther 1980. Environ Health Perspect 2004. et al. Beryllium. Ann Clin Res 1973. arsenic. Kolff WJ. and Exposures in the Glass Manufacturing industry.361:1686-1692.155(2):161-168. Blood organic mercury and dietary intake: National Health and Nutrition Examination Survey. Elinder CG. Br J Ind Med 1991.49(6):394-401. Davidson PW. Oskarsson A. Demuth S.103:2766-2679. Murata K. Mercury concentrations in urine and whole blood associated with amalgam exposure in a US military population.71(1):29-38. Satoh H.77(3):461-467. Mercury. Hernandez GT. Hightower JM. Environ Res 2004. Schutz A. Seppanen K. selenium. Lancet 2003. Korolainen A. Elinder CG. Schutz A. Clarkson TW. Korpela H. Lauwerys RR. Nyyssonen K.3(2):116-122. National Academy Press. Circulation 2000. Shamlaye CF. Rahola T.51(3):234-241. Cox C. Rahola T. Sakamoto M.iarc. Lagerkvist BJ.91:645655.Metals Grandjean P. The distribution and biological half-time of 203 Hg in the human body according to a modified whole-body counting technique. Sampson EJ. Weihe P. and multiracial groups. Rahola T. Circulation 1995. Declining risk of methylmercury exposure to infants during lactation. 1999 and 2000. Arch Environ Health 1996.70(5):310-314. Clickner RP. Burse VW. et al. Lakka TA. Kubota M. Nakai K.fr/ENG/Monographs/vol58/index. A compartmental model for the kinetics of mercury vapor in humans. Pellizzari E. Rice DC. and the risk of myocardial infarction and coronary. Elimination of free and protein-bound ionic mercury (203Hg2+) in man. Tillander M. docosahexenoic acid and docosapentaenoic acid. The US EPA reference dose for methyl mercury: sources of uncertainty. Kubota M. Hattula T. IARC Monographs on the Evaluation of Risks to Humans. Schultz A. Kantola M. Hursh JB. Kauhanen J. Rissanen K. Sandborgh-Englund G. Myers GJ. Hattula T. Environ Sci Technol 2004. Br J Ind Med 1993. Allen J. et al.114(2):173-175. and the risk of acute coronary events— The Kuopio Ischaemic Heart Disease Risk Factor Study. Bodurow CC. Br J Ind Med 1992. Sakamoto M. Toxicological effects of methylmercury. Sallsten G. Fish oil-derived fatty acids. Halbach S. Akagi H. Renal and immunological effects of occupational exposure to inorganic mercury. Hair mercury levels in U. Vesterberg O. Environ Physiol Biochem 1975. Miettinen JK. Dillon CF.5:252-257. Environ Health Perspect 2004.48:247-53. Sandborgh-Englund G. Kingman A. Needham LL. International Agency for Research on Cancer (IARC). Rissanen T. Nyyssonen K. Nakano A. The effect of ethanol on the fate of mercury vapor inhaled by man. Nakamoto S. Langworth S. lipid peroxidation. Langworth S. Salonen JT. Cernichari.13:496-501. Mehaffey KR. Liu XJ. Roels HA. Johanson G.95:406-13. Yasutake A. Sanchez-Sicilia L. 1993. Ann Clin Res 1971. Miettinen JK. Hallen IP. J Dent Res 1998.5:214-219.38:3860-3863. Fourth National Report on Human Exposure to Environmental Chemicals 225 . Salonen JT. Total and inorganic mercury in breast milk and blood in relation to fish consumption and amalgam fillings in lactating women. Ann Intern Med 1963. methylmercury transport across the placenta via neutral amino acid carrier. National Research Council (NRC). Osterloh J. Blood mercury reporting in NHANES: Identifying Asian.112(5):562-570. Palumbo D. Hirayama K. Environ Res 2002. Albertini T. Prenatal methylmercury exposure from ocean fish consumption in the Seychelles child development study.S. Intake of mercury from fish.3dimercaptosuccinic acid (DMSA).50(9):814-821. Available at URL: http:// monographs. Maternal and fetal mercury and n-3 polyunsaturated fatty acids as a risk and benefit of fish consumption to fetus. 7/15/09 Jonsson F. Acute mercurial intoxication treated by hemodialysis. and polychlorinated biphenyl and other organochlorine concentrations in human milk. McDowell MA. Ekstrand J. Matsumoto S. Bolger PM. KajiwaraY.112(11):1165-1171. Volume 58.php.

4(5):981-988. Vupputuri S. Environ Health Perspect 2007. Environ Res 2005. Goldberg J. Mooney TF. Public Health Nutr 2001. Toxicol Appl Pharmacol 1994. Amurrio A. Speciation of mercury in the primate blood and brain following long-term exposure to methyl mercury. The contribution of dental amalgam to urinary mercury excretion in children.110:129-132. Lind B. Hongo T. Farris FF. Vahter M. Am Ind Hyg Assoc J 1970. Orr MF. Amiano P. Estimation and validation of mercury intake associated with fish consumption in an EPIC cohort of Spain. Yoshinaga J. Smith PJ.Metals Sanzo JM. Martin MD.289(13):1667-1674. Acrodynia: exposure to mercury from fluorescent light bulbs. Blood mercury level and blood pressure among US women: results from the National Health and Nutrition Examination Survey 1999-2000. et al. Elevation of mercury in human blood from controlled ingestion of methyl mercury in fish. Takahashi Y. Patil LS. Am J Physiol 1990. Environ Health Perspect 2003. Azpiri MA. Guo S. Dorronsoro M. Tunnessen WW. Sinks TH. Suzuki T. Leroux BG. Blood mercury levels in US children and women of childbearing age. McMahon KJ. 1993-1998. Woods JS. Langolf GD. Pediatrics 1987. Environ Res 2005. Bernardo MF. Burbacher T.31:687-700. Leitao JG. Sherlock J. Mottet NK.37:245-252. McDowell M. Effects of exposure to mercury in the manufacture of chlorine. Methyl mercury pharmacokinetics in man: a reevaluation. Longnecker MP. Sandler DP. DeRouen TA.128(2):25125-25126. Imai H. Most B. Effects of occupational exposure to elemental mercury on short term memory. An assessment of the cord blood: maternal blood methyl mercury ratio: implications for risk assessment. Kaye WE.258(4 Pt 2):R939-945. Bolger PM. Matsuo N. The kinetics of intravenously administered methyl mercury in man. Whittle K. Smith AE. Lorscheider FL. Friberg L.48(4):221229. et al. Hislop D. 1999-2000. JAMA 2003. Arch Environ Health 1993. Daniels JL. Zeitz P. Topping G. A review of the studies of the cardiovascular health effects of methylmercury with consideration of their suitability for risk assessment.115(10):1527-1531.124:221-229. Fisher HL. Toxicol Appl Pharmacol 1994. Hall LL. Turner MD. Smith JC.98(1):133-142. Shen DD. Aguinagalde FX.40:413-419. Nakazawa M. 226 Fourth National Report on Human Exposure to Environmental Chemicals . Baser M. Smith JC. Maternal-fetal distribution of mercury (203Hg) released from dental amalgam fillings. Smith RG. Toxicol Appl Pharmacol 1996. Stern AH. et al. Public health consequences of mercury spills: hazardous substances emergency events surveillance system. Hum Toxicol 1984. Newton G. Jones RL.97(2):195-200. Stern AH. Vorwald AJ. Br J Ind Med 1983.2:117-131. Schober SE. Osterloh J. Vimy MJ.79:786789.111(12):1465-1470. Allen PV. The hair-organ relationship in mercury concentration in contemporary Japanese. Environ Health Perspect 2002.

5-46.4) 49.0 (43.7 (58.2-59.3) 37.3 (46.3) 54.6 (43.2) 52.3 (38.1 (91.9 (73.1) 35. aldehyde dehydrogenase.0) 60.6 (73..7) 75th 84. see Data Analysis section) for survey years 99-00.4-75.5-41.5 (37.5 (43.9) 34. chemical reagents in hospital laboratories.8 (67.1-59.9 (34.9 (40. and xanthine oxidase (Kisker et al.0) 84.8) 48.1-52.5 (74.0 (48.2 (61.5) 47.3 (79.6) 71.2-70.6 (40.9-82.6) 53.7) 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 78.1 (34.4-82.4) 45. and the average dietary daily intake of molybdenum is approximately 100 µg/day (IOM.5-52.9-55.1 (38.6-42.9-85.8 (82.7) 57.7-91.6) Selected percentiles ( 95% confidence interval) 50th 50.1-52.9 (32.3) 90th 135 (125-146) 124 (117-130) 111 (105-118) 95th 180 (154-216) 165 (145-176) 138 (133-146) Total 45.0) 55. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.0-38.8) 46.3-115) 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.0 (76.2 (63. hard metal widely used to add strength and hardness and retard corrosion in metal alloys.6-46.5 (67.0-62.7) 46.6 (52.7) 86.6 (40.3 (55.4 (48.2) 41.6) 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 (99.7-84.7 (36.5) 80. hydrogenation catalysts. and paints.1 (71.5 (41.7-39.2 (83. The recommended dietary allowance for adult men and women is 45 µg/day (IOM.3) 83.6-62.1) 57.Metals Molybdenum or ore deposits.7-92.5 (49.9-55.3 (37.8) 39.6) 93.2 (40.9 (37.4 (48.9 (33.4 (79.3) 85.1-48.6-58. Compounds of molybdenum are also used as corrosion inhibitors.2 (38.0 (81.3 (53. More recently.9-109) 97.1-88.0-77.3 (84. respectively.4) 42.7 (37.0) 97.1) 126 (106-147) 109 (94.9 (44.7 (44.7 (51.2) 40. 2001).0) 45.4) 52.7) 78.9) 67. Gastrointestinal absorption of molybdenum averages 8893% for dietary intakes of 22-1490 µg/day.5 (81.3 (55.8) 75.0) 62. inks.3 (64.0-71.2) 150 (128-187) 130 (120-141) 119 (112-130) 119 (105-138) 115 (104-128) 101 (97.2 (49.2 (55.0 (41.3-44.2 (69.0-110) 90.9-56.8-94.1) 60.8 (85. lubricants.1-55. 1996).7-51.6-82.2-79.2) 53.3 (71.3) 65.9-83.7) 51.7-122) 93. Fourth National Report on Human Exposure to Environmental Chemicals 227 .8) 44. Excretion occurs predominantly via the kidneys.4-52.8) 40.1) 46.9 (52.3) 47.5) 44.1) 59.4) 76.1) 82. WHO.5-52.5) 85.2) 79.3-91.9) 62.2) 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 (98.7-73.7) 77.7 (73.8-108) 87.0-100) 63.8-90.3-75.6-96.3-108) 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 47.7-41.0 (42.1-44.5-65. 2001. which exert homeostatic regulation over molybdenum balance.7 (45.5 (48.3) 41.8 (42.6 (55.0) 54. Molybdenum is a nutritionally essential trace element that enters the body primarily from dietary sources. 7439-98-7 General Information Elemental molybdenum is a silver-white.0-56.2) 37. In humans.7) 45.3-47.1-51.8. 0.3 (73. 01-02.7) 78.7-105) 69.7 (71.5-124) 108 (92.7-47.6-111) 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 52.4 (80.0-65.7-60.4 (72.6) 51.2-53.9 (78.5 (41.7-96.8-46.2 (49.0-85.5) 60.5-68.S.4 (34.8-49.5) 80. interval) 45.4-61.0-101) 82.5-91. population from the National Health and Nutrition Examination survey.6-55.5-66.4) 56. and 03-04 are 0.7-50.5.8.2-42. semiconductor and battery industries have begun to use molybdenum.2-37.0-53.6-72.0) 39. 1997).4) 41. and 1.0 (46.7-68.2-91. urinary excretion over six days CAS No.1-63.2-59.2 (56. molybdenum is a cofactor for three enzyme classes— sulfite oxidase. and in pigments for ceramics.8-106) 88.2) 48. At a daily oral molybdenum dose of 24 µg.6) 71.0 (42.3 (47. 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.6 (55.7 (50.

2-41.0) 53. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.4) 44.5 (80.9-71.2 (69.7-52.3 (37.7) 53.2) 39.5 (79.3 (58.1-38. Chronic exposure to very high levels may result in higher serum uric acid levels and a gout-like illness (Koval’skiy et al.9 (39.5 (36. 1993).6-41. Biomonitoring Information Molybdenum is an essential element for health.9 (64.5) 63.6-61.1) 40.2 (73.5 (35.3) 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 85.4) 116 (101-126) 104 (88.8 (36.4-120) 101 (84.6-63.3-102) 122 (116-147) 123 (109-139) 118 (101-134) 310 368 290 648 762 725 1299 1559 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 40..1-39.4) 122 (107-133) 109 (99.9) 92.0-46.4) 48.3) 64.7) 42.5 (83.2 (33.8 (56.9-117) 57.9) 173 (130-243) 159 (129-170) 132 (107-158) 85.9-45.2-103) 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..1-67.3) 56. dust and other fine particles produced during refining or shaping of molybdenum or molybdenumcontaining alloys are inhalational pathways of exposure.8-65.6-63.9) 44.3 (71.8 (90.S.9-40.6) 36.5 (35.6-45.1-100) 86.7) 41.3) 61.7) 45. interval) 43.5-70.2-96.6 (36.3 (36.2-40.2 (40.7) 75th 63.2 (40.0 (35.1 (38.1-40.1) 101 (83.1-127) 90.8 (57.9 (36.6) Selected percentiles ( 95% confidence interval) 50th 41.5 (59.0) 62.5-97.9-42.9 (40.7) 57.5-60.2 (57.1-45.7-120) 87.9) 31.6-76.9-87.4-41.5-69.5-99.4-107) 85.1 (42.3 (53.3 (37. A long term inhalation bioassay of molybdenum trioxide in mice yielded “some evidence” of carcinogenicity (NTP.1) 65.9-118) 91.5 (41.8-67.1-112) 78.4 (67.5-92.3-44.3-59.S.2 (36.5 (65.2-121) 107 (92.4 (55.4 (59.0) 88.5) 71.0-133) 119 (88.8 (75.6-61.6 (59.4 (78.5-35.0) 38.7 (75.1-43.9 (39.4-76.9 (35.4) 58.1 (30.7-100) 77.5 (38.3 (83.7-62.2) 37. EPA. U.9 (79.1-43.5-45.8-46. 1961.0-103) 103 (90.6) 39.8) 79.5 (39.0) 33. One case-control study suggested a possible link between occupational exposure to molybdenum and lung cancer (Droste et al.3-141) 109 (81.6-78.03 mg/kg/day in humans (IOM.6) 43.7-137) 129 (109-155) 112 (97.7 (77.4) 47.3) 37.5 (34. the Panel on Micronutrients of the Institute of Medicine identified a no observed adverse effect level (NOAEL) of 0. 1999).0-38.0) 95th 144 (125-171) 130 (120-149) 120 (107-135) Total 42.8) 37.5 (40.1 (40.2) 39.5 (39.2-65.5 (40.0) 72.1 (39. and clinical or epidemiologic evidence of adverse effects is limited.3-43.5 (41.9) 40.6 (71.0) 44.3-52.2-49.2 (40.1) 37.0 (80.2) 38.8) 38.1 (49.8-47.3) 40..3 (71.8) 45. respectively.1-81.7-43.1 (37.7) 115 (93.2-46.9-45. at daily oral doses of 95 µg and 428 µg.2) 42.4 (37.7) 62.5 (78.5 (37.3) 41.8-42.9 (73.2 (43.3-56.5-44.0) 39.4 (56.5) 90th 108 (97. 1995).5 (54.7-40.7-93.3) 57.5) 73.8) 38.3) 43.4-106) 85.4) 60.5 (50.3-45.8-66.4) 77.3 (55.0 (74.9) 41.0) 39.2) 58.5 (65.8) 61.9 mg/kg/day and established a tolerable upper intake level of 0.2) 55. In industry.5 (37. and molybdenum has not been systematically evaluated for carcinogenicity by IARC.2-47.7-38.0) 36.6 (42.1 (54.0-56.5-48.6 (38.6 (36.5-119) 90.5-46.1-109) 89.8 (37.8-52.8) 39.4) 40.1 (44.2 (50.0-120) 85.9-68.9-41.4-42. Levels of molybdenum Urinary Molybdenum (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.6 (57.1 (82. urinary excretion over six days rose to 50% and 67%.3-115) 98.Metals was 18% of the ingested dose.5-62.3-68.7 (66.5) 72.2) 37.5-50.6) 48. but available epidemiologic data are scant. and urinary levels reflect intake from all sources.9-96.4-66.8-47.1-79.8) 71.4) 61.1 (33.1) 43.1-39.7 (30.9-61.8) 62.8-118) 81.1) 56.2 (37.4) 89.1 (38.8-84.4 (53. Human health effects from molybdenum at low environmental doses or at biomonitored levels from low environmental exposures are unknown.2) 43.4-185) 106 (94.3) 44.2-96. population from the National Health and Nutrition Examination survey. Molybdenum is generally considered to be of low human toxicity. Based on studies finding adverse reproductive effects in rats and mice. of the ingested dose (Turnlund et al.3-46.4-118) 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 .4-39.0-41.0 (58.2) 42. 2001).5) 60. 1997).1) 37.4 (40.1-34.9) 79.5) 214 (154-1040) 185 (165-219) 160 (129-257) 112 (78.0-46.3 (51.7-44.9 (49.2-80.6-88.2 (52.9 (64.4 (44.3 (36.6) 39.1-41.7) 112 (95.

Van Meerbeeck JP.22(3):179-191. Vermeire PA. Weyler JJ. 4/14/09 Sievers E.. Droste JHJ. National Toxicology Program (NTP). nickel. and zinc: a report of the Panel on Micronutrients.niehs. Environmental Protection Agency (U. 1313-27-5) in F344 Rats and B6C3F1 Mice (inhalation studies) 1997 [online]. References Centers for Disease Control and Prevention (CDC).S. Zhurnal Obshchey Biologii 1961. excretion.. Available at URL: http://books. Third National Report on Human Exposure to Environmental Chemicals. Molybdenum absorption. 1996. Inductively coupled plasma mass spectrometric determination of molybdenum in urine. Aprea C. 2002. Shmavonyan DM. silicon. Analyst 1998. boron. Kristiansen J. iron. Schindelin H. TR-462. X. van Sprundel MP. molybdenum. Geneva: WHO. Food and Nutrition Board. Molybdenum-cofactorcontaining enzymes: structure and mechanism. Molybdenum 1993 [online]. 2001). White MA. Molybdenum. manganese.S. Sabbioni E. Am J Clin Nutr 1995. Turnlund JR.66:233-267. 144-154. Institute of Medicine (IOM). 1998). Occup Environ Med 1999. 2001. Sciarra G. Minoia et al. iodine. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.gov/iris/ subst/0425. Christensen JM. Sci Total Environ 1998. Dietary reference intakes for vitamin A. Occupational risk factors of lung cancer: a hospital based case-control study. White and Sabbioni. population were well characterized in NHANES 1999-2000 and 2001-2002 (CDC. Sabbioni E.123(1):81-85. 16:1313-1319. vitamin K.. and retention studied with stable isotopes in young men at five intakes of dietary molybdenum. J Trace Elem Med Biol 2001. Standing Committee on the Scientific Evaluation of Dietary Reference Intakes. Schleyerbach U. pp.nih. Washington. copper. 420-441. et al. Available at URL: http://ntp.htm.gov/index. Peiffer GL. cfm?objectid=070A72C6-E9C1-AE67-4BFAB97AD0F427E8. Trace element reference values in tissues from inhabitants of the European Union.15(2-3):149-154. Keyes WR. Gatti A. Inductively coupled plasma mass spectrometric determination of molybdenum in urine from a Danish population. arsenic. Turci R. vanadium. U. Minoia C. Ronchi A. Toxicology and carcinogenesis studies of molybdenum trioxide (CAS No. Urinary molybdenum concentrations in infants may be slightly lower than those in other age groups (Sievers et al. pp. these levels were comparable to those reported for adults in smaller European population surveys (Iversen et al. Yarovaya GA. Koval’skiy GA. Finding a measurable amount of molybdenum in the urine does not mean that the level of molybdenum causes an adverse health effect. World Health Organization (WHO). 1998. 2005. Rees DC.nap. Fourth National Report on Human Exposure to Environmental Chemicals 229 . EPA). Atlanta (GA). (DC): National Academy Press. Available at URL: http://www. Rapid Comm Mass Spectrom 2002.S.epa.php?record_id=10026&page=420. A study of 13 elements in blood and urine of a United Kingdom population.Metals in urine for the U. 4/14/09 Iversen BS. edu/openbook. 4/14/09 White MA. chromium. Schaub J. 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. Kisker C. Menne C. Molybdenum in infancy: methodical investigation of urinary excretion. 2005). Ann Rev Biochem 1997. Changes of purine metabolism in man and animals under conditions of molybdenum biogeochemical provinces.216:253-270. In: Trace elements in human nutrition and health. 56:322-327.62(4):790-796.

and as drugs (e. lustrous metal found naturally in extremely low amounts in the earth’s crust and is typically associated with sulfide-ore bodies of nickel. as oxidation catalysts in chemical manufacturing. Platinum-rhodium compounds are also used in glass and glass-fiber manufacture and in hightemperature thermocouples. strength at high temperatures. 230 Fourth National Report on Human Exposure to Environmental Chemicals . respectively. and 0. see Data Analysis section) for Survey years 99-00. 1998). Platinum compounds are used in electrodes. copper. and high catalytic activity.04.04. 01-02. the ambient air concentrations of platinum associated with its use in automotive engine catalytic converters are estimated to be thousands of times lower than occupational exposure limits.. and 03-04 are 0. and iron. which may vary for some chemicals by year and by individual sample. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.. Human health effects from platinum at low environmental Urinary Platinum Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. Higher environmental soil concentrations of platinum from vehicular emissions have been found near roadways (Farago et al. Platinum-rhodium and platinumpalladium crystals are used as catalysts in petroleum refining and in vehicular catalytic converters to control exhaust emissions. however. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th < LOD < LOD < LOD 90th < LOD < LOD < LOD 95th < LOD < LOD < LOD Sample size 2465 2690 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 340 368 290 719 762 725 1406 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1227 1335 1281 1238 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. 0. < LOD means less than the limit of detection.Metals Platinum CAS No. Important properties of platinum are resistance to corrosion. jewelry. 7440-06-4 General Information Platinum is a silver-gray.S.07. thick-film circuits printed on ceramic substrates. cisplatin. dental alloys. carboplatin) in the treatment of cancer.g. 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.

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

Iavicoli I. Schierl R. 3/31/08 Moore W Jr.Metals the International Programme on Chemical Safety at http:// www. Stilianakis NI. Moore W Jr. Turfeld M. Schierl R. Schulz C. Senofonte O. New York: John Wiley & Sons. Schierl R. Saindelle A. Seiwert M. Hysell D. Biomonitoring of traffic police officers exposed to airborne platinum. 2004). Int Arch Occup Environ Health 1997. Farago ME. 2001). et al. Pethran et al. Biological monitoring of hospital pharmacy personnel occupationally exposed to cytostatic drugs: urinary excretion and cytogenetic studies. ruthenium. et al. Influences on human internal exposure to environmental platinum.org/documents/ehc/ehc/ ehc125. Several studies have shown that background concentrations in general populations were usually less than 0. Seifert B. 1998). Platinum. pp. Jankofsky M. Campbell K. et al. Schierl. Urinary platinum levels associated with dental gold alloys. Powell CH. Br J Pharmacol 1969. and in blood and urine in the United Kingdom.S.inchem. 2003. Environmental Health Criteria 125.. Occup Environ Med 2004. Begerow J. Angerer J. Part 1: monitoring of urinary concentrations. Fries HG. Boos KS. Herr et al. Urinary excretion of platinum from platinum-industry workers. 2004) or less than 0. palladium. Gromiec JP. Patty’s Toxicology. Stara J: Biological fate of a single administration of 191Pt in rats following different routes of exposure. One study found that traffic-control officers had no greater urinary platinum concentrations than office-based control subjects (Iavicoli et al. 1991 [online]. Platinum-industry and precious-metal workers had urinary concentrations about one-thousand times higher than general populations (Schierl et al. 2000.123(3):451-454. 1997. Analyst 1998. which elevate urinary platinum by five to twelve-fold (Begerow et al. Schulz C. Rommelt H.. Stara J: Preliminary studies on the toxicity and metabolism of palladium and platinum. Finding a measurable amount of platinum in the urine does not mean that the level of platinum causes an adverse health effect. et al. Gold-platinum dental restorations were correlated with increased urinary platinum concentrations. Arch Environ Health 2001. and platinum. Parrot JL. Gieler U.. Revised and new reference values for some trace elements in blood and urine for human biomonitoring in environmental medicine. Kulka U. Allergy and histamine release due to some platinum salts. Int Arch Occup Environ Health 2003. Hauff K. Nowak D. Huber R. References Becker K. Biomonitoring Information Urinary platinum levels reflect recent exposure. Hysell D. International Journal of Hygiene and Environmental Health 2003. Int J Hyg Environ Health 2004. 2003... 1999. Raab W. Nickel. Environ Health Perspect 1975b. Biomarkers 1999. Kavanagh P. 5th ed. Cohrssen B. Ruff F: Histamine release by sodium cholorplatinate. Wilhelm et al.04 µg/L) in this Report. Environ Res 1975a.. Ensslin AS.61(7):636-9. Wilhelm M. In: Bingham E.01 µg/L (Becker et al. Occup Environ Med 1998. osmium. Hall L. Bocca B.9:152-158. 2003).35:313-321. Levels of platinum in urine for the U. and gold excretion of patients after insertion of noble-metal dental alloys.13(1):24-30. Hebert R. population were below the limit of detection (0.. 206:15-24. Ruff F: Platinum and platinosis. Grimm CH. Petrucci F. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. van de Weyer C.. 232 Fourth National Report on Human Exposure to Environmental Chemicals . Kuster W. 2003. 1998).org/documents/ehc/ehc/ehc125. Ewers U. Alimonti A. Thornton I.htm.005 µg/L (Iavicoli et al. eds.inchem. 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. Neuendorf J. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Uptake of antineoplastic agents in pharmacy and hospital personnel. Duneman L:Long-term urinary platinum. Herr CE. Schierl et al. Saindelle A. Kelly J.10:63-71.56(3):283-286.htm. J Expo Anal Environ Epidemiol 2003. Fruhmann G. Available at URL: http://www.. rhodium. Blanks R. Crocker W. Carelli G..4(1):27-36. Pethran A.207(1):69-73. 289-380. Arch Environ Health:1969. palladium.. Kaus S. International Programme on Chemical Safety (IPCS). 2004.55(2):138-140.76(1):5-10. Kazantzis G. Platinum concentrations in urban road dust and soil.70(3):205-208. Herr et al. Czerczak S. Schierl R. Pethran A. 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.19:685-691.

133-.340-.450 (.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 .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 .280 (.135-.200 (.290 (.490) Total .170-.200) .350-.150-. In the past.330-.420-.157-.182-.181-.300-.202 (.400 (.460) 861 675 618 561 657 723 801 1114 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.140-.290 (.S.240) .630) . and 03-04 are 0.460) .420) .160 (.270 (.210-.270-.430-.270 (.550 (.300) .340-.400 (.410 (.196) .250-.390 (.420) .175) .470) .243) .690) .320) .480) .200) .220 (.190 (.350-.520) .420) .200-. Elimination from the body tissues occurs slowly through urine and feces (Blanchardon et al. it has not been specifically mined or refined in the United States since 1984.220) .340) .201 (.290 (.270 (.250 (.159 (.410 (.340 (.250-.380 (.330) .370 (.490) .290) .470) .156) .400) 95th . thallium readily crosses the placenta and also distributes into breast milk.180) 75th .160-.280-.330) .640) . 01-02.240-.270) .440 (.180 (.160 (.270) .360-. 7440-28-0 General Information Elemental thallium is a blue-white metal found in small amounts in soil and in sulfide-based minerals.160 (.210) .300 (.370 (.360 (.170 (.360-.183) .300) .260 (.410) .220) .470) .160-.173-.360-.176 (.300) .390 (.239) .290) .450 (.440) .520) .370 (.290 (.190 (.144 (.200) .360) .430 (.230) .450 (.590) .167 (.201 (.187-.310 (.191 (.480) .460-.217) .200-. 0.156-.410-.190-.460 (. see Data Analysis section) for Survey years 99-00.270 (.370) .185-.200-.180-.270-.217 (.510 (.165 (.410-.158) .320) . the latter being the current major industrial consumer of thallium in this country. It is still used in relatively small amounts in pharmaceutical and electronics manufacturing.430) .147-.220 (.290-.02.420) . In addition.520 (.190 (.230-.380 (.490 (.400) .390) . and 0.330) .450 (.420-.180-.134-.220) .440 (.172) .350-.173) .470 (.420) .510) .145-.180 (.250-.250 (.300 (.218) .170 (.220) .400-.290) .280 (.330) .150-.150-.153-.160 (.215) .480) .420) .380-.170 (.330-.170-.170-.410 (.400) .440-.230) . In the United States.196) .370) .177) .220) . representing distribution into other tissues.440 (. thallium is produced in a fine particulate form that can be absorbed through inhalation or ingestion.470 (.270 (.350-.450 (.310) .260-. 2005).410 (.170-.200 (.280) .260-.370 (.500 (.450) .145 (. population from the National Health and Nutrition Examination Survey.240-.400) .390) .200 (.330-.300 (.370 (.02.240) .400 (.148-. Fourth National Report on Human Exposure to Environmental Chemicals 233 .290) 90th .250-.220 (.490) .250) .340) .200 (.400-.220 (.170-.320-.420) . From these and other sources.350-.230) .240-.178) .202 (.360 (.147-.390-.450 (.145-.150-.200-.430 (.206) .400 (.200) .210 (.Metals Thallium depilatory cosmetics.180) .400-.02.410-.310-.170-.160-.280 (.192) Selected percentiles ( 95% confidence interval) 50th .370 (.162-.210 (.260-.440 (.200) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.230 (.480) .160-.260) .230-.400 (.450 (.430) .500) .370-.220) .390-.260-.188) .420-.173) .150-.146 (.390) .370-.320 (.200) .190 (.350 (.159 (.360 (.171 (.280-.400-.490) . thallium was obtained as a by-product of smelting other metals.400-.410 (.360-.390-.330-.159 (.180-.370 (.410 (.190 (.430-. interval) .260 (.280) .160-.154-.560) .320) .410-.179-.167-. Thallium disappears from the blood with a half-life of several days.290) .430 (.184 (.590) .250-.163) .197 (.180-.230-.220-.440) .500) .197-.300) .280) .370-.420 (.167-.260 (.380-.350) .155 (.218) .156) .290 (.340-.170) .170) .160 (.420-.450 (. however.330-.149 (.170-..172 (.220 (.190 (.290 (. respectively.400) .350) .290-.180 (.520) .500) .410-.370-.172 (.360 (.200 (.225) . 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.430-.137-.250-.150-.360-.390) .230) .350-.270-.480) .430 (.330-. Thallium exposure occurs primarily from industrial processes such as coal-burning and smelting.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 .183) .390-.380) .410-.440) .200 (.250-. Human health effects from thallium at low environmental CAS No.310 (.330-.170) .350 (.185 (.310 (.202) .147-.450 (.340-.240) .250-.260-.

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

1998). Trace element reference values in tissues from inhabitants of the European community I.47(3):223-231. Intake and health effects of thallium among a population living in the vicinity of a cement plant emitting thallium-containing dust. Toxicological profile for thallium.48(4):375-389. Sci Total Environ 1998.Metals (CDC. Marcus RL. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Celier D. Kramer U. Available at URL: http://www.76(1):53-59.216:253-270.95:89-105. Minoia C. Sabbioni E. Boisson P.1 mg/m3 (Marcus. White MA. et al. 2005. Martin J-C. Int Arch Occup Environ Health 1981.. Schaller et al. Urinary concentrations of 100 μg/L in asymptomatic workers (500 times higher than median levels in the U.. Fourth National Report on Human Exposure to Environmental Chemicals 235 . Investigation of a working population exposed to thallium. Brockhaus A. Valentin H. (1981) studied 1. et al. Dolger R. 1998. Schaller KH. Finding a measurable amount of thallium in urine does not mean that the level of thallium causes an adverse health effect. Morrow JC. Gallorini M..265 people living near a thallium-emitting cement plant in Germany. Schmidt M.. Brockhaus et al. Sci Total Environ 1990. Seventy-eight percent of the urine specimens in that study contained greater than 1 μg/L. Pietra R. 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. 1990. Radiat Prot Dosim. Third National Report on Human Exposure to Environmental Chemicals. Centers for Disease Control and Prevention. Ting BG. Sampson EJ. Cassot G. with concentrations ranging up to 76.html. References Agency for Toxic Substances and Disease Registry (ATSDR).gov/toxprofiles/tp54. Apostoli P. These urine levels are generally comparable to levels observed in earlier studies of general populations (Brockhaus et al. population) are thought to correspond to workplace exposures at the threshold limit value of 0. Paschal DC. Sabbioni E. Manke G. 2005) and are shown with results from NHANES 2003-2004 in this Report.113(1):47-53.S. Long term retention and excretion of 201Tl in a patient after myocardial perfusion imaging. and serum of Italian subjects.cdc. Pozzoli L. Ewers U. Trace metals in urine of United States residents: reference range concentrations. Paschal et al. Soddemann H. et al. Challeton-de Vathaire C. J Soc Occup Med 1985. 2005. A study of 13 elements in blood and urine of a United Kingdom population. Investigations of thallium-exposed workers in cement factories.5 μg/L. 1980. blood.35(1):4-9. 7/15/09 Blanchardon E. 1992 [online]. 1985). Environ Res 1998. Atlanta (GA). Nearby residents were exposed by eating garden plants that had been contaminated by the thallium. X. 1981. Minoia et al. Wiegand H. Jackson RJ.atsdr. White and Sabbioni. Buhlmeyer G. A study of 46 elements in urine. Raithel HJ. Int Arch Occup Environ Health 1980. Pirkle JL. Trace element reference values in tissues from inhabitants of the European Union. 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.

190 (.105) .060-. Little information is available on the toxicity of tungsten.S.080 (.330 (.111-.810) .120) .200-.060 (.470) .520) .120-.100) .380-.060-.122) .280 (.410) 790 680 618 562 649 723 802 1117 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.250) .210 (.130) .290 (.130) .074-.220) .420-.230-.065 (.088) .430-.350-1.460 (.076 (.080-.070 (.270 (.230-.200 (.110-.340-.260-.070-.430 (.270-.090) .630) .100 (.100) .071-.100-.400-.310-.069) .050-.300 (.204) .04.430) 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 .350) .560) .090-.370-.310-.380-.130 (.370 (.410-.087) .137 (.050-.050-.110 (.073-.520) .113 (.090) .560) .097-.160-.160 (.130) .070-.090 (.070) .530 (.077-.800) .200) .460) 1160 1307 1281 1178 1345 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .270 (. mainly as scheelite (CaWO4).180) . and it has not been classified with respect to its carcinogenicity by either IARC or NTP.04.135) .360-.120-.180 (. Occupational exposure is from dusts released during grinding or drilling of hard metals.620) .570 (.290-.080 (.101-.230-.060 (.070 (.060-.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 . Most background environmental exposures to tungsten are from the soluble forms such as tungstate salts that may occur in drinking water.070) .090-.370) .130) .088 (. 0.360-.310) .360) .560) .390 (.260 (.082 (.440) .560 (.060-.110-.160-.107 (.126) .080) .220) .060-.470 (.190-.140 (.500) .330-.065-. and 0.060 (.350 (.330) .04.550) . 7440-33-7 General Information Tungsten is a steel-gray to tin-white metal that occurs naturally in the earth’s crust.510-.160 (.180-.070-.113 (.530 (.080-.300) .400 (.300 (.130 (.570 (.100 (.082) .180 (.180-.091) .320 (.080) .170) .086 (.100) .150 (.050-.270-.190 (.320-.460 (.140-.151) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.650) . and for producing ferrotungsten.084 (.410 (.068) .250) .830) .370 (.070-.340-.290) .360 (.116) .400 (.300-.470) .056-.093 (.100) .360 (.120) .510-1.080 (.070) .250) . bronzes in pigments.310-.400 (.360 (.340-.095-.350) .550) .430 (.100 (.620) .170) .320) .290-. Although workers occupationally exposed to tungsten carbide may develop serious lung disease (“hard metal disease”).062 (. 236 Fourth National Report on Human Exposure to Environmental Chemicals .380 (. and 03-04 are 0.250) .260-.260-.120-.230-.260 (.110) .070) .790) .090-.100) .240 (.260) .140 (.120) .130-.080 (.180-.130-.670) .800) .073) .082 (.270-. Evidence is lacking for the carcinogenicity of tungsten.510 (.056-.380) .110 (.390) .290-.160) .210 (. and as catalysts in the petroleum industry.220-.090-.230 (.550 (.490) .560) .550) . Human health effects from tungsten at low environmental doses or at biomonitored levels from low environmental exposures are unknown.090-.490 (.062 (.280-.190-.120 (.092 (.105 (.081 (.060 (.950) .064-.160 (.095-.180) .109) .180-.069-.110 (.240-.160-.087-.770 (.080) 75th .150 (.00) .270-.280 (.120-.310 (.150 (.230) .300) 95th .080) .640 (.100-. Tungsten compounds are used as lubricating agents.110 (.330-.104) . see Data Analysis section) for Survey years 99-00. their illness may stem from exposure to cobalt mixed with tungsten carbide rather than to tungsten alone.150-.100-.066-.080-.53) .070 (.380 (. Tungsten is used mainly for producing hard metals.170 (.210 (.470 (.350) .073 (.093-.420-.190-.090 (.310-.070-. 01-02.158 (.130-. population from the National Health and Nutrition Examination Survey.500 (.060 (.140 (.101 (.140 (.380-.120-.150) .123-. which are used in rock drills and metal-cutting tools.310-.113 (.230) .620 (.090 (.096-.430 (.340) .220 (.590) . which is used in the steel industry.133) .580) .370 (.110-.250) .400) .160) .100 (.090-.190-.092 (. filaments for incandescent lamps.160 (.080 (.090) .290) .093) .090) .220) .250-.092) .520) .480) Total .300 (.140) 90th .370-.113 (.690) .210 (.120-.130) .110 (.073-.096 (.110) . interval) .250-.190) .460) .060 (.210) . respectively.530 (.380-.180) .060-.500 (.210 (.130-.170) .170-.078-.450 (.470-.076 (.460 (. Urinary Tungsten Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.132) .450-.210-.Metals Tungsten CAS No.160-.058-.090-.320 (.180) .320-.140-.170 (.250) .090-.330) .430) .120) .120) .170) .071 (.460) .430-.120) .270 (.400 (.100) Selected percentiles ( 95% confidence interval) 50th .084-.084) .160 (.082-.

218 (.279 (.436-1.068-.122 (.086) .176-.217-. 1997).797) .136-.667) .075) .109 (.258-.098-.126-.080-.107-.555 (.100 (.186 (.071 (.086-.084 (.152-.253) 95th .237) .331-.28) .071 (.167-.059 (.083 (.088) .074-.284) .117) .079) .098) .439 (.138 (.392) .133) .174) .098 (.081-.061-.279 (.482 (.089 (.375) .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 .255 (.065-.439) Total .215 (..187) .060-.143-.062 (.066 (.414) .231-.065-.329 (.148 (.070 (.317) .094-.200-.144 (.272-.333-.S.136-.124-.300 (.340 (.095-.484 (.158) .079) . Nicolaou et al.739) .217-.436) .080 (.082) .085) .359 (.667 (.299 (.317-.150-.203-.058-.057-. Workers involved in grinding operations that released tungsten metal into the air had elevated urinary levels that Levels of urinary tungsten reflect recent exposure.125 (.158 (.155-.410-.300-. and 2003-2004 (Paschal et al.258 (.164 (.S.081 (.237-.074 (.103-.075 (.104-.059-.333 (.056-.339 (.S.075-.096) .333) .201 (.091) .198-.170-.205-.117 (.293 (.069-.823) . A study of 14 unexposed adults yielded values that were similar to the 95th percentiles in this Report.071) .122-.278-.294 (.181 (.439 (.086) .138 (.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 .497 (.064-.253 (. Using neutron activation analysis to 2000. 1998).426) .265 (.358) . population (CDC.106 (.500) .169 (.111 (.108) .154) ..066 (.250-.153) .093-.119-.158) .072 (.150-.167-.063-.197-.074-.065-.255 (.364 (. 2001).237) .231 (.092) .079) .426) . Biomonitoring Information median urinary levels were as much as 15-fold higher than median levels in the U.144-. 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.214-.116 (.091) .070 (. population from the National Health and Nutrition Examination Survey.081 (.067-.459) .094) .054-.069 (.354-.139-.462) .727) .245-.055-.359 (.073 (.270 (.222) .071) .122-.484) .084) . Patients with medically-inserted tungsten found at increased levels in drinking water.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 .139 (.184 (.059-.089) .211 (.199 (.300-.283) . population in the NHANES 1999-2000 slightly higher values than those found in NHANES 1999.453) .145 (.199 (.072-.353 (.216 (.385 (.279 (.151 (.143 (.082) .060-.214) .285) . (1987) found possibly due to methodologic.086) .083) .538) .075-.317 (.200-.208-.078) .255-.088) .061-.072-.267-.073 (.084) .098-.075 (.124 (.108-.146) .077) .190) .063-.198) . In whereas the tungsten-worker group had mean urine levels a Nevada community where tungsten was measured and 35 times higher.286-.091) .379 (.078 (.381) .261-.109-.080 (. 2005).065 (.215) .180-.233-.093) .360 (.216-.099-.083 (.049-.179-.071-.133) 90th .079 (.078) .130-.061-.073 (.158) .634 (.100) .880) .077) .064-.150 (.065) .090-.167) .139) .308) .267) .339 (.302-.167) .067 (.222-.165) .063-.169) .053-.154) .079) .554) . population.216 (.344-.120) .206-.326) .179-.054-.133) .315-.116-.465) .138) .148) .250 (.105 (.077-.146 (.065 (..071) .333-.074) 75th .075) .146 (.069 (.085-.383 (.209-.216-.056-.087) .333 (.341 (.582) .091 (.090-. 2001-2002.059-.347 (. measure urinary tungsten.465) .063 (.412 (.201) .136-.119 (.074) .197 (.431) .301) .301) .224) .253-.071 (.063 (.176-.125) .083) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.078-.(Kraus et al.057-.300) .063-.605) . A were more than 900 times higher than the overall geometric nonrandom subsample from NHANES III demonstrated mean of the U.333) .100) .121 (.067 (.302-.275 (.094) .197) . or exposure that a control group of non-metal workers had mean levels differences.136-.082 (.079 (.174 (.431) .091 (.080-.240-.157) .250 (.087 (.329-.073 (.084 (.333 (.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 .078 (.131-.354) .098-.105 (.153-.287) .081) .216-.188-. 2003.085 (.Metals Workplace air standards for external exposure have been established by ACGIH and recommended by NIOSH.168 (.091) .353 (.333 (.060 (.068 (.077-.431) .197) .130 (.121-.136 (.161) . similar to those in this Report (Schramel et al.386) .120) .301) .452-.095) Selected percentiles ( 95% confidence interval) 50th .116) .083-.308) . interval) .306) .

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

007-.027) .023-. 0.008 (.012 (.010 (.022-.012-.009-.040-.009) . It usually occurs as an oxide and is extracted from ores containing less than 1% natural uranium.028-.011-.037) .014 (.013-.067) .013-.023) .030 (.007-.020-.007-.009) .018) .010 (.007-.008 (.046 (.016) .021 (.036 (.013 (.158) .010-.009 (.009 (.013 (.009) .007-.031 (.015 (.036) 883 683 618 568 667 722 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.008 (.039) .008-.007 (.013) 90th .004. 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.048 (.033-.012) .021) .034) .016-.006 (.008 (.011-. Natural uranium is a mixture of three isotopes: 238 U (greater than 99%).031 (.012 (.017-.011-.020-.007 (.031 (.011) .023-.013) .034-.007-.016) .006 (.017-.007 (.015-.016) .024-.009-.009-.018) .063) .054) .018) .Metals Uranium CAS No.010) * .027-.007 (.004.006-.011) .018 (.008-.007-. human exposure occurs primarily by inhaling dust and other small particles.006-.019-.019-.066) .009) .020-.050) .027) .028 (.026 (. 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.010) .008 (.022) .029-.007-.016) .020) .060 (.008) .034-.032 (.046) .013 (.029-.027 (.014 (.012-.009-.010-.012-.015 (.047 (.005.006-.021 (.009 (. and 03-04 are 0.046 (.007-.049) .037-.006 (.042 (.072) . the primary exposure sources for nonoccupationally exposed persons are dietary (especially root vegetables) and drinking water.042) .015 (.012 (.008 (.015) .012-.031-.127) .009) .065) .038) .028 (.021-.009) * .011) .037) Total .007-.010-.013 (.009-.009) .037) .009 (.014 (.016) .005-.006-.053 (.009) .088) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.012) .020-.023-.009) . In workplaces that involve uranium mining.014 (.020 (.006-.007 (.008-.017) .067) . or processing.039-.006-.72%).012) .037 (.055 (.008-.013-.041 (.065) .008-.016 (.010) .010 (.023) .044 (.037) .054-. see Data Analysis section) for Survey years 99-00.011 (.011-.007) . DU has been used by the military in armor-piercing ammunition and as a component of protective armor for tanks.033 (.009) .026 (.011) . nuclear fuel.021-.009-.023 (.024 (.056) . 01-02.022 (.026-.007) .029 (. 235U (about 0.012 (. Fourth National Report on Human Exposure to Environmental Chemicals 239 .039) .027-.011) .009 (.019-.009 (.035) .007-.018) .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 .008) .007 (.007 (. and 0.013 (.007) .053) .017) .006-. Since the 1990’s.022-.008) .026) .035) .046-.033) .010) .010 (.019 (.011-. Uranium has many commercial uses.027 (.009-.008-.020) .008 (.006-.009) .023 (.024-.012) .051) .015) .007-.030 (. respectively.009) .017 (.062) .007) .005-.033 (.010 (.007-.011-.028-.005-.064 (.041 (.069) .036) .012-.008 (.043) .008 (.008-.010-.008 (.027 (.038 (.008) .008) .049) .008 (.019-.040 (.007 (.028 (.007 (.027-.027 (.011-.017-.008 (. milling.009-.010) . and 234U. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.017) .045) .046 (.036-.008 (. Thus.040-.014 (.036-.013 (.054) .017) . interval) .014 (.017 (.007-.007) .040) .012 (.016-.018-.026 (.026-.020-.012-.010-.013 (.005-.009 (.056) .010-.025-.007 (.018 (.017-.009) .030) .009) .023-.046 (.036) .114 (. and as an aid in electron microscopy and photography.008 (.031 (.073) . in some ceramics.279) .010) .021) .005-. Variable concentrations of uranium occur naturally in drinking water sources.040) .017-.006-.026) .045) . including nuclear weapons. 7440-61-1 General Information Uranium is a silver-white metal that is extremely dense and weakly radioactive.007) 75th .035-.S.021 (.052 (.007-.015 (.011 (.008 (.026) 95th .006-.031 (.010) .007-.008 (.021) .011) .010) * .009-.030-.036 (.024-.043 (.006-.009 (.040 (.027) .017) .016-.023) .012 (.006-.007-.050) .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 .007-.023 (.008-.010) .009-.027) .006-.009) Selected percentiles ( 95% confidence interval) 50th .017-.011) .007 (.048) . population from the National Health and Nutrition Examination Survey.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 .009 (.022-.009 (.008 (.010) .016) .030 (.006 (.

012) .039) Total .006-.007 (.010) .025-.006 (.015) .031 (.029 (.027-.009-.051 (.008 (. Radiation risks from exposure to natural uranium are very low.010) .010-.056) .024) . After long term or repeated exposure.061) .006-. the half-life of insoluble uranium in the lungs is several years (Durakovic et al.011-.007 (.025 (.011 (.029 (.034 (.146) .030 (.020-.009-.022 (. Soluble forms of uranium salts are poorly absorbed in the gastrointestinal tract.008) . the shrapnel acts as a source of chronic.027 (.008) 75th .021-.024) .028) ..009-.022 (. where limited absorption occurs (less than 5%).030) .028 (.016) .058) .008) .008) .015-.009) .016) .047) .025-.020) .007 (.010) .012) . 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.011-.035 (.012 (.006) .007-.007-.006-.007-.006-.007 (.007) .009 (.033 (.009) .012 (.010-.011-.025) 95th .008-.016) .028 (.006-.020-.009 (.030-. 240 Fourth National Report on Human Exposure to Environmental Chemicals .010) .017-.008 (.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 .012 (.009) .028) .018-.013-.032) .007 (.024) .013 (.007 (.019 (.008-.006) .008 (.050) .010-.027 (.018-.019-.009 (.007-.013 (.080) .008 (.014) .008-.030-.067) .008) .034-.034-.044) .007 (.030 (.026 (.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.005 (.016-.012 (.014 (.035 (.053) . Health effects from uranium exposure result from chemical toxicity to the kidney.010) .010) * .019 (.009) .010 (.006-.039) .009) .027 (.008 (.007 (.008) .008-.007 (.017) .027-.048) .022 (.024) .015) .018-.006-.021) .029) .006-.033 (.005 (.034 (.011 (.051) .054) .015 (.017) .007 (.016-.005-.077) .014-.020 (.011-.027-.009) * .017 (..034 (. low level exposure.006-.031-. Human health effects from uranium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.013) .011) .032) .020-.027) .022-.028) .017-.014-.024-.042-.009) Selected percentiles ( 95% confidence interval) 50th .029) .028) .018-.016-.007 (..007-.S.024-.009-.016) .006 (.016) .006 (.063) .026 (.010-.007-.043 (.013 (.029) .010) .014) . with much slower elimination from bone.005-.012 (.014) .004-.034 (.009) .011-.017) .007 (.006-. After inhalation.011) .015 (.006 (.007 (.009) .005 (.006) .005-.008) .005-.008) .029 (.006-.017-.006) .007) .006-.009 (.010-.013) .039) .033 (.010 (.013 (.037 (.042) .004-.024) . Uranium is eliminated in feces and urine.025-.024 (. 2005).051) .006-.013 (.030 (.008) .010 (.021 (.009) .007 (.008-.034 (.019-.009 (.019) .Metals impact. and bones can accumulate uranium with the largest amounts being stored in bones (Li et al.012 (.013 (.008 (.040 (.033 (.015 (.006-.050 (.021 (.029) .008-. which represents distribution and excretion.007-.010-.026-.008) .011-.006-. kidneys.007 (. about 50% of the absorbed dose is eliminated in the urine within the first 24 hours.022) .021 (.015-.020-.022-.006 (.007-.007-.059 (.011-.006-.024 (.042) .010-.027-.006-.028-.017 (.019-.015-. which can occur occasionally from high occupational exposure.011-.019) .025-.026) .009) .011-.016) .006) .008) .015 (.041) 1227 1334 1280 1237 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .010 (.019-.021 (.005-.045 (.010 (.027) .009) .015) .013 (.013 (.015-.016 (.008 (.005 (. Depending upon the specific compound and solubility. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.030) .058) .006-.017-.010-.026 (.009) .005-.008 (.053) .019 (.006-. After exposure to soluble uranium salts.074) . 2003).007 (.015) .006-.007 (.015-.100 (.007) .013 (. population from the National Health and Nutrition Examination Survey.012-.010-.016) .019-.011) .048) .051) . the initial half-life of uranium is about 15 days (Bhattacharyya et al.010-. liver. In cases of retained DU shrapnel.012) .012-.011) * .039) .024 (.006-. interval) .008 (.016-.007 (.007-.014 (.007 (.012 (.041) .014-.013) .023-.033) .1%-6% of an ingested dose may be absorbed.014) 90th .270) .018-.018) .013 (.025 (.008 (.009-.050) .005-.020 (.024-.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 .016) .008) .007 (.022-.034) .006-. Inhaled uranium-containing particles are retained in the lungs.006-.006-.018 (. 0.007 (.009-. 1992).006 (.010-.020 (.

. Third National Report on Human Exposure to Environmental Chemicals. 2005. 1978).62:562-566.S. 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.168(8):600-605. A cohort of 46 U. In 17 U. soldiers evaluated before.61 μg/g creatinine.. ingestion. Drinking water and other environmental standards have been established by U. Thomas RG. the median urinary concentration was 0. Pillai KC. but in whom no shrapnel was embedded.011 μg/L (McDiarmid et al. Stradling GN. 2002).S.S. the geometric mean urinary uranium concentration was 0. Dietz LA..78:143-146. Squibb K. 2000). Older studies have demonstrated urinary uranium concentrations that are consistent with levels in the U. population. 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. 2006). soldiers who had been injured and had embedded DU shrapnel for as long as eight years.. Mil Med 2003. References Bhattacharyya MH. Radiation protection dosimetry. 1994. had a mean urinary uranium concentration of 0. Volf V. 2000). Hamilton et al. 1992. Six workers in a depleted uranium program showed concentrations of 0. during. Information about external exposure (i. although slightly increased during and after deployment. 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. EPA. Eighty-five percent of those levels were above the 95th percentile of the NHANES 1999-2000 population..html. In the same study.. The U. Nuclear Regulatory Commission (NRC) has set an action level of 15 μg/L urinary uranium to protect people who are occupationally exposed (U. Health Phys 1992. 2004). In: Gerber GB. Uranium content of blood. Fourth National Report on Human Exposure to Environmental Chemicals 241 . 2004).. 2006).e.. A previous nonrandom subsample from NHANES III (n = 499) (Ting et al. Centers for Disease Control and Prevention (CDC).. environmental levels) and health effects is available from ATSDR at: http://www. 1991. 2004). 2006. IARC and NTP have no ratings for uranium human carcinogenicity.cdc. (Kurttio et al. Ejnik JW. NRC. Komaromy-Hiller et al. Urinary uranium measurements in 103 Canadian military personnel showed mean urinary levels slightly less than geometric mean in this Report (Ough et al.S. 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. Atlanta (GA). the median urinary uranium concentration was 2. Biomonitoring Information Levels of urinary uranium reflect recent and accumulated exposure.Metals injury associated with elevated urinary uranium levels (Kurttio et al. Determination of the isotopic composition of uranium in urine by inductively coupled plasma mass spectrometry. Byrne AR. and no consistent effects on multiple endpoints of kidney function were found. and 2003-2004 (Dang et al. 1-49... pp. Pullat VR. Metivier H. eds. In a study of 105 persons exposed to natural uranium in well water. Sci Total Environ 1991.1996.066 μg/g creatinine (Gwiazda et al.1992.atsdr. Hamilton MM. Finding a measurable amount of uranium in urine does not mean that the level of uranium causes an adverse health effect. Determining the normal concentration of uranium in urine and application of the data to its biokinetics.. urine and hair of exposed and non-exposed persons determined by radiochemical neutron activation analysis. McDiarmid et al. with emphasis on quality control. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Vol. Benedik L. Galletti. respectively. or wound contamination.. Recent studies of veterans have been conducted to examine concerns about DU exposure during military conflicts.. In a much larger study of 446 Gulf War veterans who were concerned about past exposure to DU. in that the levels were below their respective detection limits (Byrne et al. Boyd P.55 μg/L (median 0. 2002.162 μg/L) (Orloff et al. Kent (England): Nuclear Technology Publishing. et al. Tolmachev et al. 2003. Carmichael AJ. Horan P.65 μg/L). (May et al.107:143-157. urinary levels of uranium were as high as 9. Dang HS. 2006). Workplace air standards and guidelines for external exposure to soluble and insoluble uranium compounds have been established by OSHA and ACGIH. 2004).. 2001-2002. McDiarmid M. 1999) and other small populations have shown urinary concentrations that are similar to those in NHANES 1999-2000.078 μg/L (ranging up to 5.gov/ toxpro2. In two studies of a Finnish population with high natural uranium concentrations in their drinking water. 2006). Durakovic A.. Guidebook for the treatment of accidental internal radionuclide contamination of workers. 28 soldiers who may have been exposed to DU by inhalation.. Karpas et al..110 to 45 μg/L (Ejnik et al. Muggenburg BA. Breitenstein BD. Health Phys 2000.S. Zimmerman I.S. 41 (1).

Ejnik J. Hollriegl V. Hancock RG. McDiarmid MA. Nuclear Regulatory Commission (U. McDiarmid M. Heller J. Orloff KG. Am J Kidney Dis 2006. Andrews WS. Metcalf S. VI. Wahl W. Int Arch Occup Environ Health 2006. Noguchi H. Hamilton EI. U. Jackson RJ. May LM. Ting BG. Roiz J. Kuwabara J. Marino R. Sampson EJ. Salonen L. Kidney toxicity of ingested uranium from drinking water. Detection of depleted uranium in urine of veterans from the 1991 Gulf War. Kalinsky V.67(8-10):697-714. et al. 242 Fourth National Report on Human Exposure to Environmental Chemicals . Auvinen A. Scott K. Health Phys 2003. July 1978. Lorber A. An examination of uranium levels in Canadian forces personnel who served in the Gulf War and Kosovo. Oberbroekling KJ. Katorza E. Review of elements in blood. Squibb K. NRC). Marko R. Lewis BM.94:319-326. Makelainen I. Wilson PD. Harmionen A.158:165-190. Environ Res 1999. Howerton K.79(1):11-21. Clin Chim Acta 2000. Health Phys 2004. Biokinetic modeling of uranium in man after injection and ingestion.Metals Galletti M. Saha H. Salonen L.44:29-40. Oliver M. et al. Cremisini C. Pirkle JL. D’Annibale L. Environ Health Perspect 2002. et al. concentration and daily excretion of uranium in urine of Japanese. et al. Uranium and thorium in urine of United States residents: reference range concentrations. Karpas Z. J Toxicol Environ Health A 2004.47(6):972-982. Ough EA. Sabbioni E.296(1-2):71-90. Paschal DC.110(4):337-342. Shelly T.86:12-18. Smith D.S.87:51-56. Oeh U. Health Phys 2006. Squibb K. Comparison of representative ranges based on U. Roth P. Bennett LG. Nuclear Regulatory Commission (NRC) Guide 8. Health Phys 2002. Li WB. Cordero S. Engelhardt SM. Pinto V. and inexpensive method for determination of uranium in urine and fresh water: comparison with LIF. Komulainen H. Biological monitoring and surveillance results of Gulf War I veterans exposed to depleted uranium.91(2):144-153. patient population and literature reference intervals for urinary trace elements. Tolmachev S. Gwiazda RH. Englehardt SA. U.81:45-51. Health Phys 2004. Paretzke HG. Ash KO. Human exposure to uranium in groundwater. Gucer P. Kane R.S. Kurttio P. Mistry K. Halicz L. Radiat Environ Biophys 2005. Komaromy-Hiller G. Washington (DC): NRC.85:228-235.71(6):879-85. et al. Biologic monitoring for urinary uranium in Gulf War I veterans. Auvinen A. Sci Total Environ 1994. Inductively coupled plasma mass spectrometry as a simple. plasma and urine and a critical evaluation of reference values for the United Kingdom population. Jarrett JM.S. et al.22–Bioassay at uranium mills. Renal effects of uranium in drinking water. Karpas Z.82(4): 527-532. Health Phys 1996. rapid. McDiarmid MA. Uranium daily intake and urinary excretion: a preliminary study in Italy. Element reference values in tissues from inhabitants of the European community. Charp P.S. Kurttio P. Costa R. Pekkanen J. Saha H. Military deployment human exposure assessment: urine total and isotopic uranium sampling results. Environ Res 2004. Van der Venne MT.

90-6.0) 9.55) Sample size 2820 2522 01-02 03-04 01-02 03-04 01-02 03-04 4. Animal and human studies have shown that perchlorate can inhibit thyroid hormone production (NAS.80 (3.0 (8.0) 9.40-11.40 (8.30-6.70-3.08-3.90 (5. 7601-90-3 General Information Perchlorate is an inorganic chemical containing one chlorine and four oxygen atoms.01 (2.5 hours and has a small estimated volume of distribution (Crump and Gibbs.30) 6.0 (9. Other manufactured uses include fireworks. and electroplating. 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.20-12.00) 3.40-6.0-17.0 (8.93-4.32 (3.93 (4.00-6.40-5.31) 2.40) 3.20 (2.0 (12.90 (2.0) 14.30 (5.10-7.07-4. matches. Perchlorate is excreted unchanged from the human body with an estimated elimination half-life of about 7.0-15.76) 4.0 (12.70-7.70-12.90-11.20 (6.0 (11.21 (2.05 (2.0-19.50) 3.70 (3.0 (11.89-3.0 (10.20 (5.80) 12.50 (8.0-17.0) 9.40 (5.0) 13.22-5.30 (5.30 (2. Perchlorate has been characterized as a mobile and persistent ground and surface water contaminant.0-17.0) 19.05.18-3.50-7.10) 5.16) 3. 2006) and accumulate in nitrate-rich mineral deposits mined for use in fertilizers Urinary Perchlorate Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.80-15.0-17.0) 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 3.80-12.10-11.40-4.0) 374 314 828 721 1618 1487 01-02 03-04 01-02 03-04 4.20 (8.0-18.0 (11.60) 8.35 (3. Large doses of perchlorate have been used as a medicine to treat hyperthyroidism and to diagnose disorders related to thyroid or iodine metabolism.50) 5.0) 9.0 (12.0-14.40-13.40 (5.0) 1335 1229 1485 1293 01-02 03-04 01-02 03-04 01-02 03-04 4.0) 11.60-7.62 (3.12) 3.80 (3.0-15.0 (11.70-3.38) 5.0) 9.70-6.60-6.10 (7.0 (11.g.0) 13.40) 2.96 (3.90-9.65) 3.70 (3. but has strong oxidant properties in the presence of concentrated acids.90-12.20) 3.40 (3.90 (5.20-11.50-4.0 (11.00-5.19 (3.0 (12.0-17.00-6.60 (4.20-3.75-3.81-16.22 (2.70-9.90 (4.90-3.50) 6.0 (9.02 (3.0 (9.50) 11.0 (11.0) 13. small amounts of perchlorate can form naturally in the atmosphere (Dasgupta et al.60 (4.0) 14.Perchlorate Perchlorate (Urbansky.0) 11.0) 16. milk. potassium. interval) 3.50-11. certain catalytic metals.0-23.40) 90th 10.0) 15.44-4.50 (3.0) 14.40) 4.90-10.00) 5.90) 6.26 (2. 1998). 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.80 (6.0) 13.56) 3.76 (3. lettuce) can be the main sources of intake for humans (FDA.50) 5.20 (4.50-4.80) 75th 6.0) 11.40-4. 2002).0) 9.80-4.87-3.00) 3.0) 95th 14.39-4.0-29.0 (9..60) 5. see Data Analysis section) for Survey years 01-02 and 03-04 are 0.0-17.0) 13.93-3.0) 10.10 (6..10-11.30 (2.81) Selected percentiles ( 95% confidence interval) 50th 3.0 (11.10 (5.40) 3.67-5.0 (11.0 (8.46) 3.90) 5.20) 4.80) 3.90-9.90 (5.03) 3.00) 7.20 (2.S.20-4.20-4.45-4.0) 10.49-3. 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. Survey years 01-02 03-04 Geometric mean (95% conf.30-7.0) 15. Drinking water. Perchlorate was added to the U.80-4.0-18.20 (7.40 (5. 2007).80-8.0) 10.20) 7.40-7. 2001-2002 performed on surplus samples (variable unavailable of NHANES website) Fourth National Report on Human Exposure to Environmental Chemicals 243 .80 (7.80) 7.54 (3.10 (6.30-7.0-18.84) 14.0) 13.10-4. laboratory analysis.0) 8. and reducing agents.66) 3.10-12.0) 708 617 681 652 1228 1092 Limit of detection (LOD. or ammonium salt.0 (8.05 and 0.30-17.90 (3.30) 6.0 (11.50 (5. population from the National Health and Nutrition Examination Survey.70) 3.40 (4.47-4.50-3. 2005).09) 3.S.29-3.11) 4.90-3.10) 3.80-6.40) 3. It is normally found and produced as the anion of a sodium. and certain plants with high water content (e.40) 6.19-4.0) 8.0 (9.75 (3.10 (2.0 (9.0-20.30-19. leather tanning.68) 4. Perchlorate is stable under most environmental and physiological conditions.40 (3.70 (3.11) 3.70-11.10) 5. and limited applications in pharmaceutics.0 (8.0) 13.51 (3.40 (4.51 (3.S.70-5.0) 13.EPA.60) 3. 2005). In addition.20 (4.74-3.60 (7.00) 4.88) 3. fabric dyeing.10) 3.0) 12.90-11.0 (9.79 (2.0 (13.10) 12.

10 (1.75) 3.20) 8.90-20.20-3.40) 17.64-3.EPA.90 (7.87 (5.30 (3.0) 13. gender.60-11.10 (2.1) 8.40 (3.33 (7.90 (2.30) 3.56-3.20 (4.50) 6. thiocyanate.S.4 (8.39 (3.25) 5.46-13. 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.54 (2.S.14 (2.96) 2. Many factors may be important in consideration of perchlorate action on the thyroid: dose.61-10.93-7.67) 5.0) 4.47) 2.93-8.7 (11..40) 5.54 (3.02) 3.90-2. 2005). dietary iodine intake.60-3.0) 11. suggesting its tumorgenic effect is a result of a chronic increase in thyroid stimulating hormone indirectly resulting from iodine uptake inhibition. 2001.60-5.1 (11.Perchlorate inhibition (RUI).6) 20.90-9.3) 12.89 (2.60-15.00) 9.70) 10.20 (7.76 (3.04-3. U. nitrate.70-15.22-4.10 (4.73) 3.20 (3.10-7.00 (2.30-5.. Li et al.50 (3.16-3. 2006.99 (5.20) 3.0 (9.50) 2. but without effects on serum levels of thyroid stimulating hormone or thyroxine (Braverman et al.S.24 (4.70) 2..51-4. 2002.99-3.0) 6.10) 6.90 (2.00) 4.91) 4.53 (2.20-10.80-3.EPA.81-3.21 (2. although iodine intake was higher than U. levels. In the U. women with urinary levels of iodine less than 100 micrograms per day. interval) 3.0 (10.52 (8.0 (9.60) 8.87-3.1-16.S. Greer et al.30 (6.50-3.39-4.90-11.59) 3.83 (5.70 (2.37-13.24-2.1 (8. perchlorate is negative in most genotoxic assays (U.10 (4.30-5.60) 10.S.50-5.0) 7.87) 7.32) 5.00-2.8 (11.15-12.50-9. menopausal status.60-8.80) Selected percentiles ( 95% confidence interval) 50th 3.1-14. Also.0) 14.50) 5.00) 3..40 (7. up to 68% RUI has been demonstrated..40 (3.35 (4.0) 10.0 (11..43) 6.82 (5. 2005. 2007).97-5.0) 12.3-14.S.0) 374 313 827 715 1617 1476 01-02 03-04 01-02 03-04 3.0 (11.00 (4.26) 4.37 (4.41) Sample size 2818 2504 01-02 03-04 01-02 03-04 01-02 03-04 5.5 (13.90-3.39) 2.0) 12.0-17.80 (7.52-9.3) 8.70-3. NAS. population from the National Health and Nutrition Examination Survey.12 (6.20-9.20-4.07 (2.0) 12.40-10.0-19.02-4.61-5.0 (11. 2002).66) 3.29) 2.0) 13.77 (3.2) 8.0 (8.90) 5. 2003.93-5. 2005).10-3.87 (7. 2005).70 (2.90 (4.0-44.25) 5.08 (3. Though it produces follicular cell thyroid tumors in animal studies at goitrogenic doses.46 (3. chronicity of exposure.04-3. Lawrence et al.00-3.19-6. During gestation and infancy.93-5.30) 90th 9.3) 11.10) 13. 2002.35 (2.22-6.86) 4.25) 5.10) 3.00-11.0) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites 3.95 (2.36 (8.74) 7.20 (2.05 (4.60-8.30-10.4 (11.10 (6.56 (3.80-3.0) 9.0 (8.08) 3.45-2. Lamm and Doemland.30) 75th 5.4 (11.42 (3.0) 9.4 (10.71 (5.29-6.64) 5.44) 3.0) 708 616 680 648 1227 1080 2001-2002 performed on surplus samples (variable unavailable of NHANES website) 244 Fourth National Report on Human Exposure to Environmental Chemicals . However. 1999.6-17.0) 1335 1220 1483 1284 01-02 03-04 01-02 03-04 01-02 03-04 3.33-12..50) 9.1-13.22 (2.2) 8.60 (3.25 (3.87) 2.58) 2.09) 3.50) 2.18-3.76-3.40 (4.20-3.S. urinary perchlorate at environmental exposure levels were inversely associated with thyroxine levels and positively associated with levels of thyroid stimulating hormone (Blount et al..19-10. 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.84) 2. 2005. levels and sufficient in most participants (Tellez et al..4) 13.22-4. medications).35) 3.70-4.89-3. and the presence of other substances known to affect thyroid function (e.03 (2.45) 3.5) 8. 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.80 (4.60-11.g.51 (3.6) 12.70 (4.30 (5..50) 95th 12.60-5.10) 4.0-14. Short term human studies of the effect of perchlorate on RUI have been used for risk estimation (Greer et al. Steinmaus et al.09 (7.4-16. in a representative sample of U.98) 3.70-5.0 (9.33-6.61 (5.4) 8.60) 3.34-3.72 (3. congenital hypothyroidism is a condition for which nearly all newborn blood is screened.80 (7.40) 3. it is known that maternal and congenital hypothyroidism adversely effects neurological development and decreases learning capability.3 (10.0-14. 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.00 (6.46-4. age.93) 3.50 (6.41-9. 2000).0) 12.20 (6.26 (3.44-6.90-15.12-2.1-22.30) 5. Survey years 01-02 03-04 Geometric mean (95% conf.60-6.

Richman K. Barnard JC. References Blount BC. Osterloh JD.. Valentin-Blasini L. EPA reference dose (Blount et al. Has perchlorate in drinking water increased the rate of congenital hypothyroidism? J Occup Environ Med 1999. Crump KS.S. Food and Drug Administration (FDA). Chacon PM.41(5):409-411. Lawrence JE. Additional information about exposure and health effects is available from the U. Erratum in: J Occup Environ Med 2004. Primary congenital hypothyroidism. May 2007. Li Z. Kirk AB. 2005. Li FX. Available at URL: http://www. Neonatal thyroxine level and perchlorate in drinking water. and nitrate on thyroid function in workers exposed to perchlorate long-term.S.45(10):1116-1127.fda. Urinary perchlorate and thyroid hormone levels in adolescent and adult men and women living in the United States. The effect of perchlorate. Finding a measurable amount of perchlorate in urine does not mean that the level of perchlorate causes an adverse health effect. (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. Thyroid 2000. Erratum in: Environ Health Perspect 2005.114(12):1865-1871. Rutherford GW. Osterloh JD. Washington (DC): National Academy Press. Page Last Updated: 05/28/2009.10(8):659-663. Sesser DE. et al. Valentin-Blasini L.gov/Food/FoodSafety/ FoodContaminantsAdulteration/ChemicalContaminants/ Perchlorate/ucm077653.Perchlorate be unlikely to occur without overt perturbation of thyroid homeostasis. Environ Health Perspect 2006. Pirkle JL. Environ Health Perspect 2002. Blount BC. J Occup Environ Med 2000. Doemland M.S. Lamm S. Perchlorate Exposure of the US Population. 2007). Impact of smoking and thiocyanate on perchlorate and thyroid hormone associations in the 2001-2002 national health and nutrition examination survey. et al. Blount et al. thiocyanate. J Occup Environ Med 2003. CFSAN/Office of Plant & Dairy Foods. Buffler PA. Crump KS. Lamm SH. Pino S. Greer SE. National Academy of Sciences (NAS). Environ Health Perspect 2007.atsdr. Steinmaus C.42(2):200-205.17(4):400-407. The effect of short-term low-dose perchlorate on various aspects of thyroid function. most of the population is considered to be below the U.115(9):1333-1338.113(8):10011008. et al.110(9):927-937. Braverman LE. 6/2/09 Greer MA. Landingham CB. Pleus RC. epa. Abarca CR. Dyke JV. Byrd D. and environmental perchlorate exposure among residents of a Southern California community. Preliminary Estimation of Perchlorate Dietary Exposure Based on FDA 2004/2005 Exploratory Data. et al. Also. Tellez RT. 2001-2002. Braverman LE. Gibbs JP.cdc. Lau EC.htm. J Expo Sci Environ Epidemiol 2007. Pino S. Dasgupta PK.46(5):509.EPA at: http://www.11(3):295. Long-term environmental exposure to perchlorate through drinking water and thyroid function during Fourth National Report on Human Exposure to Environmental Chemicals 245 . Braverman LE.. Health Implications of Perchlorate Ingestion. Magnani B.90(2):700-706..html and from ATSDR at: http://www.html.40(21):6608-6614. Biomonitoring Information Urinary perchlorate levels reflect recent exposure. J Clin Endocrinol Metab 2005. Lamm SH. Cross M. Skeels MR.gov/toxpro2. Perchlorate in the United States. Howd R.113(11):A732. National Research Council of the National Academies. Thyroid 2001. Blount BC. 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. When these NHANES 2001-2002 urinary levels of perchlorate are used to calculate daily oral intakes for the U. 2005).gov/safewater/ccl/perchlorate/perchlorate. 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. Analysis of relative source contributions to the food chain. newborn thyroid function. He X. Jackson WA. Environ Sci Technol 2006. Compared to a previous study of pregnant women in three Chilean communities with varying perchlorate levels in the drinking water. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Caldwell KL. 2005). Deyhle GM. Lawrence J. Daaboul JJ. Health effects assessment for environmental perchlorate contamination: the dose response for inhibition of thyroidal radioiodine uptake in humans. Kelsh MA. Miller MD. Lamm SH. the women in the community with the highest drinking water levels had mean urinary perchlorate levels about 40 times greater than the geometric mean for participants in NHANES 2001-2002 aged 20 years and older (Tellez et al. Goodman G. Environ Health Perspect 2005. Low dose perchlorate (3 mg daily) and thyroid function. Benchmark calculations for perchlorate from three human cohorts. population. Mauldin JP. Pirkle JL. The levels seen in NHANES 20032004 show a similar pattern to NHANES 2001-2002.

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

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

Survey Geometric mean (95% conf. C7).. and in offspring. pancreas.S. All sources of human exposure are uncertain. by high protein binding in plasma and other proteins. The liver toxicity of several PFCs is evident by vacuolization and lipid accumulation in both rodent and monkey livers (Seacat et al. peroxisomal proliferation. C6.. PFOS and PFOA levels in archived bird eggs from Sweden have increased thirtyfold from 1968 to 2003 (Holmstrom et al. but probably include dietary sources (Kannan et al. but limited observations in humans suggest that only one-fifth of the total body clearance is renal (Harada et al. It is unclear if environmentally degraded telomer products are a major source of other PFCs. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.4. Kannan et al. may metabolize or degrade to PFOA (Dinglasan et al. 2005.. PFOA preparations used in many studies may also contain a small percentage of other chain length perfluoroalkyl acids (i. Keller et al. 2005. The PFCs often measured in human serum are listed in the table. Vanden Heuvel et al..... 2006a. population from the National Health and Nutrition Examination Survey. 248 Fourth National Report on Human Exposure to Environmental Chemicals . Unlike many organohalogen contaminant chemicals. Guruge et al. Some of the effects in animals may be mediated through peroxisomal proliferation. Excepting PFOS and PFOA. Lau et al.. in a wide variety of marine and land animals (Kannan et al. Olsen et al. Prevedouros et al. 1995. 2007a). growth retardation and delayed sexual maturation (Kennedy et al.. Tittlemier et al. but the relevance of peroxisomal pathways in humans is unclear (Kennedy et al. The elimination half-life of PFOA in humans is roughly estimated to be 3. 2007). there is limited information on the sources. approximately 4. In some cases..S. or effects of other PFCs.5 years and for PFOS. 2005)... Taniyasu et al. kidney. 2005).. thymus and spleen. human toxicokinetics.. which may vary for some chemicals by year and by individual sample.. U.. heptadecafluoro-1-decanol. 2003. 1993). endocrine and immune effects.. 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. EPA. 2003a and 2004a).. Human health effects from PFCs at low environmental doses or at biomonitored levels from low environmental exposures are unknown. but still can have long residence times in the body. PFOA has been reported to cause liver. 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.. the 8-2 telomer. 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. including immunologic effects and tumor induction. Both PFOA and perfluorodecanoic acid have been shown to reduce androgen levels in laboratory animal studies (Biegel et al. PFCs have been identified in surface coastal and ocean waters (Yamashita et al. Lau et al. 2004. 2005). The ammonium salt of PFOA has been tested at high doses in mammalian animal studies and produced altered weights of the liver. For instance. see Data Analysis section) for Survey year 03-04 is 0.8 years (Olsen et al... 2005. environmental fate. 2004. < LOD means less than the limit of detection. 2003). 2003). and in human blood and semen (Calafat et al. 2004). 2004). Bookstaff et al. 2004.. 2002.. 2006. 2004. PFOA (and probably other perfluoroalkyl acids) exist in the anionic state at physiologic and environmental pHs and their distribution in the body is determined. and β-oxidation of lipids (Kudo et al.. 1990).. 2000.e. in part. PFOA is mostly excreted in the urine in animal studies. the perfluoroalkyl acids (PFOA and PFOS) do not tend to accumulate in fat tissue.Perfluorochemicals PFOS greater than 2000-fold over aquatic levels). hepatotoxicity. C5.

2007a. 2005).800 (. and no substantial age trends were seen within adults ages 20-69 (Olsen et al. population from the National Health and Nutrition Examination Survey. 2003a)..400-.10) * 03-04 03-04 * * < LOD < LOD < LOD . 2003a. 2005).500) . which may vary for some chemicals by year and by individual sample.700 (. U.800 (.80) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD 75th . Cook et al. monkeys.600-2... Two recent cross-sectional human studies observed a negative correlation of birth weight with serum levels of PFOA (Apelberg et al. population. and changes in thyroid hormone concentrations (Grasty et al.500-1. perfluorohexanesulfonate (PFHxS).S. 2003. PFOS.800 (.00) .80) 640 1454 03-04 03-04 * * < LOD < LOD .700) .400-1. At high but non-toxic maternal doses of PFOS. 2003a.500 (<LOD-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.400-1.400 (<LOD-.40) . PFOS.50) . 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. 2003). In such studies. 2004..400-1. and humans. However.20) . At doses causing maternal toxicity.500-1. 2003a.10) .10) .. 2001.. animal and human serum PFOA levels have been compared: serum levels associated with toxic effects in animals are 66-11. Fourth National Report on Human Exposure to Environmental Chemicals 249 . Harada et al. interval) Selected percentiles ( 95% confidence interval) Sample 95th . Roughly similar levels of PFCs in serum have also been measured previously in other samples of the U. elderly and children. A study of workers chronically exposed to primarily PFOA showed no biochemical evidence of hepatotoxicity or hormonal changes (adrenal. Analysis of the NHANES 20032004 subsample demonstrated higher levels of PFOA and PFOS in males and a slight increase in levels of PFOS with age (Calafat et al. 2007).400) .400-1. 1999. Lau et al.900 (. or increased cancer rates (Alexander et al.500) 90th .900 (.500) . 2007b)..500 (. 2003.. 2003. 2003). thyroidal).Perfluorochemicals and testicular tumors in high dose animal testing (Biegel et al. 2004b).00 (.300 (<LOD-.. Due to marked intergender differences in the elimination of PFOA in rats and substantial differences in the half-life of PFOA in rats. 2007a.400-.500-1.500 (. Fei et al. 2004a.80) 485 538 962 Limit of detection (LOD.300 (<LOD-. In comparing three separate reports on adults. PFOA.500-1.400 (<LOD-..20) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD .300 (<LOD-. Olsen et al.500) .. 2004). 2003). Olsen et al. 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. hepatotoxicity.10 (.400 (<LOD-. 2007. PFOA.. Animal studies of PFOS have demonstrated weight loss.400-1. Kennedy et al. Olsen et al. Serum Perfluorodecanoic acid (PFDeA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.600 (. Slightly higher levels of PFOS and PFOA in males than females have been noted in several other studies (Calafat et al. Twelve different PFCs were measured in the sera of NHANES 2003-2004 participants. Late gestational exposure to PFOS in animal studies has also demonstrated early neonatal lethality. U. and other PFCs have not been classified as to human carcinogenicity by IARC or NTP. reproductive..600 (.300-1.600 (.00) . 1992..500-3. the potential to estimate risks to humans from animal doses is uncertain. Biomonitoring Information Serum levels of PFCs (particularly PFOA and PFOS) tend to reflect cumulative exposure over several years... 2004.. EPA.800) 1.S. developmental and teratogenic effects were demonstrated in offspring. development in offspring was stunted and hypothyroxinemia was observed.800) 1. Survey Geometric mean (95% conf.. 2003a). 2004). see Data Analysis section) for Survey year 03-04 is 0.108 times higher than background serum levels in humans (Butenoff et al. 2007b. and there was no clear evidence of excess all-cause or diseasespecific mortality.500) . EPA. the median PFCs values tend to be roughly similar in these age categories (Olsen et al..00) .800 (.500-. possibly related to lung immaturity (Lau et al.900 (..3. Thibodeaux et al. < LOD means less than the limit of detection.S. Effects on serum liver enzymes in limited observational studies of human occupational exposures are unclear..

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

Survey Geometric mean (95% conf. which may vary for some chemicals by year and by individual sample. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. < LOD means less than the limit of detection.900) < LOD .900) < LOD 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD .300 (<LOD-. Serum Perfluoroheptanoic acid (PFHpA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.400) .500) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th < LOD 90th * 03-04 03-04 * * < LOD < LOD < LOD < LOD .400 (<LOD-. 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.Perfluorochemicals Serum Perfluorododecanoic acid (PFDoA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.500 (<LOD-.300 (<LOD-. < LOD means less than the limit of detection.3. Fourth National Report on Human Exposure to Environmental Chemicals 251 .400 (.600) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .400 (<LOD-. which may vary for some chemicals by year and by individual sample.0. population from the National Health and Nutrition Examination Survey.S. interval) Selected percentiles ( 95% confidence interval) Sample 95th .S.500) 485 538 962 Limit of detection (LOD.600) < LOD .300-. see Data Analysis section) for Survey year 03-04 is 1. 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 (. population from the National Health and Nutrition Examination Survey.500-. Survey Geometric mean (95% conf.

60) 9.10 (.966 (.30) .77-2.20 (1.00 (1.900-1.00-6.50 (1.60) 2.Perfluorochemicals Serum Perfluorohexane sulfonic acid (PFHxS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.00) 3.20-1.721-1.17 (1.30-9.42 (1.60-4.90-2.00) 2.10) 1.92 (1.40) 1.30-2.40) 1.834-1.10) 8.90 (1.10 (4.30-12.800-1.90) 8.80) 5.40 (2.20) 1.50) 2.984 (.50-6.00 (1.1.1) 485 538 962 Limit of detection (LOD.62-2.900-1.00-7.50 (4.70-2.70-10.00 (1.30 (1.60-3.50-6.80) 90th 2. interval) .90) 90th 5.50-10.70) 1.900-1.80-4.56-1.05-2.70) 13.5) 8.80-3.70) 2.852 (.10) 1053 1041 03-04 03-04 03-04 .60) 1.S.30) 3.30 (3. interval) 1.80-2.700 (.60-7.14) Selected percentiles ( 95% confidence interval) Sample 95th 3.60-2.70) 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 1.30 (6.10-5.30 (7.10) 5.20 (1.80-8.40 (1.80-8.0) 8.72 (1.80 (1.900-1.80) 3.10 (.70) 2.700-1.20-3.900 (.20) 485 538 962 Limit of detection (LOD.80-4.50 (1.80-7.50 (1.90) 1.80-4. population from the National Health and Nutrition Examination Survey.900-1.20 (6.50) 2.00 (2.00) 1.826-1.09 (.90 (1.30 (1.912-1.10) 75th 3.3.51) 1.900 (.697-1.20 (1.90) 1.12) .67-2.80 (1.30) 3.40-1.00 (.60 (6.44 (2.60-4.90-10.40) 640 1454 03-04 03-04 1.00 (5.586-. Survey Geometric mean (95% conf.20 (6.86 (1.80) 1.50-3.809) 1.10) 4.20-1.40) .16) Selected percentiles ( 95% confidence interval) Sample 95th 8.90 (2. Survey Geometric mean (95% conf.40-1.30) 03-04 03-04 .50) 6.60-3.60-2.20-1.00-1.10-9.600-.10-9.91) 2.70-2.70-5.60 (1.60-2.40) 4.30-6.54) .90) 1. see Data Analysis section) for Survey year 03-04 is 0.30 (2.816-1.10) 75th 1.80-12. Serum Perfluorononanoic acid (PFNA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.00 (.50 (2.70 (2.90 (1.00-8.73-2.40 (1. see Data Analysis section) for Survey year 03-04 is 0.80) 4.S.50 (6.6) 7.20 (1.90 (1.689 (.10) 1.40) 640 1454 03-04 03-04 2.26) 2.861 (.90-19.90) 3.72) 1.01 (1.3 (9.04) .03) 1.70) 1.800 (. 252 Fourth National Report on Human Exposure to Environmental Chemicals .80-6.20) .60) 3.87-2.0) 1053 1041 03-04 03-04 03-04 1.50 (4.70) 3.70-6.10 (4.70) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 1.10 (.20) 1.50 (1.20-2.70 (1.14 (.00) 1.16) .20-1.90 (4.10) 4.30 (1.30) 3.10) 6.40 (1.00-1.835-1.30 (2.17-1.00 (1.20) 03-04 03-04 2.60 (1.963 (.40 (1.30 (1.93 (1.27) 1.90 (4. population from the National Health and Nutrition Examination Survey.5) 5.900) 1.40-3.10) 6.80-7.08) 2.60 (1.70-7.50 (6.80 (4.40) 2.900-1.10 (1.60-8.20) 2.80-3.

interval) 3.90-4.60 (6.7 (13.8) 46.70-7.9) 27.8-22.60 (6.50-4.21-3.07-4.40 (4.0-16.10 (3.95 (3.5) 18.8) 27. Serum Perfluorooctane sulfonic acid (PFOS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.2 (19.7 (19.3) 42.60-9.00 (3.40) 90th 7.30 (5.20-9.70) 6.9 (19.0-20.70 (3.2 (18.5-62.0) 21.2) 30.8-35.3 (28.5) 8.4 (19.1 (23.8 (34.3) Selected percentiles ( 95% confidence interval) Sample 95th 54.00 (5.2 (21.9-38.0) 36. interval) 20.4-25.9) 22.4) 75th 30.80 (7.40) 5.4 (17.20) 4.2 (28.8) 32.70) 4.5-33.40) 3.70) 3.9-19.18 (3.50-13.9-23.89 (3.40-6.90-4.50) 4.11 (2.2 (16.5 (28.Perfluorochemicals Serum Perfluorooctanoic acid (PFOA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.96 (3.20) 5.3) 41.27) Selected percentiles ( 95% confidence interval) Sample 95th 9.4) 20.1-24.70 (5.8 (45.7-23.7-53.4) 640 1454 03-04 03-04 23.3-61. Survey Geometric mean (95% conf.50) 7.8 (37.8-22. population from the National Health and Nutrition Examination Survey.70-10.5) 57.5) 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 21.60) 03-04 03-04 3.5-21.0 (27.30-6.6) 9.50 (4.10 (6. Fourth National Report on Human Exposure to Environmental Chemicals 253 .5 (28.4) 21.1-52.40-17.70-7.80 (6.60) 8.6) 62.67-4.6) 42.65-4.3) 485 538 962 Limit of detection (LOD.30-5.2) 640 1454 03-04 03-04 4.4-42.80 (6.7 (35.7-30.9) 9.3-22.8-22.2-57.6) 18.9) 22.3 (44.3 (35.10) 5.5) 32.80-9.40-10.30) 6.2) 45.82) 4.10 (3.70-9.85-4.6 (42.10-3.00 (5.3 (17.0) 23.8-78.6) 7. see Data Analysis section) for Survey year 03-04 is 0.20) 7.1 (24.5) 19.35) 3.60 (7.1) 15.40 (6.37 (2.2 (27.1) 57.1.7-49.70 (5.9 (13.47-4.1-36.0) 43.8-81.30-3.4 (23.60-13.00) 3.6) 1053 1041 03-04 03-04 03-04 3.9 (22.20) 7.90-12.5) 9.90 (7.0) 21.30-8.40-14.4-17.60 (4.7-69.7) 39.6 (44.6) 35.1) 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 4.60 (3.79) 4.4 (19.84-3.30 (3.S.40-6.7 (43.53) 3. population from the National Health and Nutrition Examination Survey.5) 7.90 (5.6 (19.20-4.20-5.7 (35.20 (4.5-23.50 (3.3) 28.3 (35.60-14.80) 8.0-66.80-12.2-22.0) 485 538 962 Limit of detection (LOD.6 (35.9 (17.8-30.0 (20.1-25.6-50.20) 10.30 (3.0) 03-04 03-04 19.90 (7.6) 21.6-24.6-45.4.30) 7.40) 75th 5.5) 1053 1041 03-04 03-04 03-04 14.90) 6.1-35.20 (4.91) 3.80 (5.60 (5.99-3.S.47 (4. see Data Analysis section) for Survey year 03-04 is 0.1-33.4) 56.4 (28.7 (7.70-5.1 (19.50-6.80-4.7 (43.30-11.7-33.20) 5.0) 90th 41.90 (7.60-6. Survey Geometric mean (95% conf.0-70.27) 4.2) 30.

200-.300 (.300 (. which may vary for some chemicals by year and by individual sample.400) 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD . see Data Analysis section) for Survey year 03-04 is 0.400) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th 90th . see Data Analysis section) for Survey year 03-04 is 0.300 (.300) .200-. population from the National Health and Nutrition Examination Survey.200 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.300 (.200-.500) . interval) Selected percentiles ( 95% confidence interval) Sample 95th .400 (<LOD-. 254 Fourth National Report on Human Exposure to Environmental Chemicals .300 (.500) < LOD 485 538 962 Limit of detection (LOD.200-.300 (.300 (.200-.200-.500) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD . < LOD means less than the limit of detection.200-.300 (.300) . interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th < LOD 90th * 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .S.2.300 (.300 (.300) .Perfluorochemicals Serum Perfluorooctane sulfonamide (PFOSA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.300) .300) .300-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.200-.300-.500) .300 (.300 (. Serum 2-(N-Ethyl-perfluorooctane sulfonamido) acetic acid (Et-PFOSA-AcOH) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.300) .500) 485 538 962 Limit of detection (LOD.300 (. Survey Geometric mean (95% conf.500) . population from the National Health and Nutrition Examination Survey.4.300-. which may vary for some chemicals by year and by individual sample.200-.300) * 03-04 03-04 * * < LOD < LOD < LOD < LOD . Survey Geometric mean (95% conf.300-.200-.300 (.300) . < LOD means less than the limit of detection.S.

10-1.80) 1.900 (.90) .10 (.30) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th < LOD 90th * 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD .300 (<LOD-1. population from the National Health and Nutrition Examination Survey.10-1. < LOD means less than the limit of detection. which may vary for some chemicals by year and by individual sample.30) 1.600 (<LOD-.60) 640 1454 03-04 03-04 * * < LOD < LOD .20-1.700 (<LOD-.20 (1.700 (<LOD-. population from the National Health and Nutrition Examination Survey.700 (<LOD-.70) 1.800 (<LOD-. see Data Analysis section) for Survey year 03-04 is 0.10-1.900-1.900) 485 538 962 Limit of detection (LOD.700 (<LOD-.10 (1.10 (.10) * 03-04 03-04 * * < LOD < LOD .Perfluorochemicals Serum 2-(N-Methyl-perfluorooctane sulfonamido) acetic acid (Me-PFOSA-AcOH) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.700) 90th 1.900-1. see Data Analysis section) for Survey year 03-04 is 0.10) 1.600 (<LOD-1.40) < LOD < LOD .00-1.30) 1.700) 1.700) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .30 (1.700 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.10 (.S.10) .600 (<LOD-1.30 (1.900-1.700 (<LOD-2.300-2.20) 1.700) .00 (.800) .S.600 (<LOD-1.60) 485 538 962 Limit of detection (LOD.40) 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD .900-1.10) .30 (1.800) .300 (<LOD-. Serum Perfluoroundecanoic acid (PFUA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.00 (. Survey Geometric mean (95% conf.3.500 (<LOD-.30) . which may vary for some chemicals by year and by individual sample.50 (1.00 (.00) < LOD .50 (1.10-1.40) 1.900-1.700) 1.400 (<LOD-.900-1.80) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD . < LOD means less than the limit of detection.10-1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1. Fourth National Report on Human Exposure to Environmental Chemicals 255 . Survey Geometric mean (95% conf.900) 1.6. interval) Selected percentiles ( 95% confidence interval) Sample 95th .900) .900-1.80) 1.00 (.400 (<LOD-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.50) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD 75th .900 (<LOD-1.600) .700 (<LOD-.10) 1.

Kawashima Y. Grey BE.99(2):253-261. de Voogt P. and ex vivo studies. Rev Environ Contam Toxicol 2003. Liu RC. Environ Health Perspect 2007.and perfluorinated acids. Reidy JA. Caudill SP. Morikawa A. Holmstrom KE.39(3):363-380.7(4):371-377.S. Reidy JA. et al. Apelberg BJ.38(10):2857-2864. Toxicol Appl Pharmacol 1990. Olsen J.Perfluorochemicals References Alexander BH. Katakura M.63:490496. Chemosphere 2006b. Mandel JH. Mandel JH. Regul Toxicol Pharmacol 2004. Bookstaff RC. Kannan K. Environ Sci Technol 2005. Calafat AM. Kuklenyik Z. Inoue K. Bandai N. Saito N. Suzuki E. Fluorotelomer alcohol biodegradation yields poly. Perfluorinated chemicals and fetal growth: A study within the Danish National Birth cohort. Environ Sci Technol 2005. Yamashita N. et al. The influence of time.1968--2003. Butenhoff JL. Kumar KS. Reidy JA. et al. et al. Bignert A. Peterson RE. et al. population: data from the National Health and Nutrition Examination Survey (NHANES) 2003-2004 and comparisons with NHANES 1999-2000. Biegel LB. Biegel LB. Sasaki S.40:21282134. Birth Defects Res B Dev Reprod Toxicol 2003. Mechanisms of extrahepatic tumor induction by peroxisome proliferators in male CD rats. Reidy JA. Gaylor DW. Frame SR. Cook JC. Characterization of risk for general population exposure to perfluorooctanoate. brominated. Perfluorinated organic compounds in human blood serum and seminal plasma: a study of urban and rural tea worker populations in Sri Lanka. Environ Res 2005. Rogers JM. Calafat AM. Tully JS. Environ Sci Technol 2005. 2007b. Androgenic deficiency in male rats treated with perfluorodecanoic acid. Watanabe T. Perfluorooctanesulfonate and related fluorochemicals in human blood from several countries. Environ Sci Technol 2004.34(4):351-384. Kuklenyik Z. Tarone RE. population: Data from the National Health and Nutrition Examination Survey (NHANES) 1999–2000. Loganathan BG. Burris JM. Kudo N. Needham LL. Frame SR. Yun SH. Needham LL. Calafat AM. sex and geographic factors on levels of perfluorooctanesulfonate and perfluorooctanoate in human serum over the last 25 years. in vivo. Environ Sci Technol 2007a. Taniyasu S. Chlorinated. Yoshinaga T.124(2):119-132. Environ Sci Technol 2006a.39(1):80-84. Moore RW. Calafat AM.115(11):1670-1676.115(11):1596-1602. Day RD. Toxicol Sci 2001. Mortality of employees of a perfluorooctanesulphonyl fluoride manufacturing facility. Yamashita N. Yoshinaga T. O’Connor JC. Kuklenyik Z. et al. Saito N. Cord serum concentrations of perfluorooctane sulfonate and perfluorooctanoate in relation to weight and size at birth. J Environ Monit 2005. Effects of ammonium perfluorooctanoate on Leydig cell function: in vitro. Perfluorinated chemicals in selected residents of the American continent. Polyfluoroalkyl chemicals in the U. Seacat AM. Kamiyama S. Jarnberg U. Murray SM. Toxicol Appl Pharmacol 1995.Koizumi A. McLaughlin JK. Needham LL. Prenatal window of susceptibility to perfluorooctane sulfonate-induced neonatal mortality in the Sprague-Dawley rat.113(2):209-217. Harada K. Ingall GB. Witter FR.179:99-121. Calafat AM. Lau CS. Hurtt ME. Cook JC.46(2):141-147. Seneviratne HR. Inoue K. Harada K. Cook JC.60(1):44-55. Environ Health Perspect 2007. Falandysz J. Environ Sci Technol 2004. Toxicol Appl Pharmacol 1992. Halden RU. Renal clearance of perfluorooctane sulfonate and perfluorooctanoate in humans and their species-specific excretion. Herbstman JB. Environmental and toxicity effects of perfluoroalkylated substances. Rodricks J.39(23):9101-9108.S. Koizumi A. Taniyasu S. Moore JA. Induction of Leydig cell adenomas by ammonium perfluorooctanoate: a possible endocrine-related mechanism. and perfluorinated contaminants in livers of polar bears from Alaska. Needham LL.134(1):18-25. Perkins RG. Keller JM. Kennedy GL Jr. Kannan K. Fei C. Aguilar-Villalobos M. Caudill SP. Ye Y. Induction by perfluorinated fatty acids with different carbon chain length of peroxisomal beta-oxidation in the liver of rats. Perfluorochemicals in pooled serum samples from United States residents in 2001 and 2002. 256 Fourth National Report on Human Exposure to Environmental Chemicals . Laane RW. Wong LY. et al.38(17):4489-4495. Chem Biol Interact 2000.104(2):322-333. Olsen GW. Mabury SA. O’Connor JC. Crit Rev Toxicol 2004. The toxicology of perfluorooctanoate. Grasty RC. Hekster FM. Dinglasan MJ. Environ Health Perspect.60(10):722729. Evans TJ. J Occup Health 2004. Olsen GW.115(11):1677-1682. Olsen GW.68(6):465-471.41:2237-2242. Wijeratna S. Corsolini S. Fillmann G. Mandel JS. Kannan K.39(23):9057-9063. Hurtt ME. Edwards EA. Guruge KS. Occup Environ Med 2003. Tully JS. Serum concentrations of 11 polyfluoroalkyl compounds in the U. Mohotti KM. Arendt MD. Perfluorinated compounds in the plasma of loggerhead and Kemp’s ridley sea turtles from the southeastern coast of the United States. Butenhoff JL. Temporal trends of PFOS and PFOA in guillemot eggs from the Baltic Sea. Kuklenyik Z. Hurtt ME.

54(11):1599-1611. Froehlich JW. Kawashima Y. Moisey J. Church TR. fish. perfluorooctanoate andother fluorochemicals in human blood. Rogers JM. Lau C. Grey BE. Coordinate induction of acyl-CoA binding protein. Serum perfluorooctane sulfonate and hepatic and lipid clinical chemistry tests in fluorochemical production employees. Petrick G. Available from URL: http://www. Butenhoff JL. Zobel LR. htm. Stanton ME. Burlew MM. Larson EB. EPA). Ehresman DJ. Fourth National Report on Human Exposure to Environmental Chemicals 257 . Taniyasu S. fate and transport of perfluorocarboxylates. et al. Seacat AM. Mar Pollut Bull 2005. Toxicol Appl Pharmacol 2004. Subchronic toxicity studies on perfluorooctanesulfonate potassium salt in cynomolgus monkeys. 2007a. (Erratum in: Toxicol Sci 2004. Thibodeaux JR. et al.115(9):1298-1305. Butenhoff JL.Perfluorochemicals Kudo N. Huang HY.113(5):539-545. Burris JM. A global survey of perfluorinated acids in oceans. Serum concentrations of perfluorooctanesulfonate and other fluorochemicals in an elderly population from Seattle. Hansen KJ. 2003a. and food items prepared in their packaging.perfluorohexanesulfonate. Richards JH. Reagen WK.37(12):2634-2639. Environ Sci Technol 2003. Biol Pharm Bull 2003. Preliminary Risk Assessment of the Developmental Toxicity Associated with Exposure to Perfluorooctanoic Acid and its Salts. Burris JM. Lundberg JK. Yamashita N. Horii Y. Sterchele PF. fast foods. Hanson RG.111(16):1900) Olsen GW.74(2):369-381. Thomford PJ. Hansen KJ. Ellefson ME. Olsen GW.111(16):1892-1901. Mair DC.51(8-12):658-668. Half-life of serum elimination of perfluoroo ctanesulfonate. Hansen KJ. Barbee BD. Lundberg JK. Lau C. et al. birds. Nesbit DJ. et al.68(1):249-264. Environmental Protection Agency (U.40(1):32-44. Kannan K. U. Seacat AM. Quantitative evaluation of perfluorooctanesulfonate (PFOS) and other fluorochemicals in the serum of children. Exposure to perfluorooctane sulfonate during pregnancy in rat and mouse. (Erratum in: Environ Health Perspect. J Occup Environ Med 1999. II: postnatal evaluation. Chemosphere 2007b. The developmental toxicity of perfluoroalkyl acids and their derivatives. Washington. Toxicol Sci 2002.S. Butenhoff JL. 1/15/06 Vanden Heuvel JP. Mandel JH. Induction of triglyceride accumulation in the liver of rats by perfluorinated fatty acids with different carbon chain lengths: comparison with induction of peroxisomal betaoxidation.1177(2):183-190. Taniyasu S. Miller JP. Butenhoff JL. A survey of perfluorooctane sulfonate and related perfluorinated organic compounds in water. Epidemiologic assessment of worker serum perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) concentrations and medical surveillance examinations. Exposure to perfluorooctane sulfonate during pregnancy in rat and mouse. Rogers JM. and perfluorooctanoate in retired fluorochemical production workers. Buck RC. Cao XL et al. Olsen GW.82(1):359.68:105–111. Seymour C. J Children’s Health 2004b. Thibodeaux JR. fatty acid binding protein and peroxisomal beta-oxidation by peroxisome proliferators. Chemosphere 2004a. Bronson R. Butenhoff JL. Environ Health Perspect 2003a. Case MT. Mandel JH.41(9):799-806.26(1):47-51.55:3203-3210. Preliminary evidence of a decline in perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) concentrations in American Red Cross blood donors.. Burris JM. Church TR. Burris JM. I: maternal and prenatal evaluations. Biochim Biophys Acta 1993. Ehresman DJ. Hansen KJ.S. Butenhoff JL. J Ag Food Chem 2007. Prevedouros K. Hanari N. Historical comparison of perfluorooctanesulfonate.74(2):382-392. Sources. Mandel JH. Rogers JM. Hansen KJ. Church TR.) Tittlemier SA. Gamo T. and humans from Japan. Olsen GW. Horii Y.epa. van Belle G.45(3):260-270.gov/opptintr/pfoa/pfoara. Yamashita N. Dietary exposure of Canadians to perfluorinated carboxylates and perfluorooctane sulfonate via consumption of meat. Mandel JH. Peterson RE. Burris JM. et al. Olsen GW. fish.2(1):53-76. Olsen GW.198(2):231-241. Grey BE. Pepper K. Kannan K. et al. Environ Sci Technol 2006. Toxicol Sci 2003. J Occup Environ Med 2003b. Environ Health Perspect 2005. Korzeniowski SH. Toxicol Sci 2003. Hanson RG. Cousins IT. Perfluorooctanesulfonate and other fluorochemicals in the serum of American Red Cross adult blood donors. Helzlsouer KJ. Olsen GW. 2003. Olsen GW. Olsen GW. Environ Health Perspect.

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

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

Parker MG.103:582-587. Calafat AM. Draft Update Monograph on the Potential Human Reproductive and Developmental Effects of Di(2-ethylhexyl) Phthalate (DEHP). Filser J. Mechanisms of phthalate ester toxicity in the female reproductive system. Kessler W. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Silva MJ. Reprod Toxicol 2004.106(1):23-26. Stringer WT.nih. Grote K. Research Triangle Park (NC). Leffers H. 2000b [online]. Int Arch Occup Environ Health 1993. Tsukino H.46(11):643-647. Available at URL: http://cerhr. Occurrence and daily variation of phthalate metabolites in the urine of an adult population. David RM. Andersson A-M. Boehmer S. Toxicol Appl Pharmacol 2004. Environ Health Perspect 1998. Meeker JD. Hagmar L.111(2):139-145. Available at URL: http://cerhr. Urine phthalate determinations as an index of occupational exposure to phthalic anhydride and di (2-ethylhexyl) phthalate. Reproducibility of urinary phthalate metabolites in first morning urine samples. Angerer J. Yoshimura M. Dalgaard M. Chahoud I.210:21-33. NTP-CERHR. Ryan L. Jacobsen H. Drexler H. Henttu P. 6/2/09 NTP-CERHR. Epidemiol 2005. Sumpter JP. Monograph on the Potential Human Reproductive and Developmental Effects of Din-Butyl Phthalate (DBP). Liss GM.18(1):122.195:142-153.gov/chemicals/dehp/dehp-eval. Gans G. Reprod Toxicol 2005. Jonsson BAG. Fromme H. Hoppin JA. gov/chemicals/dehp/dehp-eval. Koch HM. 2006 [online].nih.niehs.Phthalates in human urine samples. et al. and infant formula by tandem mass spectrometry (LC-MS-MS). Anal Bioanal Chem 2005. Csanády G. Ryan L.niehs. Biol Pharm Bull 2003. Brock JW. Hanaoka T. Zhang S. Research Triangle Park (NC). Environ Health Perspect 2003.382:10841092. Relative potency of xenobiotic estrogens in an acute in vivo mammalian assay. 6/2/09 NTP-CERHR. Mortensen GK. Akesson B.gov/ chemicals/phthalates/bb-phthalate/bbp-eval. Estimation of estrogenic and anti-estrogenic activities of some phthalate diesters and monoesters by MCF-7 cell proliferation assay in vitro. Sumpter JP. Ladefoged O. Hass U. et al. Skakkebaek NE.64(8):555-560. 2000c [online].105:802-811.html. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites.26(8):1219-24. Int J Hyg Environ Health 2007. Silva MJ. Monograph on the Potential Human Reproductive and Developmental Effects of Di(2-ethylhexyl) Phthalate (DEHP).11(5):381-387. Reynolds T. Hartle RW. Phthalate ester exposure—air levels and health of workers processing polyvinylchloride. Silva MJ. Wang P. Meeker JD. Jobling S. Research Triangle Park (NC). The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. Pan G.nih. consumer milk. Main KM. A variety of environmentally persistent chemicals including some phthalate plasticizers are weakly estrogenic. Richthoff J. Singh NP. The estrogenic activity of phthalate esters in vitro. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Jarfelt K. Davis BJ. 6/2/09 NTP-CERHR. Hum Reprod 2007. McKee RH. Duty SM. Environ Health Perspect 1997. Determination of phthalate monoesters in human milk.gov/chemicals/ phthalates/dbp/dbp-eval.html. Butala JH. Brock JW. 6/2/09 Okubo T. Temporal variability of urinary phthalate metabolite levels in men of reproductive age [published erratum appears in Environ Health Perspect 2004. Skerfving S. Scand J Work Environ Health 1985. Hauser R. Harris CA. Park MG. Numtip W.22(3):688-695. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. Rylander L. Suzuki T. Albro PW. Urinary phthalate metabolites and biomarkers of reproductive function in young men. Environ Health Perspect 2002. Giwercman A.112(17):1734-1740. Antiandrogenic effects in male rats perinatally exposed to a mixture of di(2-ethylhexyl) phthalate and di(2-ethylhexyl) adipate. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Kalita JC. Duty S. et al. Balasubramanian AV. Environ Health Perspect 1995.niehs.110(5):515-518. Yokoyama Y. Lovekamp-Swan T. Monograph on the Potential Human Reproductive and Developmental Effects of Butyl Benzyl Phthalate (BBP). et al. J Androl 2004. Kano I. Kano K. Milligan SR. Nielsen J. Research Triangle Park (NC).nih. Hauser R. Available at URL: http://cerhr. Calafat AM.niehs. White R. Am Ind Hyg Assoc J 1985.16(4):487-493. Borch J.html. Available at URL: http://cerhr. Environ Health Perspect 2004.25(2):293-302. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction.19(4):505-515. Blood burden of di(2-ethylhexylphthalate (DEHP) and its primary metabolite mono(2-ethylhexyl) phthalate (MEHP) in pregnant and non-pregnant rats and marmosets. Baird DD. Park S. Bolte G.html. 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 . Chen Z. 2000a [online].112(17):1740]. Davis BJ.

The plasticizer diethylhexyl phthalate induces malformations by decreasing fetal testosterone synthesis during sexual differentiation in the male rat. Zacharewski TR. Lambright CR. Examination of the in vitro and in vivo estrogenic activities of eight commercial phthalate esters. Meek MD. et al. Jackson SJ. Pratt IA.45:11-17. Toxicol Sci 1998. Barlow NJ. Bratt H. Environ Health Perspect 1986.S. Klinefelter GR. Fielden MR.112(3):331-338. Silva MJ. Reidy JA. Rusyn I. Environ Health Perspect 2004. Orton TC.114(11):1643-1648.46:282-293. Hodge CC. Modes of action and species-specific effects of di-(2-ethylhexyl)phthalate in the liver. Toxicol Sci 2000. Peters JM.36:459-479. Caudill SP. Clemons JH. Crit Rev Toxicol 2006. Urinary levels of seven phthalate metabolites in the U.58:339349. et al. Comparative pharmacokinetics and subacute toxicity of di(2-ethylhexyl)phthalate (DEHP) in rats and marmosets: Extrapolation of effects in rodents to man. Environ Health Perspect 1982. Fourth National Report on Human Exposure to Environmental Chemicals 261 . Albro PW. Matthews JB.65:299-308. Batten PL. Peck CC. Malek NA. 112(5):A270]. Barr DB. Cunningham ML. Environ Health Perspect 2006. Toxic potential of the plasticizer di (2-ethylhexyl) phthalate in the context of its disposition and metabolism in primates and man. et al.Phthalates phthalate (DEHP): a cross-sectional study in China. Abbott BD. Wu ZF. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Rhodes C. Ostby JS. Parks LG.

8-18.2 (10. 2004.2) 14.1 (55. High dose BzBP and its monoester metabolites.8 (10.8-17.9-87.3 (44.9 (22.1-35. People exposed to BzBP will excrete mono-benzyl phthalate (MBzP) and small amounts of mono-n-butyl phthalate in their urine.9-14.6-38.8-121) 79. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.0 (15.9) 15. 2000). interval) 15.6 (12.1) 13.8-17.3-74.0) 70.9) 49.4 (53.8-16.6-79.8 (30.6-92.0 (30.6) 50.6) 67.S.7-16.0) 32.6) 24.8 (14.7-25.0 (27.2-16.5-97.1 (32.3-125) Total 15.6 (13.9) Sample size 2541 2782 2605 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 39.3-18.6 (41.6-18.2) 14.4) 35.7 (70. sealants.4 (48.7) 23.2) 33. vinyl tile.7-58.0 (14.1-38.2 (19. can produce developmental and reproductive toxicity in rodents.6-150) 94. and 2003-2004 were generally similar those reported in U.8 (80.0) 20.5) 23.1 (13.6) 15.3) 15. some personal care products.1-16.9-27.1-90.9-49.8-13.0) 90th 67.3) 13.2 (19.4 (31.6) 35.1 (19.4) 38.8) 24.3-21.8 (71.5-33.3) 63.1) 29.9 (70.5) 214 (108-399) 235 (183-330) 255 (146-365) 125 (93. population from the National Health and Nutrition Examination Survey.2 (11.1-15.8-98.7 (15.0) 33.6) 35.4) 81.4) 14.2 (25.8) 14. 2001-2002.5 (26.3-122) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.8-64.2-31.6) 63.8-41.9-190) 86.6) 13.6) 95th 103 (94.0-85.4 (68.4-25.5) 15.7 (53.2-39.2) 17. including MBzP.1) Selected percentiles ( 95% confidence interval) 50th 17.7-16.3-75.2) 66.8 (28.3-12.3-27.5 (57.7-13.1-15.5-36.0 (20.4) 98.3) 23.9-16.8 (86.2-155) 91.9-28.4 (63.6) 25.2) 78.4 (10.1) 32. 262 Fourth National Report on Human Exposure to Environmental Chemicals .8) 63.9 (12.6-29.0 (55.5-94.0-130) 101 (86.8 (71.3-82.0 (43.2) 32.7 (82.6 (21..2) 12.8-48.6) 14. residents (Blount et al. and 03-04 are 0.0 (33. 01-02.Phthalates Benzylbutyl Phthalate CAS No.2) 22.6) 37.1 (10.9) 14.5 (55.9) 11.6 (32.9 (39.1-214) 166 (116-191) 145 (110-213) 88.3) 37.4-16. particularly male animals (McKee et al.8 (50.6-132) 103 (84.6-116) 122 (102-142) 101 (85.6) 13.3 (12.7 (12.7-15.7 (80.9-62.4-24.3 (12.2-19.5 (76.6 (13.2-20.4) 65.S.8-133) 89.8-35.5 (67.3-91.3-161) 99.6-17.6 (13.9 (11. Food crops take up BzBP.0) 24.2 (47. Biomonitoring Information The median levels of MBzP in NHANES subsamples from 1999-2000.4 (29.5-18.5-84.9) 43.4) 35. respectively.5-41.3-43.1) 67.7) 38.4 (13.4) 108 (96.3-18.0 (34.1 (14.9) 13.9-30..1 (14.4) 33.7 (13.5 (13.5-62. see Data Analysis section) for Survey years 99-00.5) 65.1 (20.5 (61.5 (47.9 (21.0 (26.1) 12. BzBP can be released into the environment during its production and. it can be released into the ambient air during use or disposal of the products.5) 30.4-92.3 (12. and to a lesser extent. because it is not bound to products in which it is incorporated.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 16.3 (29.2-17.4-15.0 (15.0 (23.8 (21.6 (66.5-14.2-38.1-120) 52.6-92.7 (11.6 (53.4) 49.7-16. and 0.0 (30.7) 40.2-40.5-145) 138 (106-241) 143 (127-179) 120 (99.5-35.0 (12.4 (32.1) 76.8-72.3 (30.0) 34.5-36.7-17.9 (13. in a small sample of pregnant women in New Urinary Mono-benzyl phthalate (MBzP) Metabolite of Benzylbutyl phthalate (BzBP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.8-14.3-34. and diet is the major source for general population exposure.5) 15.0) 16.7-35.2 (14.2) 13.3-130) 122 (88.3 (29.6) 14.7-119) 99.8-14.1 (58.4-120) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 13.1) 14.8 (12. car care products.1.4 (10.0) 23.2 (43.2-33.1) 31.6) 29.2-183) 101 (78.2-16.3 (22.9 (16.7 (51.1-18.6-39.3) 94.0-26. NTPCERHR.8 (53.9 (12.8-76.3) 54.7-14.1) 68.4 (27.7-170) 169 (134-198) 152 (99.8-16. 85-68-7 General Information Benzylbutyl phthalate (BzBP) is a solvent and additive used in products such as adhesives.5) 27.9) 12.2-116) 122 (102-143) 101 (84.2) 69.6-72.4-127) 80.3) 13. 2000).4) 75th 35.5) 16.8 (38. IARC considers BzBP not classifiable with respect to human carcinogenicity.6-43.4-62.4 (53.4) 12.9) 18.1-39.5-25.5) 82.6 (13.5 (66.9 (28.8) 33.5 (27.3-88.0 (11.3.8.0-106) 58.7-82.9) 14.2) 15.7-172) 103 (74.8) 28.5-40.4 (32.1-116) 122 (93.4) 80.2-115) 113 (91.3 (54.1 (13.6) 16.3 (33.9-47.1-43.4) 71.0-55.4 (59. 0.5) 55.3 (13.4) 51.4) 129 (98.1-61.1-16.

7) 11.4) 21.5-61.73-12.3) 13.8-39.S.4-27.7 (14.7) 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. 2004).4 (11.5-58.1 (14..8 (13. 2005).3) 36.7 (38.69-11.4) 17.4) 44.0) Selected percentiles ( 95% confidence interval) 50th 13.1 (23.7) 46.2 (41. 2007).6) 30.4-79..1 (15.7-20.2-12.9 (12.8) 53.7 (18.5-13.9-13. 2006).5) 17.2) 15.0 (12..5 (56.7-15. in men attending a Boston infertility clinic (Duty et al.6-99.1) 17.3) 14.4) 50.9 (9. in young Swedish men (Jonsson et al. interval) 14.7-29.8 (10.6 (36.7-56.4 (11.6-12.1) 27.1) 24.8 (64.1 (21.6 (30.2) 32.4) 90th 50.5-76.8) 33.2 (69.4-116) 73.6) 13.8) 54. 2002.7 (59.7-12. and females compared to males (Silva et al.1-79.1-35.9 (24.8) 11.5-29.1-58. 2007).7-19.4 (74.6-20.9) 64.6) 12.5) 10.0 (12.9-13.7 (13.5 (35.9 (10.3 (38. In NHANES 1999-2000.5 (48.9 (15. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.3-11.3-73.6 (30.4-23.7-31.2-15.5) 14.7 (19.9-16.9 (22.0-27. Hoppin et al.6 (15.8 (12. DC reported median urinary MBzP levels that were about twice the levels of adults and females reported in NHANES 1999-2002 (CDC.1-27.8) 16.6) 25.0) 15.4 (26.4 (25..4) 328 393 342 752 742 729 1461 1647 1534 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 12.7) 25.4 (69. adolescents compared with adults.4-93.4-14. Hauser et al.1) 142 (99.5-79.2 (27.9 (55..4) 60.4 (21.0 (11.5) 41.7-90.8-14.1 (43.4) 104 (89.5 (10.9) 12.5-26.4-60.0-53.8-69.4 (60.3) 89.0) 13.7-14.4) 28.5) 13.9-115) 57.0 (41.4-42.1 (9.6-26.8-42.9-14.6-15. 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.7 (54.8) 53.1-12.7-19.2 (40.4) 25.5) 95th 77.9) 11.5) 20.2) 67.1 (25.1 (18.2) 12.9) 12.8-85.1) 12.9) 12.8) 15. In an annual sample of German university students.9 (51.6-116) 74.6 (19.5) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Fourth National Report on Human Exposure to Environmental Chemicals 263 .9) 11.1 (11.8-13.8) 13.0) 24.7 (55.7-20.8 (69.5-16.0-51.Phthalates York City (Adibi et al.2) 26.6 (51. and in a small sample of German residents (Koch et al.6-47.4) 13. 2003).6 (24.6-13.9) Total 14.3-64.6) 58.3) 29.9 (10.3 (13. Weuve et al.3 (39..6) 38.3 (15.5 (10.1 (21.3) 55.4) 14.4-14.5-42.8 (46.3 (35.8) 26.0) 49.6) 75th 25.8-60. 2003).0) 60.1) 23.9) 52.8) 108 (75.8-15.7 (21.2-13.4) 15.8) 46.2-17.4 (11.5-38.7-15.3) 16.2 (56.4) 13.8-80.2) 11.9-104) 62.8-173) 195 (121-305) 229 (99. A small study of African-American women in Washington.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 12.2-13.5) 16.2-21.4-18.9 (29. population from the National Health and Nutrition Examination Survey..9-40.6 (34.2-15.2-51.4 (13.9-62.8-34.4) 51.4-90.7 (12.7) 56.2-57.1) 80.8-13.9 (54.7-397) 70.2-117) 95.8) 80.9 (15.8-13.4-142) 134 (116-176) 136 (85.1 (46.0-90.3) 67.6 (22.7 (11. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.3) 13.4 (10.9 (39. the adjusted geometric mean levels of urinary MBzP were significantly higher in several subgroups: children compared to adolescents and adults.5 (11.0 (62.9) 42.1-125) 86.3) 37.6 (11.5-31.3) 13.0-26.1) 35.8 (49.2-78.8 (30.2-49. 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.5-26.6-86.3-38.7 (13. 2004.4-99.4 (46.6) 12.0 (38.7-123) 77.3) 14.5 (42.1-120) 77.8-64.3) 12.9 (12. 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.4-19.0) 24.3 (24.95-14.6 (11.1-14.0 (33.7) 38.3-34.0 (41.1 (21.3 (23.9-23.8) 33.5 (49.6-81.4 (33.7-14.2) 11.0 (67.5) 46.5 (12.1 (53.8) 34.0-109) 65.2-26.5-99.1 (13.3) 73.7-61.4-102) 70.3 (12.8) 24.0 (49. 2002)..3 (60.4-17.9 (43.0 (10.4 (63.5-58.1) 39.4 (34.0-15.5) 23.0) 11.6 (14.9-28.1-12.7-69.1-29.9) 100 (80.5 (9.8-27.2) 11.8) 68.7 (11.4-15.5-213) 49.0-48.6 (11.6) 53.9) 24.5-23.7 (23. 2005.1 (21..3-16.1 (19.7 (11.5) 78.9 (24.6-40.0 (13.1 (41.1) 24.3) 21. Finding a measurable amount of MBzP in the urine does not mean that the levels of MBzP or the parent compound cause an adverse health effect.6 (57.9-83.8 (50.4) 12.5-57.9-69.8 (11..8-15. median urine levels of MBzP were about one-half the median levels in NHANES subsamples from 1999-2002 (Wittassek et al.0) 12.6) 73.8) 71.7) 19.8) 56.4 (12.1 (34.8-14.8-48.8-16.1 (13.3) 90.8 (57.3) 18.

Weuve J. et al. 2000 [online]. Green RA.Phthalates References Adibi JJ. Ryan L. Hum Reprod 2007. Bull Environ Contam Toxicol 2002. Urinary levels of seven phthalate metabolites in the U. Blount BC.25(2):293-302. Ryan L. Richthoff J. et al. et al. Rylander L. Silva MJ. Hoppin JA. Levels of seven urinary phthalate metabolites in a human reference population. Silva MJ. Urinary phthalate metabolites and biomarkers of reproductive function in young men. Dobler L. Int J Hyg Environ Health 2007. Drexler H. Atlanta (GA). Needham LL. Phthalate monoesters levels in the urine of young children. Koch HM. Helm D. Eckard R. Third National Report on Human Exposure to Environmental Chemicals. Environ Res 2003. Singh NP. Brock JW. Davis BJ. Prenatal exposures to phthalates among women in New York City and Krakow. Gans G. Duty S.gov/ chemicals/phthalates/bb-phthalate/bbp-eval. Epidemiol 2005. Koch HM. Environ Health Perspect 2000. Sampson EJ. Barr D. 2005.114(9):1424-1431. et al. Internal phthalate exposure over the last two decades—a retrospective human biomonitoring study. Giwercman A. David RM. Hu H. Jonsson BAG. Available at URL: http://cerhr. Rossbach B. Environ Health Perspect 2004. J Androl 2004. et al. Caudill SP. 112(5):A270]. Poland. Perera FP. Exposure to phthalates in neonatal intensive care unit infants: urinary concentrations of monoesters and oxidative metabolites. Duty SM. Baird DD.93:177-185. Needham LL. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. Silva MJ. Jacek R. Brock JW.niehs.110(5):515-518. Hilborn ED. Sanchez GN. Camann DE. Centers for Disease Control and Prevention (CDC). Environ Health Perspect 2002. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Schettler T. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Chen Z. Malek NA.112(3):331-338. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Wiesmuller GA.210(3-4):319-333. Silva MJ. Hauser R. Reidy JA.html. Caudill SP.108(10):979-982.22(3):688-695. Hagmar L. Reprod Toxicol 2004. Meeker JD. Pirkle JL. Angerer J.S. Calafat AM.16(4):487-493. Caudill SP. Reproducibility of urinary phthalate metabolites in first morning urine samples. Research Triangle Park (NC). Jedrychowski W. 4/20/09 Silva MJ. Butala JH. Environ Health Perspect 2006. 264 Fourth National Report on Human Exposure to Environmental Chemicals . Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine.18(1):122. Environ Health Perspect 2003. Calafat AM. et al. et al. Brock JW.nih. NTP-CERHR.111(14):1719-1722.68:309-314. Hodge CC. Wittassek M. Barr DB. McKee RH. Monograph on the Potential Human Reproductive and Developmental Effects of Butyl Benzyl Phthalate (BBP).

8) 40.80 (2.82-3. Compared with the median for 6 to 11 year olds in NHANES 1999-2004 (CDC.1) 25.20 (6.10-9.50-6.4) 12.0) 20.30-13.67 (5.3 (18.90-4.50 (3. and also in some printing inks. 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.3 (13.9 (16.00) 7.20 (7.07 (3..6-26.5) 18.3 (19. When total DBP metabolites have been measured.90) 12.1-20. Following oral administration of DBP to humans. pharmaceutical coatings.6) 10.9 (16.20-2.5 (27.90-2.5-29.90-4.7-20.6) 26.00 (7. 2003)..11-3.30-6.1) 22.30 (1.3-43.3-24. 2000.20-12.30-6. mostly as MnBP (Anderson et al.40 (7.5) 23. population from the National Health and Nutrition Examination Survey.24-8.10) 3.28-5.6-20. OSHA has established a workplace air standard for external exposure to DBP.00-11. 2000).43) 6.5-16.30) 10..4 (20.33 (2.81 (3.1-12.2-33.46 (3.72-3.30-3.6) 17.2) 5.68 (2.5 (17. Fourth National Report on Human Exposure to Environmental Chemicals 265 .6 (10.22) 3.1-17.0 (19.50-10.22 (3.3 (16.30) 2.6 (13.5) 19. Neither IARC nor NTP has evaluated dibutyl phthalates with respect to human carcinogenicity.5) 14.5-24.40 (6.3-18.1 (8.5) 25.59) 3.44-2.5) 18. they have been referred to as monobutyl phthalate (MBP).00-6.40) 5.20 (3.6-14.55 (3. DBP can produce reproductive toxicity in male rodents (McKee et al.. Small amounts of mono-3-carboxypropyl phthalate are also produced from di-n-butyl phthalate.7 (17.4-12.00) 4.6-18.6) 16.50) 18.2 (8.37) 6.7) 18.10 (4.3) 18.3.60 (5.3 (13.6 (9.10) 9. In addition. 84-74-2 Di-isobutyl Phthalate CAS No.Phthalates Di-n-butyl Phthalate CAS No.10) 2.00-4.8) 21.20-6.90 (4.3 (11.30) 6.7 (7.56 (5.50) 2.46-5.90-7.30) 5.2 (11. 2001).10 (4.73-5.6) 12.70) 3.50) 7.2-22. interval) 2.4-27.5 (10. NIOSH and ACGIH have established guidelines for workplace air exposure to di-n-butyl phthalate.17) 4.60) 3.20) 7.0 and 0.40-5.6 (13.02) 4.2 (12. about 65% to 80% of a dose is eliminated in urine within 24 hours.0-25. 84-69-5 General Information Dibutyl phthalates (both di-n-butyl and di-isobutyl phthalates.9-14.3-48.80-5. 2007).00-9.73 (2.5 (11.90 (4.9-23.3 (16.2-14.40-12.25) 01-02 03-04 01-02 03-04 01-02 03-04 4. 2005). Koch et al.5) 22..50-2.6 (11.0) 12. Biomonitoring Information Median concentrations reported in the NHANES 19992000.4 (14.1) 16.40-4.00) 4.10) 11.S..40-4.96) 3.8) 677 652 703 699 1216 1088 Limit of detection (LOD.50) 8. 2005).94) Selected percentiles ( 95% confidence interval) Sample 95th 17.50-4.0 (13.70-8.00-6.20-9.3-19.20-12.4) 5.7) 14.70) 5.46 (2.30-7.97-7. 2004.00) 6.97) 4.48 (2.0-38.1-25.6 (10.. NTP-CERHR.70-4.90 (3.10) 8.40 (2.6) 17.0 (13.91) 4.80 (5.46) 2.40-3.10-9. 2004.0 (11.60 (8.70-4.50) 5.40-17. 2003).80-5.56-4.7) 15.0) 1371 1250 1411 1355 01-02 03-04 01-02 03-04 01-02 03-04 3.3-30.5 (20.97) 2.85-6. 2005).6 (29. and insecticides.8 (9..7) 7.6 (14. Median MBP levels in two European studies were about two to six times higher than median levels in this Report (Jonsson et al.50) 90th 12. 2005. 2001-2002 and 2003-2004 subsamples were similar to MBP levels reported in U.00 (5.90 (6.7 (18. residents (Blount et al.40-9.4) 22.56) 3.3) 3.70 (2..80 (3.6-34.0) 9. Studies of children found age-related differences in urine MBP levels.0) 393 342 742 729 1647 1534 01-02 03-04 01-02 03-04 2.30 (3.9) 10. Hauser et al.0) 13. and in a small sample of Japanese adults (Itoh et al. see Data Analysis section) for Survey years 01-02 and 03-04 are 1.7 (9.0-14. in a small sample of pregnant women in New York City (Adibi et al.0-18. exposure to benzylbutyl phthalate (BzBP) will also result in small amounts of mono-n-butyl phthalate appearing in the urine. People exposed to dibutyl phthalates will excrete mono-n-butyl phthalate (MnBP) and mono-isobutyl phthalate (MiBP) in their urine.19-3.66) 2.0) size 2782 2605 Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 03-04 50th 2.60-6.55) 2. referred to as DBP) are industrial solvents or additives used in many personal care products such as nail polish and cosmetics.7-31.20) 4.30) 10.80 (2.6) 16.63) 3.26 (2.30-11. in men attending a Boston infertility clinic (Duty et al.3-20.S.5) 12.7 (16. CDC.80 (5.7-18.71 (2.80) 75th 5.70 (5.10 (3.10-2.9) 15.40 (3.7) 4.00) 10.7-31.50 (6.3) 33.40-3.49-2.0) 24.56 (3.60 (2.1 (13.17 (2.84) 4.30 (4. Survey Geometric mean (95% conf.6 (14.40 (2.5-16.60 (4.30-2.7 (17.

65-4..04-5.29-8.72) 5.28 (4.8 (9.25) 5.9 (15.59 (4.21) 10.2) 24. while MnBP declined (Wittassek et al.94 (5.80-3.86-4.1 (10.18 (1.6-19.78-8. than adults in NHANES subsamples during the same time period.32 (7.52-3.56-15.68 (2.32) 7.6 (8.86) 6.52-20. population from the National Health and Nutrition Examination Survey.66 (8.9 (11.8) 10.61-3.11-2.95) 2.20 (7.79-6.1) 11.6) 13.0-18.6) 11. to about two to fourfold higher (Fromme et al.56) 5.31) 2.05) 2.46-11.39-3.9) 12.9-26.79 (4.08) 75th 4.55-6.64-7.80 (3. Over this time.6 (12.20 (2.29-3.00-3.00 (3.18-10.5) 15.9-40.74-3.33) 3.91-6.4) 15.84 (4.3) 13.76-15.2-15. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.76 (3.7 (11.74 (4.7) 10.1-24.34 (3.1) 4.78) 9.9-16. Survey Geometric mean (95% conf.04) 3.54 (4.11) 5.95-3.1) 13.57 (3.69) 6.64-7.3 (17.69-7.0) 11.33-9.54) 2. interval) 2.20 (2. 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.37) 3.43) 3.38 (6.45) 3.57-4.31 (2. Weuve et al.65 (4.43) 3.8-36.66) 2. 2006).0) 15.93-6.76-3..9 (9.26-2.51) 5.31) 2.30) 2.17) 90th 8.51) 2..03-7.66) 10.75 (4.62 (6.2-13.51) 15.41 (2. 2004).76-3.85 (2. Urinary Mono-isobutyl phthalate (MiBP) (creatinine corrected) Metabolite of Di-isobutyl phthalate (DBP) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.01-2.10-5.7) 11.47-12.related differences in the adjusted geometric mean levels of urinary MiBP and MnBP (CDC.56) 2.1) 677 652 703 699 1216 1088 266 Fourth National Report on Human Exposure to Environmental Chemicals .96 (3.6 (10.8-18.0 (12.2) 9.46 (2.81 (6.15-4.6 (8.28-13. 2005). respectively.3) 28.69) 4.67-5.72-7.84 (8. 2004).52) 3.13 (2.82 (4.33 (2.89-5.5 (11.1-25.65-11..38-10.6) 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 2.1-12.66) 4.04) 7.S.4) 23.and gender.68) 3. samples from German university students had consistently higher median urine levels of MnBP and MiBP.7) 19.8-13.42) 2.44 (3.47-5.0 (10.1-15. 2007).58-3.97-2.75 (6.69 (2.22 (2.43) 3.27-12.7 (9.2 (10.0) 7.92 (7.98 (2.58-4.09-2.0 (8.57 (3.03 (5.6 (9. Studies measuring urinary MnBP have reported variable median values compared to the NHANES 2001-2002 and 2003-2004 subsamples.07 (2.03-11.53-5.1 (11.94-12.62-12.0) 3.81) 9.24) 3.Phthalates for neonates was lower (by about half) and the median for toddlers was higher (by about sixfold) (Brock et al.4-16.4 (12.20-3. ranging from more than one-tenth the NHANES median (Itoh et al.39) 5.56-4.8 (10.52 (2..20-4.36-2.18-4.15) 3..02 (7.33 (3. 2005).21 (5.30 (6.19 (2.7 (13.83 (2.73) Selected percentiles ( 95% confidence interval) Sample 95th 12.8-18.53-4.20-2.6-19.81) 4.08-2.18) 4.89 (3.13-6.53-3.1) 7.3) 16.7) 3.26 (2.18 (4. An analysis of NHANES 2001-2002 showed similar age.3) 18.0) 393 342 742 729 1647 1534 01-02 03-04 01-02 03-04 2.2) 8. Between 1998 and 2003.35) 3.36-7.95) 10. 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.32 (3.1) 15..7-28.7) 1371 1250 1411 1355 01-02 03-04 01-02 03-04 01-02 03-04 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. 2007).31 (7.5) 13.68) 5.4) 7.11 (5.78) 8.00-7.94) 6.81 (3. the students’ median values for MiBP levels remained relatively unchanged. 2002.07-5.54 (2.6 (15.1) 10.7 (21.64-10.88 (2.17 (2.99) 7.82) 4.02-10.00-3.47 (3.79-8.17-12.73 (5.80) 7.18) 3.99-4.2 (11.14 (4. In an analysis of NHANES 1999-2000.46) 3.00) 01-02 03-04 01-02 03-04 01-02 03-04 4.3 (13. Differences in urinary MBP population estimates by gender have also been shown (Silva et al.3) 13.8 (8.89) 6.5 (9. up to four and 13 fold.5-19.

0-26.5) 47.3-85.1 (17.1-27.7-42.5) 95.7) 124 (98.1) 36.1-24.4-25.1-92.0 (78.9-92. *In the 1999-2000 survey period.8-111) 167 (143-223) 121 (106-136) 137 (122-156) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00* 01-02 03-04 99-00* 01-02 03-04 23.6-29.9) 18.9-42.8) 19.2) 68.3 (17. respectively.1-51.7-127) 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 22.2) 20.9-114) 116 (97.8-42.2-23.2 (79.5 (59.4 (35.1 (34.8-22.9 (20.0 (17.6) 20.0-51.1 (62.7-34.8-119) 90.1.2 (19.0-21.4.0) 38.5) 36.7) 92.6) 21.1) 25.1) 31.7-124) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites 99-00* 01-02 03-04 Limits of detection (LOD.7 (70.2-114) 73.6 (65.6-69.4) 20.3-79.4-26.4-42.8) 62.9 (79.5-47.1) 30.6-33.9) 46.7-92. interval) 24.2 (18.6) 35.2) 90th 98. Fourth National Report on Human Exposure to Environmental Chemicals 267 .Phthalates Urinary Mono-n-butyl phthalate (MnBP) Metabolite of Dibutyl phthalate (DBP) and Benzylbutyl phthalate (BzBP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.6) 166 (127-279) 159 (110-290) 191 (150-243) 165 (121-227) 148 (106-185) 134 (110-158) 143 (117-161) 95.5-60.3-145) 85.7-121) 97.0) 21.5 (30.7 (38.9.5-43.0-24.5) 20.1 (51.6 (61.8 (19.4) 59.6-24.3 (51.1 (28.1) 46.3 (23.7-106) 69.6) 39.S.1 (58.1 (21.5) 21.3) 24.1) 19.4 (21.6 (32.5) 17.1 (19.0-19.5) 36.2 (78.5) 24.7 (19.4) Selected percentiles ( 95% confidence interval) Sample 95th 150 (121-169) 108 (94.6 (16.3) 26.0) 30.6) 17.6-37.1) 20.0) 31.2-33.1 (18.2) 62.5) 34.7-111) 64.5-44.6-29.7 (16. referred to as monobutyl phthalate (MBP).0 (30.2-49.8) 43.6 (26.7 (33. concentrations of mono-isobutyl phthalate and mono-n-butyl phthalate were measured together and expressed as a combined value.0 (25.8 (57.3-24.5-47.7) 28.1-122) 122 (104-137) size 2541 2782 2605 Total years 99-00* 01-02 03-04 50th 26.0 (18.9-28.9-33.2-56.5 (59.4 (72.3-40. 1.9) 26.4 (23.8) 58.1 (36.4 (35.5 (29.3) 23.5) 78.2 (58.2 (59. see Data Analysis section) for survey years 99-00.1 (26.5-42.6-20.1-29.7-42.2) 38.8-123) 101 (90.0-73.6) 71.5) 40.0 (15.0 (72.4) 64.3 (23. and 03-04 are 0.3) 19.6) 80.5-53.5-27.9) 36.6) 46.1 (19.5) 85.1) 23.7 (43.2-21.1-82.7-117) 118 (108-143) 93.2-22.5) 37. Survey Geometric mean (95% conf.1) 23.0 (20.4 (25.4-18.5 (28.6-49.3) 36.0-58.0 (23.5) Age group 6-11 years 99-00* 01-02 03-04 99-00* 01-02 03-04 41.0 (36.3 (60.3) 18.7 (28.6-48.4-44.5) 65.1 (31.7) 42.5-121) 106 (94.0) 117 (104-131) 112 (84.1) 47.2) 26.5-117) 95.5) 26.3-67.6 (90.6 (55.3 (37.0 (45.3 (30.0) 20.2) 42.4 (38.8-25.2-93.8) 23.9 (79.7-53.2) 32.4 (35.2-87.0) 120 (98.7) 52.3-96.5) 31.0-24. and 0.1 (54.3 (42.4) 22.4-31.1-75.7) 74.4 (84.7-116) 95.2-159) 92.9 (17.8-165) 167 (143-197) 138 (110-184) 144 (115-168) 142 (111-161) 107 (89.4-159) 107 (84.8-132) 95.8) 48.2 (25.4 (36.2-32.5) 19.6-36.0) 84.7-34.2 (17.3) 21.1 (19.6 (44.3-76.7 (18.1-22.1 (41.9-87.4 (35.9) 75.6-40.7-20.4 (19.2-24.4 (71.6 (22.0-32.7 (18.2 (75.3 (30.9-22.6 (48.1 (19.7 (51.7 (24.7-24.6-113) 108 (90.6) 38.2 (20.9) 29.2 (21.1) 17.7-26.8) 75th 51.9) 21.3 (56.2 (74.7 (64.9-53.0-19.7-91.6 (19.4) 52.1-20.9) 71.3-136) 137 (107-162) 119 (90.0) 27.3 (36. population from the National Health and Nutrition Examination Survey.0 (31.9-101) 77.3) 40.6-143) 127 (99.9 (17.2 (21.3-21.6-44.3-60.9-22.4-60.4-20.5 (74.9-79.2-63.1-80.7 (22.1 (16.8-29. 01-02.6-31.1) 23.

3 (19.8) 19.6) 25.7-20.1 (32.6-23.1-32.4-131) 81. interval) 22.9 (30.8) 30.3 (17.7 (57.7-23.0) 94.4 (13.6 (19.8 (22.0) 29.8 (33.8 (18.6 (61.7 (27.8-32.2-108) 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 (31.6-53.0 (71.8) 35.7-42.0 (18.1-128) 97.0 (26.4-135) 71.8) 34.3) 17.5) 91.2-16.1) 50.7-26.4) 20.9 (16.1) 37.8 (65.0-38.9 (20.0-92.1 (15.6 (29.3-71.8) 20.6) 39.1) 22.1-83.8) 13.8) 22.5 (15.9-14.9-56.9-26.2-22.3) 20.4 (31.6-19.9) 30.2) 74.0-113) 104 (83.5 (14.2-28.2-73.4-164) 96.0) 59.0-75.0 (69.4 (45.3 (17.3-18.8-43.3) 21.9-84.6 (57.3-49.7 (43.6-74.1) 44.6-139) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00* 01-02 03-04 99-00* 01-02 03-04 21.6-16.5-142) 89.9 (35.S.0 (20.7 (54.9-105) 85.6-28.7 (28.2) 159 (102-263) 147 (93.6) 83.4) 16.6) 64.4-72.7-37.1-115) size 2541 2782 2605 Total years 99-00* 01-02 03-04 50th 21.9-68.6) 37.0-90.0) 26.6) 65.1 (29.1-62.1) 20.8 (18.9 (21.8) 17.3-114) 328 393 342 752 742 729 1461 1647 1534 12-19 years 20 years and older 99-00* 01-02 03-04 Gender Males 99-00* 01-02 03-04 99-00* 01-02 03-04 17.4 (17.6-119) 63.7-19.0 (61.1 (34.4) 62.5-41.2-86.5) 21.4 (23.9) 14.5-21.7 (19.2 (83.7 (20.0) 25.2-22.8) 17.5-142) 81.6-43.7 (81.9) 52.6) 31.0 (27.1) 61.9) 19.2-21.5-37.5-23.1) 21.3-106) 74.2) Age group 6-11 years 99-00* 01-02 03-04 99-00* 01-02 03-04 41.6-24.6 (25.0) 108 (71.4 (50.2) 65.4-65.0 (18.3) 35.0) 19.4-61.6-24.9) 91.9 (19.7 (73.4) 15.7-19.3-32.0-19.1-99.0) 70.7-51.9) 20.3) 59.3 (52.4 (20.8) 40.6-22.1) 53.4) 21.4-47.0) 28.8) 28.0 (43.4 (16.5-70.7 (16.4 (50.4 (47.4-76.6-23.9 (58.5-18.5) 134 (93.6 (41.2) 31.5 (18.9-68.9-38.3) 67.9-100) 86.3 (76.3-20.9) 24.3-23.3) 33.9 (30. concentrations of mono-isobutyl phthalate and mono-n-butyl phthalate were measured together and expressed as a combined value.2) 59.8) 34.5) 90th 68.3-39.6 (27.6) 38.3 (71.3 (60.7 (60.2-27.8 (17.5 (81.8-23.5-16.3 (42.7-28.5-76.3) 52.4) Selected percentiles ( 95% confidence interval) Sample 95th 97.4 (56.3 (55.1-23.1) 42.0) 53.6 (31.3-38.4 (68.2-179) 84. 268 Fourth National Report on Human Exposure to Environmental Chemicals .6-32.0 (16.7) 36.7 (60.6 (17.3) 19.7) 20.1 (46.0 (19.5) 82.0 (34.4 (31. population from the National Health and Nutrition Examination Survey.2-48.3-17.2-106) 64.6-155) 91.0 (52.3 (46.6-42.5) 17.7-39.9 (30.5 (18.1-99.7-80.3) 33.3 (52.3-81.6) 14.2-18.3-26.8) 17.0) 81.0-60. Survey Geometric mean (95% conf.3-21.3 (17.1) 17.9-70.1 (61.6) 24.2 (16.5) 84.9) 49.4 (17.5-15.9 (35.6) 24.3 (21.7) 42.9) 28.4 (53.4 (16.0 (70.5-30.6-50.4-24.9 (37.1 (56.3-21.1 (21.3 (16.0) 35.6) 23.5-22.7-21.4) 53.2 (19.7) 19.9-34.5 (30.4 (19.0) 75.8 (18.6-26.3 (48.2 (19.6-27.9 (64.8-24.5-64.1) 35.6) 18.4 (18.9 (56.7 (14.8) 75th 38.5) 60.2 (35.9 (39.0 (50.6) 34.4) 19.3 (28.0) 41.8 (16.8) 23.2-61.2) 21.3-78.4 (37.4-34.3-40.7-78.0-47.6 (72.2) 16.9-36.0-17.5) 39.6-44.4-103) 117 (83.3 (24.9-49.6-128) 96.7 (12.8 (13.0-41.0) 55.6 (25.1) 20.3 (69.6-44.9) 39.5 (64.Phthalates Urinary Mono-n-butyl phthalate (MnBP) (creatinine corrected) Metabolite of Dibutyl phthalate (DBP) and Benzylbutyl phthalate (BzBP) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.6-92.8-24.9) 62.4) 51.2-85.2-22.1-21.9 (73.8 (50.3) 19.1-18.3) 18.4) 15.8) 63.0 (15.6 (74.8 (25.8-235) 137 (108-198) 88.2 (38.4 (33.8) 20.

Reprod Toxicol 2004. Scotter MJ. Hum Reprod 2007. Jonsson BAG. Massey RC.Phthalates References Adibi JJ. 112(5):A270]. Ryan L. Boehmer S. et al. Pirkle JL.112(3):331-338. Dobler L. Brock JW. Silva MJ. Wiesmuller GA. Occurrence and daily variation of phthalate metabolites in the urine of an adult population. Research Triangle Park (NC).gov/chemicals/ phthalates/dbp/dbp-eval. Malek NA. Int J Hyg Environ Health 2007. Environ Res 2003. Phthalate monoesters levels in the urine of young children. Environ Health Perspect 2000. et al. Evaluation of the effect ofa governmental control of human exposure to two phthalates in Japan using a urinary biomarker approach. Itoh H. Exposure to phthalates in neonatal intensive care unit infants: urinary concentrations of monoesters and oxidative metabolites. Prenatal exposures to phthalates among women in New York City and Krakow. Environ Health Perspect 2003. Centers for Disease Control and Prevention (CDC). et al. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. David RM. Caudill SP. Epidemiol 2005. Angerer J. Koch HM. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Chen Z. 4/20/09 Silva MJ. NTP-CERHR. 2005.22(3):688-695. Koch HM. Levels of seven urinary phthalate metabolites in a human reference population. McKee RH. Wittassek M. et al. Hodge CC. Jacek R. Jedrychowski W. Gans G. Giwercman A.114(9):1424-1431. Environ Health Perspect 2004. Camann DE. Caudill SP. Weuve J. Sanchez GN. Angerer J. Poland. Sampson EJ. Silva MJ. Monograph on the Potential Human Reproductive and Developmental Effects of Di-n-Butyl Phthalate (DBP). Available at URL: http://cerhr. et al.16(4):487-493. Duty S. Ryan L. et al. Third National Report on Human Exposure to Environmental Chemicals. Meeker JD. Drexler H. et al. Duty SM. Koch HM. Food Addit Contam 2001. Perera FP. Eckard R. Calafat AM.208:237-245. Rylander L. Silva MJ. Hagmar L.html.18(12):10681074.nih.210:21-33. Springall C. Helm D. Needham LL. Green RA.108(10)979-982. Silva MJ. Barr DB.68:309-314. Environ Health Perspect 2006. Rossbach B. Yoshida K. et al. Butala JH. Urinary phthalate metabolites and biomarkers of reproductive function in young men.111(14):1719-1722.niehs.S. Brock JW. Caudill SP. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Needham LL. Blount BC. Bull Environ Contam Toxicol 2002. Schettler T.210(3-4):319-33. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. Hilborn ED. Internal phthalate exposure over the last two decades—a retrospective human biomonitoring study. Int J Hyg Environ Health 2007. Hauser R. Castle L. Fromme H. Fourth National Report on Human Exposure to Environmental Chemicals 269 . Anderson WA. 2000 [online]. Hu H. Urinary levels of seven phthalate metabolites in the U. Int J Hyg Environ Health 2005. J Androl 2004. Singh NP. A biomarker approach to measuring human dietary exposure to certain phthalate diesters. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction.25(2):293-302. Richthoff J. Barr D. Atlanta (GA). Drexler H. Reidy JA. Masunaga S.18(1):122. Bolte G. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. Calafat AM.93:177-185.

00-3.50) .300 (.300-. Neither IARC nor NTP has evaluated DCHP with respect to human carcinogenicity.200-.400-.70) .500) 1.400 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.500) .300-.400 (.200-.300 (.200-.500 (.400) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.500 (.300 (.400-.2.400) < LOD < LOD .Phthalates Dicyclohexyl Phthalate CAS No.400) size 2541 2782 2605 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .500) < LOD < LOD .600) .400 (<LOD-. 84-61-7 General Information Dicyclohexyl phthalate (DCHP) is used to stabilize some rubbers.400 (<LOD-.300) < LOD .400 (.600 (.500 (.300 (.900-1.80) .600) < LOD .400 (.400-.300 (<LOD-.00 (<LOD-1. which may vary for some chemicals by year and by individual sample.70 (1.700) .500) < LOD < LOD . resins.300-. 0.400-. and 03-04 are 0.400-.200-.00-2.500 (.00 (<LOD-1.300-. People exposed to DCHP will excrete mono-cyclohexyl phthalate (MCHP) in their urine.500) < LOD * * * Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1.300 (.200-. respectively. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.300) 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 .300-. In this Report.10 (<LOD-1.500) 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 .90) . see Data Analysis section) for Survey years 99-00. 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) .00 (<LOD-1.10 (<LOD-2.500) .500 (. and polyvinyl chloride.3. < LOD means less than the limit of detection. 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. 270 Fourth National Report on Human Exposure to Environmental Chemicals .600) .500 (. and polymers. 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.20) .500) 1.500) 1.400) < LOD 1.300-.500 (.300-.500) < LOD 1.300 (.70 (1.400 (.9.400-.300-. population from the National Health and Nutrition Examination Survey. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 01-02.200-.400 (<LOD-.300 (.700) .10 (.400) 1.S.400 (. Urinary Mono-cyclohexyl phthalate (MCHP) Metabolite of Dicyclohexyl phthalate (DCHP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.70) . polyvinyl acetate.500 (.700) .300-. only levels at or above the 90th percentile could be characterized.500) .10) .500-.00) .600) .50) .500 (. and 0. Survey Geometric mean (95% conf.10 (<LOD-1.500) .400) 1.300-.400-.600) .400 (.400 (<LOD-.300) < LOD . including nitrocellulose.200 (<LOD-.

880 (.630 (<LOD-.290-.16 (<LOD-3.670-1.360-.33) .530 (.220 (<LOD-.67 (1.770-1.690) < LOD * * * Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1.690) < LOD < LOD .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 .11) .690) < LOD 2.530-.670 (<LOD-.16) .54) .370 (<LOD-.800-1.22 (<LOD-1.590 (.790-1.82 (1.44) .510-.740) < LOD < LOD .400-. interval) Selected percentiles ( 95% confidence interval) Sample 95th 3.380-.940 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.910 (.54 (<LOD-2.250 (.05) . population from the National Health and Nutrition Examination Survey.310) < LOD .610 (.53) .36-1.14 (<LOD-3.18) .560) 1.530-1.910 (.350-.500) size 2541 2782 2605 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .170-.950 (.S.43 (1.82) .690 (.830) 1.310-.710) .660) .470 (.770-1.450 (.770 (.74) .390 (.500-.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.510 (.590) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .690-1. Fourth National Report on Human Exposure to Environmental Chemicals 271 .620) < LOD .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.530) 1.450 (.420-.910 (.53) .34) .260-.490) .410 (.330 (.590 (<LOD-.270) < LOD .740) .06) .770-1.00) .06) .54-6.17) .480 (.12-1.33 (<LOD-3.500) 3.400-.420-.470) 3.770) < LOD 2.10) .630 (<LOD-.330 (.660) < LOD < LOD .240-. Survey Geometric mean (95% conf.380 (.00 (<LOD-3.420-.500 (.910 (.

9..9-92. a sample of young Swedish males entering the military had median urinary MEP levels that were somewhat higher than males in the NHANES subsamples.S. see Data Analysis section) for Survey years 99-00.2.. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. 01-02. population from the National Health and Nutrition Examination Survey. soaps.3-110) 211 (160-278) 197 (159-243) 225 (187-270) 190 (164-219) 191 (171-214) 205 (176-238) 75. shampoos. and hand lotions. and 0. 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. respectively.7) 71.5) 81.Phthalates Diethyl Phthalate CAS No. 0. 2007). 2003) and African-American women in Washington. Products that may contain DEP include perfumes.3 (74. Neither IARC nor NTP has evaluated DEP with respect to human carcinogenicity. 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.7 (70.1 (71. 2002). and 03-04 are 1. DC (Hoppin et al. particularly those containing fragrances. Biomonitoring Information MEP levels in the NHANES 1999-2000.4 (62.2-102) 95. and also in men attending a Boston infertility clinic (Hauser et al. deodorants.8-111) 85. 2001-2002..3 (82. 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. colognes. 84-66-2 General Information Diethyl phthalate (DEP) is a solvent used in many consumer products.4. People exposed to DEP eliminate mono-ethyl phthalate (MEP) in their urine. Workplace air guidelines for external exposure to DEP have been established by ACGIH and NIOSH.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.9 (61. 272 Fourth National Report on Human Exposure to Environmental Chemicals . In contrast.1-93.

9-110) 96.0-117) 142 (119-169) 152 (126-184) 168 (141-201) 179 (161-199) 181 (164-200) 197 (174-223) 79.7-110) 81. 2003) were slightly lower than levels found in NHANES 2001-2002. Analysis of NHANES 2001-2002 showed similar findings.6 (77.2 (66. 2002). Survey years 99-00 01-02 03-04 Geometric mean (95% conf..5-114) 101 (87. 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.5-113) 122 (93. 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.. 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.9 (82. 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.S. 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. population from the National Health and Nutrition Examination Survey.Phthalates 2002 (Brock et al. 2004)..0 (66. with adjusted geometric mean levels of urinary MEP that increased with age (CDC.6 (65. Other population estimates also differed by sex and race ethnicity (Silva et al. interval) 163 (149-178) Selected percentiles ( 95% confidence interval) 50th 141 (129-157) 148 (133-162) 153 (137-177) 75th 360 (307-422) 388 (330-435) 452 (386-504) 90th 905 (753-1180) 969 (805-1180) 1110 (889-1290) Total 167 (150-185) 181 (163-202) Sample size 1950 (1670-2310) 2536 1840 (1450-2200) 2782 2040 (1640-2540) 2605 95th Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 92. In an analysis of NHANES 1999-2000. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.0-156) 140 (111-180) 150 (123-184) 154 (136-177) 160 (146-182) 177 (147-202) 165 (127-208) 177 (135-224) 180 (145-203) 364 (275-495) 330 (249-409) 363 (292-485) 390 (336-452) 419 (363-486) 512 (423-632) 341 (219-554) 512 (290-802) 470 (310-596) 879 (676-1260) 808 (590-1100) 791 (589-1080) 1010 (803-1460) 1060 (884-1320) 1230 (989-1610) 625 (400-784) 843 (512-1320) 719 (470-1330) 1760 (1000-2000) 1330 (868-1840) 1470 (987-2220) 2170 (1790-3350) 2120 (1520-2790) 2290 (1770-3200) 328 393 342 752 742 729 1456 1647 1534 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 141 (124-159) 148 (130-168) 154 (139-171) 187 (165-211) 187 (166-210) 211 (180-248) 120 (107-134) 126 (110-147) 127 (108-150) 158 (142-179) 171 (148-188) 181 (148-217) 324 (249-415) 352 (282-425) 390 (341-465) 377 (307-495) 407 (355-473) 508 (379-634) 1000 (693-1480) 1100 (839-1480) 1070 (852-1360) 822 (697-1170) 860 (712-1100) 1120 (889-1400) 1950 (1460-2900) 2120 (1490-3030) 2000 (1610-2410) 1930 (1170-3410) 1430 (1190-2010) 2250 (1440-3330) 1214 1371 1250 1322 1411 1355 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 164 (142-190) 213 (182-249) 241 (213-271) 208 (183-236) 247 (226-271) 254 (225-287) 149 (135-165) 157 (142-173) 165 (144-189) 154 (136-174) 199 (164-242) 233 (202-270) 196 (166-228) 227 (185-270) 212 (188-246) 128 (111-142) 136 (124-150) 135 (120-158) 382 (314-472) 461 (396-572) 533 (417-665) 443 (390-505) 557 (478-618) 619 (476-791) 313 (239-387) 338 (288-402) 386 (338-485) 814 (673-974) 1080 (860-1650) 1230 (956-1610) 1030 (762-1700) 1240 (961-1480) 1530 (1200-1970) 856 (655-1390) 919 (712-1160) 989 (831-1330) 1330 (974-1920) 1940 (1410-2630) 2270 (1810-3140) 1920 (1230-2590) 2090 (1550-2800) 2590 (2160-3500) 1950 (1480-2740) 1590 (1320-2170) 1920 (1400-2780) 813 677 652 603 703 699 908 1216 1088 Non-Hispanic blacks Non-Hispanic whites Fourth National Report on Human Exposure to Environmental Chemicals 273 . 2005).3-105) 87.

2005. Silva MJ.S. Duty S.112(3):331-338. 274 Fourth National Report on Human Exposure to Environmental Chemicals . Jacek R.111(14):1719-1722. et al. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Reidy JA. Rossbach B. Reproducibility of urinary phthalate metabolites in first morning urine samples. Drexler H.68:309-314. Barr D. Bull Environ Contam Toxicol 2002. Hilborn ED. Brock JW.Phthalates References Adibi JJ. Needham LL. Singh NP. Barr DB. Koch HM.93:177-185. Ryan L. Hodge CC. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Hum Reprod 2007. Caudill SP. et al. Caudill SP. Prenatal exposures to phthalates among women in New York City and Krakow. Hoppin JA. Malek NA. Angerer J. Urinary levels of seven phthalate metabolites in the U. Silva MJ. Third National Report on Human Exposure to Environmental Chemicals. Jedrychowski W. Phthalate monoesters levels in the urine of young children. Brock JW. Baird DD. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. 112(5):A270]. Environ Health Perspect 2002. Centers for Disease Control and Prevention (CDC). Camann DE. Environ Health Perspect 2004. et al. Perera FP.110(5):515-518. Meeker JD. Hauser R. Atlanta (GA). Environ Res 2003.22(3):688-695. Environ Health Perspect 2003. Poland. Davis BJ. Silva MJ.

7-32.7 (14.23 (2.8-47.31-4.5 (12.0) 23.6-38.60 (5.49 (3. DEHP present in medical devices and parenteral delivery systems results in the diester rather than the monoester form being directly introduced into the blood.2 (10.61 (3.9-28.0) 39.40 (4.1) 22.6-25.90) 7.10-5.9-57.80 (4.6 (11.0-18.70 (8.50-16.6) 39.6) 15.3) 28.90 (3.50 (3.60) 4.5 (30.80) 9.5-17.Phthalates Di-2-ethylhexyl Phthalate CAS No.8 (17.80 (1.10-3.68 (3.16-3.0 (18.0.40-8. as glucuronide conjugates (Albro et al.50-2. 1982.3-64.0-84. Concentrations in plastic materials may reach 40% by weight.70 (1.10) 8.92) 4.96-5. MEHP is primarily formed by the hydrolysis of DEHP in the gastrointestinal tract and then absorbed.54) 4.4) 15.90-8.3) 13.2 (11.1-29.50 (2.8-50. and blood product storage and intravenous delivery systems.16 (2.9 (29.3 (15.6) 9.41) 3.20 (1.0 (13.0) 35. mainly polyvinyl chloride.46) 3. Urinary Mono-2-ethylhexyl phthalate (MEHP) Metabolite of Di-2-ethylhexyl phthalate (DEHP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.70-4.0-29.50 (8.40) 2.30-6. 2002.4 (16.63-4.39) 3.40) 11.3 (24. and in humans.7-58.0) 31.9 (17.00-4.51) 4.4) 22.0) 23. and 0.2) 29.6) 14.40-9.0 (17.26-2.80-3.5-28.7) 35.9) 5.10-11. interval) 3. mono(2-ethyl-5-oxohexyl) phthalate (MEOHP).40-8.20 (3.4) 5.5 (25.9 (16.6 (9.5 (31.00-3.30 (7.00 (2.86) 2.80) 6.5 (11.7 (17. mono-(2-ethyl5-hydroxyhexyl) phthalate (MEHHP) and mono-(2-ethyl5-carboxypentyl) phthalate (MECPP).89-3.9 (15.1-17.83) 2.4) 6.42) 3.7) 6.50 (3.60-7.70 (3.10-5.10) 3.4) 7.30) 2.10) 2.5 (20.4 (13.6) 95th 23.10 (3.6 (41.5 (18.70-6.9) 27.2) 6.60) 4.9) 13.2-39.80-4.0 (9.4-27.6-130) 31.0 (14.3-25.30 (3.80-4.1982). population from the National Health and Nutrition Examination Survey.84-4. After parenteral administration.9-48.98) 2. DEHP has been removed from or replaced in most toys and food packaging in the United States.25-3.5 (12.5-27.4) 13.50) 4.40) 4.9) 15.50-11.34 (2.67-4.10) 2.50-20.10-3.3-49.50-3. 1.90-3.90) 4.1-27.0 (19.40 (2.23) 3.9 (7.4) 22.90-4.35 (1.7) 18.69) Selected percentiles ( 95% confidence interval) 50th 3.0) 23.80 (2.80-27. Four metabolites were measured in this Report: mono-(2-ethyl-5-hexyl) phthalate (MEHP).9) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.30-11.80 (8.20 (3.6) 14.90) 1.57-7.27) 2.2-28.5) 19. see Data Analysis section) for S