2009

Fourth National Report on Human Exposure to Environmental Chemicals

Fourth National Report on Human Exposure to Environmental Chemicals

2009

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

Contents

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

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

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

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

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

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

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

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Introduction

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

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

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5.2'3.5.2'4.html.gov/exposurereport/chemical_selection.6-Pentabromodiphenyl ether (BDE 100) 2.4’.2'.3-Dichlorobenzene (m-Dichlorobenzene) 1.cdc.5'-Hexabromodiphenyl ether (BDE 153) 2.1.4’-Trichloro-2’-hydroxyphenyl ether) Non-dioxin-like Polychlorinated Biphenyls 2.4-Dichlorobenzene (p-Dichlorobenzene.5.2-bis[4-Hydroxyphenyl] propane) 4-tert-Octyl phenol (4-[1.3’.4.4’. Total Arsenic (V) acid Arsenobetaine Arsenocholine Arsenous (III) acid Dimethylarsinic acid Monomethylarsonic acid Trimethylarsine oxide Disinfection By-Products (Trihalomethanes) Bromodichloromethane Dibromochloromethane (Chlorodibromomethane) Bromoform (Tribromomethane) Chloroform (Trichloromethane) Environmental Phenols Benzophenone-3 (2-Hydroxy-4-methoxybenzophenone) Bisphenol A (2.4.3'.and p-Xylene o-Xylene 2 Fourth National Report on Human Exposure to Environmental Chemicals .What’s New in this Report What’s New in this Report In this Fourth Report.5'-Tetrachlorobiphenyl (PCB 49) 2. The process for selection is described at http://www. Paradichlorobenzene) 1.3.1.2-Dichloropropane 2.2'.5-Dimethylfuran Ethylbenzene Hexachloroethane Methyl-tert-butyl ether (MTBE) Nitrobenzene Styrene 1.2-Dibromo-3-chloropropane (DBCP) Dibromomethane 1.1-Trichloroethane (Methyl chloroform) 1.2'.3-Tetramethylbutyl] phenol) Triclosan (2.4. Table 1.4'-Tetrabromodiphenyl ether (BDE 66) 2. 2009 Acrylamide Adducts Acrylamide Glycidamide Total and Speciated Arsenic Arsenic.4'-Tribromodiphenyl ether (BDE 28) 2.2-Dichloroethene trans-1.2-Dichloroethane (Ethylene dichloride) 1.2'.2'.5'-Hexabromobiphenyl (BB 153) Volatile Organic Compounds (VOCs) Benzene Chlorobenzene (Monochlorobenzene) 1.2-Dichloroethene Dichloromethane (Methylene chloride) 1.2'.4'.5’.4'.4.4.4'.4.5-Pentabromodiphenyl ether (BDE 99) 2.6'-Hexabromodiphenyl ether (BDE 154) 2.4.4'.5'-Tetrachlorobiphenyl (PCB 44) 2.6-Heptabromodiphenyl ether (BDE 183) 2.2.4'-Tetrabromodiphenyl ether (BDE 47) 2.2-Tetrachloroethane Tetrachloroethene Tetrachloromethane (Carbon tetrachloride) Toluene 1.1.2'.4.4-Tribromodiphenyl ether (BDE 17) 2.2'. Chemicals reported for the first time in the Fourth National Report on Human Exposure to Environmental Chemicals.4'.5'.4.1.4.4.2-Trichloroethane Trichloroethene (Trichloroethylene) m.3.2-Dichlorobenzene (o-Dichlorobenzene) 1.6'-Decachlorobiphenyl (PCB 209) Perchlorate Perfluorinated Compounds Perfluorobutane sulfonic acid (PFBuS) Perfluorodecanoic acid (PFDeA) Perfluorododecanoic acid (PFDoA) Perfluoroheptanoic acid (PFHpA) Perfluorohexane sulfonic acid (PFHxS) Perfluorononanoic acid (PFNA) Perfluorooctane sulfonamide (PFOSA) Perfluorooctane sulfonic acid (PFOS) 2-(N-Ethyl-Perfluorooctane sulfonamido) acetic acid (Et-PFOSA-AcOH) 2-(N-Methyl-perfluorooctane sulfonamido) acetic acid (Me-PFOSA-AcOH) Perfluorooctanoic acid (PFOA) Perfluoroundecanoic acid (PFUA) Phthalate Metabolite Mono-(2-ethyl-5-carboxypentyl) phthalate (MECPP) Polybrominated Diphenyl Ethers (PBDE) and Polybrominated Biphenyl 2.6.4'-Pentabromodiphenyl ether (BDE 85) 2.5.4.3.1-Dichloroethane 1.3.1-Dichloroethene (Vinylidene chloride) cis-1.2'.2’. 75 new chemicals are added for the 2003-2004 survey period and are listed in Table 1.

urinary 2.. and polycyclic aromatic hydrocarbons (PAHs) for one or more of the 1999-2002 survey periods.g.. five results that all have the value 90. Data for other pesticides are included only for 1999-2000 and 2001-2002.What’s Different in this Report What’s Different in this Report The Fourth Report uses a new procedure to estimate percentiles when the percentile estimate falls on a value that is repeated multiple times (e. Only slight differences should be noted when one compares the recomputations to previous releases of the Report. and these data will be included in the next release of the Report. Percentiles for all three NHANES survey periods (1999-2000.5-dichlorophenol for the 1999-2002 survey periods. 2001-2002. 2003-2004) have been re-computed by use of this improved procedure.1). 2003-2004 data for these other pesticides will be provided on this website as soon as they are available. Details of this procedure are provided in Appendix A. the presence of an interference) that produced results of inadequate quality. 2003-2004 data for the organochlorine pesticides and the dialkyl phosphate organophosphorus insecticides are included in the Report. Explanations for each change are provided in Appendix B.g. Affected analytes were serum beta-hexachlorocyclohexane for the 2001-2002 survey period.4-dichlorophenol and 2. Some results reported previously have been changed or removed due to improvements in analytical measurement or recognition of an analytical issue (e. Fourth National Report on Human Exposure to Environmental Chemicals 3 .

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

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

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

Therefore. Quality Assurance of Chemical Measurements. 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. Taylor JK. Boca Raton (FL). All data from 1999-2004 have been reanalyzed using this new procedure to handle situations where the percentile falls on a repeating value. This improved procedure makes each repeated value unique by adding a unique negligibly small number to each repeated value. we have improved the procedure for estimating percentiles to better handle this situation. Appendix A gives the details of the new procedure for estimating percentiles.Data Sources and Data Analysis Report. Lewis Publishers.

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

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

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

7) 96.Acrylamide Acrylamide CAS No.6) 90th 141 (124-155) 03-04 03-04 03-04 03-04 03-04 03-04 03-04 59.2 (62.4) 100 (89. acrylamide is synthesized and used in the production of polyacrylamide polymer.7) 54.1) 46. 217 million pounds of acrylamide were produced commercially in the U.2-70. see Data Analysis section) for Survey year 03-04 is 3.5) 58.2-59.9-61. Natural substances in the food are converted to acrylamide. EPA reference dose of 0.S. (NTP-CERHR.S. the main source of exposure is from the diet. 2006).2) 57. 2005).1-64. In 1997. 2002). and peripheral neuropathy following chronic Acrylamide Geometric mean and selected percentiles of hemoglobin adduct concentrations (in pmol/g hemoglobin) for the U.7-60.2 μg/kg/day (U.8-55. 2005).7-64. as an absorbent in disposable diapers.1 (52.4 (54. drinking water. but can covalently bind to form adducts with proteins. Fourth National Report on Human Exposure to Environmental Chemicals 11 . and cosmetics (NTP-CERHR. 1994).1 (83. 2005.4 (59.1) 53. People may be exposed to acrylamide from foods.1 (73.9-52. it was discovered that acrylamide is formed when starch-rich foods. In humans.3-2. 2006.8 (81. and from dermal contact with products that contain residual acrylamide. widely distributed in tissues.4) 57. such as potatoes and some grains.7) 75th 79. and in some cosmetics. Acrylamide is not thought to accumulate in the body at environmental doses. Estimated intakes in children are about twice that of adults (DiNovi and Howard.S.S.9 (60.2) 57. Survey Geometric mean (95% conf.0-58.0-49. in some sealing grouts.3) 86.1 (47. environmental releases of acrylamide can enter aquatic systems and soils where it degrades within days and does not bioaccumulate (U.4 (51.5) 66.6) 73.1) 62.3-71.0 (53.6-75.5-80.0 μg/kg for adults (FAO/ WHO. population from the National Health and Nutrition Examination Survey..6) 90. in permanent press fabrics. Tareke et al. soil conditioners.0 (69.6 (81.8 (52. EPA.6-66. acrylamide has produced upper airway irritation following inhalation of high levels.4) 57. FAO/WHO. These estimated intakes are hundreds of times lower than occupational exposures..0 (67.0 (57. gels.9) 58.2-118) 98.8-57. 2005).9 (54. interval) 61.9) 57. Animal studies indicate that acrylamide is well absorbed.4-89. mineral processing. 79-06-1 General Information Acrylamide is a small organic molecule existing as a white crystalline powder in its pure state.6-61.4 (54. Polyacrylamides are useful water-compatible polymers used in water treatment.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. are heated at temperatures used for frying and baking.0) 57.7) 58.1) 101 (95.5-85.3) 70.. Smaller scale applications of polyacrylamides include additives to paperboard used for food packaging. 2005). EPA. and is either metabolized to the reactive epoxide.5 (44. although additional exposures from cosmetic products could add a similar amount (NTP-CERHR.0.5 (74.2 (75.2 (58. smoking. pulp and paper production. or to glutathione conjugates (Calleman et al.2-67. Recently.7 (55. ocular and dermal irritation from direct contact with acrylamide containing materials.8 (91.4-60.0-108) 152 (139-175) 126 (111-142) 108 (86.7 (58. FDA.3) 63.1) 55.6) 50.1-57.4 (53.7 (63. glycidamide. and an average daily intake is estimated as 0.7-64. and well below doses known to cause nerve damage or carcinogenicity in animals.1-61.2-114) 163 (147-191) 96. Fennell et al.1 (88.0-115) 156 (120-203) 146 (129-163) 149 (125-179) 218 (172-271) 197 (172-223) 1792 1874 2994 Limit of detection (LOD. 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.S.2-93.6 (56.7 (65.7) 73.9 (69.5 (79. Commercially.9) 63. but are generally above the U. 2004).4-60. and in the synthesis or compounding of dye materials. 2004.6-108) 61. 2005).4-83. and binding agents.0-66.2-91.0) 85.3 (55. 1990.6 (51.1-64.8 (57. Since acrylamide has limited volatility and high water solubility.6) 71.6-104) 82.2-77.9-105) 86. In the general population.6-65. Elimination occurs mainly in the urine as mercapturic acid conjugates.5 (52.3 (53.4-76.9) 75.4) 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.

4 (57. most non-smokers had levels less than about 100 pmol/gram hemoglobin.6 (90.2) 87.9-77..2-91.7) 60. Survey Geometric mean (95% conf..1-60.who.1 (56.7 (84.2-90. 2005). Several of these studies have shown that smokers have adduct levels that are three to fourfold higher than non-smokers.4-65. EPA at: http://www.8-48. NTP-CERHR. IARC classifies acrylamide as probably carcinogenic to humans.4 (51. although different analytic methods can affect results.9) 59. Maniere et al. gov/iris/ and from the Food and Agriculture Organization of the United Nations and WHO at: http://www.1-62.4) 46.7 (57.7 (87.7 (61.5) 87.pdf. and to increase DNA reactivity when glutathione availability is reduced (Klaunig et al.2-68. 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.. 2005. scrotal.1 (66.4 (81.5) 118 (110-129) 121 (108-140) 136 (124-149) 152 (135-170) 159 (129-204) 172 (157-194) 1841 1954 3044 Limit of detection (LOD. 1997.4 (56. respectively) are markers of integrated acrylamide exposure over the preceding few months.8 (44.5 (42.0) 118 (103-126) 121 (112-134) 113 (94. 2004). 2006) have been demonstrated after acrylamide dosing.3) 59.8 (51.1) 62. Vesper et al. and cancer (mammary.5) 71. 2001).9-64.9) 75. Puppel et al.6-64. and neuronal DNA reactivity (Doerge et al.4) 53.1 (70. 2005. 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.9-78.7) 90. thyroid. probably through its epoxide metabolite. Rice. 2005).0-93.1 (82.5 (83. altered gene expression in testicular tissues (Yang et al. Klaunig et al.1 (57.1) 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 59.2 (56.6 (66. Vesper 2005) and smoking (Bergmark.5-64.9-62.1-70. 2003.7) 74...1) 56.S.Acrylamide occupational exposures.0 (80.2 (72. 2005. 2006).8) 60.9 (81. Acrylamide is clastogenic and can produce dominant lethal mutations. Mucci et al. 2005). 2005. Adducts are formed when either acrylamide or glycidamide react to form a permanent covalent bond with hemoglobin in the blood.4 (61.2) 65. EPA.5-92. Animal studies have shown that acrylamide can cause nerve damage (neuropathy).1) 60.8-61.4 (90.7-62. Puppel et al.3) 59.7-86.S. 2005)... 2005.S.. 2008).3-78. Schettgen et al.4-103) 79.7-64.. In addition. see Data Analysis section) for Survey year 03-04 is 4. Axonal degeneration. Younger children may have slightly higher levels possibly due to increased intake of acrylamide-containing foods relative to body size (Dybing et al. 2006..3) 59.8) 45.0-62.1-56. 2005. dominant lethality). U.S. glycidamide (NTP-CERHR. 2004..9 (57. fetal death. 2005. to increase the unscheduled synthesis of DNA in tumor susceptible tissues (Klaunig et al.0 (52.5) 75th 85..5 (59.4-98. After exposure ceases.. adrenal.7) 61. 2005.2 (63.9 (58.0 (75. population from the National Health and Nutrition Examination Survey.9) 65.9) 87. Glycidamide Geometric mean and selected percentiles of hemoglobin adduct concentrations (in pmol/g hemoglobin) for the U. 2002.0-103) 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 64.5-94. 1997.3) 85.. Biomonitoring Information Acrylamide and glycidamide hemoglobin adducts (AHA and GHA.. 2005) and sperm DNA adducts (Xie et al. EPA. Schettgen et al.epa.9-138) 143 (130-159) 96. U.0. male germinal cell injury.3-101) 95.0 (70. 2006).8-49. Glycidamide has been shown to react with DNA (Doerge et al.4) 83.6-90. AHA levels have been shown to increase with dietary intake (Hagmar et al. 2005.5) 90th 130 (120-141) 03-04 03-04 03-04 03-04 03-04 03-04 03-04 71.4-59. uterine. levels of AHA adducts decline but may remain detectable for several months (Hagmar et al..int/ ipcs/food/jecfa/summaries/summary_report_64_final.9-76.. interval) 59. 12 Fourth National Report on Human Exposure to Environmental Chemicals .. 2005) have been demonstrated in animals.3 (56. and other sites) (FAO/WHO. 2002. reproductive effects (reduced litter size. Hagmar et al.2) 55.. 2008).5 (56.0) 94.6-62. Additional information is available from U. 2005. presynaptic nerve terminal binding (LoPachin.. 2005.5-66. 2009).

html#u1004. AHA levels were several fold to several hundredfold higher than levels in non-exposed non-smokers (Bergmark et al.. Fennell TR. April 13-15. morphological and molecular endpoints in animal models. July. smoking habits and gender. Wirfalt E. Mutat Res 2005. Uncertainties. Costa LG. Mechanisms of acrylamide induced rodent carcinogenesis. Available at URL: http://www. Hagmar et al. 2006. and Research Strategies. [Epub ahead of print] Dybing E.56. February. Tornqvist M. Chem Res Toxicol 1990.fda. Illinois. McDaniel LP. Laurentie M.580(1-2):157-165. 2/3/09 Hagmar L. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Granath F. Fennell TR. CFSAN/Office of Plant and Dairy Foods. Calleman CJ. Osterman-Golkar S.nih.. symptoms of numbness or tingling in the extremities did not occur in exposed workers whose AHA levels were below 510 pmol/gram hemoglobin. Adv Exp Med Biol 2005. Summer SCJ. Adv Exp Med Biol 2005. Simultaneous analysis of hemoglobin adducts of acrylamide and Fourth National Report on Human Exposure to Environmental Chemicals 13 . Wu Y. Toxicol Sci. J Agric Food Chem 2008. Acrylamide is metabolized to glycidamide in the rat: evidence from hemoglobin adduct formation. Available at URL: http://cerhr.who. Farmer PB. Doerge DR. 1999). Rosen I. DNA damage and DNA adduct formation in rat tissues following oral administration of acrylamide. Survey data on acrylamide in food: individual food products.gov/chemicals/ acrylamide/Acrylamide_Monograph. 6013-6019. 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. Bridson WE. Maniere I. NIH Publication No.Toxicol Appl Pharmacol 1994.580(1-2):119-129. Axmon A.3:406-412. DNA adducts derived from administration of acrylamide and glycidamide to mice and rats. Center for the Evaluation of Risks to Human Reproduction (NTP-CERHR). Differences in hemoglobin adduct levels of acrylamide in the general population with respect to dietary intake. Yang JS. The Updated Exposure Assessment for Acrylamide. et al. Bergmark E. Toxicol 2005. Hemoglobin adducts of acrylamide and acrylonitrile in laboratory workers. In another study. Alexander J. 2004 Acrylamide in Food Workshop: Update Scientific Issues.Acrylamide In occupational settings. Haugen M. Aprea P. 2001). Magnusson AL. 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. Twaddle NC.10(1):78-84. and 39% of workers with levels above 1000 pmol/gram hemoglobin had these symptoms (Hagmar et al. 2/3/09 Perez HL. Food Chem.int/ipcs/ food/jecfa/summaries/summary_report_64_final. Food and Drug Administration (FDA).561:21-37. Acrylamide neurotoxicity: neurological. References Bergmark E. Toxicol Sci 2005. 64th Meeting: Summary and Conclusions (FAO/WHO). Available at URL: http://www. et al. Scand J Work Environ Health 2001.pdf. Churchwell MI. Perez et al.580(1-2):131-141. Bergmark E. 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. Mutat Res 2005. da Costa GG. Cheong HK.. Mutat Res 2005.561:49-62. Nordander C. Tornqvist M. He F.pdf. Chicago. Relationships between biomarkers of exposure and neurological effects in a group of workers exposed to acrylamide. Metabolism and hemoglobin adduct formation of acrylamide in humans. gov/~dms/acrydata. Chem Res Toxicol 1997 Jan. Burgess J. 2004.cfsan. Italy. Paulsson B. 2009 Jan 8. et al. He F.niehs. Bergmark E. Biomarkers of human exposure to acrylamide and relation to polymorphisms in metabolizing genes. 054472.27(4):219-226. National Toxicology Program. Bjellaas T. Costa LG. Paulsen JE. Spicer R. Monograph on the Potential Human Reproductive and Developmental Effects of Acrylamide. Andersen M. 2/3/09 Klaunig JE. 2005. Joint FAO/WHO Expert Committee on Food Additives.. 8-17 February 2005. Human exposure and internal dose assessments of acrylamide in food. Bruze M. Kamendulis LM. Zhang S. Malmberg B. Toxicol Appl Pharmacol 1993.. Churchwell MI. Wilson KM. 1993. DiNovi M and Howard D. Health effects of occupational exposure to acrylamide using hemoglobin adducts as biomarkers of internal dose. Becher G. et al. smokers and nonsmokers.120(1):45-54. Guffroy M. Beland FA. Doerge DR. Duale N.43:365–410. Calleman CJ. Tian G. 1994).126(2):361-371. Determination of hemoglobin adducts in humans occupationally exposed to acrylamide. Calleman CJ. et al. Snyder RW. LoPachin RM. Hagmar L. Rome.85:447-459. Kautiainen A. 2001. Godard T. Acrylamide intake through diet and human cancer risk. Mucci LA.

Ospina M.txt. Reprod Toxicol 2005. Toxicol Lett 2006. Rapid Commun Mass Spectrom 2006. Myers GL.580(1-2):3-20. U. Available at URL: http://www. Vesper HW. Acrylamide. 1994.207(6):531-9. Rydberg P. Drexler H. Smith A.S. Benetou V. Angerer J.gov/iris/subst/0286. Anal Biochem 1999. Kutting B.htm. Toxicological effects of acrylamide on rat testicular gene expression profile.19(4):527-34. Meyers T. Office of Pollution Prevention and Toxics. Adduction of biomacromolecules with acrylamide (AA) in mice at environmental dose levels studied by accelerator mass spectrometry. 2/3/09 Vesper HW.206(1):9-14. et al. Angerer J.S. The carcinogenicity of acrylamide. Han DU. Hemoglobin adducts of ethylene oxide. Chemical Summary for Acrylamide. Lee SH. Drexler H. Sun H. propylene oxide. Pilot study on the impact of potato chips consumption on biomarkers of acrylamide exposure. A first approach to estimate the internal exposure to acrylamide in smoking and non-smoking adults from Germany. Lee MH. Ingham L. Choi JH. 2/3/09. Drexler H. EPA). Xie Q. Analysis of acrylamide.580(1-2):71-80. Schettgen T. Integrated Risk Information System (IRIS). Environmental Protection Agency (U. Int J Hyg Environ Health 2003. Available at URL: http://www. Rice JM. Puppel N. Tornqvist M.163(2):101-8. Toxicol Lett 2002. Rossbach B. Cross-sectional study on acrylamide hemoglobin adducts in subpopulations from the European Prospective Investigation into Cancer and Nutrition (EPIC) Study. Liu K. Hallmans G. Chae C. Mutat Res 2005. Jin Y. Vesper HW. Angerer J. Gray JG.50(17):4998-5006. Automated method for measuring globin adducts of acrylamide and glycidamide at optimized Edman reaction conditions. 14 Fourth National Report on Human Exposure to Environmental Chemicals . Mutat Res 2005 Feb 7. Eriksson S. Broding HC. Schettgen T. Schettgen T. Tjønneland A. Slimani N.274(1):59-68. September. revised 1/3/06.epa. et al. Yang HJ. DNA strand breaking capacity of acrylamide and glycidamide in mammalian cells. Tjaden Z. Fueller F.56(15):6046-53. Fu D. Marko D. Agudo A. Letzel S. Determination of haemoglobin adducts of acrylamide and glycidamide in smoking and non-smoking persons of the general population. EPA). Washington (DC). acrylonitrile and acrylamide-biomarkers in occupational and environmental medicine. U. J Agric Food Chem 2008. Karlsson P. Adv Exp Med Biol 2005. a carcinogen formed in heated foodstuffs. Liu Y.134(1-3):65-70. Weiss T. Han CH.561:89-96. Licea-Perez H. Ding X. Ospina M. Int J Hyg Environ Health 2004.Acrylamide glycidamide by gas chromatography-mass spectrometry.gov/chemfact/s_acryla. Tareke E.20(6):959-64.epa. J Agric Food Chem 2002.S. Environmental Protection Agency (U.S. Meyers T.

21-1.570 (.77 (1.570-1.077) .140 (.44 (1.92) 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 .12-4.50-1.120 (. The consequences of smoking and of using smokeless tobacco products are well known and include an increased risk for several types of cancer.860 (.080-.22) 2789 3152 2937 3210 3667 3383 Females Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 * . 2006).050-.470-.060 (.50-4. population from the National Health and Nutrition Examination Survey.990) .210 (.188) .164 (.92 (1.34 (1.62 (2.066-.020-.20) .370-.040-.14) .17 (1.30) 2.88 (.030-.01) 3.139) * .080 (.05 ng/mL. Cigarettes contain about 1.09-3.320) .111-.220) .81-2.164 (.621-1.060) .520 (.106-.21 (. and various other disorders (U.094) .060-.48-3.110) .77 (1.533-.060 (<LOD-. 2004).110-.740-1. Survey Geometric mean (95% conf.14-1.070) 75th .142-.180) .080-.44 (2.84-3. acute respiratory infections.120 (. and 03-04 are 0.88 (1.49) 1.030-.930 (.540 (.580 (.14) . DHHS.350-.50) 3.05. and more than 50 compounds present in ETS are known or reasonably anticipated to be human carcinogens (NTP.17) .190-.44) 2.505 (.430-1.110 (.990 (.163 (.39) 3.087) < LOD < LOD .70) 2.180 (. < LOD means less than the limit of detection.015 ng/mL.670) .23-2.160 (.187) . Children exposed to ETS are at increased risk for sudden infant death syndrome.108) * .62) 2. 1998).120) .050 (<LOD-.77 (2.167 (.600-1.163) .050-.800 (.09-2.230 (.047-.068) .234) .910-1. Persons exposed to secondhand tobacco smoke (environmental tobacco smoke [ETS]) may have adverse health effects that include lung cancer and coronary heart disease. DHHS.23 (1.630 (.145) .580) .39 (1.050) .040 (.26-1.110) .066 (.63 (2..050 (<LOD-.220-.68) 2.94) 1.54 (1.312) .050) .400-.32-2.96-4.216 (.071 (.080-.126) .500 (.220) .96) 2.950-1.054 (.230) .S.12 (2.23 (.061) < LOD .15) 2.63-2.198) * .410) .89) 1.059-.070 (<LOD-.01 (1. Fourth National Report on Human Exposure to Environmental Chemicals 15 .071) .19) .23 (2. maternal exposure during pregnancy can result in lower birth weight.30) 2.137-.084) . respectively.043-.30) * .180) .190-.00) 1. see Data Analysis section) for Survey years 99-00.080) < LOD < LOD .066) .124 (.620-1.960-1.690 (.260) 1.00) .080) < LOD .059-.190-.5% nicotine by weight (Kozlowski et al. ear problems.160) .68 (1.110 (.68) .770) .12) 1.080 (.48-2.350 (.090-.200) 1.920 (.15 (2.131 (.040 (.47-3.57) 2.99) 2.154-.130 (.310-1.070) .087 (.175 (.115-.350-.850 (.240 (. producing roughly 1–2 mg of bioavailable nicotine per cigarette (Benowitz and Jacob.140 (.060 (.506 (.87-3.20-2.900-1.820) .33-2.55-2.213) .790) .S. cardiovascular disease.09-3.280 (.19) 1.180) .S.02) 1.310) .Cotinine Cotinine CAS No. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.99) 2.580-1.150) .201) .21-1.040 (.120-.625) .04 (1.308 (.11) .180 (.32) 1.79) 3.49) 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.130) .110 (.030 (.062 (.068) .080-.052 (<LOD-.070-.540-.090-.070) .180) .93) .75) 1.100-.96 (1.050 (<LOD-. 83% of measurements had an LOD of 0.060-.55 (1.770-1.144 (.28) .60-2.66) 1.140-.19-2.54) 1.20 (.110 (.42 (1.43 (1.50 (1.70-2.150) .090-.997-3.83-2.12 (1.620 (.052 (<LOD-.05) 1. stroke.85 (1.480-.20) 1.160) .050 (. and exacerbated asthma (U.302) .077) .030-.120 (.104-.193) .45) 1.060 (<LOD-.66 (1.66-3.050 (<LOD-.32-2.49) 1.770) .54 (1.047-. and 17% had an LOD of 0.063) .140-.726) .058 (.040-.015.360) .180) .20 (1.300) .02 (.630 (.78) 2. 2004). emphysema.02) 1.44) 2.840) 3.110-.310) 90th 1.28-1.35 (2. acute respiratory illness.18-3.42-4.480-1.110 (.087-.076-.38-2.260-1.16) .088-.057-.740-1.120 (.060-. and 0.075 (.660) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.428-.53-4.17 (.450-.153-.53 (1.089) Age group 3-11 years 99-00 01-02** 03-04 . The smoke produced by burning tobacco contains at least 250 chemicals that are toxic or carcinogenic.65 (1.710 (.40) .160 (.086 (.137 (.54) size 5999 6819 6320 Total years 99-00 01-02** 03-04 50th .110-.197) .053 (<LOD-.148-. ** In the 2001-2002 survey period.073) < LOD .160 (.22) 2.120 (.160-.730 (.510 (. 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.95) 1.950 (.120-.310-1. 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.630 (.76 (1. which may vary for some chemicals by year and by individual sample.

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

Herrera B. Vol 38. Summary of Data Reported and Evaluation [online] 1986. Jacob P.S. National Toxicology Program (NTP). Health Effects of Exposure to Environmental Tobacco Smoke: The Report of the California Environmental Protection Agency. Tobacco related exposures. IARC Monogr Eval Carcinog Risks Hum. Jacob III P.fr/ENG/Monographs/ allmonos90. Pollack HA. Modin G. Am J Public Health 2004. 4/13/09 International Agency for Research on Cancer. Exposure of the U. Maurer KR. Smoking and Tobacco Control Monograph 10 [online]. Benowitz NL. Decrease in the prevalence of environmental tobacco smoke exposure in the home during the 1990s in families with children. 4/13/09 Iwase A.fr/ENG/Monographs/allmonos90.275:1233-1240.4:313-316. Aiba M.S.niosh. Tob Control 2006. IARC Monogr Eval Carcinog Risks Hum. Tob Control 1998. Smoke-free laws and secondhand smoke exposure in US nonsmoking adults. Jacob P III.63:139-43. Centers for Disease Control. Dollery CT.57(1):79115.nih. Available at URL: http:// cancercontrol. Fong I. Trends in the exposure of nonsmokers in the U. Mehta NY.280:135-140. Pirkle JL. National Center for Fourth National Report on Human Exposure to Environmental Chemicals 17 . International Agency for Research on Cancer. Schober SE. 1991. Schwartz SS. Etzel RA. Coordinating Center for Health Promotion. Perez-Stable EJ. Jarvis MJ. Warner K.291(3):1196-1203. U. Sweeney CT. Benowitz NL. Pickett MA. Epidemiol Rev 1996. 11th ed. Respiratory nicotine absorption in non-smoking females during passive smoking. DHHS). DHHS). June. Hukkanen J. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Benowitz NL. In Report on Carcinogens. Soliman S. Curtin LR. Bernert JT.pdf. U. BMJ 1975.S.php. 4/13/09 National Cancer Institute (NCI).7:369-375. Third National Report on Human Exposure to Environmental Chemicals. Herrera B. 1999. Absorption and metabolism of nicotine from cigarettes. JAMA 1998. Environ Health Perspect 2006. the United Kingdom. Available at URL: http://www. Benowitz NL. Pharmacol Rev 2005.gov/tcrb/monographs/10/. Summary of Data Reported and Evaluation [online] 2004. George CF. [online].S. Flegal KM.surgeongeneral. 1988-1991. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Metabolism and disposition kinetics of nicotine. Giovino G. Vol 83. Available at URL: http://monographs.cancer. National Center for Chronic Disease Prevention and Health Promotion. iarc. Metabolism of nicotine to cotinine studied by a dual stable isotope method. Current Intelligence Bulletin 54: Environmental tobacco smoke in the workplace. U. Pechacek TF. and the United States. Kira S. Strauss WJ. Department of Heath and Human Services.56:483-493. Biomonitoring data can also help scientists plan and conduct research about exposure to ETS and about its health effects. Filter ventilation and nicotine content of tobacco in cigarettes from Canada. Ethnic differences in N-glucuronidation of nicotine and cotinine. 4/13/09 U. Department of Heath and Human Services. 4/13/09 Centers for Disease Control and Prevention (CDC). cigarette smokers: the Third National Health and Nutrition Examination Survey. population to environmental tobacco smoke: the Third National Health and Nutrition Examination Survey.S. Centers for Disease Control and Prevention. et al. Racial/ethnic differences in serum cotinine levels among adult U.94(2):314-320. Nicotine metabolism and intake in black and white smokers. Pirkle JL. Tobacco Smoke.Cotinine and public health officials determine whether people have been exposed to higher levels of ETS than are found in the general population.gov/ntp/roc/eleventh/profiles/ s176toba. available at URL: http://mtn.15:302-307.S Department of Health and Human Services (U. Office on Smoking and Health [online] 2006.gov/eid/rmca/critdocs/ criteriadoc/33. J Pharmacol Exp Ther 1999. JAMA 1996. Richter PA. Cotinine as a biomarker of environmental tobacco smoke exposure. Sosnoff CS. Vogler GP. Houseman TH.niehs. Int Arch Occup Environ Health 1991. 1988-1991. Caudill SP. 2004. Lewis PJ. References Armitage AK.iarc. 4/13/09 Perez-Stable EJ. Tobacco Smoke and Involuntary Smoking. Giovino GA. Kozlowski LT. Available at URL: http://monographs.S. Clin Pharmacol Ther 1994. Pechacek TF.S. Bernert JT.php. National Institute for Occupational Safety and Hygiene (NIOSH). JAMA 1998. Brody DJ. The Health Consequences of Smoking: The Surgeon General’s Report—Executive Summary. population to secondhand smoke: 1988-2002. Brody DJ. Atlanta (GA): 2005.pdf. Mowery PD.18:188-204. 1999-2002. Turner DM.280:152-156.114(6):853-858. Coordinating Center for Health Promotion. Caraballo R. Centers for Disease Control and Prevention. The Health Consequences of Involuntary Exposure to Tobacco Smoke: A Report of the Surgeon General — Executive Summary. Available at URL: http://ntp. et al.cdc.S Department of Health and Human Services (U. Benowitz NL.gov/library/ secondhandsmoke/. Jacob P III.

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

140-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.120-.S.EPA.520) < LOD . Fourth National Report on Human Exposure to Environmental Chemicals 19 .110 (<LOD-. One survey detected DEET in 74% of sampled streams in the U. DEET is not genotoxic.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 .180) < LOD .160) < LOD . 1998). see Data Analysis section) for Survey years 99-00 and 01-02 are 0. Its use is recommended for prevention of several vector-borne diseases. DEET has low acute toxicity.100 (<LOD-.N. DEET is metabolized via hydroxylation and dealkylation pathways and eliminated in the urine within approximately 24 hours (Selim et al.110 (. DEET is also used in combination with dermal sun screens (U. but higher DEET concentrations and different formulations may result in greater absorption (Sudakin and Trevathan.560) < LOD .140) < LOD .130-. About 3-8% of dermally applied DEET is absorbed.130-.S.150) < LOD . have been reported as result of self-poisoning by ingestion or excessive dermal application.N-Diethyl-meta-toluamide (DEET) N.110-. General population exposure to DEET occurs from skin application and from inhalation of aerosol formulations.140) < LOD .EPA. 2003).180 (. Sudakin and Trevathan. 2002).220 (. Urinary N.190) < LOD . (U.110-.110 (.100-. Additional information is available from U.110 (. EPA.1.S.130 (.N-diethyl-meta-toluamide (DEET) is an insect repellent that was first marketed in 1957. Most reports of adverse effects from overexposure to DEET involve skin reactions (Bell et al.EPA at: http://www.140) < LOD .N-Diethyl-meta-toluamide (DEET) CAS No.130) < LOD . and they range in concentration from 4% to 100%.130-.449 and 0.180 (.180 (.240) < LOD . and it has not been rated by IARC or NTP with respect to human carcinogenicity.100-. There are over 225 insect repellents brands containing DEET.S.100-. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD . 2005).S. including seizures and encephalopathy. People in outdoor occupations may apply DEET more frequently or use higher concentration formulations resulting in higher levels of exposure.N-Diethyl-meta-toluamide (DEET) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.130) < LOD .epa.100-.110 (.130 (.270) 688 678 518 700 598 956 Limit of detection (LOD.130-.210) 480 580 672 829 825 1126 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .170 (.gov/pesticides/. 2002). Exposure can also occur from consuming food contaminated by DEET on hands or that was sprayed nearby. (Kolpin et al.130 (.100-. 1998). 2003). Neurological effects in humans.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 .210 (.120-. DEET can be applied to clothing and the skin to repel biting insects.250) < LOD .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 .100-.110 (<LOD-. Survey Geometric mean (95% conf. 134-62-3 General Information N. < LOD means less than the limit of detection. DEET is not a developmental or reproductive toxicant in animals (U. population from the National Health and Nutrition Examination Survey... 1995. which may vary for some chemicals by year and by individual sample. Human health effects from DEET at low environmental doses or at biomonitored levels from low environmental exposures are unknown.140 (.S. DEET is not registered for use on agricultural commodities.170 (.. After absorption.

170-.270) < LOD . Finding a measurable amount of DEET in urine does not mean that the level of DEET causes an adverse health effect.250) < LOD .240) < LOD .N-Diethyl-meta-toluamide (DEET) Biomonitoring Information Urinary levels of DEET reflect recent exposure. population from the National Health and Nutrition Examination Survey.640 (.550) 688 678 518 699 598 956 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD .200 (.S.690 µg/L were measured in eight park employees who applied 71% DEET once a day (Smallwood et al.130 (<LOD-.190-.93) < LOD .N.350-.S.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 . Urinary N.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 . 20 Fourth National Report on Human Exposure to Environmental Chemicals .410 (. 1992).270 (.250 (.280-1.190 (<LOD-. In this survey period.480 (.190 (.230-.280 (.240-.150-.490) < LOD .350) < LOD . representative subsamples from NHANES 2001-2002.320 (. 2007).150) < LOD .410 (.140-.500 (. Survey Geometric mean (95% conf.290-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.500) 480 580 672 828 825 1126 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . DEET was detected in 10% of 60 Latino children in eastern North Carolina farm worker households (Arcury et al. Urinary DEET levels as high as 5.440) < LOD .350) < LOD .230-. Urinary levels of DEET were characterized only at the 90th and 95th percentiles of the U.370-..N-Diethyl-meta-toluamide (DEET) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.320) < LOD .250-.230) < LOD .390-.300) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .330 (..270 (<LOD-.300 (. 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.410-. 2005).370) < LOD .630) < LOD . the limit of detection was lower than for the NHANES 1999-2000 survey period (CDC.330 (. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.190 (.270-.

U.pdf. streams. Third National Report on Human Exposure to Environmental Chemicals. Reregistration Eligibility Decision (RED): DEET. Barber LB.115(8):1254-1260. Environ Health Perspect 2007. Furlong ET.gov/oppsrrd1/REDs/0002red. Environ Sci Technol 2002.41(6):831-839. Washington (DC): U. Available at URL: http://www. Sudakin DL. Trevathan WR. Page BC. Human exposures to N.S. Gabriel KL. Schoenig GP. 1-118.S. hormones. Pesticide urinary metabolite levels of children in eastern North Carolina farmworker households. and other organic wastewater contaminants in U.epa. EPA 738-R98-010. Diethyltoluamide (DEET).EPA). DeBord KE.S. Toxicity and Exposure Assessment in Children’s Health. J Anal Toxicol 1992.N-Diethyl-meta-toluamide (DEET) References Arcury TA. 2005 Kolpin DW. Thurman EM.EPA. Centers for Disease Control and Prevention (CDC). and excretion of N. Pharmaceuticals.gov/teach/chem_summ/ DEET_summary. Available at URL: http://www. Veltri JC. Absorption. Chemical Summary.N-diethyl-mtoluamide insect repellents reported to the American Association of Poison Control Centers. 1999-2000: a national reconnaissance. DEET: a review and update of safety and risk in the general population. Smallwood AW. 2005. Lowry LK. EPA.N. September 1998.S. Atlanta (GA). Zaugg SD. 1993-1997. metabolism. Quandt SA.S. J Toxicol Clin Toxicol 2003. U.N-diethyl-mtoluamide following dermal application to human volunteers. Environmental Protection Agency (U. Meyer MT.epa. Bell JW. pp. pdf.25:95-100. et al. Hartnagel RE Jr. Osimitz TG. Fundam Appl Toxicol 1995. Chen H.N’-diethyl-mtoluamide (m-DET): analysis of an insect repellent in human urine and serum by high-performance liquid chromatography. Grzywacz JG. Int J Toxicol 2002. Barr DB. Selim S.S. Environmental Protection Agency (U. N. Tapia J.2:341352.36(6):1202-1211. 4/9/09 U.EPA).S.16(1):10-13. 4/9/09 Fourth National Report on Human Exposure to Environmental Chemicals 21 .

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

Joint Research Centre Institute of Health and Consumer Protection.312(2):441-448. Furukawa M. Sottas CM. An evaluation of the possible carcinogenicity of bisphenol A to humans.J. Gender differences in the levels of bisphenol A metabolites in urine. Rubin C. Nippon Eiseigaku Zasshi 2004.gov/chemicals/bisphenol/BPAFinalEPVF112607. Available at URL: http://ecb.pdf. Watanabe S. Thomas BF. Endocrinology 2004. Needham LL. 2/4/09 National Toxicology Program’s Report of the Endocrine Disruptors Low-Dose Peer Review (NTP).nih. Tsugane S. DirectorateGeneral Health and Consumer Protection.780(2):365-370. 32 Fourth National Report on Human Exposure to Environmental Chemicals . Bisphenol A. Howdeshell KL. 2008. Chem Res Toxicol 2001. Reidy JA. Cha SW. Kroes R. Regul Toxicol Pharmacol 2002. Koh WS. Available at URL: http://ntp. Park S. et al. Proc Natl Acad Sci USA 2005. hormones.S. Kiguchi M. Fujii S. 2007.68(1):121-146. National Institute of Environmental Health Sciences. Richter CA. Cunha G. Ema M. National Institutes of Health. Munro IC. Cohen JT. Needham LL. 2/4/09 National Toxicology Program Center for the Evaluation of Risks to Human Production (NTP-CERHR). European Commission. Estimation of intake level of bisphenol A in Japanese pregnant women based on measurement of urinary excretion level of the metabolite.pdf .pdf. Szigeti-Buck.europa.14(2):149-157.59(9):625-628. et al. Furlong ET.Environmental Phenols References Akingbemi BT. NC. Koulova AI.10:875-921. Kim JC. NTP-CERHR Panel Report on Reproductive and Developmental Toxicity of Bisphenol A. Three-generation reproductive toxicity study of dietary bisphenol A in CD Sprague-Dawley rats. bisphenol A glucuronide.gov/chemicals/bisphenol/bisphenol. Myers CB. Twomey K. Han SS. Rhomberg et al. 2002. Kolpin DW. Barr DB. Ecotoxicity and the Environment (CSTEE). and Hardy MP. with estrogen receptors alpha and beta. Calafat AM. Research Triangle Park. McConnell EE. and other organic wastewater contaminants in U. Environ Health Perspect 2008.145:592-603. Yoshinaga J.pdf. K.102(19):7014-7019. Serizawa S.137(3):353-362.Scientific Committee on Toxicity. Ispra. streams.eu/ health/ph_risk/committees/sct/documents/out156_en. Han SY.113(4):391-395. Wong LY. Barber LB. Evaluation of developmental toxicity in rats exposed to the environmental estrogen bisphenol A during pregnancy. Environ Health Perspect 2005. Marr MC. Biochem Biophys Res Commun 2003. Haighton LA.S. Arakawa C. et al.nih. Keimowitz AR. Joskow R. National Toxicology Program.59(4):403-408. Toxicol Sci 2002. niehs. U.4’-Isopropylidenediphenol (Bisphenol-A) Summary Assessment Report.S. Ye X. Exposure of the U. Harazono A. Kim YH.. Kawamura N. In vitro and in vivo interactions of bisphenol A and its metabolite. Estrogenic chemicals in plastic and oral contraceptives disrupt development of the fetal mouse prostate and urethra. Tyl RW. Timms BG.jrc. Reidy JA. Rat two-generation reproductive toxicity study of bisphenol A.36(6):1202-1211.pdf . Gray GM. Bisphenol A prevents the synaptogenic response to testosterone in the brain of adult male rats. J Chromatogr B Analyt Technol Biomed Life Sci 2002.35(2 Pt 1):238-254. Urinary concentrations of bisphenol A and 4-nonylphenol in a human reference population. Ikka T. Human Health. NTP-CERHR Panel Report on Reproductive and Developmental Toxicity of Bisphenol A. J Am Dent Assoc 2006. Endocrinology 2008. National Toxicology Program Center for the Evaluation of Risks to Human Production (NTP-CERHR). Barr JR. Watanabe C. 4. August 2001. November 26.nih. Shin HC. Lynch BS. Reprod Toxicol 2001. Belgium. 2/4/09 Ouchi K. MacLusky.. C. and Hajszan. Hara K. Imai H.it/DOCUMENTS/ Existing-Chemicals/RISK_ASSESSMENT/SUMMARY/ bisphenolasum325. Available at URL: http://ec. Needham LL. Thurman EM. Hlywka JJ. 1999-2000: a national reconnaissance. Brussels. Italy. Yang M. Chung MK. Exposure to bisphenol A from bis-glycidyl dimethacrylatebased dental sealants. Measurement of bisphenol A in human urine using liquid chromatography with multi-channel coulometric electrochemical detection. Leranth. Pyo MY. population to bisphenol A and 4-tertiary-octylphenol: 2003-2004. Klinefelter GR. Zacharewski TR. 2/4/09 Fujimaki K. Weight of the evidence evaluation of low-dose reproductive and developmental effects of bisphenol A. N. Hanaoka T. vom Saal FS.niehs. 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. Matthews JB. September.116(1):39-44. Barton L. Ekong J. Calafat AM. Kim CS. Brine DR.. 2003. Department of Health and Human Services. Available at URL: http://cerhr. T.149:988-994. Calafat AM. 2/4/09 European Commission.69(22):2611-2625. Available at URL: http://cerhr. Zaugg SD. Occup Environ Med 2002. Meyer MT. 5: 505-523. May 22. niehs. Pharmaceuticals. Life Sci 2001. Doull J. Bradley S. Urinary bisphenol A and plasma hormone concentrations in male workers exposed to bisphenol A diglycidyl ether and mixed organic solvents. Kuklenyik Z. Environ Sci Technol 2002. Hum Ecol Risk Assess 2004. Caudill SP. Hughes C.gov/ntp/htdocs/liason/ LowDosePeerFinalRpt.

Vom Saal FS. Endocrine mechanisms mediating effects of bisphenol A at levels of human exposure. Endocrinology 2006.44(4):546-51.Environmental Phenols Volkel W. Dekant W. Jang JY. Lordo RA. Yang M. Metabolism and kinetics of bisphenol A in humans at low doses following oral administration. bisphenol-A. Sheldon LS. Welshons WV.113(8):926-33. Kim SY. An extensive new literature concerning low-dose effects of bisphenol A shows the need for a new risk assessment. Biological monitoring of bisphenol a in a Korean population. Kawamoto T. Nagel SC. Morgan MK. Environ Health Perspect 2005. Large effects from small exposures. Colnot T.147(6 Suppl):S56-69. Chuang JC. Food Chem Toxicol 2002. III. Filser JG. An observational study of the potential exposures of preschool children to pentachlorophenol. Chem Res Toxicol 2002. Fourth National Report on Human Exposure to Environmental Chemicals 33 . Hughes C. Lee SM. and nonylphenol at home and daycare. Wilson NK. Arch Environ Contam Toxicol 2003.15:12811287. Witorsch RJ. Low-dose in utero effects of xenoestrogens in mice and their relevance to humans: an analytical review of the literature. Chang SS. vom Saal FS.40(7):905-12. Csanady GA. Environ Res 2007.103(1):9-20. et al.

Environmental Phenols 4-tert-Octylphenol CAS No. over 500. Disposition in humans has not been studied sufficiently.500) . impaired steroidogenesis. Human exposure to alkylphenols and alkylphenol ethoxylates may occur through ingestion of contaminated foods (e.600-1.10) 1.400 (.400 (. did not bioaccumulate. leading to inhalation as another potential exposure route (Rudel et al. and the polyethoxy chain may consist of up to 50 ethoxy units..274-. testicular atrophy.60-3.80 (1.40) 2.600) . < LOD means less than the limit of detection.20) 2..10) 2. In 1999-2000.20-2. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2. These high dose parenteral effects of 4-tert-octylphenol have included altered sex hormone levels and hypothalamicpituitary suppression. In the 1990s.20-2.900 (. Alkylphenols also have been used as plasticizers and antioxidants in plastics and resins. altered neonatal sexual development. and was quickly eliminated from the blood (Certa et al.600-1.40) 1.477) .600-1. 2000.500-1.30) 1.300 (<LOD-. through sewage. 34 Fourth National Report on Human Exposure to Environmental Chemicals .70 (1.20) 314 715 1488 03-04 03-04 * * .300 (<LOD-. Bian et al.20-2.70 (1.300-.50-2. 2002). The alkylphenols can bioaccumulate in some fish. Blake and Boockfor..268-.500) .800-1.90) 2.500 (. 2004).90) 2. Several alkylphenols.g.50) 1.600-1.00 (.300 (<LOD-.g. Survey Geometric mean (95% conf. industrial cleaners.30 (1.S. orally administered 4-tert-octylphenol was well absorbed. outdoor air may have detectable levels of 4-tert-octylphenol and 4-tert-octylphenol monoethoxylates. and through manufacturing waste streams (Warhurst.80 (1. altered estrus cycles and reproductive outcomes.10 (.000 tons of alkylphenol ethoxylates were produced annually worldwide.. The alkylphenol ethoxylates enter the environment through human use of products containing them.60-3.30) 90th 1.40 (1.20-2. Indoor and to a lesser extent..60-3.497) * .30 (1.300 (<LOD-.60-3. several European nations banned the use of alkylphenol ethoxylates in domestic detergents and other uses.2.900 (.900 (. Saito et al. streams in 30 states (Kolpin et al..50) 1.5% of 139 U. Nonylphenol ethoxylates are more commonly used than octylphenol ethoxylates. and some of their degradation products are toxic to aquatic life. Laws et al.60) 1.600) 1. Less frequently.600-1.30 (. including 4-tert-octylphenol.60) .S.50) .900 (. 1997. fish) and drinking water.10-2. and impaired spermatogenesis (e. and some personal care products. 140-66-9 General Information 4-tert-Octyphenol.500) . 2000. 2006.10 (1.600) .30 (1.500-1. an alkylphenol.200-.00) 1229 1288 03-04 03-04 03-04 * .. textiles.20 (1.30) 2.80 (1. have demonstrated estrogenic effects particularly when injected at high doses in animals. 2003. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.389 (.20) 1. They are biodegraded to the corresponding alkylphenol (octylphenol or nonylphenol).40) * 03-04 03-04 03-04 .30-2..900 (.00 (1.1. 4-octylphenol monoethoxylate was detected in 43. which may vary for some chemicals by year and by individual sample.600) .400) 1.50 (1. the various alkylphenols have also been used as emulsifiers and modifiers in paints.700-1. 1996). Urinary 4-tert-Octylphenol (4-[1. Human health effects from 4-tert-octylphenol or the corresponding octylphenol ethoxylates at low environmental doses or at biomonitored levels from low environmental exposures are unknown.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 .3-Tetramethylbutyl] phenol) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. population from the National Health and Nutrition Examination Survey..300-.70 (1. 2002).369 (.60-3.40) 2.3. Octylphenols and nonylphenols can also enter the environment directly from manufacturing waste streams.60-3.00 (. pesticides.507) * < LOD .50) 1. In rats. During the 1980s and 1990s.357 (.299-. and emulsifiers. 1995. Ying et al. see Data Analysis section) for Survey year 03-04 is 0.300 (<LOD-.60) 613 652 1092 Limit of detection (LOD.400 (.40) 1..10 (. Katsuda et al.600-1.20-2.50-3.80) 2.20-2.30 (1.200-. is used to manufacture alkylphenol ethoxylates. and to alkylphenoxycarboxylates. which are anionic surfactants used in detergents.50) . Commercial formulations of alkylphenol ethoxylates usually contain a mixture of oligomers and isomers. to shorter chain alkylphenol ethoxylates. and from contact with some personal care products and detergents.70 (1.500) 75th .

08) 1.S.33 (2.20 (1.43-3.420) .64 (. 4-tert-Octylphenol is not considered directly genotoxic.85 (1.14) 314 713 1487 03-04 03-04 * * .40 (1.320 (<LOD-.15) 1.160-. Kawaguchi et al.00 (.60 (1.06 (2.24) 612 651 1091 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. 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.96-4. Nagao et al.78) 1228 1286 03-04 03-04 03-04 * ..78 (1.270-.22) .199-.29) 2.540-1.370 (<LOD-.05-2.68) 2. Biomonitoring Information Urinary levels of 4-tert-octyphenol reflect recent exposure.530) .17 (.71) 2. 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. 2003.11-2.450) .850 (.260 (<LOD-..43) 1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.410 (. Calafat et al.460 (.62 (1.00) 2.276 (.03 (1.11) 2.59 (1. representative subsample of NHANES 2003-2004.81 (1.59) 1.170-. IARC and NTP have not rated octylphenol. at lower or environmentally relevant doses (Blake et al.384) * .. (2008) showed that urinary levels of 4-tertoctyphenol were detectable in slightly greater than half of the participants of the U.860 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.380 (<LOD-. nonylphenol.33) 3.620) .10-2.50 (2.1.570) . 2000. 2004.78) 3. Tyl et al.470-1.640-1.207-.76 (2.470-1.349) * < LOD .62 (1.470) 75th .31-2.00) 1.740 (.630-1. In a small number of adult Japanese volunteers.25) 2.11) 1.270 (. Survey Geometric mean (95% conf.550-1.68-2.910 (.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 ..300 (<LOD-.3. Sweeney et al. It is unclear if estrogenic or other effects occur in animals through oral dosing.Environmental Phenols Myllymaki et al.62) .18-4.67-2.610) .43) 1.00 (.730-1.560) . population from the National Health and Nutrition Examination Survey.65-3.31 (1.400) . 2001). 2004).03 (1. 2005.25-2.40-4.890-2.280-.500-1. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. the urinary concentrations of 4-tert-octyphenol were near or below the detection limit (Inoue et al.740 (..269 (.620-1.337-. 1999).450) 1. Yoshida et al.270 (.770 (. or their corresponding ethoxylates with respect to human carcinogenicity.53-3.435 (.02-4.73) 2.41) .03-6.00) 2.36-3. Fourth National Report on Human Exposure to Environmental Chemicals 35 . 2001. Urinary 4-tert-Octylphenol (4-[1.3-Tetramethylbutyl] phenol) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.S.25) 90th 1..54) * 03-04 03-04 03-04 .

Two-generation reproduction study with para-tert-octylphenol in rats. Brody JG. Takenaka A. Taya K. Myers CB.18(1):43-51. 2003. Xu L. Inoue K. 1995. Effects of neonatal exposure to a high-dose p-tertoctylphenol on the male reproductive tract in rats.141(7):2667-2673. streams. et al. An environmental assessment of alkylphenol ethoxylates and alkylphenols. Nair-Menon JU. Arch Toxicol 1996. Sakui N. Camann DE. pesticides. Laws SC. Indoor air pollution by alkylphenols in Tokyo. Available at URL: http:// www. Katsuda S.Environmental Phenols References Bian Q.28(3):215-226. Infantile 4-tert-octylphenol exposure transiently inhibits rat ovarian steroidogenesis and steroidogenic acute regulatory protein (StAR) expression. Song L. McCoy GL. Nakagomi M. Saito I. population to bisphenol A and 4-tertiary-octylphenol: 2003-2004. Estrogenic activity of octylphenol. Makino T. Thurman EM.57(2):255-266. Izumi S. Roche JF. hormones. 2/4/09 Ying GG.799(1):119-125.30(2 Pt 1):81-95. Barber LB. Raychoudhury SS. nonylphenol. Marr MC. Effects of 4-tert-octylphenol given in drinking water for 4 months on the male reproductive system of Fischer 344 rats. Toxicol Lett 2001.121(1):21-33.37(20):4543-53. Blake CA. Tyl RW.S. Furlong ET. Phthalates. Seely JC. Maekawa A. Reprod Toxicol 2004. Qian J.S. Myllymaki SA. Bolt HM. Kawaguchi M. Korn LR. Food Chem Toxicol 2006. Ito R. Anal Chim Acta 486:41-50. Okada F. Katsuda S. et al. Yoshimura S. Watanabe G. Maternal exposure to octylphenol suppresses ovine fetal follicle-stimulating hormone secretion. and sertoli cell number.co. Pharmaceuticals. Toxicol Appl Pharmacol 2000. Environ Int 2002.36(6):1202-1211. Regul Toxicol Pharmacol 1999. Williams B. Ono H. Zaugg SD. Environ Sci Technol 2003. Kawaguchi M. Calafat AM. Reproductive effects in male and female rats from neonatal exposure to p-octylphenol. 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. Environ Health Perspect 2008.15(6):683-692. Blake CA. Seto H. Wong LY. and other endocrine-disrupting compounds in indoor air and dust. 1999-2000: a national reconnaissance. Paranko J.pdf. Measurement of 4-nonylphenol and 4-tert-octylphenol in human urine by column-switching liquid chromatography-mass spectrometry. Karjalainen M. Taya K. Brooks AN. Exposure of the U. Wang X. Bodman GJ. Kookana R.165(3):217-226. Kolpin DW. Usumi K. Needham LL. Cooper RL. testis size. Endocrinology 2000. and testosterone.71(1-2):112-122. J Chromatogr B Analyt Technol Biomed Life Sci 2004. Takai N. Toxicokinetics of p-tert-octylphenol in male Wistar rats. alkylphenols.207(1):59-68. Reprod Toxicol 2001. Boockfor FR. Carey SA. Environmental fate of alkylphenols and alkylphenol ethoxylates--a review.54(1):154-167. Fail PA. polybrominated diphenyl ethers. Nicol L. Spengler JD. Toxicol Appl Pharmacol 2005.116(1):39-44. Brine DR. Ferrell JM. Watanabe G. Reidy JA. Environ Sci Technol 2002. Horie M. Muller AM. Fedtke N. Saito Y. Chen J. 36 Fourth National Report on Human Exposure to Environmental Chemicals . Indoor Air 2004.folliclestimulating hormone.uk/resource/reports/ethoxylates_alkylphenols. Toxicol Sci 2000. Inoue K. Irreversible effects of neonatal exposure to p-tert-octylphenol on the reproductive tract in female rats.14(5):325-332. Ye X. Maekawa A. Biol Reprod 1997. The toxic effects of 4-tert-octylphenol on the reproductive system of male rats. et al. Yoshida M. Certa H. Boockfor FR. Warhurst AM. Sweeney T. Millette CF. prolactin. and other organic wastewater contaminants in U.44(8):1355-1361. Toppari J. Yoshimura Y. Nagao T. Wiegand HJ. bisphenol A and methoxychlor in rats.foe. Meyer MT. et al. Chronic administration of the environmental pollutant 4-tert-octylphenol to adult male rats interferes with the secretion of luteinizing hormone. Haavisto TE. Rudel RA. Onuki A. Yoshida M.

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

7 (28.20 (7.0) 49.4.Environmental Phenols Urinary Triclosan (2.54 (8.50-10.5) 13.4 (11.0) 65.8) 9.1 (15.6-14.4) 51.20 (7.2-14.8-63.7-318) 224 (186-272) 236 (115-336) 356 (169-580) 385 (308-506) 314 713 1487 03-04 03-04 13.6-15.1) 9.1) 14.4) 90th 249 (188-304) 03-04 03-04 03-04 8.7) 123 (36. see Data Analysis section) for Survey year 03-04 is 2.6 (10.8) 7.4-19.2 (27.45-13.5) 66.6 (9.2-58.45-10.2 (37.6 (30.55 (4.94 (7.20-11. Survey Geometric mean (95% conf.00 (4.5-14.7 (39.48 (8.9-61.2 (11.43-13.9) 75th 47.6) 10.8) 116 (39.2) 9.2 (13.3-31.9) 7.7) 10.3) 6.4) 357 (225-456) 203 (87.6-111) 33.4’-Trichloro-2’-hydroxyphenyl ether) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. Survey Geometric mean (95% conf.0-15.16 (6.3-15.1) 50.0-73.90-10.92-12.1) 13.38-18.70-16.22-10.6-14.0-213) 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 .3 (9.2 (25.2) 12.6) 12.1 (8.S. Urinary Triclosan (2.9 (8.4.6-20.74 (5.18 (5.60 (8.5-86.0-15.2-46.86-12.6-37.8 (21.1-39.50) 10.5) 11.0 (36.7) 292 (151-432) 132 (78.60 (6.9) 8.6) 31.93 (7.4-18.4) 7.00-8.7 (14.2) 13.3-67.S.5) 20. interval) 12.72-13.0-19.4) 75th 43.6 (12.9-236) 193 (90.4 (12.32-14.8) 14.3 (11.9 (11.29-12.20-10.20-13.3.6) 90th 212 (172-241) 03-04 03-04 03-04 9.9 (50. population from the National Health and Nutrition Examination Survey.48-10.4’-Trichloro-2’-hydroxyphenyl ether) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.5-341) 245 (163-334) 597 (372-992) 450 (254-750) 461 (383-527) 613 652 1092 Limit of detection (LOD.3) 10.9) 32.10) 84.8-60.3) 47.40-11.45 (5.0 (34.6-65.3 (26.4-163) 304 (134-566) 261 (198-317) 157 (113-380) 655 (310-890) 472 (406-522) 314 715 1488 03-04 03-04 16.89-11.1) 9.1) 7.1 (45.8-85.7 (11.82 (8.2 (10.80 (5.6) 237 (175-294) 182 (138-217) 384 (294-506) 336 (225-480) 1228 1286 03-04 03-04 03-04 13.0) 9.9 (33.8-112) 30.5 (11.21 (6.3 (8.0 (8.2-58.7 (9.0 (11.0 (26.8-127) 37.4 (32. population from the National Health and Nutrition Examination Survey.5-250) 574 (461-716) 380 (258-430) 1229 1288 03-04 03-04 03-04 14.1) 9.4) 25.6) 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) 39.40-17.4 (38.4) 317 (231-433) 144 (96.10-9.1) 9.3-35.30-14.4) 73.1) 11. interval) 13.11-11.1) 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.

Ye X. et al.66:1052-1056. 4’-trichloro-2’-hydroxydiphenyl ether. Hirano M. Consumer antibacterial soaps: effective or just risky? Clin Infect Dis 2007. Biol Pharm Bull 2005. Leonard PA. population: 2003-2004. Pilot study of urinary biomarkers of phytoestrogens. Furia T. Skirrow RC. Adolfsson-Erici M. Readman JW. Nagao Y.36(6):1202-1211.S. Meyer MT. J Invest Dermatol 1976. Clapson DJ. Aranami K. Watanabe N. Mezcua M. streams. Benson WH. Gilbert RJ. Pharmacokinetics of triclosan following oral ingestion in humans. 1999-2000: a national reconnaissance.4. Britton JA. Lyman FL. Foran CM. Ekstrand J. Kanetoshi A. Environ Health Perspect 2007. Wigmore H. J Toxicol Environ Health A 2006. Toxicology of 2. Food Chem Toxicol 2000. Matsumura N. Larson EL.524:241-247. Bodey GP. Fernandez-Alba AR.. Photolytic degradation of triclosan in freshwater and seawater. Wong LY. Veldhoen N. Ferrer I. Levy SB. phthalates. Gunderson MP. Katsura E.23(5):579-583. Hong HC. Environ Health Perspect 2008. Shiratsuchi H. Evidence of 2.38(2):64-71. et al. Ogawa H. Sandborgh-Englund G. Teitelbaum SL.80(3):217-227. Triclosan: applications and safety. and other organic wastewater contaminants in U. Kolpin DW. Bhargava HN.69(20):1861-1873.116(3):303-307. et al. Barber LB. Erratum in: Aquat Toxicol 2007. hormones. Ishibashi H. Br J Clin Pharmacol 1987.Environmental Phenols References Aiello AE. Reidy JA. The oral retention and antiplaque efficacy of triclosan in human volunteers. Gomez MJ. The bactericidal agent triclosan modulates thyroid hormone-associated gene expression and disrupts postembryonic anuran development.17(5):637-644. Chelimo C. Williams FM. Arch Environ Contam Toxicol 1988.115:116-121.S. Odham G. Osachoff H.7/2. Pinney SM. Pharmaceuticals. Kaneshima H.24(3):209-218. 4. Calafat AM. Ebersole R. Okui T. Wolff MS. Zaugg SD. Aguera A. et al.4’-trichloro-2’hydroxydiphenyl ether). Fourth National Report on Human Exposure to Environmental Chemicals 39 . Windham G.83(1):84.67(4):532-537. Developmental evaluation of a potential non-steroidal estrogen: triclosan. and phenols in girls. Aquat Toxicol 2006. Urinary concentrations of triclosan in the U.8-dibenzodichloro-pdioxin as a photodegradation product of triclosan in water and wastewater samples. IMS Ind Med Surg 1969. Percutaneous penetration and dermal metabolism of triclosan (2. Am J Infect Control 1996. Needham LL. Hernando MD. Howes D. Furlong ET. Randomized trial of a hexachlorophene preparation and P-300 bacteriostatic soaps.38(4):361370. Anal Chim Acta 1004. Effects of nonylphenol and triclosan on production of plasma vitellogenin and testosterone in male South African clawed frogs (Xenopus laevis). Bennett ER.28(9):1748-1751. Environ Sci Technol 2002. Williams PE.45 Suppl 2:S137-S147.50(1-5):153-156. Mar Environ Res 2000. Thurman EM. Disposition and excretion of Irgasan DP300 and its chlorinated derivatives in mice. Moss T. Chemosphere 2007.

Kohli et al. water and sediments because of the large amounts that were produced and used historically. has been restricted.350) 90th . mollusicide.390 (.860-2.350) < LOD .350) < LOD .350) . PCP is distributed to most tissues and is not extensively metabolized. The parent compound and conjugates.510-3.37) .47-3.350) < LOD .70) .54-2.48 (.350-.350-2.350 (. Effects including hyperthermia.350-.30 (1. which may vary for some chemicals by year and by individual sample.g.00) 2.350-. 1976.58-2. Since 1984.350-.350 (.23 (. other polychlorinated benzenes.350-1.350-. plants. Human health effects from PCP at low environmental doses or at biomonitored levels from low environmental exposures are unknown.350-.30) 1.. are eliminated in the urine.10) 1.350-.350-.94 (1. Workers who manufacture or apply PCP may Urinary Pentachlorophenol Also a Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.650 (. so it is relatively non-persistent.350) < LOD .25 and 0.00) 1. < LOD means less than the limit of detection. ingestion of contaminated food or water. 40 Fourth National Report on Human Exposure to Environmental Chemicals .350-. PCP is absorbed rapidly and well by all exposure routes.350) < LOD . and metabolic acidosis were observed in CAS No.350 (. along with small amounts of tetrachlorohydroquinone and conjugates.850-2. PCP also may be eliminated in urine as a metabolite of hexachlorobenzene.76) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .510-5.350-..67) 1.64) 1. PCP use in the U.350) < LOD < LOD 75th .10 (1.75) 2.350-.08-3.5. Acute. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.680-1.10 (.890 (.91 (1.48-2. high dose exposure to PCP can induce a hypermetabolic state and excessive heat production as a result of uncoupling mitochondrial oxidative phosphorylation.350 (.90) 1. PCP has been detected in soils.350-1.350) < LOD . with repeated or chronic exposure.350) < LOD .960) 1.660 (.350-1.78) 1. and animals.65 (. PCP cannot be used on wood in residential or agricultural buildings. After a single dose. the elimination half-life may be a week or more (Uhl et al.350-.650) 1.350-1.33) .73 (1.350 (. PCP is degraded by sunlight and metabolized rapidly by microorganisms.10) 1.350) < LOD .350-.630 (.350) < LOD .350) < LOD ..390 (.500-2.350 (. and dermal contact with PCP-treated products.990 (<LOD-2.350-.350) < LOD .350-.980 (.90 (1.350 (.30) 1.350 (.70) 2.350-.00 (. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.33-2.18 (<LOD-1.30) .51) 1.890-1.350 (.58-2.350-2. utility poles and fence posts).350 (.350-.350 (.42) 973 1190 1021 1338 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .990-2.350) < LOD . hypertension.83 (2. 2002.30 (.53) 482 577 681 826 831 1125 99-00 01-02 99-00 01-02 * * * * .S.32 (.350 (. 1979). After absorption.350-2.350) < LOD .350 (.98 (1. algaecide and insecticide. PCP is eliminated over a few days (Braun et al.350 (.350) < LOD .42) 696 680 521 696 603 951 Limit of detection (LOD.350 (.60) 1.Fungicides Pentachlorophenol inhale it or absorb it through exposed skin. In the environment.50) 1.04) 1.350-2.. 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.90) 2.47-5.01 (<LOD-1.350 (. population from the National Health and Nutrition Examination Survey..590-1.53) 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 . 1986).30 (.09) .76) .10 (<LOD-1. General population exposure to PCP may occur by inhalation of contaminated air.40 (. 1997).350 (. To-Figueras et al.530) 1.350-.350-.480-2.65 (. and it is used primarily as a preservative for wood to be used outdoors (e.76) 1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.45-2. air.350 (.350 (.350 (. herbicide.350) < LOD . Survey Geometric mean (95% conf.80) . bactericide.62 (.350) < LOD . Human exposure to PCP has become less common. and possibly of lindane (IPCS.350-.94 (1.770 (.37 (.350-.00) 1.350-.350 (.S.350-2.60) 1.

67 (1. environmental levels) and health effects is available from the U.420) < LOD . More information about external exposure (i.S.67-3.18 (1.67 (1.40) 1. respectively) (Becker et al.25-2.52) 1.350) < LOD . In animals.gov/ pesticides/ and from ATSDR at: http://www. chronically administered high doses of PCP were hepatotoxic.08 and 5.35) 1.94 (1. 2004. or skin absorption.35-2. Urinary PCP levels at the 95th percentile in this Report are approximately half the corresponding 95th percentile values found in German adults evaluated in 1998 (Becker et al.95) 3.35) 1. In NHANES 2001-2002 subsamples.30) 1.470 (..250 (.340-.11) 2.560-.67-2.79) 1.67 (1.55) 973 1190 1021 1337 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .atsdr.99) 482 577 681 825 831 1125 99-00 01-02 99-00 01-02 * * * * .310) < LOD .19) 2.260 (.650) 90th 1.0 mg/L.25 (1. Survey Geometric mean (95% conf. 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 (4.06) 1.320) < LOD < LOD 75th .52 (<LOD-1.650 (. 1995).06-3.560) < LOD .580-.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 . van Raaij et al.650 (.990 (.610 (.21 (.510-.cdc.. carcinogenic. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.570 (.360 (. inhalation.92) 1.S.00-1. 2003).360-. 1989).09-1.57 (1.18) .730) < LOD . Death can result from seizures and cardiovascular collapse.19) 2.630 (.25-1. IARC has determined that pentachlorophenol is possibly carcinogenic to humans.590-1.850 (. 2003).35-2. 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.67-3.84) 1.S.510-.370 (.09 (<LOD-2. Among adults in the NHANES 1999-2000 subsample.19 (1.270-.40) 1.920 (.500 (.. The U.29-3. 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.30-2.94-3.40) 1.82) 1.94 (1.90) 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.epa.250 (.21-2.25 (1..590) < LOD .40) 1. Fourth National Report on Human Exposure to Environmental Chemicals 41 . 2000).320) < LOD .75) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .950-1.500-1..26 (1.400 (.83 (1.290-.560) < LOD .Fungicides adults and children severely exposed to PCP through ingestion.75) 1.16-1.e.67 (1.51) 1.300 (. EPA has developed standards for PCP in drinking water and the environment. OSHA has established an occupational standard. respectively) (Seifert et al. Pentachlorophenol is not mutagenic or teratogenic.780-1.6 and 14.430-.220-.52 (<LOD-1.S.760 (.700-2.84 (1.10 (1.gov/ toxpro2.16 (.320 (. In a small sample of U.78) 1.08) 696 680 521 695 603 951 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.9 mg/L.30) 1.950-1.800-1.290-.25-2.710-1.82 (1.67 (1..84-4. and adversely affected thyroid function (U.440 (.300 (.34 (.800) < LOD 1.73 (1.55) 1.00) 1.430) < LOD .40) 1.html..13 (.500-. 1989).40-2.220-.26 (1. population from the National Health and Nutrition Examination Survey.490) < LOD .10-2.830) < LOD .900-1. EPA at: http://www. 1991). children in the 1980’s.910-1.380-.300 (.52 (1.19) 2.290) < LOD .36) .48-2.06 (.320) < LOD .280) < LOD .EPA.75 (<LOD-2.57 (. 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.30 (.310-.25) 1.78) 1. and the FDA has established a standard for bottled water.240-.69 (1.330-.950-1.00-1. the median and 95th percentile urinary PCP levels were approximately three times lower than comparable values in German adults (2.270-..S.56) 1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.780) < LOD .

Safe A. et al. Environ Res 1995.Fungicides Finding a measurable amount of PCP in urine does not mean that the level of PCP causes an adverse health effect. Phillips DL. To T. Head SL. Lindane. 4/21/09 Kohli J. 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. et al. Krause C.54(3):203-208. van den Berg KJ. Santiago-Silva M. 4/21/09 van Raaij JA. Seifert B. References Becker K. Chenoweth MB. Barrot C. The metabolism of higher chlorinated benzene isomers. htm. International Programme on Chemical Safety (IPCS). Environ Health Perspect 1997. Environmental Protection Agency (U. Hill RH. 42 Fourth National Report on Human Exposure to Environmental Chemicals . 11/30/2004. PCP: Human Risk Characterization [online]. Seifert B. Bragt PC. Baker S. Sala M. available at URL: http://www. Smith SJ. Pentachlorophenol measurements in body fluids of people in log homes and workplaces. Kaus S. Effects of hexachlorobenzene and its metabolites pentachlorophenol and tetrachlorohydroquinone on serum thyroid hormone levels in rats. Uhl S. Schlatter C. Seiwert M. Arch Toxicol 1986. Bailey SL. Blau GE. Notten WR. 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. EPA). German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Metabolism of hexachlorobenzene in humans: association between serum levels and urinary metabolites in a highly exposed population. Braun WH. Jones D. house dust.S. 206:15-24. The German Environmental Survey 1990/1992 (GerES II): reference concentrations of selected environmental pollutants in blood. Arch Environ Contam Toxicol 1989. Schulz C. Engel R. To-Figueras J.10:552-65. Otero R.inchem. urine. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children. Cline RE. Shealy DB. Gregg M. Holler JS. Hill RH Jr. Pesticide residues in food-2002-Joint FAO/WHO meeting on pesticide residues. Arch Environ Contam Toxicol 1989. Hill RH Jr. Int J Hyg Environ Health 2003. U. Schmid P. Helm D. et al. Needham LL. Fast DM. Can J Biochem 1976. J Expo Anal Environ Epidemiol 2000. Rodamilans M. r e g u l a t i o n s .18:475-481.58:182-186. Biomonitoring data can also help scientists plan and conduct research about PCP exposure and health effects.4:289296. hair. The metabolism/ pharmacokinetics of pentachlorophenol in man and a comparison with the rat and monkey.105(1):78-83. 2002.org/documents/jmpr/jmpmono/2002pr08. Becker K. Dev Toxicol Environ Sci 1979. Toxicology 1991: 67(1):107-16. Pesticide residues in urine of adults living in the United States: reference range concentrations. Needham LL. drinking water and indoor air.S. Available at URL: h t t p : / / w w w.18(4):469-474. Schulz C. Seiwert M. Pharmacokinetics of pentachlorophenol in man.71:99108.

20-3. 1998).567 (.00) < LOD .30 (1.470 (<LOD-.S.950) < LOD .750-2. sodium ortho-phenylphenate (SOPP).30) < LOD 1.638) * .00 (1.90) 1.61) 2. are antimicrobial agents used as bacteriostats.600) < LOD 1.970 (.500-2.410-.3.630) < LOD .60 (1. SOPP is applied topically to the crop and then rinsed off.14 (<LOD-3.10) 1.600) < LOD .90) .40-5.10) .50) < LOD .420 (<LOD-.493 (.490 (<LOD-.820 (.80-3. which may vary for some chemicals by year and by individual sample.50-2.22) 2.50) < LOD .30) < LOD .30-2.Fungicides ortho-Phenylphenol CAS No.389-.836) * .23) 695 680 520 695 603 953 Limit of detection (LOD.02) 1.10) 1.20) < LOD 2.85) size 1991 2529 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th .90 (1.00 (1.20) 2.450 (<LOD-. or apply these chemicals may be more highly exposed than the general population.50) 1.600-1.03) 1.40-2. Cnubben et al.490 (<LOD-.370-.710-2.370-. 2006).402-. Estimated human intakes have been below recommended intake limits (U.EPA.552 (. EPA.EPA.10 (1. OPP is considered to be moderately toxic after acute oral doses in animal studies.600-1.28 (. 2006).740 (.386-.10 (1.860) * 99-00 01-02 99-00 01-02 99-00 01-02 . and it is eliminated rapidly from the body as OPP glucuronide and sulfate conjugates (Bartels et al.350-1.570 (. General population exposure can occur via dermal.760-2. formulate.696) * .770 (. or 2-phenylphenol) and its water-soluble salt. Workers who manufacture.90 (1.610 (.50-4.433-.76) 1. < LOD means less than the limit of detection.91) 973 1190 1018 1339 99-00 01-02 99-00 01-02 99-00 01-02 .509 (.800-3.00-2.790) 2.10) 2.540-2. 2002.560-8.370-.636) * . OPP is volatile. it was used in home sanitizers for surfaces.780) < LOD .632) Selected percentiles ( 95% confidence interval) Sample 95th 2.860 (.50 (1.20) < LOD 1.600) < LOD .850 (.80) 1.92 (.27 (.07 (.570 (.520 (.50) < LOD .23) 480 577 681 827 830 1125 99-00 01-02 99-00 01-02 .85) 2.80) 1. OPP was detected in 40 of 60 different canned beers at concentrations in the low parts per billion (Coelhan et al.670) 2.40-7.710) 3.20 (. on ornamental plants and turfs.80 (2.50-3.880-2. 1998..17 (.364-. Fourth National Report on Human Exposure to Environmental Chemicals 43 . interval) .30) 1.600) < LOD 75th . In the past.90) 2. 2006).00) . and as a wood preservative.50 (1.09) 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.3 and 0. Available evidence suggests that OPP does not accumulate in the body.550-1.450 (<LOD-.490 (<LOD-. 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.50 (1.40 (. Timchalk et al.60-2.20 (1.28-3. or oral routes from residential use and by ingesting treated food or food that was in contact with treated surfaces or equipment. inhalational..34) 1. 90-43-7 General Information Ortho-phenylphenol (OPP.480-1. small amounts of OPP have been measured in human adipose tissue (Onstot and Stanley. leaving the chemical residue OPP.570-1.389-.490 (<LOD-.580-1. OPP is efficiently absorbed from the gastrointestinal tract and through the skin.S. however. whereas SOPP is not volatile and is more water soluble.508 (. fungicides.930 (.10) .30-7.S. in paints.20 (1.60-3.590-2.498 (. population from the National Health and Nutrition Examination Survey. Survey Geometric mean (95% conf. Most agricultural food applications have been revoked.390-. 1989).645) * . but OPP and SOPP are still used on pears and citrus (U.570-.890 (.690) < LOD .600-1.88) 1. Human health effects from OPP at low environmental doses or at biomonitored levels from low environmental exposures are unknown. and it has limited water solubility.50) .624) * .S.90) .742) * . OPP is still used as a disinfectant fungicide for industrial applications.349-.10-2.60 (1.466 (. such as fruits and vegetables.621) * .60 (1.640) < LOD .690-1.890) 1.570-2.30) < LOD 90th 1. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.40-5.496 (.10-1.770 (. and sanitizers.33 (.497 (. Both have been used in agriculture to control fungal and bacterial growth on stored crops.10) .20-2.840-1..830 (.19 (.00 (1. Both chemicals degrade within hours to weeks in the environment (U.890 (.450 (<LOD-. 2006).22 (.490 (<LOD-.00 (1.610-1.00) .

343 (.510 (<LOD-. Biomonitoring studies on levels of OPP provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of OPP than are found in the general population.38-3.470 (<LOD-.440 (.43) 3.670 (.380 (.24-2.900-1.670 (.470) < LOD .. Bomhard et al.12) < LOD 1. Smith et al.514 (. Pathak and Roy.560) < LOD 75th .58) 2. by possible genotoxic mechanisms (Hagiwara et al.550 (. U.690 (.61 (2. and it has classified OPP as not classifiable with respect to human carcinogenicity.51-3.484) * .96 (1.940-2.550) < LOD . Zhao et al.38) 1..248-.770-2.EPA 2006).670) < LOD .47) .980 (.93) .410 (<LOD-.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 .33) .06-5..4) 3.590) * .84 (1. population from the National Health and Nutrition Examination Survey.S..53) 1.600-1.810-1.69 (1.780-14.656) * . 1999.291-.11 (. 2000.43-2. Urinary ortho-Phenylphenol (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.420 (<LOD-.860 (. Detectable levels were seen in over half the U. Ito et al.96 (1. 1993.93) .980 (<LOD-1.311-.43 (1.270-. Brusick.29) 1.21) 1.382 (.750 (. 1998.. 1984.46) < LOD 1.810) < LOD .910 (<LOD-1. 2005.08-1.18) 2.91 (1.29) 1. Volunteers exposed to 0..05-2. or developmental toxicity was observed (Bomhard et al. IARC has classified SOPP as a possible human carcinogen..EPA 2006).780 (.97 (2. Biomonitoring Information Urinary OPP levels reflect recent exposure.08) 1.40-13.910-1.02 (..444 (.20) < LOD 3.. less likely.640-1. 2005).75 (1.17) 2.750-2.361-. OPP or SOPP produced carcinomas of the bladder only after phase II detoxification pathways were saturated.666) * .13) 1.970) 1.74 (1.52 (.28 (<LOD-4.910 (.580) < LOD . 2002.09-3.568) * .510-.900) < LOD .360 (<LOD-.86 (1. leading to production of two metabolites.17) * 99-00 01-02 99-00 01-02 99-00 01-02 .17 (.26) 1.S.61 (.11) 4.88-4.460-.301-. Kwok et al.990) < LOD .31) < LOD . U.453 (. In high dose animal studies.89 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. or.62) .0) 1. Murata et al. Additional information is available from U.33-2.24-2.64 (2.96) 1. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.06 (1.Fungicides anemia.558) Selected percentiles ( 95% confidence interval) Sample 95th 2.840 (.38) 973 1190 1018 1338 99-00 01-02 99-00 01-02 99-00 01-02 . These metabolites may induce carcinogenicity via nongenotoxic regenerative hyperplasia of the bladder (Appel. 1999.385 (.550-. but no neurologic.61 (1.27) < LOD .17 (. OPP was not found to be mutagenic.950) < LOD .800-1.880-1.791) * . 1997.11) < LOD 90th 1.78 (2.08-2.473) * .580-1.496 (.25-6.353-.01) 1. ortho-phenylhydroquinone and ortho-phenylbenzoquinone.12-2. Finding a measurable amount of OPP in urine does not mean that the level of OPP causes an adverse health effect.93) 1.620-1.00 (1. reproductive.07) 2.44 (1.96-4.860 (.28 (2. Survey Geometric mean (95% conf.43-2.650-1. Dermally applied OPP was not carcinogenic in a 2-year experimental study in animals (NTP. 1986). 1984.91) 695 680 520 694 603 953 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. Nakagawa et al.480-. 2002.04-4.620-1.S.570) < LOD 1. CDC.32) 1. 2005).508) * .. 1992.38) 2.21-2.75 (1.560-2.11 (.59) .21 (.06-4.320 (<LOD-.329-. 2002).11-1.gov/pesticides/.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.500) < LOD .S.81) 1.403-.420 (<LOD-.610) < LOD 1.EPA at: http:// www.750 (.00 (.410 (<LOD-.09-6. population in the subsamples from NHANES 1999-2000 and 2001-2002 (CDC.59) 1.455-.epa.93 (1. 44 Fourth National Report on Human Exposure to Environmental Chemicals .32) 3.09 (1.30) 480 577 681 826 830 1125 99-00 01-02 99-00 01-02 . interval) .S.

Ito N. Regul Toxicol Pharmacol 2002. July 28. Environmental Protection Agency (U. Xenobiotica 1998. et al. 1989.28(6):579594. Turteltaub KW. Identification of SARA compounds in adipose tissue. J Agric Food Chem 2006. 4/13/09 Onstot JD. Centers for Disease Control and Prevention (CDC). O-phenylphenol and its sodium and potassium salts: a toxicological assessment. Bormett GA. Bartels MJ. EPA). Herbold BA.gov/oppsrrd1/REDs/ phenylphenol_red.epa. Toxicol Appl Pharmacol 1998. Christenson WR. Timchalk C. Arnold LL. J Agric Food Chem 2002.nih. Glas K. Inoue S. National Toxicology Program (NTP). Crit Rev Toxicol 2002. Office of Toxic Substances.S.159(1):18-24. Bromig KH. Zhao S. Timchalk C. Available at URL: http://www. Environ Mol Mutagen 2005. Fukushima S.S. Carcinogenesis 1999. Oxidative damage to cellular and isolated DNA by metabolites of a fungicide orthophenylphenol.gov/ntp/htdocs/LT_ rpts/tr301. Roy D. The pharmacokinetics and metabolism of 14C/13C-labeled ortho-phenylphenol formation following dermal application to human volunteers.niehs. Vogel JS.20(5):851-857. Sangha G. Bartels MJ. EPA-560/5-89-003. Moore GA. Ito N. Brzak KA. In vivo genotoxicity of sodium orthophenylphenol: phenylbenzoquinone is one of the DNA-binding metabolite(s) of sodium ortho-phenylphenol. Fukushima S. Hagiwara A. Brendler-Schwaab SY. St John MK. Mendrala AL. Shirai T.S. Determination of orthophenylphenol in human urine by gas chromatography-mass spectrometry. Coelhan M. U. Brusick D.54(16):5731-5735. Cnubben NH. 4/9/09. NTP Technical report on the toxicology and carcinogenesis studies of ortho-phenylphenol (CAS No. Moldeus P. Fourth National Report on Human Exposure to Environmental Chemicals 45 . 2005.S. Hakkert BC. van de Sandt JJ. 2006. Hirose M. Food Chem Toxicol 1984. Richter M.703(12):97-104. Kwok ES. Hum Exp Toxicol 1998. Analysis of genotoxicity and the carcinogenic mode of action for ortho-phenylphenol. Bomhard EM.EPA).35(2 Pt 1):198-208. Atlanta (GA). Bartels MJ.74(2):61-71. rat and man. Available at URL: http://ntp. Detection and characterization of DNA adducts formed from metabolites of the fungicide ortho-phenylphenol. March 1986. Comparative metabolism of orthophenylphenol in mouse.22(10):809-814. food additives and natural products as promoters in rat urinary bladder carcinogenesis. Determination and levels of the biocide ortho-phenylphenol in canned beers from different countries. Long-term toxicity and carcinogenicity study of sodium o-phenylphenate in B6C3F1 mice. The carcinogenicity of the biocide ortho-phenylphenol. Shibata M. Urinary physiologic and chemical metabolic effects on the urothelial cytotoxicity and potential DNA adducts of o-phenylphenol in male rats.286(2):309-319. Pathak DN. Bartels MJ. Gierthy J. Tayama S. Roberts AL. Elliott GR. Meuling WJ. Nakagawa Y.50(11):3351-3358. J Chromatogr B Biomed Sci Appl 1997. Environmental Protection Agency (U.17(8):411-417.43(7):14311437. EPA 739 R-06004. Cano M. Narang A. Selim S. IARC Sci Publ 1984. Toxicol Appl Pharmacol 1999. Eastmond DA. Biochem Pharmacol 1992. U.45(5):460-481.pdf. Dose-dependent binding of ortho-phenylphenol to protein but not DNA in the urinary bladder of male F344 rats. Buchholz BA. et al. Comparative in vitro-in vivo percutaneous penetration of the fungicide ortho-phenylphenol. Moriya K. Mutat Res 1993. Arch Toxicol 2000. Leser KH. Third National Report on Human Exposure to Environmental Chemicals. Hagiwara A. Relationship between metabolism and cytotoxicity of ortho-phenylphenol in isolated rat hepatocytes.150(2):402-413.. Kawanishi S. 90-43-7) in Swiss CD-1 mice (dermal studies). Sangha GK. Christenson WR.32(6):551-625. Reregistration Eligibility Decision (RED) for 2-phenylphenol and salts (Orthophenylphenol or OPP). Freyberger A.(56):399-407. McNett DA. Smith RA. Imaida K. Murata M.pdf. Stanley JS.Fungicides References Appel KE. Drugs. Eadon G.

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

. 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. 1994.. 2005. the latter which may account for some observed effects (Coleman et al. and thyroid (U. Acetochlor degrades in water to acetochlor sulfonic acid and acetochlor oxanilic acid. 1998). remains in soils for up to 3 months.S.. 2000.5 to 449 μg/L were measured in commercial applicators within 24 hours following its application (Barr et al. 1996). Fourth National Report on Human Exposure to Environmental Chemicals 47 . 2006).. 2005). 2-hydroxyethyl-6-methylaniline. in some species and at doses above maximum tolerated doses. 2000). Davison et al.S. 2006). Hladik et al.. Jefferies et al. environmental levels) is available from U.. mainly corn. Acetochlor is moderately toxic to fish and honey bees. Human health effects from acetochlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown. and neurologic movement abnormalities (U. In animals.EPA. It is absorbed by plants and inhibits plant protein synthesis. this metabolite is not a marker of exposure to most plant metabolites or environmental degradates. People exposed to acetochlor will excrete acetochlor mercapturate in their urine. however.EPA 2000.EPA considers acetochlor likely to be carcinogenic in humans.S. 2006). 2000.epa.gov/ pesticides/. 2000. Plants can degrade acetochlor to 2-ethyl-6-methylaniline. including one that produces 2-methyl-6ethylaniline and its reactive metabolite.0 μg/L (Curwin et al. CAS No. but other pathways occur. However. Urinary acetochlor mercapturate levels of 0. 2006). which are often more prevalent in the environment. but it has produced testicular atrophy. Additional information about external exposure (i. Estimated human intakes of acetochlor have been below recommended limits (U. Kolpin et al. nasal epithelia. 34256-82-1 General Information Acetochlor is a chloroacetanilide type herbicide with restricted usage for preemergent control of grasses and broadleaf weeds on agricultural crop land. Acetochlor has low acute toxicity. Finding measurable amounts of acetochlor mercapturate in the urine does not mean that the levels of acetochlor mercapturate cause an adverse health effect. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 1989. Acetochlor mercapturate was measured in the urine of farmers actively spraying the pesticide and the geometric mean was 8. Urinary levels of acetochlor mercapturate were generally not detectable in the NHANES 2001-2002 subsample (CDC. animals have demonstrated tumors of the lung. and it is unlikely to be genotoxic at relevant doses (Ashby et al.e.S. Feng and Wratten.Herbicides Acetochlor Biomonitoring Information Urinary levels of acetochlor mercapturate reflect recent exposure. General population exposure to acetochlor may occur through diet or drinking water. and hydroxymethyl ethyl aniline (U. Acetochlor is microbiologically degraded. EPA at: http://www. renal injury.S.. 2005). Acetochlor is not mutagenic. U. and has been detected in watersheds of agricultural lands (Battaglin et al. 2007).EPA.EPA. a major pathway for acetochlor metabolism involves mercapturate conjugation.. NTP and IARC do not have ratings regarding human carcinogenicity. Acetochlor has not shown developmental or fetal toxicity in chronic animal studies..S..

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

Number 15.108(12):1151-1157. and other herbicides in rivers. Alavanja MC. Environ Health Perspect 2003.248(2-3):123-133. Environ Sci Technol 2005.gov/oppsrrd1/reregistration/REDs/acetochlor_tred.cornell. Burkhardt MR.248(2-3):115-122. Whyatt RM. Hladik ML. 2005. Sanderson WT. Peter CJ. pages 3682-3690. et al. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa.html. Sci Total Environ 2000.S.S. Hines CJ. Chem Res Toxicol 1998.15(6):500-508. EPA). Identification of human urinary metabolites of acetochlor in exposed herbicide applicators by high performance liquid chromatography-tandem mass spectrometry. Sci Total Environ 2000. J Expo Sci Environ Epidemiol 2007. Hodgson E. Wratten SJ. sulfonamide. Kolpin DW. Barr DB. Report of the Food Quality Protection Act (FQPA) Tolerance Reassessment Progress and Risk Management Decision (TRED) for Acetochlor.S. Roberts AL. Fourth National Report on Human Exposure to Environmental Chemicals 49 . In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. Striley CA. Finding minimal herbicide concentrations in ground water? Try looking for their degradates. 5/30/06 U. Feng PCC. Federal Register: January 24. Available at URL: http://www.11(4):353359. EPA). epa. Third National Report on Human Exposure to Environmental Chemicals. Davison KL. Reynolds SJ. Kier L. Hum Exp Toxicol 1996. Curwin BD. Atlanta (GA). Occurrence of sulfonylurea. Battaglin WA. Jefferies PR. Acetochlor (Harness) Pesticide Petition Filing 1/00. Comparative metabolism of chloroacetamide herbicides and selected metabolites in human and rat liver microsomes.S. Kinney PL. Casida JE. and metolachlor herbicides in rats. Evaluation of the potential carcinogenicity and genetic toxicity to humans of the herbicide acetochlor. Camann DE. Barr DB. reservoirs and ground water in the Midwestern United States. Available at URL(non U. Environmental Protection Agency (U. et al.24(10):1003-1012. acetochlor. Xenobiotica 1994.cce. Olsson AO. Lefevre PA. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. Linderman R. Barr JR. J Expo Anal Environ Epidemiol 2005. Wilson AG. U.Herbicides References Ashby J. Barr DB. et al. Environmental Protection Agency (U.S. J Agri Food Chem 1989. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. EPA 738-R-00-009. Comparative metabolism and elimination of acetanilide compounds by rat. Bravo R. Hein MJ.111(5):749-756.39(17):6561-6574. Furlong ET.37(4):10881093. 2000. Tinwell H. Larsen GL. Linhart SM. Quistad GB.edu/profiles/herbgrowthreg/24-d-butylate/acetochlor/acetochlor_pet_100. Volume 65. Rose RL. Hsiao JJ. Deddens JA.pdf. Ward EM. 1998. March 2006. Environ Health Perspect 2000. 5/30/06. Feil VJ. Thurman EM. imidazolinone.15(9):702-735. Green T. Coleman S. Heederik D. Centers for Disease Control and Prevention (CDC). Andrews HF. Dialkylquinonimines validated as in vivo metabolites of alachlor.17(6):559-566.EPA): http://pmep.

corn cropland was treated with alachlor. mean values of urinary concentrations of alachlor metabolites. 15972-60-8 General Information Alachlor is a chloroacetanilide type herbicide with restricted usage for preemergent control of grasses and broadleaf weeds on agricultural cropland. WHO. ranged from 0. 1994. 1998). Kolpin et al. Alachlor has low potential for acute toxicity. In a study of applicators and workers exposed to alachlor. but not likely at low doses. 50 Fourth National Report on Human Exposure to Environmental Chemicals . U. but another metabolic pathway can produce 2. It is both metabolized in plants and degraded microbiologically in agricultural soils into as many as 19 metabolites and degradates. Estimated human intakes have been below recommended limits (U.S.Herbicides Alachlor CAS No. 1998.EPA. as measured through conversion to deethylamine.S.epa.. IPCS. 1996). It is absorbed by plants and inhibits plant protein synthesis.EPA. Alachlor is highly toxic to freshwater fish and slightly toxic to birds and some invertebrates.S.. whereas 60% of applicators had detectable amounts. People exposed to alachlor will excrete alachlor mercapturate in their urine (Driskell et al.S. Alachlor has a soil half-life of a few weeks. including corn. the dermal exposure route is potentially significant for applicators.. 1989. In chronic animal testing.S. 1997. and field workers. In 1993-1995. 1988.. Animal carcinogenicity studies have demonstrated tumors of the nasal turbinates. but shows little bioaccumulation.1 mg/L at various collection times (Sanderson et al. WHO.. Alachlor and its degradates are leachable from agricultural soils and have been detected in watersheds of agricultural land including ground and surface waters (Battaglin et al.. General population exposure to alachlor may occur through consumption of contaminated food or drinking water. Hines et al. and on non-crop land for general weed control..6-diethylaniline and its reactive metabolite. about 20-25% of the U. Alachlor itself is not considered mutagenic.EPA considers alachlor to be a probable human carcinogen at high doses. 1996. but has not shown developmental or reproductive toxicity in mammalian systems (U. 1998. 1999.EPA. (2003) showed that 2. though positive genotoxic results are reported for several metabolites of alachlor (Brown et al. EPA at: http://www. soybeans. WHO...S.S.EPA. 1998. 2000. U.S. Finding measurable amounts of alachlor mercapturate in the urine does not mean that the levels of alachlor mercapturate cause an adverse health effect. 2003). Since the late 1980s alachlor use has been declining. USGS. 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. Human health effects from alachlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 1995). 1995. Because it can be absorbed through skin. Tessier and Clark. 1998). Additional information about is available from U. alachlor is quickly absorbed after oral doses and mostly excreted as metabolites within a week (IPCS. 2003). 1998). 2005. peanuts and other crops. Hladik et al. Biomonitoring Information Urinary levels of alachlor mercapturate reflect recent exposure.EPA.1 to 1. but this metabolite is not a marker of exposure to most plant metabolites or environmental degradates which are often more prevalent in the environment. In animals. the latter may account for some observed effects (Davison et al. mercapturate conjugates were predominant metabolites. and uveal degeneration. U. alachlor has demonstrated hepatotoxicity. Jefferies et al. 1996. 1999 and 2007. U. formulators. stomach. 2003). 2005). Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Feng and Wratten. WHO. hemosiderosis. Hill et al. Urinary levels of alachlor mercapturate were generally not detectable in the NHANES 2001-2002 subsample (CDC. 2000. NTP and IARC do not have ratings regarding human carcinogenicity.2% of a reference population had detectable alachlor equivalents by immunoassay in their urine. In animal studies. and thyroid only at either maximum tolerated doses or related to species-specific pathways (Heydens et al.gov/pesticides/..

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

S. EPA 738R-98-020.56(6):853-859.39(17):6561-6574. World Health Organization.43(9):2504-2512.gov/oppsrrd1/ REDs/0063. Gilliom RJ). who. Quistad GB. December 1998. Kier LD. U. Identification of a major human urinary metabolite of alachlor by LC-MS/MS. Am Ind Hyg Assoc J 1995.111(5):749-756. Sanderson WT.24(10):1003-1012. J Ag Food Chem 1995. Environmental Protection Agency (U. Kinney PL. reservoirs and ground water in the Midwestern United States. Available at URL: http://www. Mutat Res. Wilson AG. Third National Report on Human Exposure to Environmental Chemicals. 1999. Available at URL: http:// www. Hines CJ. Hill AB. Linhart SM. California.org/documents/pds/pds/pest86_e. 2007.pdf. Hum Exp Toxicol. 2003. Sci Total Environ 2000. Chem Res Toxicol 1998. Casida JE. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models.S. WHO/ FAO Data Sheets on Pesticides. J Agri Food Chem 1989. Andrews HF. 2/27/09 U. Davison KL. Burkhardt MR. imidazolinone. Biagini R. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. Occurrence of sulfonylurea. Tessier DM. Geneva. Hull RD.inchem. Thurman EM. Ann Occup Hyg 2003. Biagini RE.Herbicides References Battaglin WA. Sacramento. Casida JE.usgs. Geological Survey (USGS). Kimmel EC. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. Environ Sci Technol 2005. Striley CA. Dialkylquinonimines validated as in vivo metabolites of alachlor.11(4):353359. Feil VJ. Deddens JA. Casida JE.248(2-3):123-133. 86. Available at URL: http://water. 4/2/09 U. The Quality of Our Nation’s Waters Pesticides in the Nation’s Streams and Ground Water. 2005. and metolachlor herbicides in rats. Whyatt RM. Available at URL: http://www. Wratten SJ. An evaluation of the carcinogenic potential of the herbicide alachlor to man. et al. Centers for Disease Control and Prevention (CDC). 1999. Hines CJ. Erratum in: Life Sci 1989. Clark JM. DNA adduct formation by alachlor metabolites. Shealy DB. Furlong ET. World Health Organization (WHO). Henningsen G. ALACHLOR. March 2006.395(2-3):159-171. Alachlor in Drinking-water. sulfonamide. Quistad GB. Thake DC. Atlanta (GA).47(6):503-517. Driskell WJ. MacKenzie B. EPA). 2/27/09 Jefferies PR. 98-4245 (by Barbash JE.gov/nawqa/pnsp/pubs/circ1291/ supporting_info. Biological monitoring of commercial pesticide applicators for urine metabolites of the herbicide alachlor. Jefferies PR. Thelin GP. Finding minimal herbicide concentrations in ground water? Try looking for their degradates. Bull Environ Contam Toxicol 1996.18(6):363-391.int/water_sanitation_health/dwq/chemicals/en/alachlor. Shoemaker DA.44(18):1325. Circular 1291. Quantitative assessment of the mutagenic potential of environmental degradative products of alachlor. Sci Total Environ 2000. Hsiao JJ. Martens MA. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. Tolos W. Brown MA. Dialkylquinoneimine metabolites of chloroacetanilide herbicides induce sister chromatid exchanges in cultured human lymphocytes. Heydens WF. 1996.S. Brown KK. Reregistration Eligibility Decision (RED) Alachlor.56(9):883-889.S. acetochlor. Kolpin DW.htm. and other herbicides in rivers. Barr JR. 1992-2001.248(2-3):115-122. Water-Resources Investigations Report: Distribution of Major Herbicides in Ground Water of the United States Water Resource Investigations Report No. Camann DE. Background document for development of WHO Guidelines for Drinking-water Quality. et al. Roberts AL. Feng PCC. Hill RH Jr.epa. Life Sci 1988.43(25):2087-94. Barr DB. 2/27/00 52 Fourth National Report on Human Exposure to Environmental Chemicals . International Programme on Chemical Safety (IPCS). Lau H. Supplemental Technical Information (available on-line only). Larsen GL.pdf. Kolpin DW. Hladik ML. 1998. Comparative metabolism and elimination of acetanilide compounds by rat. Peter CJ. No.37(4):10881093. Geological Survey (USGS). Xenobiotica 1994. 1997. Environ Health Perspect 2003. revised February 15.php.

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

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

Tapia J..115(8):1254-1260.. In the NHANES 2001-2002 subsample. The effects of atrazine on female wistar rats: an evaluation of the protocol for assessing pubertal development and thyroid function. Gillis JH. Schmid J.. Wetzel LT. Sanborn JR. Toxicol Sci 2003. Pesticide urinary metabolite levels of children in eastern North Carolina farmworker households. World Health Organization.. Heederik D. urinary concentrations ranged from 5-1756 μg/L (Lucas et al. Collins A. Toxicol Sci 2000. Perry et al. Freeman NC. Atrazine disrupts the hypothalamic control of pituitary-ovarian function.58(2):366-376. Toxicological profile for atrazine. Maroni M. Hermaphroditic. et al. Determination of atrazine metabolites in human urine: Fourth National Report on Human Exposure to Environmental Chemicals 55 . Proc Natl Acad Sci USA 2002.2 μg/L in 15 farmers studied several days after spraying the pesticide (Curwin et al. the urinary geometric mean levels for herbicide applicators in Ohio and Wisconsin were about 6 μg/L (Hines et al. Hein MJ. Quandt SA. J Toxicol Environ Health 1994. Striley CA. In small studies of Maryland residents in 19951996 (MacIntosh et al. Biagini RE. Finding measurable amounts of atrazine mercapturate in urine does not mean that the levels of atrazine mercapturate cause an adverse health effect.61(4):331-355. J Toxicol Environ Health 1994. Available at URL: http:// www.. et al.htm.. Laws SC. diamino-S-chlorotriazine and hydroxyatrazine.64(9):672-678. ATRAZINE. Hines CJ. Goldman JM. 1999) and 83 Minnesota children with multiple urine collections during 1997 (Adgate et al.inchem. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. Cooper RL. Brown KK. Bradway DE. Pubertal development in female Wistar rats following exposure to propazine and atrazine biotransformation by-products. Grzywacz JG. Extrom PC. Ferioli A. Gammon DW. 2003. The mammary tumor response in triazine-treated female rats: a thresholdmediated interaction with strain and species-specific reproductive senescence.gov/toxprofiles/tp153. Determination of urinary residue levels of the N-dealkyl metabolites of triazine herbicides. Agency for Toxic Substances and Disease Registry (ATSDR).atsdr. The geometric mean of urinary atrazine mercapturate was 1. Geneva. Aldous CN. A risk assessment of atrazine use in California: human health and ecological aspects. Lucas AD. Short-term effects of chlorotriazines on estrus in female Sprague-Dawley and Fischer 344 rats. Seiber JN.69(2):217-222. Stuart AA. Stoker TE. Deddens JA. Pfeifer KF. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample.76(1):190-200. Environ Health Perspect 2001. Ferrell JM. 2005).53(2):297-307. Ferrell JM. 3/11/09 Laws SC. 1993). 2005.Herbicides Biomonitoring Information Urinary levels of atrazine mercapturate reflect recent exposure.99(8):5476-5480. Carr WC Jr. Biological monitoring of human exposure to atrazine. Moseman RF. Pest Manag Sci 2005. atrazine mercapturate was infrequently detected at the detection limit of < 1 μg/L. In a small number of field workers. Saiz SG. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. Chen H. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Toxicol Lett 1993. et al. Bersani M. Available at URL: http://www.30(2):244-247. Environ Health Perspect 2007. Eberly LE. Barbieri F. Jones AD. Cooper RL.html. 2000). 2005). Goodrow MH. Reynolds SJ. Vonk A. Third National Report on Human Exposure to Environmental Chemicals. International Programme on Chemical Safety (IPCS). Sanderson WT.15(6):500-508. Through immunoassay atrazine equivalents (detected mostly as atrazine mercapturate).109(6):583-590. 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. Barr DB. Gillis JH. Breckenridge CB. Mendoza M. Ann Occup Hyg 2003. Short-term effects of chlorotriazines on estrus in female Sprague-Dawley and Fischer 344 rats. Clayton CA. Lioy PJ. Simpkins JW. 3/11/09 Arcury TA. References Adgate JL. Hayes TB. Eldridge JC. atrazine was detected in only four children (Arcury et al. Steroids 1999.org/documents/pds/pds/pest82_e. WHO/ FAO Data Sheets on Pesticides.43(2):155-167. Curwin BD. 82. Shoemaker DA. McElroy WK. levels of atrazine mercapturate were generally not detectable (CDC. No. Cooper RL. demasculinized frogs after exposure to the herbicide atrazine at low ecologically relevant doses. In a study of 60 farm worker children. 2001 [online].cdc. J Expo Anal Environ Epidemiol 2005. 2007). 2001). Catenacci G. Cottica D.43(2):155-167. Atlanta (GA). Stevens JT.. Noriega N. Toxicol Sci 2000. Centers for Disease Control and Prevention (CDC). Eldridge JC. et al. Stoker TE. Blewett C. et al. Lee M. Fleenor-Heyser DG. Barr DB. Barr DB.47(6):503-517. et al. J Agric Food Chem 1982. Tyrey L. 1996. Wetzel LT. Stoker TE.

gov/scipoly/sap/meetings/2003/june/ finaljune2002telconfreport. Wetzel L. Available at URL: http://water. A longitudinal investigation of selected pesticide metabolites in urine. Sanderson JT. A review of epidemiologic studies of triazine herbicides and cancer. Cooper RL. Lansbergen GW. Dagenhart D. Determination of the effect of tridiphane on the pharmacokinetics of [14C]-atrazine following oral administration to male Fischer 344 rats.pdf. March 2006.epa. Toxicol Sci 2002.gov/oppsrrd1/REDs/ atrazine_ired. Available at URL: http://www.195(1):23-34. 3/11/09 U. van den Berg M. Sathiakumar N. Toxicol Appl Pharmacol 2004. Needham LL. Pesticides in the Nation’s Streams and Ground Water. Stoker TE.61(1):27-40.pdf. 0062. Geological Survey (USGS).php. Osborne DW. EPA). Dryzga MD. Timchalk C.S.67(2):198-206. Kastl PE. Interim Reregistration Eligibility Decision For Atrazine. Available at URL: http://www.S. Langvardt PW. J Expo Anal Environ Epidemiol 1999. EPA Office of Pesticide Programs.10(7):479. Crit Rev Toxicol 1997.S. A risk characterization for atrazine: oncogenicity profile. Stevens JT.56(2):69-109. Case No. Environmental Fate and Effects Division. Perry M. Cooper RL. Environmental Protection Agency (U. Laws SC. Boerma J. Toxicol Appl Pharmacol 2002. Fenton SE.Herbicides development of a biomarker of exposure.9(5):494-501. Hammerstrom KA. Circular 1291. EPA). J Toxicol Environ Health A 1999. 6/1/09 U. MacIntosh DL. Wood C. Induction and inhibition of aromatase (CYP19) activity by various classes of pesticides in H295R human adrenocortical carcinoma cells. 2007. The effect of atrazine on puberty in male Wistar rats: an evaluation in the protocol for the assessment of pubertal development and thyroid function. Supplemental Technical Information (available on-line only). Delzell E. 4/2/09 56 Fourth National Report on Human Exposure to Environmental Chemicals . May 2003a.27(6):599612. Environmental Protection Agency (U. Stoker TE. Pesticides and Toxic Substances. Rayner JL.182(1):44-54. 1992-2001. Office of Prevention. Ryan PB.usgs. Guidici DL. Singzoni B. Toxicology 1990.epa.S. White paper on potential developmental effects of atrazine on amphibians.58(1):50-59. Washington (DC). Laws SC. Christiani D. Toxicol Sci 2000. revised February 15. Urinary biomarkers of atrazine exposure among farm pesticide applicators.S. Ann Epidemiol 2000. Chem Res Toxicol 1993.gov/nawqa/pnsp/pubs/ circ1291/supporting_info. Tortorelli J.6(1):107-116. 2003b. Guidici DL. The effects of atrazine metabolites on puberty and thyroid function in the male Wistar rat. Exposure parameters necessary for delayed puberty and mammary gland development in LongEvans rats exposed in utero to atrazine. Breckenridge CB. The Quality of Our Nation’s Waters. U.

S.16) < LOD .210-.S..670-1. 2.4-D) controls broadleaf weeds in residential. MCPA.43) 1. 2007).S. 1974.560-.420) < LOD . Intentional overdoses and unintentional high dose exposures to chlorophenoxy acid herbicides have resulted in weakness.27 (.EPA in 1948. Acid and salt forms are much less toxic to fish and aquatic invertebrates than the ester forms.07 (.10) < LOD 1.30 (<LOD-2. and by consuming food or drinking water contaminated with 2.410) < LOD .890) < LOD . 2.910) 1.27 (1. Kohli et al. and delayed Urinary 2.260 (<LOD-. with a half-life of several days to several weeks... which may vary for some chemicals by year and by individual sample.560-1. although dermal exposure may be significant for herbicide manufacturing plant workers exposed to high concentrations of 2.24 (. in 2001 (U. and aquatic environments.10 (<LOD-1.930 (.02-1.690 (.550-1. < LOD means less than the limit of detection. but at higher levels they are herbicidal.22) < LOD . As much as 62 million pounds of 2.690-1.660) 1. headache. Sauerhoff et al.EPA.40) 1.740 (.250 (<LOD-. nausea. 1989. renal and hepatic injury.250 (<LOD-.810-1. myotonia.05-2.4-D is rapidly absorbed via oral and inhalation routes.4-Dichlorophenoxyacetic Acid CAS No.4-dichlorophenoxyacetic acid (2.540-. these herbicides can enhance plant growth. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 1.EPA.210 (<LOD-. population from the National Health and Nutrition Examination Survey.80) 1.2. It is rarely detected in ground waters (USGS.310) < LOD .55 (1.4-D has low acute toxicity. It is poorly bound in soils.27-2.330 (.400) < LOD . the chlorophenoxy herbicide 2. Fourth National Report on Human Exposure to Environmental Chemicals 57 .13) < LOD .49) 477 546 677 797 823 1070 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD . dizziness. 94-75-7 General Information Widely used throughout the United States.03) 695 659 520 668 589 892 Limit of detection (LOD.890 (.910) < LOD .60) 1. it acts as a plant growth hormone.930-1. by direct contact with agricultural and residential areas after applications. and mecoprop). and it is often mixed with other chlorophenoxy acid herbicides (such as dicamba. hypotension. 2005).4-D is eliminated mostly unchanged in the urine with an elimination half-life ranging from 10 to 33 hours (Arnold et al.51 (1. Similar to other chlorophenoxy herbicides.32 (1.610 (. It is not well absorbed through the skin.680-1.230-.22) 962 1135 1015 1278 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD . Survey Geometric mean (95% conf.4-D at low environmental doses or at biomonitored levels from low environmental exposures are unknown.320) 90th .910) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .4-D or exposed for prolonged periods. Human health effects from 2. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.S. 2004). 1977).490 (. agricultural.960-1.350) < LOD < LOD < LOD .420-.310 (. General population exposure to 2. abdominal pain. It was first registered with U.952 and 0.490) < LOD < LOD < LOD . Once absorbed. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.730 (.S.21) 1.4-D may occur during residential applications.610-. 2.4-D can be applied either as an aqueous salt or as oil-soluble esters.10 (<LOD-1.4-D have been below recommended intake limits (U.4-D were used in the U.230 (<LOD-.08) < LOD .70) 1.66) < LOD 1.440-1.370-.20 (.690 (. 4-D.690 (.00-2. 2.760 (.20 (<LOD-1.48) < LOD 1. At low levels.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 .Herbicides 2. Recent estimates of chronic intakes of 2.4-Dichlorophenoxyacetic acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.

890-1.17 (.520-.05) .56) .350 (<LOD-. 2003.Herbicides neuropathy (Bradberry et al. 2006.19) .27-1.08 (.780) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .330-. IOM.920) < LOD 1.270-. 1996. IARC considers the chlorophenoxyacetic acids group of chemicals as possibly carcinogenic to humans.410 (<LOD-.3. Knopp et al. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 1. with the exposure to chlorophenoxy herbicides as defoliants or contaminated herbicides.14 (.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 .390) < LOD < LOD < LOD .4-Dichlorophenoxyacetic acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.610-.EPA 2005).590 (<LOD-1.590 (<LOD-1. or to contaminants in the herbicide formulations (specifically 2.820-1..73) .930-1. or teratogenic effects in chronic rodent studies (Charles et al.4-D reflect recent exposure. 2005.. 58 Fourth National Report on Human Exposure to Environmental Chemicals .S.990-1.560-.S.340-. U..380 (<LOD-.550-. U.13 (. 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. myotonia.640 (.470) < LOD . In previous samples of the U.40) 695 659 520 667 589 892 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. 1985.670 (. urinary 2.EPA. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.4-D levels were detectable in less than a quarter of the individuals studied.780) . 1994).490 (. 2. Kutz et al. 2002. such as soft tissue sarcoma and non-Hodgkin’s lymphoma. adrenals and gonads (NTP.29) 477 546 677 796 823 1070 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD . developmental.660) < LOD . in small samples of children (Hill et al. 2005).. 2. 2005).670 (.4-D does not have significant reproductive.08 (. The acid and salt forms of 2.340 (.570) < LOD .610-.. thyroid. eyes.S. 2005).16) 1. liver.890) < LOD 1. 1992).EPA.410) 90th . 1995.08 (.8-tetrachlorodibenzo-pdioxin) (Garabrant and Philbert.740 (.EPA.4-D had urinary levels several hundred to several thousand times higher than the 95th percentiles of the NHANES subsamples (CDC. 1996..680) < LOD .480 (. 2005.980) < LOD 1.620-.4-D was not found to be genotoxic or carcinogenic in animal studies (Garabrant and Philbert. and evidence of histological injury to the kidneys. 2001.410) < LOD 1. It is unclear whether these associations are related to the chlorophenoxy herbicides.S. U. IPCS.810-1.790) < LOD . Hill et al.410) < LOD < LOD < LOD .850) < LOD . and of adults and children (Baker et al. 2000). Post-application levels in farmers and home gardeners were dependent on Urinary 2. population (Hill et al.EPA at: http://www.270 (<LOD-. 2005.gov/pesticides/.7.S. U. 1996.epa.780 (..24) 1. population from the National Health and Nutrition Examination Survey.780-1. 1980. 2005).. Survey Geometric mean (95% conf.S. IPCS. IPCS.S.700 (.810-1. 2002.41 (1. 2.440 (. 1989). Acute high doses administered to laboratory animals produced ataxia.380) < LOD . Kolmodin-Hedman and Erne.26) 962 1135 1015 1277 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD . 2005.560-.35) < LOD .32 (<LOD-2.660 (. Epidemiological studies have reported associations of several types of cancer. 2004). Biomonitoring Information Urinary levels of 2.39) < LOD 1. Average post-application urinary levels of 2. Frank et al. 1995).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..790) 1.720 (.4-D are eye irritants.380 (<LOD-.4-D production plant workers and a few forestry workers spraying 2. Pearce and McLean.380-. other exposures. Additional information is available from U. CDC.580-.13 (..670 (<LOD-1.

Selected pesticide residues and metabolites in urine from a survey of the U. Alexander BH. Needham LL. TOX-63: TOXICITY REPORT CURVES.4-D): exposure and urinary excretion.31 Suppl 1:98-104. et al. Heederik D. Board on Health Promotion and Disease Prevention.4-dichlorophenoxyacetic acid in the chemical industry: results of a five year biological monitoring study. Carter-Pokras OD. Scand J Work Environ Health 2005. Exposure of homeowners and bystanders to 2.4 dichlorophenoxyacetic acid (2. Reynolds SJ. Veterans and Agent Orange: update 2002. Arch Environ Contam Toxicol 1985. Arch Toxicol Suppl 1980.nih. Frank R. Review of 2. 2005). Toxicol Sci 2001. the amount of pesticide applied.4-D.inchem. Hill RH Jr. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. Environ Res 1995. Pesticide residues in urine of adults living in the United States: reference range concentrations.org/documents/jmpr/jmpmono/v96pr04. Mandel JS. In farm families. Chapman P. The pharmacokinetics of chlorinated phenoxy acid herbicides: a literature.4-D will result in an adverse health effect. Biomonitoring for farm families in the farm family exposure study. Erne K. Dhar MM. Head SL. Hill RH Jr. the number of acres to which it was applied (Curwin et al. Ritter L. Scand J Work Environ Health 2005. Tables. 2003. Kutz FW..gov/index. et al. Barr DB. geometric mean urinary levels of 2. Wilson RD.60(1):121-131.4:318-321. Khanna RN. Curwin BD.4-Dichlorophenoxyacetic Acid).37(2):277-291.S.4-D than levels found in the general population. 3/17/09 Fourth National Report on Human Exposure to Environmental Chemicals 59 . Gregg M. Cook BT.4-D) epidemiology and toxicology. Baker BA. National Toxicology Program (NTP). Philbert MA. 2005. Atlanta (GA). Estimation of occupational exposure to phenoxy acids (2. Tandon JS. 3/17/09 Institute of Medicine (IOM). et al.51(3):152-159. Ripley BD. Holler JS. Washington (DC): National Academies Press.nap. Forestry workers involved in aerial application of 2. Crit Rev Toxicol 2002. Biomonitoring of herbicides in Ontario farm applicators. Smith SJ. Hanley TR Jr. Bus JS.18(4):469-474. 2005).4:427-435. Available at URL: http://ntp. 3/17/09 Knopp D. Baker SE.. Beeson MD. J Toxicol Environ Health 1992. Survival and Growth Curves from NTP Toxicity Studies. Absorption and excretion of 2. Centers for Disease Control and Prevention (CDC). To T. J Environ Sci Health B 1992. Vet Hum Toxicol 1989.4:97-100. Brody D.4-dichlorophenoxyacetic acid (2. Available at URL: http:// www.4. 2005. 1992). Honeycutt R. Garabrant DH.27(1):23-38. Bailey SL. Kolmodin-Hedman B. Arnold EK. Mandel et al. Solomon KR. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children.71(2):99-108. Occup Environ Med 1994. Committee to Review the Health Effects in Vietnam Veterans of Exposure to Herbicides (Fourth Biennial Update.4-D and 2. Harris SA. 914.4-D were highest in the farmers who applied the 2. van Ravenzwaay B. TOX-63 Peroxisone Project (2. Quantification of selected pesticide metabolites in human urine using isotope dilution high-performance liquid chromatography/ tandem mass spectrometry.php?record_id=10603. Gupta BN.niehs. general population. cfm?objectid=06FF8DA6-E5A1-90CD-3F26562CEC5CDDE5.4-dichlorophenoxyacetic acid (2. Barr DB.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. Campbell RA. Available at URL: http:// www. Kohli JD. Pesticides residues in food: 1996 evaluations Part II Toxicology.4-dichlorophenoxyacetic acid in man. International Programme on Chemical Safety-INCHEM (IPCS). Xenobiotica 1974.15(6):500-508.32(4):233-257. Driskell WJ.31(2):121-125. Updated March 7. 2. Shealy DB. J Expo Anal Environ Epidemiol 2005 Nov. Stephenson GR. Sanderson WT. Assessment of exposure to 2.edu/catalog.10(6 Pt 2):789-798. Arch Environ Contam Toxicol 1989. Biomonitoring studies of 2. 2005 Charles JM. 2006. Sircar KP.4-. Hein MJ.Herbicides the time since application.31 Suppl 1:90-97. Sirons G J. other family members had levels ranging only slightly higher than the 95th percentile levels in NHANES 1999-2000 and 2001-2002 subsamples (CDC. Developmental toxicity studies in rats and rabbits on 2. Baker S. and the use of protective clothing or equipment (Arbuckle et al. Finding a measurable amount of 2. J Expo Anal Environ Epidemiol 2000.4-dichlorophenoxyacetic acid and its forms. Needham LL.5-T). Fast DM.. Harris et al. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.4-D). References Arbuckle TE. Murphy RS.htm.. Cole DC. Acquavella JF.4-D in urine does not mean that the level of the 2. Dichlorophenoxyacetic acid. Third National Report on Human Exposure to Environmental Chemicals. Beasley VR.

Environmental Protection Agency (U. 4/2/09 U.epa.gov/oppsrrd1/ REDs/factsheets/24d_fs.usgs. gov/oppbead1/pestsales/01pestsales/market_estimates2001. revised February 15.S. 60 Fourth National Report on Human Exposure to Environmental Chemicals .8:3-1U.S. Circular 1291.S.htm.S.Herbicides Sauerhoff MW. Office of Prevention Pesticides and Toxic Substances.4-D) following oral administration to man. Available at URL: http://water. Geological Survey (USGS). Gehring PJ. Environmental Protection Agency (U.EPA). 1992-2001.2000 and 2001 market estimates. June 2005. May. The Quality of Our Nation’s Waters.S.pdf. Supplemental Technical Information (available on-line only). Braun WH. Pesticides in the Nation’s Streams and Ground Water.4-dichlorophenoxyacetic acid (2. 3/17/09. The fate of 2.epa. Blau GE. 3/17/09 U. 2007. March 2006. EPA 738 F-05-002. Washington (DC): U.4-D RED Facts. Toxicology 1977. 2. S. 2004.gov/nawqa/pnsp/pubs/ circ1291/supporting_info. Pesticide industry sales and usage .EPA).php. Available at URL: http://www. Available at URL: http://www.EPA.

2000. 2000. People exposed to metolachlor will excrete metolachlor mercapturate in their urine. Gilliom. Additional information is Urinary levels of metolachlor mercapturate reflect recent exposure. 2003). Salivation. 2007. and it was not mutagenic in mammalian cells (U. General population exposure may occur through the consumption of contaminated food or drinking water. Human health effects from metolachlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown.S. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.. Urinary levels of metolachlor mercapturate were generally not detectable in the NHANES 2001-2002 subsample. USGS. sorghum and other crops..S. WHO. Davison et al. 1995). (2003) showed that 2. The geometric mean metolachlor mercapturate was 4. Metolachlor has low potential for acute toxicity (U. including corn. 2007. It is absorbed by plants and inhibits plant protein synthesis. Fourth National Report on Human Exposure to Environmental Chemicals 61 . Metolachlor or its degradates can leach from soils and have been detected in watersheds of agricultural land. 1995. 2005). and field workers may have significant exposures via this route. Occasionally in the past. and convulsions were observed at lethal doses in animal studies. In animals. Estimated human intakes have been below recommended limits (U. 2003). but another metabolic pathway can produce 2-methyl-6-ethylaniline and its reactive metabolite which may account for observed effects (Coleman et al. 2005. 1994. Metolachlor has a soil half-life of a few weeks to three months and is degraded microbiologically and photochemically to at least five different products. EPA at: http://www..Herbicides Metolachlor available from U.gov/pesticides/. Hines et al. lacrimation. mercapturate conjugates were the predominant metabolites. and eliminated in urine and feces over two to three days (WHO. and on non-crop land for general weed control.S. This metabolite is not a marker of exposure to either plant metabolites or environmental degradates of metolachlor which can be present in the environment..S. though the 95th percentile for males was 0. Jefferies et al. 2005). 1995).200 μg/L (CDC. Kolpin et al.EPA.7 μg/L in the urine of farmers after they had sprayed metolachlor (Curwin et al.S.EPA. Hladik et al. 1999. in both ground and surface waters (Battaglin et al. formulators. Biomonitoring Information CAS No. WHO.EPA.2% of a small reference population had detectable metolachlor equivalents by immunoassay in their urine. whereas 60% of applicators had detectable amounts. In animal studies. metolachlor was quickly absorbed after dermal or oral doses.epa. 1998).. Biomonitoring studies on levels of metolachlor mercapturate provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels metolachlor than are found in the general population.S. Metolachlor shows little potential to bioaccumulate but is moderately toxic to fish. metolachlor levels in water have exceeded lifetime human health advisory levels (U. 2003). 51218-45-2 General Information Metolachlor is a chloroacetanilide type herbicide that is applied for preemergent control of grasses and broadleaf weeds on agricultural crop land.EPA considers metolachlor to be a possible human carcinogen. 1995). Finding measurable amounts of metolachlor mercapturate in the urine does not mean that the levels of metolachlor mercapturate cause an adverse health effect. so applicators. Feng and Wratten. 1989. U.. NTP and IARC do not have ratings regarding human carcinogenicity. EPA. Metolachlor did not show developmental or reproductive toxicity in chronic animal studies. Metolachlor is well absorbed dermally. soybeans..

Herbicides Urinary Metolachlor mercapturate Metabolite of Metolachlor Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. population from the National Health and Nutrition Examination Survey. Urinary Metolachlor mercapturate (creatinine corrected) Metabolite of Metolachlor Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.220) < LOD 1192 1346 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result. < LOD means less than the limit of detection.2. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2537 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 580 830 1127 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD .440 (<LOD-.500) < LOD 1192 1345 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . which may vary for some chemicals by year and by individual sample.670 (<LOD-. Survey Geometric mean (95% conf.S.200 (<LOD-.S. 62 Fourth National Report on Human Exposure to Environmental Chemicals . Survey Geometric mean (95% conf. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. population from the National Health and Nutrition Examination Survey.240) 679 701 957 Limit of detection (LOD.200 (<LOD-. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2538 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 580 831 1127 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD . see Data Analysis section) for Survey year 01-02 is 0.740) 679 700 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.

gov/nawqa/pnsp/pubs/circ1291/ supporting_info. The Quality of Our Nation’s Waters Pesticides in the Nation’s Streams and Ground Water. Occurrence of sulfonylurea.39(17):6561-6574. Biagini RE. and metolachlor herbicides in rats.pdf. World Health Organization (WHO). Camann DE. Brown KK. Supplemental Technical Information (available on-line only). Environmental Protection Agency (U. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. Barr DB. Reregistration Eligibility Decision (RED) Metolachlor. Available at URL: http://water.gov/nawqa/pnsp/pubs/files/051507.11(4):353359. Deddens JA. Third National Report on Human Exposure to Environmental Chemicals. sulfonamide. Gillion. Roberts AL. Barr JR. 1999. EPA). 4/2/09 U. Hodgson E. Heederik D. 3/27/09 Fourth National Report on Human Exposure to Environmental Chemicals 63 . Finding minimal herbicide concentrations in ground water? Try looking for their degradates. Available at URL: http://www. Jefferies PR.pdf 3/30/09 Hines CJ. Sci Total Environ 2000.37(4):10881093. Background document for development of WHO Guidelines for Drinking-water Quality. Casida JE.47(6):503-517. et al. Environ Sci Technol 2007. Andrews HF.S. Linderman R. Metolachlor in Drinkingwater. streams and groundwater.int/water_sanitation_health/dwq/chemicals/ metolachlor. Thurman EM.usgs. Kolpin DW. Comparative metabolism of chloroacetamide herbicides and selected metabolites in human and rat liver microsomes. Quistad GB. 2005. Curwin BD. Geological Survey (USGS). Coleman S. Chem Res Toxicol 1998. Atlanta (GA). Feng PCC. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. Linhart SM.who. and other herbicides in rivers. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. Feil VJ. Thelin GP. Environ Health Perspect 2003. Striley CA. Environ Sci Technol 2005. Dialkylquinonimines validated as in vivo metabolites of alachlor. Wratten SJ.111(5):749-756. Barr DB. Burkhardt MR. Available at URL: http://water.html. 3/26/09 U. Geological Survey (USGS). Furlong ET. Available at URL: http://water. reservoirs and ground water in the Midwestern United States. Rose RL. Peter CJ.pdf. 2007.248(2-3):115-122. Kinney PL. et al.S. EPA 738R-95-006. Gilliom RJ). Sacramento. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. 1998.S. Water-Resources Investigations Report: Distribution of Major Herbicides in Ground Water of the United States Water Resource Investigations Report No. acetochlor. 1992-2001.15(6):500-508. Xenobiotica 1994.usgs. Davison KL. Comparative metabolism and elimination of acetanilide compounds by rat.S. Larsen GL.24(10):1003-1012.41:3409-3414. Sci Total Environ 2000.108(12):1151-1157. California. April 1995. 6/1/09 Whyatt RM. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. 2003. revised February 15.gov/nawqa/ pnsp/pubs/wrir984245/text.gov/oppsrrd1/ REDs/0001.ESTfeature_gilliom. Hein MJ. Ward EM. J Agri Food Chem 1989. Hladik ML. imidazolinone. usgs.Herbicides References Battaglin WA. Reynolds SJ. Available at URL: http://www. Centers for Disease Control and Prevention (CDC). Environ Health Perspect 2000. R. Alavanja MC.S. 98-4245 (by Barbash JE. Hsiao JJ.php.248(2-3):123-133. Ann Occup Hyg 2003. Sanderson WT. Shoemaker DA. U. Kolpin DW. Pesticides in U. J Expo Anal Environ Epidemiol 2005. March 2006.epa. Circular 1291.

5-T at low environmental doses or at biomonitored levels from low environmental exposures are unknown.4.. Epidemiological studies have reported associations of several types of cancer. such as soft tissue sarcoma and non-Hodgkin’s lymphoma. < LOD means less than the limit of detection. 93-76-5 General Information 2. myotonia. with the exposure to chlorophenoxy herbicides as defoliants Urinary 2.4.4-D were used as defoliants in the Vietnam War (e..4.4.5-T (Holson et al.5-T degrades to 2.4. Mohammad and St. dizziness. Although 2. Omer.5-T) is a chlorophenoxy acid herbicide that is no longer registered for use in the United States. the general population is unlikely to be exposed to it.5-T in soil varies with conditions. 1974).. and concern about contamination with 2. Nelson et al. Survey Geometric mean (95% conf. Once absorbed into the body.Herbicides 2. 64 Fourth National Report on Human Exposure to Environmental Chemicals .4. 2.5-Trichlorophenoxyacetic acid (2.1..4. Chlorophenoxy herbicides act as plant growth hormones. headache.5-T. 1992. nausea.4. with an elimination half-life of approximately 19 hours (Arnold et al. Human health effects from 2.5-Trichlorophenoxyacetic Acid CAS No. population from the National Health and Nutrition Examination Survey. these herbicides can enhance plant growth.5-trichlorophenol and other degradates.S. 1986.4. 2007).5-T use as a herbicide in 1985. 2.4. abdominal pain.4.5-T and 2.4. 2. and delayed neuropathy (Bradberry et al. Intentional overdoses and unintentional high dose occupational exposures to chlorophenoxy acid herbicides have resulted in weakness. The half-life of 2.4. 1992). it is not well absorbed through the skin.4.g. see Data Analysis section) for Survey years 99-00 and 01-02 are 1.8-tetrachlorodibenzo-p-dioxin (TCDD) led to the discontinuation of 2. Ester forms of 2. Kohli et al. At low levels. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 1989. ranging from several weeks to many months.7. 2004). 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. hypotension.5-T is eliminated mostly unchanged in the urine.3. renal and hepatic injury. Teratogenic and developmental effects have been reported in studies of multiple rodent strains treated with high doses of technical grade 2. Agent Orange).2 and 0. Given the commercial unavailability of 2.5T is rapidly absorbed via oral and inhalation routes. 2.5-T was once applied as either an aqueous salt or as an oil-soluble ester.4.5-Trichlorophenoxyacetic acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. but higher levels are herbicidal.. which may vary for some chemicals by year and by individual sample.5-T has been rarely detected in ground waters (USGS.

4.7.4. Additional information is available from U. or to contaminants in the herbicide formulations (specifically 2. similar to results of NHANES II (19761980).5-T reflect recent exposure. Finding a measurable amount of 2.5-T than levels found in the general population. 2005). Survey Geometric mean (95% conf. 2003.4. other exposures. 1992).000 times higher than the detection limit for the NHANES 2001-2002 data (Kolmodin-Hedman and Erne. It is unclear whether these associations are related to the chlorophenoxy herbicides.3. Pearce and McLean. Urinary 2.4.5-T measured after a day of exposure in a few asymptomatic herbicide applicators were 35.4.5-T were generally below the limit of detection.4.5-T itself is not mutagenic.EPA.5-Trichlorophenoxyacetic acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. Biomonitoring studies on 2.4.8-tetrachlorodibenzop-dioxin) (Garabrant and Philbert. 2002. 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. population from the National Health and Nutrition Examination Survey.S.5-T also were below the limit of detection (Kutz et al. 2. Fourth National Report on Human Exposure to Environmental Chemicals 65 .S. IPCS. Biomonitoring Information Urinary levels of 2. IOM. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. urinary levels of 2. 2005.S. 1996.4.EPA at: http://www. in which urinary levels of 2.Herbicides or contaminated herbicides.. In the NHANES 1999-2000 and 2001-2002 subsamples (CDC. IARC considers the chlorophenoxyacetic acids group of chemicals as possibly carcinogenic to humans.4.5-T does not mean that the level will result in an adverse health effect. Mean urinary levels of 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.epa. U. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 2004).gov/pesticides/.

5-trichlorophenoxyacetic acid (2. Estimation of occupational exposure to phenoxy acids (2.5-trichlorophenoxyacetic acid (2.S. Nelson CJ. Fundam Appl Toxicol 1992.epa. Holson JF.31(2):121-125.S.EPA. Gaylor DW.S. 3/17/09 66 Fourth National Report on Human Exposure to Environmental Chemicals .4. general population.4.19(2):298-306. Pesticide industry sales and usage .edu/catalog. Beasley VR.4. Pearce N. Selected pesticide residues and metabolites in urine from a survey of the U. Gupta BN. II. Mohammad FK.org/documents/jmpr/jmpmono/v96pr04.5-trichlorophenoxy acetic acid in man. Cook BT. et al. Carter-Pokras OD.4-D and 2. The pharmacokinetics of chlorinated phenoxy acid herbicides: a literature. Agricultural exposures and non-Hodgkin’s lymphoma.19(2):286-297. 2. Third National Report on Human Exposure to Environmental Chemicals. Sircar KP.4-. Neurobehav Toxicol Teratol 1986.4-D) epidemiology and toxicology. LaBorde JB. Kolmodin-Hedman B. Washington (DC): National Academies Press.4:318-21. Poisoning due to chlorophenoxy herbicides.4.37(2):277-91. Committee to Review the Health Effects in Vietnam Veterans of Exposure to Herbicides (Fourth Biennial Update. J Toxicol Environ Health 1992. Brody D. St Omer VE. Behavioral and developmental effects in rats following in utero exposure to 2. Available at URL: http://www. Gaines TB. Arch Int Pharmacodyn Ther 1974. Bradberry SM.pdf.32(4):233-257.php?record_id=10603. Kutz FW.2000 and 2001 market estimates.4-D/2. Erne K. Toxicol Rev 2004.inchem.8(5):551-60. Available at URL: http:// www. Dhar MM. Board on Health Promotion and Disease Prevention. discussion 5-7. 2004. U.4.31 Suppl 1:1825. Review of 2. Arch Toxicol Suppl 1980. McLean D.5-T). 210:250-255. Developmental toxicity of 2. Washington (DC): U. Absorption and excretion of 2. 2005. 3/17/09 Institute of Medicine (IOM).5-T). Wolff GL. Vet Hum Toxicol 1989.nap.4. Scand J Work Environ Health 2005. Available at URL: http:// www. Dichlorophenoxyacetic acid. et al. 3/17/09 Kohli JD. Tandon JS. Philbert MA.4-dichlorophenoxyacetic acid (2. Proudfoot AT. May. Crit Rev Toxicol 2002. S.htm. gov/oppbead1/pestsales/01pestsales/market_estimates2001. Garabrant DH. LaBorde JB.4.EPA). 914. Fundam Appl Toxicol 1992. Nelson CJ. Khanna RN. Environmental Protection Agency (U.4. 2003. Atlanta (GA).Herbicides References Arnold EK.5-T). Office of Prevention Pesticides and Toxic Substances. Murphy RS. Sheehan DM. Multireplicated dose-response studies in four inbred strains and one outbred stock of mice. Multireplicated dose-response studies with technical and analytical grades of 2. Veterans and Agent Orange: update 2002. I. International Programme on Chemical Safety-INCHEM (IPCS). McCallum WF.5-T in four-way outcross mice. Holson JF.5-t mixture.23(2):65-73. Developmental toxicity of 2. Centers for Disease Control and Prevention (CDC). Gaines TB. Vale JA. Pesticides residues in food: 1996 evaluations Part II Toxicology.

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

Carbamate Insecticides

Carbofuran

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

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

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

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

Selected percentiles
( 95% confidence interval)

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

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

years 99-00 01-02

50th < LOD < LOD < LOD < LOD

75th < LOD < LOD

90th

* *

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

* * * * * *

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

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

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

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

482 578 681 827 831 1125

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

* * * *

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

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

973 1190 1021 1340

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

* * * * * *

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

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

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

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

696 680 521 696 603 953

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

68

Fourth National Report on Human Exposure to Environmental Chemicals

Carbamate Insecticides

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

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

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

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

Selected percentiles
( 95% confidence interval)

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

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

years 99-00 01-02

50th < LOD < LOD < LOD < LOD

75th < LOD < LOD

90th

* *

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

* * * * * *

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

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

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

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

482 578 681 826 831 1125

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

* * * *

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

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

973 1190 1021 1339

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

* * * * * *

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

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

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

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

696 680 521 695 603 953

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

Fourth National Report on Human Exposure to Environmental Chemicals

69

Carbamate Insecticides

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

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Carbamate Insecticides

Propoxur

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

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

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Carbamate Insecticides

Urinary 2-Isopropoxyphenol
Metabolite of Propoxur

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

Selected percentiles
( 95% confidence interval)

Sample 95th < LOD < LOD size 1917 2503

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

years 99-00 01-02

50th < LOD < LOD < LOD < LOD

75th < LOD < LOD

90th

* *

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

* * * * * *

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

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

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

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

456 574 655 820 806 1109

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

* * * *

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

936 1178 981 1325

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

* * * * * *

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

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

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

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

664 677 500 696 585 931

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

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Fourth National Report on Human Exposure to Environmental Chemicals

Carbamate Insecticides

Urinary 2-Isopropoxyphenol (creatinine corrected)
Metabolite of Propoxur

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

Selected percentiles
( 95% confidence interval)

Sample 95th < LOD < LOD size 1917 2502

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

years 99-00 01-02

50th < LOD < LOD < LOD < LOD

75th < LOD < LOD

90th

* *

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

* * * * * *

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

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

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

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

456 574 655 819 806 1109

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

* * * *

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

936 1178 981 1324

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

* * * * * *

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

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

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

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

664 677 500 695 585 931

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

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Carbamate Insecticides

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

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Fourth National Report on Human Exposure to Environmental Chemicals

Organochlorine Pesticides

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

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

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

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

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

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

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

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

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

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Organochlorine Pesticides

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

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Fourth National Report on Human Exposure to Environmental Chemicals

Organochlorine Pesticides

Aldrin

CAS No. 309-00-02

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

Dieldrin

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

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

Selected percentiles
( 95% confidence interval)

Sample 95th < LOD < LOD size 2275 1946

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

years 01-02 03-04

50th < LOD < LOD < LOD < LOD

75th < LOD < LOD

90th

* *

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

* * * *

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

756 588 1519 1358

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

* * * *

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

1057 946 1218 1000

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

* * * * * *

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

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

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

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

559 456 512 485 1045 881

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

Fourth National Report on Human Exposure to Environmental Chemicals

77

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

0-21.6 (14.098 (.7 (<LOD-15.0 (15. population from the National Health and Nutrition Examination Survey.077 (.080-.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 8.090-.064) 90th .160) .060) .124) .130) .096-.103 (.100) .6 (15.062-.S.140) .6) 19.090-.177) Sample size 2159 1952 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD .1) 20.075) < LOD .9-38.9 (14.7 (15.112) 95th .9-22.110) .190) .9 (13.202) 539 456 484 487 980 885 < LOD means less than the limit of detection for the lipid adjusted serum level.101) .0 (11.056-.2) 11.9 (12.0 (10.8 (9.1) 14.086-.9 (13.4) 539 456 484 487 980 885 Limits of detection (LOD.5) 15.049-. Survey years 01-02 03-04 Geometric mean (95% conf.4) 95th 20.4) 20.6) 16.6) 9.6-24.138) .8-17.117) < LOD .109-.S.50) 15.113 (.103 (.054-.6-33.110) .059 (.077-.8-17.150 (.1 (13.2) Sample size 2159 1952 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD 10.150 (. 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 9.140 (.063-.80-10.069) < LOD < LOD .5-17. Fourth National Report on Human Exposure to Environmental Chemicals 79 .8-19.180) .090 (<LOD-.10 (<LOD-16.089 (.120-.00 (8.8) 15.080 (.3 (14.2-15.5-17.40-10.3 (13.160 (.50 (8.8-24.100) .4) 21.7) 716 587 1443 1365 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD 9.30 (8.80-9.120) .130) .40-9.110-.3-21.8 (11.5) 21.080) .1) < LOD 9.8) 14.3 (19.116) .5) 19.0 (10. Survey years 01-02 03-04 Geometric mean (95% conf.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 .054-.108-.5 and 7.138 (. population from the National Health and Nutrition Examination Survey. which may vary for some chemicals by year and by individual sample. which may vary for some chemicals by year and by individual sample.3 (18.109 (.064 (.0-25.4 (12.7-19.158) .100-.110 (.8 (18.9 (12.8) < LOD 8.130 (.073-.182) 716 587 1443 1365 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD .0) 21.130) . 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 .4 (12.242) .100-.093) .6 (15.9-23.062 (.1) 15.084-.190) .100-.130-. < LOD means less than the limit of detection.7) 15. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.070) .180) .80 (<LOD-10.1-16.130-.139 (.1-18.5 (16. see Data Analysis section) for survey years 01-02 and 03-04 are 10.8.112-.130-.00-14.90) 90th 15.048 (<LOD-.090-.110 (.055 (.070-.70 (7.1-24.5-15.2) 14.1) 15.070 (<LOD-.1) 13.1 (18.6-24.0) < LOD 9.088-.139 (.140-.8-25.120 (.100 (.120 (.4) 19.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.7-22.5 (<LOD-11.2) 12.102 (.083-.110 (.4) < LOD < LOD 16.149) .058) < LOD .1-19.090 (.160 (.1) 10.4) 14.147 (.0) 19. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.062 (.4-18.053 (<LOD-.3 (18.4-17.2) 15. 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.054-.30 (8.7 (14.170) .109-.120 (.60-10.

103(Suppl 7):113-122. Revised Feb.org/documents/ehc/ ehc/ehc91. Serum organochlorine levels and breast cancer: a nested case-control study of Norwegian women. 2 Classes of Pesticides. Available at URL: http://www.html. Buckland SJ. Mink PJ. No:429-436.htm. Psychopharmacology (Berl) 1987. PA. Serrano FO.91(1):122-126. Turner W. toxicology. Grajewski B. 731-915.109(Supp1):113-139.inchem. et al.9:1357-1367. Edwards JW. 2007 [online]. Organochlorine insecticides in substantia nigra in Parkinson’s disease. Six high-priority organochlorine pesticides. McIntosh LJ. and epidemiology in the United States. Li AA. New York. Jr and Laws ER. Smith AG. FDA Pesticide Program Residue Monitoring 1993-2006 [online].47:1059-1087. Tully DB. pp. Lancet 1998. 15. Chung KL. David VL.fda. Part A 2000.html. bioaccumulation. Grandjean P. Dieldrin-induced neurotoxicity: relevance to Parkinson’s disease pathogenesis. Jorgensen T. et al. Exposure to low doses of the environmental chemical dieldrin causes behavioral deficits in animals prevented from coping with stress. 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. Olea N.64-65 Spec. Facca A. Mumtaz MM. Food and Drug Administration (FDA). Available at URL: http://www. Pesticides in the Nation’s Stream and Ground Water.150:263-271. Chapin RE. Basit A. Chlorinated Hydrocarbon Insecticides. 6/1/09 Ward EM. and lymphocyte sister chromatid exchange. Anantharam V. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Neurotoxicol 2005. Narahashi T.Organochlorine Pesticides in the NHANES 2001-2002 and 2003-2004 subsamples (Edwards and Priestly 1994).54:1431-1443. are nonestrogenic in transfected HeLa cells. Roy ML. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. Sanchez-Ramos J. Effect of occupational exposure to aldrin on urinary D-glucaric acid. either singly or in combination. 1989. Wienburg CL. Kitzazwa M.26:701-719.66(4):229-234. Aldrin and Dieldrin [online].atsdr.14:95-102.gov/toxprofiles/ tp1. Teta MJ. Stehr-Green. 80 Fourth National Report on Human Exposure to Environmental Chemicals . Inc. Academic Press.27:405-421.59:229-234.gov/~dms/ pesrpts. Organochlorine exposure and risk of breast cancer. Cox. J Occup Environ Med 2005.352:1816-1820. Demographic and seasonal influences on human serum pesticide residue levels. Frey JM.cfsan. VT. Evaluation of epidemiologic and animal data associating pesticides with Parkinson’s disease. Ginsburg KS. Hartvig HB. Available at URL: http://pubs. Patterson DG Jr. Song S. Environmental Health Criteria 91.usgs. Daniel SE. In Hayes WJ. Toxicological profile for aldrin/dieldrin [online]. Shore RF. International Programme on Chemical Safety (IPCS). Schulte P. 1992-2001. J Toxicol Environ Health 1989. Reprod Toxicol 2000. 4/21/09 Bates MN. Sodium and GABA-activated channels as the targets of pyrethroids and cyclodienes. Int Arch Occup Environ Health 1994. Chemosphere 2004. Brock JW. Handbook of Pesticide Toxicology. Patterson DG Jr. Toxicity of dieldrin for dopaminergic neurons in mesencephalic cultures. Andersen A. Eds. Environ Health Perspect 2001. Corrigan FM. August 2008. Rosellini RA. Available at URL: http://www. 1991. Exp Neurol 1998. Soto AM. References Agency for Toxic Substances and Disease Registry (ATSDR). Fernandez MG. Environ Health Perspect 1995. Mann D. Vol. Ellis H. Carlson JN. United States Geological Survey (USGS). J Toxicol Environ Health. 4/21/09 Hoyer AP. Finley B. September 2002. 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. Priestly BG. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Kanthasamy A. Aldrin and dieldrin: A review of research on their production environmental deposition and fate. The E-SCREEN assay as a tool to identify estrogens: an update on estrogenic environmental pollutants. Sonnenschein C. Garrett N. Jr. Kanthasamy AG. 4/21/09 Jorgenson JL. Toxicol Lett 1992. Needham LL.gov/ circ/2005/1291/. plasma dieldrin. Cancer Epidemiol Biomarkers Prev 2000.cdc.

3) 41.8) 52. 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.0) 21.4-40.2-49.5) 21.2 (28.7 (10. 01-02.4 (22.0-33.4) 29.7) 31.3-45.9 (15.1-25.3 (<LOD-19. Fourth National Report on Human Exposure to Environmental Chemicals 81 .8 (17.9 (29.0-18.8 (10.7 (<LOD-32.1) 22.6) 48.6) < LOD 11.7) 9.7-25.3-49.1-65.7 (42.6-24.6) 36.1 (25.4-51.9 (26. Heptachlor and chlordane and their metabolites bioaccumulate in fatty animal tissues.6) 9.3) 10.2) < LOD 11.4) < LOD < LOD < LOD 23. Since 1992.4) 37.1 (17.7 (43.2 (10.7 (17.2 (41.70 (<LOD-10.0 (20.8-33. population from the National Health and Nutrition Examination Survey.9 (26. in addition to trace amounts of numerous other related compounds (ATSDR. and 03-04 are 14.9) 47.1) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * 12.S.1 (<LOD-12.2 (39.36-11.3 (26.2) 34.1) * 11.7-56.8-33.6 (43.6 (25.8 (17. < LOD means less than the limit of detection.1-50.0-67.9) 37.1) < LOD < LOD < LOD < LOD < LOD 8.9-38.6) 9.9-40.6-18.4 (<LOD-12.7 (<LOD-13.9 (17.2-26.0) 41.5-38.6) 20.20-11.9) 23.8-32.0) 27.10 (8.10-11. Survey Geometric mean (95% conf.7-14.5) 38.2-56.7 (19.8-73.3) 10.7) 42.4 (35..20-10.3 (25.3 (11.3 (9.0) 31.0) 75th 20.6) 49.5-32.1 (44. which may vary for some chemicals by year and by individual sample. Heptachlor was used as a soil and seed treatment and for termite control in and around buildings until 1988.4) < LOD 11.5-13.9 (18.8.4 (30.5) < LOD < LOD 9.9 (15.5) 44. lawns.5-47.5-65.1-19.1-15.9) 23.8-31.7) 35.2 (37.5) < LOD < LOD < LOD < LOD 13.63 (8.8) 18.0 (32.6) 48.7) 19. 2007).5-41.1) 90th 34.7 (34. heptachlor use has been limited to treatment of fire ants near power transformers.0 (<LOD-12.5) 793 1049 963 868 1200 1015 Females 99-00 01-02 03-04 Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * 11.8 (18.7) 28.3) 18.1 (<LOD-12.1-25. see Data Analysis section) for Survey years 99-00.3) 37.0-25.2 (21.8-43. and in soil.1 (16.90 (8.30-11. buildings.3-24.7 (34.6-45.2) 36.8-61.6-53.7-70.4) 22. fish.8) 44.6-12.10-18.8-42. and dairy products are the usual sources of exposure to these chemicals in the general population.4 (30.4-21.5 (41.5-44.8) 27. 57-74-9 Heptachlor CAS No.6) 39. 76-44-8 General Information Chlordane and heptachlor are structurally related organochlorine pesticides and were used in the U.2) 46. 1994.6) 8.9) 13.7) 19.5 (8.4-14.2-28.9) 11.9) 31. 2007).9 (11.3-32.20 (<LOD-11.5 (<LOD-12.4) 18.5) 10.4-45.5-43.9-42.5 (34.9) 11.0 (37.1) * 11.4) 12.5 (33. Until 1988.9 (11.6-24.0-12.9) 39.0-13.5.3-45.3) 18.4 (31.2-21.6 (9. chlordane was used to kill termites and other insects on agricultural crops. the technical grade product of each chemical contains 10%-20% of the other chemical.5) 9. 1994).0-61.8-20.5.Organochlorine Pesticides Chlordane CAS No.0) 20.5-40. Both of these chemicals and their metabolites can cross the placenta and are excreted into breast milk.1-51.8) 663 752 595 998 1497 1383 20 years and older Gender Males 99-00 01-02 03-04 * 11.0 (26.2) 22. Chlordane is not currently produced or used in the U. Technical grade chlordane had contained 7% trans-nonachlor.0) 37.6 (9. 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.82-11.1) 30.3-43.7-39.9 (21. 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) 23.4 (10.9-21.69-10.8) size 1661 2249 1978 Total years 99-00 01-02 03-04 50th < LOD 11.9-21.0 (16.3 (20.5) 56. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.S. and 7.5) 37.9) 36. foods high in fat such as meat.89-10.2) 33.1 (40.5 (31.6) 11. from the early 1950’s until the mid-1980’s.2) * 12.8) 53.1 (15.7 (32.8 (42.1 (11.8 (10.3 (21.9) 17.8 (40. As a result of the manufacturing process.8-23.6 (16.2 (36.5-42.1 (27.74 (<LOD-10.9) 10.S.5) 628 557 462 350 501 493 559 1031 898 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.4) 39.8) 52.9 (31.37 (8.2) < LOD 11.1 (<LOD-12.9 (36. interval) Selected percentiles ( 95% confidence interval) Sample 95th 44.1 (20.2 (9. 10.1) 30.3 (28.1) 16.2-49.3 (27. respectively.7-12.2) 37. Consequently.

300) .180) .140-.240-.060 (<LOD-.208 (. which may vary for some chemicals by year and by individual sample.140 (.148) . Chlordane is metabolized primarily to oxychlordane and to a lesser extent.100 (<LOD-.148-.070-. EPA has established environmental criteria for chlordane and heptachlor. 1986). which is also persistent in the body (ATSDR.160) . characterized by seizures and paralysis.230) . FDA established allowable residues of chlordane.063 (.150-.400) .Organochlorine Pesticides (Dallaire et al.300 (.410) .119 (.190-.348) . 1991).180) .130 (. and NIOSH and ACGIH have recommended workplace exposure levels for each pesticide.170) .160) .049 (<LOD-.053-.240-.231) .330 (.061-.170) . and breast milk is a major excretion route in lactating women.062) < LOD .063 (.290) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.150 (.200-.320) .258-.080) .250 (.100-. In laboratory animal studies.286 (.286 (.320 (.450) .066-.280-.350) . 1986).320 (.200-.320) .130-.077) .320 (. to heptachlor.136) .070-.373) .290 (.200 (.180-.216-.246-. Epidemiologic studies have not demonstrated teratogenic or developmental effects (Baker et al.310) .270 (.207) . 1981)..146) .053-.242-.106-.058 (.260 (.225 (.063) * .230 (.115-.130 (.079) .168-.070 (<LOD-.190-. both chlordane and heptachlor induced hepatic cytochrome P450 enzymes and increased the incidence of liver tumors (NTP.213) * .302) .140-.210 (.320) 663 752 595 998 1497 1383 20 years and older Gender Males 99-00 01-02 03-04 * .199-.360) .070-.130) .050-.110 (<LOD-.066 (.230-. 2002.120-. 1996.260 (.091) .066 (<LOD-.450) .108-. interval) Selected percentiles ( 95% confidence interval) Sample 95th .065-.320 (.115 (.073) < LOD < LOD < LOD < LOD .126) .310-. and the U.140) .240 (.120-.130) . 2007. 82 Fourth National Report on Human Exposure to Environmental Chemicals .104-.140 (. Rogan.075 (.073 (.350 (. and heptachlor epoxide in foods and bottled water.315 (.510) .370 (. Human health effects from either chlordane or heptachlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown.092) .310) .189 (.310 (.063 (. The U.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. Smith.055-.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 * * * * . 2007). chronic doses of heptachlor have produced liver enlargement and injury. Le Marchand et al.133) 90th .128 (. Elimination of all these chemicals from the body occurs over months to years.140 (..083) .260-. OSHA has established occupational exposure criteria. 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.190-.070 (<LOD-.370 (.068) 75th .077) .058-.130-.100 (.430) .280-.223) .070 (<LOD-.070) < LOD < LOD < LOD < LOD < LOD .340) .S.080 (.291) size 1661 2249 1978 Total years 99-00 01-02 03-04 50th < LOD .290-. Chlordane and heptachlor are absorbed after oral.140 (.270 (.104) .090) . Survey Geometric mean (95% conf..220-.200-. IARC. heptachlor.110-.057) * .070 (<LOD-. IARC considers chlordane and heptachlor as possibly carcinogenic to humans.070) . Chronic feeding studies with either chlordane or heptachlor have demonstrated reduced fertility.090) .070 (.269 (. 1977a. and inhalation exposure.064) < LOD . Acute. No clear evidence of excessive cancer rates was demonstrated in human epidemiologic studies (ATSDR.290-.210 (.560) .230-.204 (.170-.165-.058-.280 (.300) .270 (.245-.380) .227) < LOD .440) .126 (.047 (<LOD-.048-.280) .080) .290) . The major metabolite of heptachlor is heptachlor epoxide.258 (.077) .056 (.100-.082 (. and alterations in immune function of offspring.280 (.130-.150 (.271 (.240) .150) .067 (. population from the National Health and Nutrition Examination Survey. 2001.066-.130 (.230 (.149 (.130-.112 (.203-. 2006).230-.080 (.350 (.370 (.063-. Takahashi et al.079) < LOD < LOD < LOD .076) < LOD .057-.083 (.071 (.400) .074-.300) .062) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * .160) . 1991.087-.287) .077) .340) .120-.057 (.170) .170) . 1977b.068) .430) .068-.290-.130-.310) .146) < LOD < LOD . dermal. Shindell and Ulrich.050 (<LOD-. high doses of either chlordane or heptachlor block inhibitory neurotransmitters and result in central nervous system toxicity.170) .S.180-.120 (.189-.253-.080) .300-.220 (.063) .S.220-.280-.069 (<LOD-.090-. Subtle neurodevelopmental effects have been observed rodents after prenatal exposure to heptachlor (IPCS.210-.150 (.250-. neonatal mortality.300) .063 (..260 (.250 (.207 (.160 (.

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

1 (19.0) size 1589 2259 1963 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th 90th 15. respectively.4 (11.3 (<LOD-25.5) 598 553 460 336 503 490 539 1041 888 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.1) 23.8) 19.9 (12.7-19.0) 13.2) 15.2) 26.3 (13.0-16.4) 21.9 (15.6) 14.7 (16.2 (<LOD-16. 84 Fourth National Report on Human Exposure to Environmental Chemicals .3) 16.6.8) 20.3) 10.6 (8. which may vary for some chemicals by year and by individual sample.20 (<LOD-9.5) < LOD 14.2-17.6 (12.2 (<LOD-62.8) 19.4 (11.2-27.8) 21.7 (10.9) * * * 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 8.5 (<LOD-32.4 (<LOD-54.8) 16.5 (<LOD-21.8 (13.3) 18.5 (11.8 (18.6 (13.1) 20. 01-02.9-16.6) 22.0-19.0 (15.3) 27.5. Survey Geometric mean (95% conf.50) < LOD < LOD < LOD 17. see Data Analysis section) for Survey years 99-00.8) 14.8.6) < LOD < LOD < LOD 27.10-13.8-24.3) 23.90 (<LOD-9.9-29.8-23.6 (<LOD-27.3-18.6 (14.0-17.5) 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. population from the National Health and Nutrition Examination Survey.2) 13.8-24.8 (15.5 (11.7-18.8) 14.8) 13.0-54.2 (18.1 (16.3) 18.8 (13.8-24. and 7.9-23.1-15.5 (10.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.9-25.6 (16.8-46.1-29.6-21.5) 19.2 (<LOD-25.0-17.9) 15.8 (<LOD-23.3) 22.S.5 (18.6-17.4 (15.7 (13.3) 18.7-25.2-27. < LOD means less than the limit of detection.2-16.1-16.40) 15.0) 638 741 592 951 1518 1371 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 13.4 (<LOD-19. interval) Selected percentiles ( 95% confidence interval) Sample 95th 24.1-38. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.2) 20. 10.8 (18.6) 13. and 03-04 are 14.4) 18.9-29.0 (11.6 (16.8) 13.8) 15.1) 13.6 (11.

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

6) 34.1) 18.8) 51.0 (16.5.7-22.1-34.1-18.6 (<LOD-14.2) < LOD 10.7 (13.4) 48.5) 22.7) 56.6) 56.2) 17.1 (17.0-22.0 (48. population from the National Health and Nutrition Examination Survey.9) 922 1062 955 1011 1224 1000 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 * 11.1-126) 67.7-21.7-34.2-18.2) 59.2 (19.6-19.4-22.9-40.9) 51.7 (28.0 (15.5 (45.2 (15.5-111) 68.10 (<LOD-11.5) 30.9 (29.7) 35.0) < LOD < LOD 8.9 (16. 01-02.8 (28.8 (26.9-35.0 (42.4-62.3 (49.8-19.4-36.4-67.7-32.0) 75th 31.1 (65.5 (15.6 (56.0) 18.3) 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.7-38.7) 78.2 (26.9-58.8-90.9 (36.3 (58.9 (15.6) 84.3) 19.1 (47.3-39.2-17.6-54.8 (71.6) 54.5-19.3) 32.7) 15.4-35.7 (35.1) 17.70 (<LOD-12.7 (16.7-20. respectively.2 (60.1) 17.86-13.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.6) 25.1) 31.3-50.S.3) 32.0 (19.7-23.2) 34.9 (47.1-22.1-34.6-20.1 (48.0) 664 758 589 1269 1528 1366 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 17.6) 10.2) 30.5) 36.3) 18.3 (17.0) Selected percentiles ( 95% confidence interval) Sample 95th 79.2-23.7) 73.4-18.1) 78.6-88.7-17.5) 14.0) 19.1 (22.9) 14.3 (14.0-93.6) 82.8-79.9 (51.8 (26.9 (51.5-20.7) 28.0-143) 112 (68.5) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * 20.8 (13.8 (<LOD-20.8 (28.0-68.9 (19.8-90.7-160) 86.1) 17.7 (59.8-110) 59.5) 78.0-123) 74.3-30.8 (17.7 (18.0 (13.0) 40.0-113) 68.4 (16.9) 51.1 (41.3-74.8 (42.7-29.1) 17.4 (45.4 (12.0-24.7) 78.8-129) 74.1) 14.0 (15.7 (74. and 7.1) 17.1) 62.8-77.8 (45.1-16.0 (14.2) 19.5 (25.2 (14.8.0-23.3) 30.0-37.7 (59.9-36.1) 32.8-19.0-23.8-67.4 (28.6-82.8 (16.3 (14.3) 18.8 (49.8 (13.2 (59.8 (15.1) 17.8 (12.3 (16.4) 59.4 (30.8-41.1) 78.7-113) 68.9-64.2-18.0) 13.2) 20.3) 30.2-21.9-65.6) 13.5) 90th 55.0 (16.8) 47.7) 17.5 (44.5) 77.5) 20.0 (13.9-20.3) 25.2) 39.3-57. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.2-37.2 (36.2 (25.1) 16.8-16.4-52.5-87.8) 19.1) 17.9-69.1) 18.3-21.6) 60.0 (42.6 (15.6-22.0) 33.4 (67.0) 49.1 (10.8-21.0-20.5 (15.1-55.4) 20.7 (11.7-18.1) 30.8) 80. and 03-04 are 14.9 (66.8 (11.0-93. which may vary for some chemicals by year and by individual sample.4) 107 (84.6) 56.3-86.5-17.6-66. interval) 18.7 (30.5) 48.3-32.0 (29.2-88.7-77.7) 52.4) 55.7-35.0 (60.7) 14.6 (57.3) size 1933 2286 1955 Total years 99-00 01-02 03-04 50th 17.0-38. 86 Fourth National Report on Human Exposure to Environmental Chemicals .3 (56.4) 16.9) < LOD < LOD < LOD 20.1-51.5-95.9-65.8 (30.8-16.2 (14.5) 19.9 (15.2 (27.5-69.6 (12.2 (7.9-89.6 (52.5 (13. < LOD means less than the limit of detection.3-58.2-16. Survey Geometric mean (95% conf.5) 9.0 (62.1-20.3 (45.3) 36.3) 16.5. see Data Analysis section) for Survey years 99-00.5) 14.4 (11.4) 19.5) 26.5-36.6 (32.9 (<LOD-14. 10.9-45.9-22.6 (56.6 (50.0-59.1-28.5) 35.9) 14.4-23.3) 15.7) 59.8 (26.1-16.6 (16.8 (19.9 (28.2 (64.8 (28.

565) 922 1062 955 1011 1224 1000 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 * .310-.099-.092 (.520 (.190-.520 (.240-.310 (.234) .220 (.161) .085-.350-.106 (.120-.490-.135 (.098-.110 (.160-.20) .093-.110 (.250) .089 (.120) .220 (.260) .390-.110-.470 (.220 (.085-.111 (.071 (<LOD-.324 (.087 (.390 (.117) .079-.210 (.062 (.090-.680) .126) .490) .106 (.390 (.417 (.360-.091-.210 (.125 (.093-.390 (.106 (.116-.690) .210-.630) .310-.490 (.119) < LOD < LOD < LOD .490 (.120 (.330-.800) .285-.211) 90th .400) .580 (.202 (.130) .110 (.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.190-.390) .510-. Survey Geometric mean (95% conf.150) .103 (.096-.250) .240) .108 (.186-.110 (.180-.122) .360-.210) .470-.120) .317 (.830) .090-.390 (.395) .190-.090-.090) .081 (.310-.355 (.127) < LOD < LOD .420) .405) .580 (.090-. Fourth National Report on Human Exposure to Environmental Chemicals 87 .129) .116) .150) .100-.096) .559) .510 (.540) .684) .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 .232) .410-.161-.061-.119) Selected percentiles ( 95% confidence interval) Sample 95th .080) .110 (.600) .272-.090-.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.098 (.099-.060 (<LOD-.191 (.370 (.240 (.113) < LOD .104-.069-.461 (.080-.098) .079-.130) .116 (.310-.250) .690) .069) .130 (.310) .130) .098 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.565) .134) .960) .594) .460) .301-.220 (.340-.590 (.112 (.340-.093) .400 (.237) .220 (.220 (.497-.409-.840) .380 (.170 (.320-.340) .270-.260) .078 (. interval) .343 (.097) .109 (.090-.397-.041 (<LOD-.160 (.220 (.370 (.100) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * .290-.190-.400-.141) .110 (.047-.110) .130 (.210 (.080 (.210) .130) .220) .100 (.190-.279-.300-.440-.091) .460-.100-.288 (.500) .131) .930) .145-.205 (.390) .177-.082) .470 (.130) .680 (.120 (.760 (.070 (.640 (.092 (.410-1.470-.280) .120) .140) .520) .240) .109 (.090 (.430-.210-.470 (.081-.242) .180-.450) .440) .130) .180-.558) size 1933 2286 1955 Total years 99-00 01-02 03-04 50th .111-.573 (.590) .124) .651) .395-.078-.125) .400-.094 (.300) .830) .095-.060) .120) .141) .237) .158-.080-.458 (.171-.240) .068-.103 (.093-.100-.120 (.350 (.420 (.414 (.084-.371) .114) .330-.120-.080-.113) .105 (.190-.286-.186 (.130) .100-.430-.096-.580 (. which may vary for some chemicals by year and by individual sample.108) .210) .320-.108) 75th .367) .100 (.590 (.630) .060-.600 (.104 (.085-. population from the National Health and Nutrition Examination Survey.S.327 (.090 (<LOD-.055 (<LOD-.080-.128 (.430-.112 (.183 (.400 (.330 (.550 (.230 (.220 (.460) .122) .173-.630) .120-.054-.480) .288-.

org/site/foundation/ research/projects2. National Toxicology Program (NTP).372:20-31. Sci Total Environ 2004. Trends in birth defects for a Hawaiian population exposed to heptachlor and for the United States.111:349355. 79.84:151-161. An evaluation of serum pesticide residue levels and liver function in persons exposed to dairy products contaminated with heptachlor. 2 Classes of Pesticides. Arch Pediatr Adolesc Med 1996. 1963-1967.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Environ Health Perspect 2003. Eds. Mortality of workers employed in the manufacture of chlordane: an update. Siegel BZ.259(3):374-377. Jr.150:981-990. gov/toxprofiles/tp12.8:1-123. Laliberte C. Covaci A. August 2007. Chlorinated Hydrocarbon Insecticides. Head SL.pdf. Available at URL: http://www. New York. Tartter P. Inc. Academic Press. Hertz-Picciotto I. Jr and Laws ER. et al. 1993.cdc. Barker J.html.gov/toxprofiles/tp31. Wong L. 2001. Sci Tot Environ 2006. Jaraczewska K. Vol. Pollutants in breast milk. Kolonel LN.Summaries & Evaluations. Environ Health Perspect 2002. Dendle WH.nih. Bioassay of chlordane for possible carcinogenicity.cdc. Van Oostdam JC. Available at URL: http://www. LeMarchand L.110:617-624. 1986. J Occup Med 1986. 4/21/09 Baker DB. Estimation of Human Exposure to Heptachlor Epoxide and Related Pesticides in Hawaii. Glynn AW.28:497501. KalubaSkotarczak A.41:145–148.nih. Aune M. Drews K. Royce W. Evaluation of human exposure to the heptachlor epoxide contamination of milk in Hawaii. Saidein D. 6/1/09 Rogan WJ. International Agency for Research on Cancer (IARC) . Environ Res 2000. Arch Environ Health. 1991 pp.110(8):835-838. Natl Cancer Inst Carcinog Tech Rep Ser 1977a. Circumpolar maternal blood contaminant survey. Bull Environ Contam Toxicol 1981:27:506-511. Determinants of serum polychlorinated biphenyls and organochlorine pesticides measured in women from the child health and development study cohort. In Hayes WJ. 4/21/09 Dallaire F.html. Poland. et al. JAMA 1988. Baker DB. Muckle G. A Report to the Hawaii Heptachlor Research and Education Foundation. 2006. Organochlorine exposures and breast cancer risk in New York City women. Bioassay of heptachlor for possible carcinogenicity. Bjerselius R.inchem. International Agency for Research on Cancer (IARC). Available at URL: http://www. Environ Health Perspect 2002. Concise International Chemical Assessment Document 70 Heptachlor [online]. Bleiweiss IJ. Available at URL: http://www. Toxicological profile for heptachlor and heptachlor epoxide [online].org/ documents/cicads/cicads/cicad70. Vol. Distribution of polychlorinated biphenyls. Organochloride pesticide residues in human milk in Hawaii. 6/1/09 National Toxicology Program (NTP).html.atsdr. Keller JA. Wolff MS. et al.atsdr. Takahashi W. Organochlorines in Swedish women: determinants of serum concentrations. 88 Fourth National Report on Human Exposure to Environmental Chemicals . organochlorine pesticides and polybrominated diphenyl ethers in human umbilical cord serum. Charles MJ. Atuma S. 1994-1997 organochlorine compounds. 4/21/09 Agency for Toxic Substances and Disease Registry (ATSDR). Canada). Available at URL: http://www.9:1-109. Toxicological profile for chlordane [online]. Hawaii Med J 1991. Handbook of Pesticide Toxicology. 9/25/07 International Programme in Chemical Safety (IPCS). Granath F. Senie R. Wohlleb JC. Loo S. Temporal trends of organochlorine concentrations in umbilical cord blood of newborns from the lower north shore of the St. Ayotte P. Gilman A.niehs. Natl Cancer Inst Carcinog Tech Rep Ser 1977b. Takei G. Darnerud PO. Brower S. Chashchin V.htm. Lulek J.inchem. Dewailly E. 4/21/09 James RA. Hansen JC. 731-915. maternal serum and milk from Wielkopolska region.htm.gov/ntp/ htdocs/LT_rpts/tr009. Berkowitz GS.pdf.heptachlor. Available at URL: http://ntp.50(3):108-118. Dewailly E. Willman E.niehs. Smith AG.gov/ntp/ htdocs/LT_rpts/tr008. Stehr-Green P. Chlordane and heptachlor [online].org/documents/iarc/ vol79/79-12. 1979-1980. Available at URL: http://ntp. May 1994. et al. Lawrence River (Quebec. Odland JO. Shindell S and Ulrich S. Voorspoels S.330:55-70.

8) 30.1 (23. population from the National Health and Nutrition Examination Survey.3-236) 24.8-26.1 (<LOD-39. which is a mixture containing p.2) 30.6-33.6 (22. food. respectively.6 (31. 01-02.0-155) 83.0) 19. DDT usually refers to the technical product.2 (<LOD-40.2-dichloroethenylidene)-bis[4-chlorobenzene] (DDE) and 1.0 (10.1-71. air.5 (23.9) 29. Fourth National Report on Human Exposure to Environmental Chemicals 89 .0-37.3) 22. < LOD means less than the limit of detection. DDT and DDE are distributed to all body tissues with the highest concentrations found in adipose tissues (ATSDR. In the body.S. DDT and DDE can cross the placenta.3) 21. as well as in plant and animal tissues.3 (27.4) < LOD < LOD < LOD 61.9) 14.9 (10. The biodegradation half-life of DDT in soil varies from 2 to 15 years.3-590) 293 (104-541) 48.8.0-53.8-23. DDT is converted in the environment to other more stable chemical forms. 2008.7. and trace amounts of several related compounds.4. after World War II until 1972.8) 36.p’-DDD (4% or less).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. DDT was used at one time as a treatment for head and body lice.7-16. p.8) 15. Only a small proportion of DDT is metabolized and excreted (Smith.5 (14. population. It was produced and used in the U.2-bis(p-chlorophenyl) ethane (DDD). sediments.2) < LOD < LOD 9. or dermal exposure. particularly meat. and 03-04 are 20.3) 21.5) 25.3 (<LOD-31. inhalation. see Data Analysis section) for Survey years 99-00.9 (10. continues to be the primary source of DDT exposure. fish. o.p’-DDT (65%-80%). interval) Selected percentiles ( 95% confidence interval) Sample 95th 28.5 (23. Food imported from countries that still use DDT may contain the chemical or its residues. depending on conditions. and 7.Organochlorine Pesticides Dichlorodiphenyltrichloroethane (DDT) CAS No. 17.10 (<LOD-12.10-13. and dairy products.0-15.2) 155 (59. It is still used in some countries.90 (<LOD-12.0-27.0 (18. 2002. Both Serum p.0 (18. DDT is converted to DDE and several other metabolites. 1991).2-95.5 (15.7) 12.0) 26.p’-DDT (15%-21%).9) < LOD < LOD 9.1’-dichloro-(2.0-35.7) < LOD 18.S.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 12.4) < LOD 17. when virtually all use of it was banned. 50-29-3 General Information Dichlorodiphenyltrichloroethane (DDT) has been used widely as a broad spectrum insecticide in agriculture and for control of vector-borne diseases.1-27.8-39.5) 23. Survey Geometric mean (95% conf.2 (11.5) 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) 40. which may vary for some chemicals by year and by individual sample.9 (21. particularly for endemic vector and malaria control.9) 17.7) 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.S.6 (9. These chemicals are highly persistent in soil.6) 635 566 461 356 514 490 564 1061 890 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.50-11.3) 28.1) 31.4 (23.1’-(2. including 1. Gunderson. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.00 (<LOD-10.0) 20.5-36.70 (8.2-65. although DDT and DDE intakes have decreased over time (FDA.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 8.9-34. In the general U.7 (15.6 (25. resulting in fetal exposure.9-28. 1988).9 (10.8-17.0 (21.1 (33. DDT can be absorbed after ingestion.3-16.5-54. Smith.9 (<LOD-20.6 (<LOD-25. 1991).5) < LOD < LOD 9.3 (<LOD-21. and water.7 (19.

098-. which may vary for some chemicals by year and by individual sample. reproductive organ abnormalities. Human health effects from DDT at low environmental doses or at biomonitored levels from low environmental exposures are unknown.106) .230) .074-. 1997).250 (. In laboratory animals.190-1. Longnecker et al. DDT may bind to estrogen receptors (Chen et al.201 (.063 (<LOD-.120-. population from the National Health and Nutrition Examination Survey.061) < LOD < LOD < LOD .313 (.146 (. accidental exposures.150) .190 (.069) ..g.064 (.078 (.114-. polychlorinated biphenyls.180 (.00) .203) .112 (.130 (<LOD-. 2002.167) size 1679 2305 1965 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * * .220) .080-.068-.140-.S. 2002.. Reproductive effects in humans affecting birth weight.180-.180 (.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 .290) ..180) .400 (.059-. Gray et al. dioxins and furans). both DDT and DDE may induce specific cytochrome P450 isozymes (Nims et al. and duration of lactation.. 2006).120 (<LOD-. lung cancer.420) .343) < LOD .130-.180) .240) .142 (.250-1..078-. 90 Fourth National Report on Human Exposure to Environmental Chemicals . resulting in exposure to nursing infants (Rogan.00 (.071-. 2001).190 (. Survey Geometric mean (95% conf. tremor.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 . A workplace standard for DDT has been established by Serum p.26) 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.170) . 1998). Epidemiologic studies of children with environmental exposure to DDT and DDE have not demonstrated neurologic or developmental abnormalities (Gladen et al. fertility.189-. 2001). and altered behavior after neonatal exposure (Eriksson and Talts. Jusko et al.. Animal studies reported reduced fertility.. although the risk for preterm delivery may be related to maternal DDE levels (Longnecker et al. In high dose. Jusko et al.079) < LOD < LOD .150-.150 (<LOD-. 1956).627) .230) . 2006.530 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th . 1996). Hayes et al..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 .530) . 2004. other organochlorines. and leukemia have also been inconclusive (ADSDR. Calle et al. have not been consistently demonstrated (Beard.106-.01) .051 (<LOD-.p’-DDD and p.220) .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.086 (.150-... Snedeker.330-4.200 (.130 (<LOD-.108 (.260) .140) . 2006).Organochlorine Pesticides chemicals are excreted in breast milk. 1995.054-.p’-DDE can produce anti-androgenic effects (Gray et al.106) < LOD < LOD .146 (.150 (<LOD-.065-.240 (. 2006. 2006). 2001). Studies of DDT exposure and pancreatic cancer.170 (. 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. 2002. 2002.400) .34) . 2006. 2001).075) 1.160-.170-. and seizures.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.128 (. overt signs of acute human toxicity include vomiting..048 (<LOD-. Gladen and Rogan.. Several reviews of cancer epidemiologic studies have concluded that a link between DDT and breast cancer is inconclusive (Beard.143) < LOD < LOD .132-.087 (.130 (<LOD-.071 (.095) < LOD . and o. premature delivery.570-4.62 (.105-. It is difficult to attribute outcomes in human studies solely to DDT because of potential co-exposure to other persistent organohalogen chemicals (e. Beard.084 (. 2000. Mariussen and Fonnum.

for males and females in the NHANES 19992000 subsample (Pavuk et al. mean serum levels of DDT and DDE in the U. Heudorf et al. population declined by about fivefold to tenfold. 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. and 03-04 are 18. 01-02. Stehr-Green. the lipid-adjusted geometric mean levels of DDT and DDE were each fivefold to tenfold higher than the 95th percentile and geometric mean levels.3. 2002. 2003). 1989)..Organochlorine Pesticides OSHA and a guidance established by ACGIH.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.html. and the most recent median levels for German adults and children are similar to levels in this Report (Becker et al. mean DDE levels were about fivefold higher among women of southern Spain exposed by virtue of Serum p.. and 7. 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. In a population-based sample of men and women from eastern Slovakia. Declining DDE levels over time have also been observed in the German population.. 2004). EPA at: http://www.7-119) 113 (100-140) 93. 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.gov/ toxpro2.p’-DDT) as a possible human carcinogen.. Fourth National Report on Human Exposure to Environmental Chemicals 91 . Smith. Survey Geometric mean (95% conf.. respectively. compared to levels observed in this Report (Anderson et al.gov/ pestcides/ and from ATSDR at: http://www. 2003. so serum DDE levels may be an indicator of historic exposure and may be higher than DDT levels in the same person.e. 8. NTP considers DDT as being reasonably anticipated to be a human carcinogen.S. 1998. Link et al. Biomonitoring Information DDE persists in the body longer than DDT.6. Compared to females in the NHANES 1999-2000 subsample.cdc. Since the 1970’s..epa.7-129) 297 (256-344) 338 (303-376) 268 (217-332) 108 (97.0-114) 269 (213-323) 285 (249-337) 233 (175-314) 185 (141-237) 213 (172-253) 167 (123-240) 608 (530-693) 695 (595-798) 557 (420-734) 339 (243-479) 319 (282-389) 341 (211-586) 1260 (1030-1550) 1480 (1310-1700) 1270 (877-1800) 528 (339-812) 456 (343-722) 522 (313-1430) 2020 (1520-2730) 2550 (1980-3080) 1990 (1500-2470) 686 758 588 1278 1540 1368 20 years and older Gender Males 99-00 01-02 03-04 249 (220-283) 285 (252-323) 235 (193-288) 270 (226-322) 305 (273-341) 241 (193-301) 223 (182-262) 248 (222-285) 200 (164-262) 234 (184-302) 256 (219-297) 207 (161-281) 494 (380-578) 520 (441-627) 466 (331-653) 601 (492-711) 708 (567-844) 539 (386-735) 1010 (789-1130) 1160 (937-1360) 1000 (763-1400) 1350 (1040-1720) 1480 (1410-1710) 1250 (813-1900) 1430 (1080-2160) 1900 (1580-2490) 1610 (1210-2320) 2210 (1570-2810) 2670 (1940-3300) 2010 (1500-2450) 937 1069 955 1027 1229 1001 Females 99-00 01-02 03-04 Race/ethnicity Mexican Americans 99-00 01-02 03-04 674 (574-792) 652 (569-747) 444 (362-545) 295 (241-362) 324 (262-400) 262 (233-295) 217 (189-249) 253 (226-284) 208 (165-263) 624 (545-701) 561 (455-690) 373 (283-522) 251 (199-313) 248 (223-296) 216 (173-267) 194 (162-238) 225 (203-254) 177 (148-238) 1350 (1090-1660) 1400 (1050-1950) 875 (608-1170) 668 (492-874) 762 (583-999) 589 (453-747) 438 (355-507) 463 (402-558) 417 (302-564) 3090 (2040-4950) 4110 (2520-6550) 2150 (1520-2470) 1850 (1040-2220) 1620 (1180-2980) 1620 (1130-2310) 825 (647-1010) 1150 (878-1340) 907 (574-1480) 4950 (3070-9350) 7080 (3080-15600) 3290 (2380-9240) 2300 (1560-5680) 3260 (1270-6900) 2860 (1880-3440) 1160 (1010-1350) 1640 (1410-1940) 1490 (909-2300) 657 566 457 416 515 487 732 1053 888 Non-Hispanic blacks 99-00 01-02 03-04 99-00 01-02 03-04 Non-Hispanic whites Limit of detection (LOD.6 (81.atsdr. 2002. see Data Analysis section) for Survey years 99-00. In general.. 2004). respectively. 1991).S. More information about external exposure (i. environmental levels) and health effects is available from the U.8. 2005). IARC classifies DDT (p..S. levels of DDT and DDE increase as a person ages as a result of cumulative exposure (ATSDR. population from the National Health and Nutrition Examination Survey.

p’-DDT were below the limits of detection.37-4.56-2.76) 1.18-1.07) 1.97 (3.4) 13.534-.06) 1.13 (1.9 (26.30 (1.80) 1.25) 8. Consumers of Great Lakes sport fish had mean serum DDE levels that were only slightly higher than nonconsumers.8 (13.44) 1.51) 1.13) 4. 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.35) 1.4) 9.2 (9.02 (2.00 (6.27) 3.87-16.9) 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 3.23 (7.24-17.14) 2. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.04 (6.72) 1.635) 1.60-13.52 (1.37-16.91 (6.90) 22. 2004).01-1.05 (3.12 (6.79) Selected percentiles ( 95% confidence interval) Sample 95th 11.20 (.34) 2.01-11.25 (1.76) 1.01) 1.03-4.8 (9.63 (1.16-1.91-2.63 (1.71) 12.01) 1.516 (.27-1.48-4.80) 3.34) 6.56-6.3) 16.82 (1.59 (1.47 (1.39-2.18-1.54 (1.30 (1.71 (5.6 (9.31-12.17 (3.25 (.419-.18) 1.6) 8.8-90.34-3.84-3.22 (7.3-43.32) 1.06) 3.2) 19.80 (2.4 (8. 2004).10-5.69 (.57 (1.71) 32.26-10.5) 16. 309 versus 268 ng/g lipid.81 (7.58) 1.965-1.611-1.68) 2.6 (7.49 (6.81 (1.46 (1.0) 657 566 457 416 515 487 732 1053 888 Non-Hispanic blacks 99-00 01-02 03-04 99-00 01-02 03-04 Non-Hispanic whites 92 Fourth National Report on Human Exposure to Environmental Chemicals .51 (1.24) 1.66) 1.54-7.1) 12.860 ng/L) and DDE (about 14.5) 22.14-9.6 (17.63 (6.31 (1.09-1.488-.32-1.72) 1.22-1.9-17. 1989).36) 3.03-1.3) 13.46 (1. less than one percent had detectable serum levels of o.29 (1.12 (.37-10.2 (19.85-4.14-1.26-2.81) 11.600) .9-38.25-16.8) 686 758 588 1278 1540 1368 20 years and older Gender Males 99-00 01-02 03-04 1.385-.83 (1.726) .91-3.64) 3.07 (5.21) 3..41 (1.53-15.00-1.38 (1.6) 9.2 (9.77 (1.45 (1..81-18.65) 1.5) 7.6 (8.07) 1.01-15.14 (1.39) 1.870 (.40-4.68-4.1) 7.54) 8.646) .32-9.40-8.57-3.92) 1.02) 1.69) 4.75) 2.69) 8.6) 12.12-1.90-8.7) 16.5) 10.490 ng/L) were found many years ago in a study of pesticide workers in Argentina (Radomski et al.65 (1.43-4.32-1.36-2.93 (7.1) 40.01-5. o.85 (1.36-11.59) 3.0 (12.63-15.6) 13. interval) 1..56-3.8) 15.61-2.34 (7. In a subsample of NHANES II (19761980) participants.41-12.4-19.84 (3. High mean levels of whole blood DDT (about 3.796 (.7) 9. 2001-2002 and 2003-2004 subsamples.10-1.7-19.Organochlorine Pesticides nearby agriculture (Botella et al.50-17.51-49.88 (2.16 (2.79) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 .61 (1.890-1.55-9.45 (1.456 (.30-1.1 (9.91) 3.0) 2. which is similar to the overall geometric mean of 260 ng/g lipid in the NHANES 1999-2000 subsample (Bloom et al.26 (1.21) 90th 7.53 (2.18 (6.76-3.30-1.85-10.62-6.88-35.1 (8.31-2.7) 13.36 (3.75 (8.680-1.22) .7-20.96) 1.6) 11.99) 1.59 (1.17-3.96) .8 (13.34-11.9 (15.19) 4.25-14.590 (.78 (4. serum levels of o. 2005).79) 4.11-1.46-2.57-2. Survey Geometric mean (95% conf.820-1.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.4) 14.97-4.69 (2.57 (1. Serum p.15-4.75) 6.87 (5.2-32.25) 1.10) .01-1.9) 7.04-1.70) 1. considerably higher than levels in this Report (Smith.14) 2.57) 2.0) size 1964 2298 1956 Total years 99-00 01-02 03-04 50th 1.58) 1.76 (2. 1971).49 (1.68 (2.53) 7.52 (3.69 (1.75) 1.p’-DDE in serum does not mean that the level of the chemical causes an adverse health effect.81-5.47) 3.57-13.52-6. Workers involved in production or application of DDT developed neurologic abnormalities associated with blood levels around 100-300 mg/L.51-8.S.557) 1.6) 9.53) 1.37 (1.43-8.66) 1.994-2.7-48.p’-DDT. population from the National Health and Nutrition Examination Survey.730) .p’-DDT.2 (6.00 (.56) 2.40-4.2) 26.7 (8.92 (3.37-1.49) 8.66) 4.32 (1.963-1.59 (4.51-15. In the NHANES 1999-2000.66-17.10) 2.4 (12.51) 3.28) 1.82) 1.5) 5. or p.43 (5. 1991).500-. 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 (3.24 (1.55 (2.3 (8.57 (3..80) 1.38 (1.66-2.18-4.75 (4.430-.26) 3.59) 6.49 (1.40 (3.66) 3.520 (.18-3.561 (.623 (.11 (2.39 (3.02-8.58) 75th 3.64-2.77 (1.33-1.39-1. Finding a measurable amount of p.6) 9.05) 1.00) 7.6) 9.8 (14.50 (2.70-3.0 (9.3 (9.13-2.32 (1.01-11.48 (6.19-14.71 (6.43-4.66-4.3) 10.p’-DDT (Stehr-Green.36-1.

see Data Analysis section) for Survey years 99-00. 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. Survey Geometric mean (95% conf. < LOD means less than the limit of detection.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. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Fourth National Report on Human Exposure to Environmental Chemicals 93 . population from the National Health and Nutrition Examination Survey. and 03-04 are 20. respectively.Organochlorine Pesticides Serum o. 01-02.8. 17. which may vary for some chemicals by year and by individual sample. and 7.7.S.4.

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

Organochlorines and breast cancer risk.358:110-114. 4/21/09 Gladen BC.111:349355.155(4):313-322. Gray KA. Vorojeikina DP. Needham LL. Moysich KB. Exposure of women to organochlorine pesticides in Southern Spain. Environ Res 2004. Cerrillo I. Bhatnagar VK. lindane (g-HCH). Zoellner I.85:504508. Furr J. Ostby J. Hum Reprod Updat 2001. Maternal DDT exposures in relation to fetal and 5-year growth. Darnerud PO. J Assoc Off Anal Chem 1988. Rogan WJ. Savitz DA. et al. Zhou H. Klebanoff MA. et al. August 2008. Rivas A. and polythelia among male offspring. Jusko TA. April 1982 to 1984. Baker RJ. Krause C. Environ Health Perspect 2003. et al. Association between maternal serum concentration of the DDT metabolite DDE and preterm and small-for-gestational-age babies at birth.72:261265. Brock JW.cdc. Bull Environ Contam Toxicol 2004. Link B. Organochlorines in Swedish women: determinants of serum concentrations. DDE. et al. Biomonitoring of persistent organochlorine pesticides. Chemosphere 2004. Gladen BC. et al. Cueto C. Parks L. Toxicological profile for DDT. Profiles of ortho-polychlorinated biphenyl congeners. Hayes WJ. 4/21/09 Anderson HA. Hurd C. Available at URL: http://www. et al. Becker K.1-dichloro2. Longnecker MP. Vena JE. Chen CW.97(2):178192. Current internal exposure to pesticides in children and adolescents in Germany: blood plasma levels of pentachlorophenol (PCP). Durham WF. Olea-Serrano MF. Jr. Longnecker MP. et al. Beard J. Hanrahan L. hexachlorobenzene. The Great Lakes Consortium. Bates MN. Herrman T.58:1185-1201. and Mirex among male Lake Ontario sportfish consumers: the New York State Angler cohort study. a biostable metabolite of dichloro(diphenyl)trichloroethane (DDT). CA Cancer J Clin 2002. Lepom P. and other chemicals. Swanson MK. Crespo J. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Saiyed HN. Transcriptional activation of the human estrogen receptor by DDT isomers and metabolites in yeast and MCF-7 cells. Willman EJ. Gray LE Jr. Epidemiology 2006. Environ Res 2005. Henley SJ. Kashyap R. Fourth National Report on Human Exposure to Environmental Chemicals 95 . Eriksson P. Piechotowski I. Talts U. Kaus S.2-bi(p-chlorophenyl)ethylene and risk of cryptorchidism. Atuma S. Lancet 2001. Thun MJ. Int J Hyg Environ Health 2003. selected elements. DDT and human health.52:301-309. Arnold SF.7(3):248-264. Am J Public Health 1995.96:34-40. Neonatal exposure to neurotoxic pesticides increases adult susceptibility: a review of current findings. and dichloro(diphenyl)ethylene (DDE).17(6):692-700. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. dichlorodiphenyldichloroethylene. Garrett N. Needham LL. Klebanoff MA. Botella B. The effect of known repeated oral doses of chlorophenothane (DDT) in man. Olson JR. Angerer J. Biochem Pharmacol 1997. Prenatal DDT exposure in relation to anthropometric and pubertal measures in adolescent males. Environ Health Perspect 2004. Neurotoxicol 2000. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. Effects of environmental antiandrogens on reproductive development in experimental animals. Environ Health Perspect 1998.162:890-897. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. Seiwert M. Food and Drug Administration (FDA). Patterson DG Jr. and HCB residues in human blood in Ahmedabad. Brock JW. Needham LL. et al. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. Hediger ML.106(5):279-289. HCH. Int J Hyg Environ Health 2002. Schulz C. Frumkin H. dietary intakes of pesticides.206:485-491. Jr. Gabrio T. Charles MJ. Greenfield TA. India.71(6):1200-1209.atsdr.cfsan. and DDD [online]. Chemosphere 2005. Falk C. Katz SH. Barr DB. Olea N.21(1-2)37-48.gov/ toxprofiles/tp35. et al. Koepsell TD. Glynn AW. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Notides AC. Drexler H. Bloom MS. Calle EE. Klebanoff MA. Aune M.355:7889.205:297-308. Heudorf U. FDA total diet study. Levels of DDT.fda.53(8):1161-1172. Available at URL: http://www. Ellis H. Maternal serum level of 1. Am J Epidemiol 2002. Sci Tot Environ 2006. Granath F. Davis MD. Buckland SJ. Gunderson EL. Wolf CJ.gov/~dms/ pesrpts. Bjerselius R.. DDE and shortened duration of lactation in a northern Mexican town. Paepke O.112(17):1761-1767.html. Kulkarni PK. Olson J. JAMA 1956. September 2002.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Zhou H. Lambright C. Zaidi SS. hypospadias.54:1431-1443. Burse VW.html.

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

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

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

Sodium and GABA-activated channels as the targets of pyrethroids and cyclodienes. et al. Perinatal toxicity of endrin in rodents. Saleem M. Chernoff N. et al. Cerrillo I. Fetotoxic effects of prenatal exposure in hamsters.64-65 Spec. Smith AG.13:155-165. Ginsburg KS. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Rowley DL. Available at URL: http://www. Chemosphere 2004. Handbook of Pesticide Toxicology. 4/21/09 Bates MN. et al.cfsan. Environmental Health Criteria 130. Rivas A. Patterson DG Jr. Rogers E. Roy ML. Garrett N. Buckland SJ. Rab MA. Academic Press. Cancer Epidemiol Biomarkers Prev 2000. Burse VW.9:1357-136. Schulte P.21:141-150. 1992. New York. 4/21/09 Kavlock RJ.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Gray JA. Food and Drug Administration (FDA). Andersen A. Toxicology 1979. Pediatrics 1987. Ward EM. 4/21/09 International Programme on Chemical Safety (IPCS).79(6):928-934. Serum organochlorine levels and breast cancer: a nested case-control study of Norwegian women. Narahashi T. Exposure of women to organochlorine pesticides in Southern Spain. No:429-436.fda. Frey JM. Liddle J. Fetotoxic effects of prenatal exposure in rats and mice.gov/~dms/ pesrpts.cdc. II. Toxicology 1981. Jr and Laws ER. Jr. Whitehouse DA. Sokal D. Vol. 2 Classes of Pesticides. Botella B. et al. Available at URL: http://www. Turner W. Grajewski B. August 1996.96:34-40. Chernoff H. Patterson DG Jr. Olea N. Hanisch RC. Environ Res 2004.htm.inchem. In Hayes WJ. Available at URL: http://www.atsdr. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Toxicological profile for endrin [online]. I. Toxicol Lett 1992. Olea-Serrano MF. Crespo J. Chlorinated Hydrocarbon Insecticides. pp. Inc.gov/toxprofiles/tp89. Endrin [online]. Ellis H. August 2008. Eds. Fourth National Report on Human Exposure to Environmental Chemicals 99 .org/documents/ehc/ehc/ ehc130. Kavlock RJ. 1991.54:1431-1443. Convulsions caused by endrin poisoning in Pakistan. Gray J. Hanisch RC. Gray LE. 731-915. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. Perinatal toxicity of endrin in rodents.html.html. Needham LL. Gray LE. Hardjotanojo W.

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) 24.7-16. Urinary metabolites include pentachlorophenol (PCP). EPA cancelled its use in 1984. 100 Fourth National Report on Human Exposure to Environmental Chemicals .5-trichlorophenol (2. 1988).5 (13.9 (25. water.3-22.4 (18.6) < LOD < LOD 25.9) < LOD < LOD 19.6) < LOD < LOD 26.8.8 (26. It is a persistent chemical and bioaccumulates in both aquatic and terrestrial food chains (ATSDR. Therefore.5 (13.6-19.3-20.0-16. 1997).1) * * 15.3) < LOD < LOD 20.7-22.3 (14. < LOD means less than the limit of detection. Workers in chemical manufacturing industries may be exposed to HCB via inhalation or dermal pathways.1 (14.7 (15. and accumulates in fatty tissues where it persists for years.5-18.2 (14.4 (11. 2.5-14.7-15.2 (14. HCB has been detected in fewer foods since the 1980s (FDA..2) < LOD < LOD 13. HCB is well absorbed after oral administration.6-trichlorophenol (2.7-30. breast milk is an additional route of elimination in nursing women.3) * * 15.9-20. HCB may be created as either a byproduct or an impurity in the manufacturing process for certain chemicals and pesticides.4 (22. and 03-04 are 118. and 7.0) * * 15. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD 28. 2002)..5-15. these metabolites can also be produced after exposure to other chlorinated compounds (Kohli et al.6-26.0-28.2) < LOD < LOD 29.0) < LOD < LOD 15.9-17.5) < LOD < LOD 18. Although it is not manufactured as an end-product in the U.6 (24.0.9) < LOD < LOD 15.4. 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.4) < LOD < LOD 22.S.5 (14. and foods with a high fat content.4) < LOD < LOD 19. air.7) < LOD < LOD 24.8 (15. HCB is slowly metabolized.9) < LOD < LOD 28.8-15.2-15.0) < LOD < LOD 24. respectively. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.4. and has been detected in soil.2-15.4.2-31.9-30.8) size 1702 2277 1961 Total years 99-00 01-02 03-04 50th < LOD < LOD 14.6) < LOD < LOD 24. 01-02.6 (21.0 (25.5-TCP) and 2. primarily as a fungicide and seed treatment until the U.3) < LOD < LOD 29.0 (18. The general population may be exposed to HCB through diet.9 (14.7 (27. 1976).5-14.1 (17.3 (16. Gunderson.2 (24.7-29.1-16. and elimination occurs by renal and fecal routes. particularly by consuming fish. 31. 2008.0 (18.S.1) < LOD < LOD 15.3 (20.0) < LOD < LOD 15.3 (22.7-26.8) 583 554 460 350 511 488 636 1052 888 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.9-24.S.9) < LOD < LOD 16.7) < LOD < LOD 75th < LOD < LOD 90th * * 15. 118-74-1 General Information Hexachlorobenzene (HCB) was used from the 1930’s to the 1970’s in the U.5-33. wildfowl.9) 19.7-21.5-15.9-15.3 (12.7 (15.1 (13. and sediment (Barber et al.1 (14.9 (25. which may vary for some chemicals by year and by individual sample. Hexachlorobenzene has entered the environment as a result of industrial activities and pesticide applications.6-44.S.4.6 (23..7) * * 14.4) < LOD < LOD 33.2 (13.0 (14.9) < LOD < LOD 20.3 (22.4-16.3-26.6) < LOD < LOD 14.4 (18.6-33. or game taken from areas with HCB contamination. distributes widely throughout the body.4-15.0-19. see Data Analysis section) for Survey years 99-00. population from the National Health and Nutrition Examination Survey.8 (22.9 (23.1-20.8) < LOD < LOD 27.4. Survey Geometric mean (95% conf.4) < LOD < LOD 18.2 (17.9) < LOD < LOD 20.6) < LOD < LOD 26..6-TCP) (To-Figueras et al.4) < LOD < LOD 14.0-25.4) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * 13.7 (19.9-32. 2005).Organochlorine Pesticides Hexachlorobenzene CAS No.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 * * 14.7-16. The FDA dietary surveys have shown that over time.4) < LOD < LOD 23.6-32.

157 (.173) < LOD < LOD .S.epa. More information about external exposure (i.111-. environmental levels) and health effects is available from the U.077-. Human health effects from HCB at low environmental doses or at biomonitored levels from low environmental exposures are unknown. In humans.159-.069) < LOD < LOD . anorexia.118) < LOD < LOD .148-. and the FDA has established a bottled water standard for HCB.123 (..174-.123 (.062-.129) < LOD < LOD .100) < LOD < LOD .171 (. as well as hypertrichosis. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD . immunologic abnormalities.152) < LOD < LOD .120 (.163 (.114-. 1960).225 (.081 (.064 (.083) < LOD < LOD .087 (. and weakness.182 (.203) < LOD < LOD . 2002).086-.167) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * .086) < LOD < LOD .147-.html.Organochlorine Pesticides chemical. IARC classifies hexachlorobenzene as possibly carcinogenic to humans.156 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.gov/toxpro2.107) < LOD < LOD .186 (. The U.212) size 1702 2277 1961 Total years 99-00 01-02 03-04 50th < LOD < LOD .226) 807 1058 957 895 1219 1004 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * .085) * * . a consequence of these heme abnormalities is a condition known as acquired porphyria cutanea tarda.088-.S.190 (. reproductive and developmental toxicities. which may vary for some chemicals by year and by individual sample.155) < LOD < LOD . Fourth National Report on Human Exposure to Environmental Chemicals 101 .125 (.135-.147 (. 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. 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.090 (.078 (.065 (.095-.089-.258) < LOD < LOD .130) < LOD < LOD .091-.127-. and many died before 2 years of age (Peters et al.104 (.072-.079 (. arthritis.145-. population from the National Health and Nutrition Examination Survey. very high.073-. EPA has established a drinking water standard. and NTP classifies hexachlorobenzene as reasonably anticipated to be a human carcinogen.169-.098 (. Survey Geometric mean (95% conf.163) < LOD < LOD .e.082-.102 (.167 (.094) < LOD < LOD . With chronic exposure.095) * * .122) < LOD < LOD . 1982.157-.095 (.107-.gov/pesticides/ and from ATSDR at: http://www.140 (.095) < LOD < LOD 75th < LOD < LOD 90th * * .090-.090 (.069) * * . acute doses produce central nervous system depression and seizures. ACGIH has developed workplace exposure limits for HCB.113-.111) < LOD < LOD .179 (.126) .178-. EPA at: http://www. This condition.121 (.089-.095 (..092 (.223) 591 747 588 1111 1530 1373 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * .097) < LOD < LOD . HCB interferes with normal heme synthesis.094 (.092-.118-. thyromegaly.115 (.163-.176) < LOD < LOD .S. Infants were exposed transplacentally and through breast milk. Chronic feeding studies in animals have demonstrated kidney injury. Schmid.191 (.160 (.203) < LOD < LOD .141) < LOD < LOD .060-.088-.123 (.099) < LOD < LOD .081-.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.118-.132) < LOD < LOD .176-. and liver and thyroid cancers (ATSDR.102) < LOD < LOD .099) < LOD < LOD .088-.145-.143-.097 (.099) < LOD < LOD . which is manifested by increased deltaaminolevulinic acid synthase activity and decreased uroporphyrinogen decarboxylase activity.092 (.cdc.097) .atsdr. Biomonitoring Information Serum concentrations reflect the body burden of HCB.086-.114-.175) < LOD < LOD .109) * * .092 (.196) < LOD < LOD .085-.090 (.

Lecha M.110(8):835-838. Kaus S. levels. Organochlorines in Swedish women: determinants of serum concentrations.44 mg/L. factory workers chronically exposed to HCB and residents near the factory had serum HCB levels that were 150 to 50 times higher.54(3):203-208. et al. Eskenazi B. References Agency for Toxic Substances and Disease Registry (ATSDR). The metabolism of higher chlorinated benzene isomers.fda. Available at URL: http://www.205:297-308.. Granath F. Hexachlorobenzene in the global environment: emissions. Polychlorinated biphenyls and hexachlorobenzene in full-term neonates. Hexachlorobenzene content in human whole blood and adipose tissue: experiences in environmental specimen banking. Reference values updated. trends and processes. August 2008. Factors predicting organochlorine pesticide levels in pregnant Latina women living in a United States agricultural area. 1986. Krause C. 4/21/09 Glynn AW. Toxicological profile for hexachlorobenzene update [online]. Gocmen A. 2002. 2003).81(2):82-85. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Biomonitoring of persistent organochlorine pesticides. HCB detection in serum also was proportional to age. selected elements.html.349:144. Environ Health Perspect 2003. Temporal trends of organochlorine concentrations in umbilical cord blood of newborns from the lower north shore of the St. Becker K. Available at URL: http://www. 2002. Aune M. Finding a measurable amount of hexachlorobenzene in serum does not mean that the level of the hexachlorobenzene causes an adverse health effect. Seiwert M. Food and Drug Administration (FDA).. Lawrence River (Quebec. but overall. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Herrero C. Bertram et al. et al. Gunderson EL. April 1982 to 1984. Bjerselius R. Holland NT.cfsan. than the limits of detection (on a whole weight basis) in NHANES 19992000 and 2001-2002 (Herrero et al. Over the past two decades. Cripps DJ. J Assoc Off Anal Chem 1988. J Exp Sci Environ Epidemiol 2007. Arch Neurol 1982.58:1185-1201. but approximately five times higher than the overall geometric mean level in 2003-2004 (Becker et al.. Lackman. et al.135(4):400404.. Lepom P. 1999). Gabrio T. Chemosphere 2005. declines in background HCB levels ranging from around 50%90% have been documented in studies using cord blood (Dallaire et al. 2006). Int J Hyg Environ Health 2002. Environ Health Perspect 2002. Dewailly E. only 4. Schwartz JM. Piechotowski I. 2002) and among children (Link et al.. In Spain. 2005.. and the geometric mean concentration of HCB in whole blood was 0. 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. Jones KC. 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. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population.. Sci Tot Environ 2005. Bertram HP. FDA total diet study. 2002. 102 Fourth National Report on Human Exposure to Environmental Chemicals .Organochlorine Pesticides in the NHANES 1999-2000 and 2001-2002 subsamples. Kohli J. Residency near industrial or agricultural areas has been associated with higher serum HCB levels (Barber et al. Bradman et al. 2005). Barr DB.. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. In a representative sample of the 1998 German adult population.cdc. Laliberte C. Ozalla D. van Wijk D. et al.39(12):744-749. more HCB levels were quantified. Safe A. Dogramaci I. 4/21/09 Barber JL. Can J Biochem 1976. Lackmann GM. Lackmann. Darnerud PO. Dallaire F.71(6):1200-1209.gov/~dms/ pesrpts. Paepke O. Schulz C. Otero R. Biol Neonate 2002. Glynn et al. IARC Sci Publ 1986. Ayotte P.gov/ toxprofiles/tp90. 2002. lower than the limit of detection (on a lipid adjusted basis) in NHANES 1999-2000 and 20012002. 1989).17:388–399. Zoellner I. Sala M.atsdr. Muckle G. Urinary porphyrin excretion in a human population highly exposed to hexachlorobenzene. Peters HA. September 2002. Sweetman AJ. dietary intakes of pesticides. Bradman A. Jones D. Arch Dermatol 1999. and other chemicals. HCB levels were directly related to age.html.111:349355. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. distribution. Kemper FH. Herrman T. however. 2002). Bryan GT.77:173182.. Epidemiology of hexachlorobenzene-induced porphyria in Turkey: clinical and laboratory follow-up after 25 years. As a result of the lower limit of detection in NHANES 2003-2004. Agerelated increases of HCB in body fat and serum have been consistently noted in general population studies (Becker et al. Muller C. Link et al. Link B. 2005).. Canada). respectively. In the 1976-1980 NHANES subsample. Santiago-Silva M. Atuma S. Fenster L..9% of participants had quantifiable levels (Stehr-Green.

Demographic and seasonal influences on human serum pesticide residue levels. Otero R. et al. Metabolism of hexachlorobenzene in humans: association between serum levels and urinary metabolites in a highly exposed population. Cutaneous porphyria in Turkey. Barrot C. To-Figueras J. J Toxicol Environ Health 1989. PA.263:397-398. Environ Health Perspect 1997.27:405-421. Fourth National Report on Human Exposure to Environmental Chemicals 103 . Rodamilans M. N Engl J Med 1960. Stehr-Green. Santiago-Silva M.105(1):78-83.Organochlorine Pesticides Schmid R. Sala M.

4-45.3-85.8) 39.4) < LOD 9.7-166) 70.90-8.90-8.0-70.1) 31.0) 71. population from the National Health and Nutrition Examination Survey.2) 9.9-81.70-19.4) 21.9 (26. water. see Data Analysis section) for survey years 99-00.9 (62. exists in several isomeric forms.S.0-111) 70. gamma.1 (16. Lindane has a half-life of about two weeks in soils and water.7-96. EPA cancelled agricultural uses of lindane (ATSDR.5) 632 563 460 403 513 487 702 1051 887 Non-Hispanic blacks Non-Hispanic whites Limits of detection (LOD.3) 34. interval) 9.8) 27.8 (9.4 (8.7) 10.4) 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 21.8) 52.6 (10.30-11.7-69.6 (16.1 (21.7) 18. Technical grade HCH is a mixture of all four isomers.9) 45. and 7.8 (32.4-111) 84.09) < LOD Gender Males 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD 14.36.0-23.9-24.3-38.2-67.6-37.56-12.3 (26.1 (30.8 (10.Organochlorine Pesticides Hexachlorocyclohexane CAS No.6) 653 758 589 1240 1533 1370 20 years and older 10.4 (16.0 (33. beta.70 (8. particularly alpha and gamma have been detected widely in air.2 (34.0 (14.1) 71.4 (12. HCH does not bioaccumulate to an appreciable extent in plants (ATSDR.3 (42.66-12.0-20.5528.9 (50. In 2006.4) 901 1067 952 992 1224 1007 Females 11.2-87.5) 90th 42.89 (<LOD-9.76.7 (<LOD-16.6-18.1-49.1-27.2 (31.7) 56.80 (<LOD-14.3-56.6) 35.8-87.6-14.7 (13.5) 40.9-21.1-32.2) 142 (99.1 (27.0) 17.7) 73.0) 8. The gamma isomer. can be used as an insecticide and has been used to kill soil-dwelling and plant-eating insects.7-20.2-22.6) 18.0-70.0 (<LOD-12.5) 29.7 (53.8 (21. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.6) 36.7) < LOD < LOD < LOD < LOD < LOD < LOD 37.4-73.8) * * * * * * 15.4 (11.1-15.8 (64. containing about 64% alpha and 10%-15% gamma isomers.3) 37. and sediment as a result of historic production and use.8-19. See the section “What’s New” at the beginning of this Report for details.5 (37.8-16.43 (<LOD-9.70-12.8-199) 134 (85.5-29.7) 23.90) 7.3) 25.70 (6.9 (9.0) 7. and have been used either as fungicides or to synthesize other chemicals.7) 10.1-36.04-10.6-135) 69.46-11.8 (17.6-89.5 (8.7-69.1) 12.3 (62.2 (18. **In survey period 2001-2002.5) 14.9 (32.60-13.80 (6.0 (35. which may vary for some chemicals by year and by individual sample. so they can accumulate in fatty tissues of animals.9-51. the U.6 (22.87 (9.9 (40.8) 12. The other isomers can be formed during the synthesis of lindane. General population Serum beta-Hexachlorocyclohexane (lipid adjusted) Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U.1) 12.1) 13.2) 13. As pesticide applications of HCH were increasingly restricted or eliminated.0) 35.6) 50. each result has been multiplied by 1.6-42.4-50. and 03-04 are 9.2-17.9 (30.8 (23.S.4) < LOD < LOD < LOD 46.5 (43.68 (<LOD-10.5 (11. environmental levels declined.5 (14.5) 22.9 (11.5 (16.7 (62.6 (17.1-16.7-96.1-37.5) 11.9-178) 48.0 (19. respectively.8-54.50) 8. 2005).4 (50.45) < LOD Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 99-00 01-02** 03-04 16.1-32. 319-85-7 gamma-Hexachlorocyclohexane CAS No. 01-02.9-56.6-47.8-68.9) 15.6 (33.6 (40.6-20.7-26.5-123) 49.6) 47.2 (48.5) 67.S. and delta. HCH isomers.2-55.5) 16.8) 95th 68.2) 62.2-52. However.1 (9.6) 16.2 (9.4) 10.0 (37.7) 27. Lindane (1%) lotion and shampoo are available by prescription for singleuse application to treat human scabies and head lice.4 (52.9) 17.3) 51. soil.7) 32.1 (18.9-14. It is no longer produced or sold in the U.0 (8.4) 51. Survey years 99-00 01-02** 03-04 Geometric mean (95% conf.7 (35.2-46.5 (24. 6.9) 81.8) 7.2-98.7) 97.3 (13.2-20.2 (29. 2005).2 (50.1 (11. formerly referred to as benzene hexachloride.4) 11.61-12.6-62.7 (29. 58-89-9 General Information Hexachlorocyclohexane (HCH).1 (12.9) Selected percentiles ( 95% confidence interval) Total * * 50th < LOD < LOD < LOD 75th 19.0-34.4) 27.7 (30. 104 Fourth National Report on Human Exposure to Environmental Chemicals .2) 36.7 (25. including alpha.0-21.8.1 (9.3 (42. < LOD means less than the limit of detection.8 (33.8) < LOD 10.3) 14. HCH isomers are lipophilic.20-16.4) 44. commonly known as lindane. 608-73-1 beta-Hexachlorocyclohexane CAS No.2-42.0) 41.

058 (<LOD-.048 (<LOD-..139 (.140 (.410-.086) < LOD < LOD < LOD < LOD < LOD < LOD .680) .144 (.110) .050 (.170-.250 (.37) 1.118 (.064) . Acute high dose toxicity in rodents affects the central nervous system producing decreased activity.058) < LOD Gender Males 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD . 2002).083 (.250) .120) .119) .081-.110-.390-.587) 653 758 589 1240 1533 1370 20 years and older .210-.062 (.319) . FDA pesticide monitoring program has shown a temporal decline in the detection of lindane..412 (. Rogan.05) . Acute high doses of lindane after ingestion or excessive skin application of the 1% lotion have produced seizures in humans.120 (.070-.103 (.100) .072 (.280-.190) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.840) .070) .400) .220-.140) .057 (<LOD-.050-.175 (.064 (. and nephropathy developed (IPCS.050 (.234 (.230-.051 (<LOD-.600) .220) .254) 95th .150 (. Distribution is mainly to fatty tissues.620) .330-.191-.210) .310) .146-.460 (.250 (.050 (<LOD-. 1971.360 (.062 (.100 (.410) .092 (. enlarged livers.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 .140) .080-.700) .103-.210 (.050) .190-1.120-.160) .080-. **In survey period 2001-2002.068-.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.140) .5528. population from the National Health and Nutrition Examination Survey.01 (. resulting in a half-life of about seven years.080 (.300-.222 (.124-.380 (.057-.220 (. 1981). for lindane. 2008.S.050-.130) .070 (.065 (.480) . HCH crosses the placenta and is also excreted in breast milk (Radomski et al.710) .065 (.190-.260-.120-.470 (.221-..100-.350 (.080) * * * * * * .080-. which may vary for some chemicals by year and by individual sample. When animals were chronically fed lindane at high doses. After dermal application of lindane 1% lotion.050-. and FDA has established a bottled water standard and food residue tolerances for lindane.32) .080 (. and seizures.294-.420-. 1986).210 (.521 (. hepatic enzyme induction. HCH isomers are absorbed after inhalation.057) < LOD Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 99-00 01-02** 03-04 .270 (.290 (.330 (.260) .100 (.051-.370-.078 (.180-.060) .331 (.050-.103) 90th .814) .410) . from 6% of samples in 1982-1984 to 2% in 1994 (FDA.560 (. Survey years 99-00 01-02** 03-04 Geometric mean (95% conf.080) .110) .214) .260) .174) .118-. and memory loss (Nigam et al.191-.372 (. Gunderson 1988). The beta isomer accumulates in fatty tissues and is metabolized more slowly. Human health effects from HCH isomers at low environmental doses or at biomonitored levels from low environmental exposures are unknown.090 (.131-.580 (.382-. the serum half-life was about 20 hours among children (Ginsburg et al.Organochlorine Pesticides exposure to HCH is through the diet.360) .620-1. Fourth National Report on Human Exposure to Environmental Chemicals 105 .661) 901 1067 952 992 1224 1007 Females .047-. Pesticide applicators or agricultural workers could be exposed to HCH by inhalation and dermal pathways.450-.910 (.216 (.410 (.390 (.350) .057-.125) < LOD < LOD < LOD .360-.096) .173-. HCH isomers are metabolized to chlorophenol metabolites that are excreted in the urine (Angerer et al. tremors.170-. interval) .250 (.480 (.280-. 1996. each result has been multiplied by 1.510) .089-.200-. The U.160 (..200 (.297-.120) .220-.290) .069) .100-.130-.290 (.450 (. Workers who directly handled HCH have complained of headache.091) .501) . respectively.090 (. See the section “What’s New” at the beginning of this Report for details.090 (. or dermal exposure.250-. 1977).150-.290) .150) .310) .690) .120 (.110) .240-.250-.340-. Saxena et al.287 (. ataxia.130 (.580-1.120 (.070-. IARC classifies Serum beta-Hexachlorocyclohexane (whole weight) Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U.090-..200-.089) .073-.050 (<LOD-.100-.160-.083) .040-.450) .059-.310 (.098 (.290 (. ingestion.470) .077) < LOD .100) . probably by blocking inhibitory neurotransmitters in the central nervous system.S. paresthesias.442 (.281 (.240 (.066) Selected percentiles ( 95% confidence interval) Total * * 50th < LOD < LOD < LOD 75th .120-.056-.570 (.067 (.480 (. OSHA and ACGIH have established workplace standards and guidelines. U.167 (.190) .S.056-.077) < LOD . EPA has established a drinking water standard.460) .560) .067) .404) .070 (.320 (.308-. 1983).244-.400) .150) .340) .070-.305) .

S.epa.. and 03-04 are 14.cdc. 2005. which may vary for some chemicals by year and by individual sample. In an earlier (1996-1997) sample of German children. serum levels of lindane were generally below the limits of detection. environmental levels) and health effects is available from the U.atsdr.8.. 1989. male sex. 1998). respectively. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Link et al. Stehr-Green.. respectively. 106 Fourth National Report on Human Exposure to Environmental Chemicals . 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.e.gov/toxpro2.. Sturgeon et al. Kutz et al. < LOD means less than the limit of detection. 2002. Stehr-Green. and 2003-2004. which were considerably lower (as much as twentyfold) than mean levels reported in small studies of adults in Spain (Botella et al. 2005. studies in populations with environmental exposure have reported lindane levels below the limit of detection in most persons (Anderson et al. 2004. 1989).Organochlorine Pesticides hexachlorocyclohexane isomers as possibly carcinogenic to humans. 2004) and India (Bhatnagar et al. 10. In NHANES 1999-2000.html. 1991. Survey Geometric mean (95% conf.. Bates et al. Becker et al.5. 1991. Kutz et al. EPA at: http://www. and 7. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD < LOD size 1799 2280 1960 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD < LOD 90th * * * Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 660 758 593 1139 1522 1367 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 863 1060 952 936 1220 1008 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 631 563 461 380 509 490 646 1045 884 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.S.... Radomski et al. In populationbased studies of New Zealand adults and German adults and children. In recent years. aged 9-11 years.5. and a diet that includes meat (Becker et al. Studies of general populations have shown declining beta-HCH levels since the 1970s (ATSDR. and NTP classifies hexachlorocyclohexane isomers as reasonably anticipated to be human carcinogens. see Data Analysis section) for Survey years 99-00. 01-02. were similar to the 95th percentiles in this Report.. 2002). beta-HCH may be detected in a higher percentage of the general population than are the other HCH isomers. the maximum and 95th percentile beta-HCH values.gov/pesticides/ and from ATSDR at: http:// www.. 1971. population from the National Health and Nutrition Examination Survey. 2004). 2001-2002. Biomonitoring Information Because of its longer half-life. 1998. Additional factors associated with higher beta-HCH levels include rural residence. More information about external exposure (i. older age...

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

20(2):186-193. 2002. gov/toxprofiles/tp43. Exposure of women to organochlorine pesticides in Southern Spain.9(4):417-424. Siddiqui MKJ. Bai KM. Saxena MC. Karnik AB. Bates MN. Ellis H. Atuma S.72:261265.120:1-82. and other chemicals. HCH. India. 4/21/09 Anderson HA. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. available at URL: http://www.atsdr. Toxicological profile for hexachlorocyclohexanes update [online]. Environ Res 2004. Gunderson EL. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Pesticide residues in food-2002-Joint FAO/WHO meeting on pesticide residues. Becker K. Lindane. Brinton LA. J Toxicol Environ Health 1989. Krishna Murti CR. Darnerud PO. Blood levels of organochlorine pesticides in Argentina: occupationally and nonoccupationally exposed adults. PA. Needham LL. Glynn AW. Potischman N. Metabolism of gammahexachlorocyclohexane in man.58:1185-1201. Reisch JS.cdc. Chemosphere 2005. Burse VW. International Programme on Chemical Safety (IPCS). et al. Rivas A. Bhargava AK.inchem. et al. Sturgeon SR.html. VI. Rothman N. Botella B. Aune M. Organochlorines in Swedish women: determinants of serum concentrations. Nigam SK.htm. Lepom P.91:998-1000. Serum hexachlorocyclohexane residues in workers engaged at a HCH manufacturing plant. et al. Zaidi SS. Saiyed HN. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. 4/21/09 Kutz FW. Kashyap R. Available at URL: http://www. Arch Pediatr Adolesc Med 1996.27:405-421. Seiwert M.52(1):59-67. 4/21/09 Ginsburg CM. Occupational exposure to hexachlorocyclohexane.cfsan. Int J Hyg Environ Health 2002.54:1431-1443. Stehr-Green. Paepke O. Absorption of lindane (g benzene hexachloride) in infants and children. Visweswariah K. Cancer Causes and Control 1998. Radomski JL. Olea N. selected elements. Schulz C. Bjerselius R. Bull Environ Contam Toxicol 2004. et al. Link B. Brock JW. Biomonitoring of persistent organochlorine pesticides. Granath F. Lowry W. Demographic and seasonal influences on human serum pesticide residue levels. Kulkarni PK. Toxicol Appl Pharmacol 1971. Environ Health Perspect 2003. Bhatnagar VK. J Assoc Off Anal Chem 1988. Falk C. Buckland SJ.150:981-990. Needham LL. dietary intakes of pesticides.111:349355. Serum concentrations of organochlorine compounds and endometrial cancer risk (United States). Olea-Serrano MF. Krause C. org/documents/jmpr/jmpmono/2002pr08. April 1982 to 1984. Olson J. et al. Raju GS. Astolfi E. Bottimore DP.48:127-134. Int Arch Occup Environ Health 1986. et al. Arch Toxicol 1981.106(5):279-289. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. children and newborn infants. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods.205:297-308.96:34-4Food and Drug Administration (FDA). Deichmann WB. Wood PH. The Great Lakes Consortium. 108 Fourth National Report on Human Exposure to Environmental Chemicals . et al. Hanrahan L. Crespo J. Rev Environ Contam Toxicol 1991. Organochlorine pesticides and polychlorinated biphenyls in human adipose tissue. Chemosphere 2004.gov/~dms/pesrpts. Kutty D. Rey AA. Angerer J. Maass R.57(4):315-320. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. Piechotowski I.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Needham LL. Majumder SK. Gabrio T. and HCB residues in human blood in Ahmedabad.fda. Patterson DG Jr.html. Available at URL: http://www. Int Arch Occup Environ Health 1983. August 2008. Pollutants in breast milk.71(6):1200-1209. Heinrich R. Levels of DDT. Zoellner I. Kaus S. Garrett N. Placental transfer of pesticides in humans. Environ Health Perspect 1998. Herrman T. J Pediatr 1977. August 2005. FDA total diet study. Cerrillo I. Rogan WJ.

10.1 (<LOD-65.1 (13.S. and foods. 1985.8) < LOD 15.0) * * * 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 19.1) 659 728 592 1194 1529 1359 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 16.5 (<LOD-42.6 (<LOD-108) 9. see Data Analysis section) for Survey years 99-00.8.7) 8.6-305) 15.70-24..4 (8. Mirex is not metabolized in the body.3) 887 1052 949 966 1205 1002 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 13.5.S.6) size 1853 2257 1951 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th 15.4) 617 548 459 398 500 484 688 1049 884 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. it is a highly persistent chemical in the environment.S. where it has a half-life of 12 years. 1995). resulting in exposure to newborns and nursing infants.2) 51.3-225) 15..70 (<LOD-15. especially those from persons living in the southeastern U.7 (12.2-230) 13.2 (7.70-40. where it was applied directly to soil and by aerial spraying.40 (<LOD-13. 1991).S. animals. 2385-85-5 General Information Mirex has not been produced or used in the U.6) 9. mirex was detected in human adipose samples.10-37.6 (<LOD-23.5-291) 11. or pesticide application.4) < LOD 15. Mirex is absorbed through the skin and from the gastrointestinal tract. (Kutz et al.Organochlorine Pesticides Mirex CAS No. aquatic organisms.0 (14. Mirex binds strongly to soil.3 (15. and 7.8 (<LOD-73. < LOD means less than the limit of detection.3) < LOD < LOD < LOD < LOD < LOD < LOD < LOD 15. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 57.4) < LOD 63. Mirex can cross the placenta and be excreted in breast milk. 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.5-82. EPA have issued public health advisories or warnings that fish from contaminated lakes and rivers may contain mirex.6 (<LOD-31. since 1977. Ingested mirex that is not absorbed is eliminated in the feces within about 48 hours. sediments.0 (12.1 (<LOD-104) < LOD < LOD < LOD < LOD 39. water.10 (<LOD-15.7) < LOD 66. after which it is widely distributed in the body and stored in fat. which may vary for some chemicals by year and by individual sample. and 03-04 are 14. Mirex has been detected in air. In studies conducted in the 1970’s and 1980’s. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.5 (9. Human health effects from mirex at low environmental doses or at biomonitored levels from low environmental Serum Mirex (lipid adjusted) Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U.3 (15. disposal.5-425) 40.S.1 (8. Mirex contamination of Lake Ontario and adjacent waterways has been well documented (ATSDR. 01-02.0-374) 11. Formerly.0 (<LOD-108) < LOD < LOD 50.5 (<LOD-115) 153 (30.6) < LOD < LOD < LOD < LOD 71.6. Some states and the U. Fourth National Report on Human Exposure to Environmental Chemicals 109 .7 (<LOD-47. population from the National Health and Nutrition Examination Survey.90-29. respectively. Occupational exposure is limited to workers at sites where mirex contamination is present. its major uses were as a flame retardant additive and as a pesticide to kill fire ants and yellow jackets in the southeastern U.4-230) 18. soil. Survey Geometric mean (95% conf.8 (12.

090-1.090-1. population from the National Health and Nutrition Examination Survey.7 ng/g of lipid.090 (<LOD-. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD . IARC classifies mirex as possibly carcinogenic to humans. developmental abnormalities including cataracts and edema in the offspring have been reported (ATSDR.8. 110 Fourth National Report on Human Exposure to Environmental Chemicals .062-.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 .256 (.100 (<LOD-.089-. 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. EPA has established environmental standards for mirex. In addition. which may vary for some chemicals by year and by individual sample.106 (.240) < LOD < LOD < LOD < LOD < LOD < LOD < LOD .73) .170-3.html.atsdr.059 (<LOD-.S.gov/toxpro2. 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.090 (<LOD-. The U.690) .070-1.106) < LOD . Smith.470 (.093 (.02) .054 (<LOD-. 1991).052-. 1989).140 (<LOD-.090-1.084) * * * 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 .170) size 1853 2257 1951 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .450 (.635) < LOD .080-1. and the FDA monitors foods for pesticide residue and has established an action level for mirex in fish tissue. environmental levels) and health effects is available from the ATSDR at: http://www.450) 1.310 (. Laboratory animals fed high doses developed liver enlargement and liver tumors. The geometric mean mirex levels of the Inuit mothers were 8... and 4. 2004).220 (<LOD-. as well as in a subsample of NHANES II (1976-1980) participants. More information about external exposure (i.110 (<LOD-.510) < LOD < LOD . 7.79) .470) .470) .170) 887 1052 949 966 1205 1002 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . reproductive toxicity included decreased fertility and testicular damage.100 (<LOD-.37) .610) < LOD < LOD < LOD < LOD .79) .92) .S. In samples obtained between 1994 and 1997. and NTP classifies mirex as reasonably anticipated to be a human carcinogen.e. 2005).410 (.430 (.102) < LOD < LOD < LOD < LOD .053-.41) .055-.108 (.170) < LOD .080-1.cdc.077 (<LOD-.064 (<LOD-.090 (<LOD-. and 2003-2004 subsamples.268) < LOD . 2001-2002. 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.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. Survey Geometric mean (95% conf. serum mirex levels were generally below the limits of detection (Stehr-Green. Biomonitoring Information In the NHANES 1999-2000.08 (.112 (.Organochlorine Pesticides exposures are unknown. 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..079 (<LOD-.220) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.370 (. 1995.

Moysich KB. et al. J Toxicol Environ Health 1985.97(2):178192. Olson JR.cdc. Gilman A. Toxicological profile for mirex and chlordecone [online]. 1994-1997 organochlorine compounds. The human body burden of mirex in the southeastern United States. Swanson MK. Smith AG.15:385-394. Carra JS. August 1995. Jr. Profiles of ortho-polychlorinated biphenyl congeners. PA. Inc.330:55-70. Bottimore DP. Stroup CR. J Toxicol Environ Health 1989. Strassman SC. 4/21/09 Bloom MS. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Chlorinated Hydrocarbon Insecticides. Stehr-Green. Handbook of Pesticide Toxicology. Circumpolar maternal blood contaminant survey. Leininger CC. Environ Res 2005. et al. 2 Classes of Pesticides.atsdr.27:405-421.120:1-82. Vena JE. Available at URL: http://www. 1991 pp. Sci Total Environ 2004. Demographic and seasonal influences on human serum pesticide residue levels. Watts DL. Vol. dichlorodiphenyldichloroethylene. Kutz FW. New York. References Agency for Toxic Substances and Disease Registry (ATSDR). Jr and Laws ER. Organochlorine pesticides and polychlorinated biphenyls in human adipose tissue.Organochlorine Pesticides effect. Kutz FW. and Mirex among male Lake Ontario sportfish consumers: the New York State Angler cohort study. 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. hexachlorobenzene. 731-915.html. Eds. In Hayes WJ. Van Oostdam JC. Hansen JC. Odland JO. Fourth National Report on Human Exposure to Environmental Chemicals 111 . Rev Environ Contam Toxicol 1991. Chashchin V. Dewailly E. Wood PH. Academic Press.gov/toxprofiles/ tp66.

40 (.6-trichlorophenol (2.0) < LOD 11.940-3. 2.57 (<LOD-15.0) 14.00 (2.9 (<LOD-121) 9.5-trichlorophenol (2. EPA.0) 2.30-40.0 (3. soils. Both chemicals have been detected in air.30 (.7.0) 2.20) < LOD 1. recent sampling of U.30-3.S.0 (4.40) < LOD 6.3. < LOD means less than the limit of detection. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.80) < LOD 1.90-33.980-3.4. other organochlorines.0 (4.4.30-27.00-3. 88-06-2 Metabolites of Organochlorine Pesticides and Other Environmental Chemicals General Information The chlorophenols.20-36.40) < LOD 4.30-44.4.5-Trichlorophenol Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. and polychlorinated benzenes (Kohil et al.6-TCP was also used as a wood preservative and may still be used in production of some fungicides (ATSDR.0) 2.00 (3.40 (2. including hexachlorobenzene and hexachlorocyclohexanes.0 (3.4.0) 2.0) 5. 112 Fourth National Report on Human Exposure to Environmental Chemicals .00-8.6-Trichlorophenol CAS No.0) < LOD 973 1178 1021 1319 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * . Environmental sources of these compounds include industrial discharges or run off from pesticide facilities or disposal sites. General population exposure may occur by ingesting contaminated food or water and by inhaling contaminated air.5TCP and 2. 1999).20) < LOD 5.0 (8.920-3.8-tetrachlorodibenzo-p-dioxin occurs during the synthesis of 2.0 (4.900-2.4.40 (1.0) < LOD 5. and sediments. Trichlorophenols are no longer manufactured commercially.4.0) < LOD 5.980-3.50 (2.71 (<LOD-8.60 (2. usually at herbicide production or waste incineration facilities. Occupational exposures.42 (<LOD-12.19 (<LOD-6. 95-95-4 2.4.9.0) 2. surface water.30) < LOD < LOD < LOD < LOD < LOD 1. 2006). Historically.60-18.4.4.5-Trichlorophenol CAS No.40 (1. 2.S.8) 21.6-TCP were used as intermediates in the production of certain pesticides.50 (1.40-18.Organochlorine Pesticides 2.9 and 0.50) < LOD 1.30) < LOD 4.6-TCP).40-11.0 (5. Survey Geometric mean (95% conf.27) 482 570 681 815 831 1112 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD 1.50-16.40 (2.60) < LOD 8. Small amounts of trichlorophenols also can be produced during combustion of natural materials and the chlorination of drinking water or waste water that contains phenols.60 (4.0) 2.40) < LOD 1. 1976).42 (<LOD-8.31 (<LOD-9.6-TCP in any of the samples (U.4.03) 9.5-trichlorophenol. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. public drinking water systems did not detect 2.27) 696 661 521 696 603 939 Limit of detection (LOD.30-27. are metabolites of several organochlorine chemicals.0) < LOD 21. interval) Selected percentiles ( 95% confidence interval) Sample 95th 16.950 (<LOD-1.60-8.60 (.0) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 1..30-27.4.0) < LOD 5. hexachlorobenzene.72) < LOD 1. Such workers would probably Urinary 2.63) 18.20) < LOD 90th 5.80 (1.40 (.00-3.0) < LOD 11. however.S.10-3. but they may be produced as by-products during manufacturing of other chlorinated aromatic compounds.40 (2.4.20-71. Exposure to trichlorophenols also may result from metabolism of lindane.40 (2.71 (<LOD-8. 1999).80-41.5-TCP) and 2.7) 24. may occur by inhalation or dermal routes.50-25. 2. Formation of 2.50 (. which may vary for some chemicals by year and by individual sample. population from the National Health and Nutrition Examination Survey.20 (4. Trichlorophenols have been detected in fish taken from waters near waste water treatment and industrial discharges (ATSDR.30-11.50-63.80 (2.27) 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.

93-11.81 (<LOD-9.62-20.67 (1.29 (1. was similar to the corresponding percentile for 6-11 year olds in NHANES 1999-2000 (Hill et al. Biomonitoring Information In the NHANES 1999-2000 and 2001-2002 subsamples.6-TCP levels at the 95th percentile were up to eight times higher than 3.4 (6.e. At lower doses.. but almost twenty times higher than 95th percentile values reported in German adults aged 18-69 years (Becker et al.4) < LOD 3.24) < LOD 5.4.05-8.33) < LOD < LOD < LOD < LOD < LOD 2.28-25.19-12.37) 696 661 521 695 603 939 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.44 (1.00) < LOD 4.75 (3.3 (5..8) < LOD 9.27-17.67 (1. More information about external exposure (i.4. urinary 2.78-19.3 mg/L in a nonrandom subsample from NHANES III (Hill et al. and other chlorinated compounds.15) < LOD 2.44 (. and lymphomas.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.11) 482 570 681 814 831 1112 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD 1.46 (1.88-16. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.4. Neither 2. furans.32) < LOD 4..53-3. Urinary 2. 1989). the 95th percentile urinary 2.13-13.95 (3.6-TCP had increased rates of hepatic tumors.4.9 (5.4.5-TCP among adults in this Report and in a nonrandom subsample from NHANES III (Hill et al.47-8. Human health effects from 2..1) 2.9) 12.7 (4.37-11.5-TCP.50) < LOD 2. The 95th percentiles for 2.4.24-11..4.78) < LOD 1.6-TCP were developmental or reproductive toxicants in animals (ATSDR 1999). Fourth National Report on Human Exposure to Environmental Chemicals 113 .68 (<LOD-8. recent small studies have not demonstrated increased exposure to trichlorophenols in workers who dredged contaminated soils or incinerated waste materials (Agramunt et al. 1995) and up to 19 times higher than the 95th percentile value of 1.820-2.11) size 1994 2496 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD 75th 2.90 (4. Radon et al. 7. IARC classifies combined exposures to polychlorophenols. as being possibly carcinogenic to humans.24 (3.69-18.3) < LOD 973 1178 1021 1318 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .00-19.57 (3.3 mg/L reported in German adults aged 18-69 years (Becker et al.6-TCP as reasonably anticipated to be a human carcinogen.74) 11.4. leukemias.html.5) < LOD 12.4) 5.60-3.68-4.8 (5. population from the National Health and Nutrition Examination Survey.gov/toxpro2....6) 4.6-TCP.78 (3. However.83-12. which includes trichlorophenols.1 (<LOD-58.4.2 (2. 2003).4. Survey Geometric mean (95% conf.4.0 mg/L.4.8) 4. interval) Selected percentiles ( 95% confidence interval) Sample 95th 11.75 (<LOD-6.64 (4.0) 7. 1995) were similar. 2003).19-4. 2003.24) < LOD 1.49 (1.05-17. 2004).4.980 (<LOD-1.43) < LOD 12.S.80 (1.4) < LOD 3.5-TCP nor 2.6) 4.24) < LOD 6.6-TCP at low environmental doses or at biomonitored levels from low environmental exposures are unknown.55 (4.5-TCP or 2.Organochlorine Pesticides be exposed to mixtures of chlorophenols.57 (<LOD-7.20-6. Among 6-11 year old children in NHANES 1999-2000.02) < LOD 7.31) < LOD 2.00-29.6-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. animals showed hepatocellular abnormalities. NTP classifies 2.82 (<LOD-32.57 (<LOD-7. In the same 2-6 year old children.37) 16.2) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 2.. environmental levels) and health effects is available from ATSDR at: http://www.5) 11.5-TCP and limited for 2.36 (1.16) < LOD 90th 5.2) < LOD 5. 1989).53-3.69 (2. the 95th percentile urinary 2.73 (<LOD-8.atsdr. IARC considers the experimental evidence for animal carcinogenicity inadequate for 2. Laboratory animals chronically fed high doses of 2.6) 4.17) 9.43 (2.920-2.86 (3.16 (. in addition to dioxins.2) 2.02-3.cdc.79-4.

58-3.33-4.95) 3.0 (14.5-46.2 (14.40-7.44) 75th 4.80) 1.60) 6.6-TCP than are found in the general population.3-26.5-TCP or 2.0 (11.20 (3.0-43.4.7-3.6-TCP (0.2-0.49 (6.5-TCP and 2.9 (11.10) 6.0) 11.84) 2.60 (3..46-3. 2004).40) 2.0-18.0 (13.20) 4.Organochlorine Pesticides A small study of adults who ate Great Lakes sport fish reported a mean urine 2.8) 32.91-4.4. for males in NHANES 19992002 (Agramunt et al.7) * 99-00 01-02 99-00 01-02 99-00 01-02 4.9 (13.3 (11.32-4.9) 694 677 519 696 602 931 Limit of detection (LOD.7 (9.80 (2.24 (2.0-38.20-6.36-5.4.09) 15.0-44.4.4 (10.5-TCP and to the median 2.65 (5.6 (12.0) 9. which may vary for some chemicals by year and by individual sample.6 (11.0-41.95-6.4.36 mg/g creatinine.78 (2. < LOD means less than the limit of detection.9) size 1989 2503 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th 2.0) 15.65) 15.89 (3.0 (7.31 (3.0 (14.85 (2.8-15.0 (16.00-21.56 (3.4 (17.0) 6.6) 970 1178 1019 1325 99-00 01-02 99-00 01-02 99-00 01-02 2.0 (15.14 (2. Urinary 2.85) * 3.26 (2.60) < LOD 5.40) 4. Biomonitoring studies on levels of 2.1 (10. see Data Analysis section) for Survey years 99-00 and 01-02 are 1.0) 19.60 (2.45 (5.6-TCP were monitored in a group of hazardous waste incinerator workers from 19992002.5-TCP and 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.4.68 (<LOD-2.4. 2003).0-54.0 (14.0 (4.0-50.70 (2.09-7.59) 4. respectively.50 (2.6-22.31) * 2.79 (5. Mean values of 2.4.9) 13.0) 13.78 (2.0) 17. In harbor workers exposed to chlorophenol-contaminated river silt. Sawmill workers exposed to chlorophenol wood preservatives had urinary 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.10) 2.40) 3.6TCP values.36 (1.6-17.80-25.0) 10.6) 21.70-3.87-14.1) 16.4.57 (<LOD-2.00 (1.70 (2.98-11.8 (9.0) 10. Biomonitoring data will also help scientists plan and conduct research about 2.90 (4.7) 33. the median urinary 2.5-TCP (0.20-3.10-3.58 (1.4..40-2.8) 18.28) * 2.40-14.2) 25.4 (9.6-19.74 (2.01-6.30-33.0) 13.20-23.0) 7.70-6.0) 12.00 (4.90) 2.20 (3.75 (8.53) 4.28) 24.67-12.4.0 (9.0) 13.5-TCP or 2.0 (15.53) 2.66 (8.0-37.45-9.07 (<LOD-3.30-11.80 (2.92 (2.0 (6.0 (20.18-3.0 (12.3) 37.4.55-3.0) 14.0) 13. 1998).04) 2.3 (11..S.0) 14.0) 11.6-TCP exposure and health effects.52-3.69 (3.40 (2.70) 5.4.32) * 3.45) < LOD 11.4 (8.80 (3.10 (5.35-3. 1991).40-4.6TCP causes an adverse health effect.70-6.40 (2. was about six times lower than the median urinary levels for males in this Report (Radon et al.1 (8.4.40-32.63) 90th 15.80-20.30) 4.12) 2.8-24.60-37.59-6.95 (4.4.5-TCP level of 0.70) 5.0) 19.40-2.6-Trichlorophenol Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.7-16.08 (2.4. 0.00-4.23) 3.98-7.90-8.51-12. 114 Fourth National Report on Human Exposure to Environmental Chemicals .6) 26.02) 2.0 (8. population from the National Health and Nutrition Examination Survey.10-2.5-TCP or 2.6-TCP provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of 2.80-7.45 (2.2) 12.0) 9.1-25.2) 481 574 678 820 830 1109 99-00 01-02 99-00 01-02 2.0 (6.4. interval) 2.0-38.60-3.40) 2.67) 4.00 (2. Urinary 2.3) 20.18) Selected percentiles ( 95% confidence interval) Sample 95th 25.60-21.4-17.0) 17.32) 3.5 mg/g creatinine) were similar to the limit of detection for 2. similar to the limit of detection for this Report (Anderson et al.10-3.4.6-TCP level.6-TCP in urine does not mean that the level of 2.30-2.70) 1.4.25-11.3.76) 3.8-13.0) 7.3) 23.4.5-TCP or 2.06) * 2.74-3.7) 21.30-2. Finding a measurable amount of 2.80-6.0 (20.23-2.90 (3.52 (2.0 and 1.6 mg/g creatinine) and 2.99) 6.3-17.60 (3.23) 2..50-5.48-26.7 (13.72-10.0-68.73-9.70) 3.7 mg/L.0 (6.89-6.0 (8. Survey Geometric mean (95% conf.54) 6.47 (3.

92) 4.52 (3.33 (1.49-3.26-13. Survey Geometric mean (95% conf.81-9.08-2.41-6.25-15.71 (3.02 (1.67-17.90) 2.83-6.99-2.00 (3.88) * 2.88-7.52) 2.83-5.9 (9.77-4.63 (<LOD-2.89-2.26) * 99-00 01-02 99-00 01-02 99-00 01-02 4.43 (2.8) 19.27-9.90 (1.6) 970 1178 1019 1324 99-00 01-02 99-00 01-02 99-00 01-02 2.3-37.32 (2.38 (2.72) 32.63-13.19-5.87) 2.9-32.73-22.51) 18.63-15.4 (12.5) 8.4) 4.78 (2.87 (3.35 (3.09-3.91 (3.25 (3. population from the National Health and Nutrition Examination Survey.6 (22.63) * 4.8 (7.9) 7.5) 11.4) 8.5 (8.77) 2.Organochlorine Pesticides Urinary 2.56 (7.7) 25.50-8.18-2.2 (12.63) 4.3-23.83-6.6 (12.88) 5.22 (3.24 (1.38-5.48-2.88) 4.20-2.9 (9.76) 4.6) 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 2.05 (6.1 (13.05 (3.22 (<LOD-2.2) 19.22-2.0 (11.33 (7.3) 8.22-9.9) 481 574 678 819 830 1109 99-00 01-02 99-00 01-02 2.42) 2.16-10.95-2.6-Trichlorophenol (creatinine corrected) Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.0) 10.81) Selected percentiles ( 95% confidence interval) Sample 95th 21.5) 12.6 (10.56-5.82) 2.8) 11.68) 2.49) 4.81) 2.00) 4.13 (1.S.5-28.28-4.26 (6.42 (2.38) 22.38 (4.65) 18.82 (8.51-21.88 (2.78) 90th 12.5 (7.1) 14.6-31.8 (8.52 (5. Fourth National Report on Human Exposure to Environmental Chemicals 115 .53 (3.82-2.23 (1.62-15.22 (1.3 (9.7-36.88) 1. interval) 2.9-29.52) 2.98 (1.89) 10.06) 11.6) 13.98) 10.5) 9.9) 8.60 (4.00 (2.10 (6.0 (9. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.00) 4.83 (3.43 (<LOD-2.65-2.1-32.54 (2.04-16.9-34.17) 13.76) 2.0 (6.25 (3.4 (11.76) 1.1) 694 677 519 695 602 931 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.18-4.53) * 2.4.91 (7.1-21.82 (3.15 (6.6 (9.51 (2.11) 10.63 (2.68) 2.9) 19.6 (6.55-2.14-2.06) 4.60-2.21-11.56) < LOD 11.8) 12.25-17.50 (2.6) 12.46-14.33) * 2.88) 4.87) * 2.17-4.58 (4.1) 11.2 (8.6 (9.0) 8.17) 2.96) < LOD 4.32-19.7 (14.53) 4.10-9.29-4.47-5.66-4.79-17.30-2.65-21.43-7.75) 75th 4.13-6.70-9.23) 4.02) 3.5) 11.44 (3.06-2.40 (2.2 (7.73) 5.78) 2.6 (5.94-13.1 (8.9) 8.6) 8.76-8.8) 21.29-4.53-11.04-2.33-2.40 (7.15 (1.59 (2.01 (3.14-13.2 (13.10) 4.41 (3.5 (10.87-6.4) 9.9-64.87-7.25-2.65) 2.72-16.29 (6.91-2.7) 6.

Available at URL: http://www. July 1999. et al. Environ Health Perspect 1998. December 2006 Draft. Int J Hyg Environ Health 2003. et al. Jarvisalo J. Schulz C. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. To T. Can J Biochem 1976. Fast DM. Toxicol Lett 2003. Holler JS. Available at URL: http://www. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine.epa. Urinary excretion of chlorinated phenols in saw-mill workers. Environ Res 1995.146:83-91. html. Szadkowski D.gov/toxprofiles/tp107. U. 5/19/09 116 Fourth National Report on Human Exposure to Environmental Chemicals . Pekari K. The analysis of occurrence data from the first unregulated contaminant monitoring regulation (UCMR 1) in support of regulatory determinations for the second drinking water contaminant candidate list [online]. Hill RH Jr. Am J Ind Med 2004. Jones D. Safe A. Domingo A. Hill RH Jr. Seifert B. S. Kohli J. Domingo JL. Wegner R. Pesticide residues in urine of adults living in the United States: reference range concentrations.18(4):469-474. Aitio A. Int Arch Occup Environ Health 1991.63:57-62. Falk C.pdf.45:440-445. Baker S. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children. The Great Lakes Consortium. The metabolism of higher chlorinated benzene isomers. Needham LL. 206:15-24. Environmental Protection Agency (U.54(3):203-208. 4/21/09 Agramunt MC. Lindroos L. Becker K. Burse VW. Needham LL.gov/safewater/ccl/pdfs/reg_determine2/report_ ccl2-reg2_ucmr1_occurrencereport.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Chlorophenol exposure in harbor workers exposed to river silt aerosols. Anderson HA. Luotamo M. Shealy DB. Heinrich-Ramm R. Arch Environ Contam Toxicol 1989. Hanrahan L.71:99108. Gregg M. Head SL. Radon K.S. Seiwert M. Olson J. Corbella J.atsdr.106(5):279-289. Smith SJ.EPA). Kaus S. Poschadel B. Baur X. Toxicological profile for chlorophenols [online]. Monitoring internal exposure to metals and organic substances in workers at a hazardous waste incinerator after 3 years of operation. Bailey SL.cdc. et al.

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

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

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

52) * * 1.290 (<LOD-1.81) 11. < LOD means less than the limit of detection.1-17.579-1.8) 7.0 (5.0 (7.50-36.80-24.1) 95th 13.81) 11.39 (3.3) 17.07-10.1 (10.58 (5.60-18.2-20.2 (7.3-15.52-11.74 (8.58 (3.80 (2.623-1.26 (5.00-12.670-1.14) * * .63) 1.20-7.76 (2.1) 10.56 (4.86-15.82-12.20 (.717-1.37 (3.5-17.0) 11.860-2.70-14.79-7.13 (2.44-3.2 (14.34-3.61 (3.0) 10.0 (7.46) 10.7 (12.20 (.5 (11.8 (8.45 (2.0) 5.22 (.58 (2.0 (8.20 (.0 (8.840-1.12-19.60-11.20-30.67) 3.40-1.70 (2.1.72) 5.20 (2.5) 20. 0.71-9.80) .05-7.0) 7.2 (7.00 (5.48-7.2) 14.620-1.9) 8.955 (.7 (14.0) 11.0 (8.9) 14.42) .810-1. see Data Analysis section) for Survey years 99-00.4) 17.44 (2.90-4.10 (.530 (<LOD-2.4) 20.1 (9.70-19.56 (6.08-15.5 (8.90-5.60 (5.8-32.11 (.23-5.8 (14.85 (3.42-3.40-16.2 (9.90) 2.32 (.91) 4.40-11.2.80-4.96-3.0) 10.599-1.10 (2.10 (2.70) .9) 952 1187 928 997 1333 1003 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.00) 3.970-2.60 (1.757-2.86 (1.19) 9.80-22.30-4.8) 11.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.00-12. population from the National Health and Nutrition Examination Survey.03 (.700-1.70 (4.2) 16.490-2.97) 8.7) 11.80) 2.71 (2.73) * * .70) < LOD < LOD 1.52) 6.08-2.35-11.66) * * 1.15-12.290 (<LOD-.29) * * 1.16 (2.4 (9.50) 2.15) 14.S.08 (<LOD-2. 01-02.0) 6.99 (5.2) 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 1.89) 9.02) 4.2 (14. and 03-04 are 0.38-5.30 (4.80) 3.0) 11.80) 2.830 (<LOD-3.4 (9.981 (.95) 5.8 (12.04) < LOD 1.954 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.54 (3.10) < LOD < LOD 4.97) 90th 7.90 (1.4 (7.00-27.0) 10.3) 14.8) 19.27-3.90) 3.0 (9.93 (4.21) 9.4) 18.94) * * .0-27.43-12.01) * * 1.34-7.40-5.16) 4.00-19.79 (5.80) 11.8 (9.94) 3.6) 18.1-23.2.0) 20.780) < LOD 3.2 (7.60) .70) < LOD < LOD 75th 3.0) 6.17-3.50 (2.0 (9.0 (6.81) 1.5) 15.13 (2.0 (7.40-19.80 (4.0 (12.33 (5. respectively. which may vary for some chemicals by year and by individual sample.35-12.26-6.53) 4.80) 4.2 (11.98-12.47) 5. and 0.0 (7.47) * * 1.00-27.36-4.74 (8.0) 12.80) 2.9-18.26-8.0-28.30 (2.82) 10.98-5.2) 16.0) 11. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.0) 10.3) 16.40-14.50 (4.00-7.40 (.9 (8.61) 4.0) 6.890 (<LOD-2.93-24.600 (<LOD-1.44-38. 120 Fourth National Report on Human Exposure to Environmental Chemicals .33-18.740-2.4 (7.10-7.30-6.750-1.2) 672 678 473 509 696 578 595 948 752 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.55-6.60) < LOD < LOD 4.20 (.758-1.5-16.51) 2.0) 10.56-13.02-5.80) .20-4.56 (1.00 (4.0) 5.6) 7.2 (9.8) 7.30 (2.57-7.32) 1.83 (5.58) Selected percentiles ( 95% confidence interval) Total * * 50th 1.10 (.68-7.50-5.70-23.0) 15.50 (.13-2. interval) 1.2) 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 1.39 (8.0) 9.0 (4.12) 4.28) 1.60-25.0 (6.00 (1.55-8.27-15.35-16.10) < LOD .1) 13.0) 5.21 (.70-11.00) 3.

9) 12.30) 2.61 (1.5) 7.42 (3.40) < LOD < LOD 75th 2.68) < LOD < LOD 3.98) 9.1-15.75 (7.71-2.93-5.66-34.533-1.8) 8.30 (1.03) 2.430-1.69 (4.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.7 (9.54-11.00-19.79-9.20-8.570-1.05 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.00) 8.74) 90th 7.57 (6.7) 471 576 308 664 821 699 814 1122 921 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .55-20.04-6.90-8.620-1.2) 9.35) < LOD < LOD 3.41) .80 (2.57 (4.71) 10.05) .39 (2.75) 2.8) 6.5-32.5 (4.440 (<LOD-2.855 (.3) 16.50) 7.7 (8.540-1.5-16.94 (2.0) 6.75-7.6) 9.52) 4.870-2.94-23.960 (.820 (.00-13.9 (5.3) 12.1) 4.47) 2.28 (2.608-1.25) 6.75) 14.54-2.78 (2.66 (2.4) 4.510-1.40-12.54) .1 (11.6) 11.6 (9.34) * * .1) 4.790 (.5-20.19 (4. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.4) 13.24-3.87-5.37 (4.98-5.05 (1.2 (8.94-9.09 (.45-5.28-9.47) * * .920 (. population from the National Health and Nutrition Examination Survey.773-1.93-9.77 (6.6 (10.01-2.98-22.2 (10.13) 4.93) 9.710 (<LOD-1.54-15.72) 11.34) < LOD < LOD .9) 16.61-13.02 (2.82-6.82-14.3) 5.2) 95th 12.06-2.37) 9.890 (<LOD-1.45-5.84 (5.89-3.95) 2.574-1.29) * * .94-22.51-5.9 (9.43) 2.57-10.27) < LOD 2.67) 1.03 (7.98) .560-1.60-9.633-1.69) 4.69-10.88 (5.76) < LOD .43 (3.29 (2.7) 18.43 (. interval) .28 (4.60) * * .960 (<LOD-2.85) 2.87 (3.900 (.80 (7.00 (4.11-6.04 (1.46) 2.98) .82-26.89) * * 1.883 (.750 (<LOD-1.780 (<LOD-1.7) 12.15-10. Fourth National Report on Human Exposure to Environmental Chemicals 121 .92-5.09) 2.03 (2.56) 4.818 (.88-10.3) 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 1.40 (3.56-13.1 (6.0) 7.84) 7.37-3.26) * * .02-14.996 (.46-5.64-5.549-1.02 (7.6) 13.28) 10.58) * * 1.66-15.860 (.1 (7.85 (6.21-23.88) 2.42) 12.7 (10.47 (1.5-13.61-29.53-11.3) 15.98 (3.2) 13.83) 8.03-6.7) 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.41) Selected percentiles ( 95% confidence interval) Total * * 50th .45-11.92-2.924 (.14 (3.09-11.2 (6.890 (<LOD-1.4 (9.00 (4.82-14.6) 8.32-12.37 (5.40-3.2) 8.62-5.38) .81-5.73 (1.8) 7.932 (.54-4.34 (6.0 (8.47 (3.9) 11.56) 7.650-1.10 (3.7) 5.1 (10.60) 2.57) 4.75 (3.5) 7.8 (10.69) 2.830-1.40-14.40) 4.5) 12.2) 7.94-10.37-5.1 (8.1) 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 1.56) .83 (7.18 (.40-5.62) .4) 4.95 (3.10-13.79-3.90-5.31 (3.81 (1.1 (9.80 (6.88-15.34 (6.80) 9.02-2.74) 4.2) 5.66 (1.41-12.28 (5.40-28.36) * * 1.07 (.61 (1.47 (3.566-1.31-14.67) 4.23 (4.38 (1.03) 2.53 (6.87 (1.9-28.8) 16.23) 4.8) 12.25) < LOD .44 (2.00-17.5) 11.66 (5.76-4.53) 9.4 (4.9 (9.500-1.S.67-19.68-4.35 (1.5) 8.2) 5.94 (4.

0) 11.0) 14.75 (2.34-5.31-12.27) .0 (9.58.80 (2.00) < LOD .75 (3.67-10.9-15.60 (2.20) .06 (2.7) 15. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th .61 (3.10) 6.95 (5.80-8.3 (6.18) * * * * * * * * 1.22 (6.90 (1.33-11.0 (8.67) 3.0-33.0) 9.49-4.96) 90th 7.40 (2.2 (7.5) 21.16-1.0) 19.66-13.8) 8.84-4.00-16.7 (11.6 (10.0) 14.0 (10.3 (11.39 (5.45 (3.95 (2.80 (5.53 (3.6) 11.20 (<LOD-2.99 (3.4 (10.51) < LOD 1.3 (9.7-19.5.1-23.96) 3.35-3.970 (<LOD-2.88) 10. 122 Fourth National Report on Human Exposure to Environmental Chemicals .00) 7.4) 672 678 498 509 695 579 595 948 757 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.0-29.30) 3.31-7.0) 6.0 (10.18 (3.40 (2.0) 11.59-3.00) 3.5) 471 576 310 664 822 717 814 1121 938 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * .31) 1.1 (10.24 (2.0 (9. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.40) < LOD < LOD 75th 2.90-15.670 (<LOD-1.97-4.27) 4.90 (6.0) 9.670 (<LOD-1.4) 11.25 (2.0-24.70-8.3 (7.22-12.0) 12.9) 16.89 (2.27 (7.00-18.92) 9.0) 12.6) 14.00-4.0) 7.10 (.0) 13.15-2.0 (13.740 (<LOD-1. population from the National Health and Nutrition Examination Survey.5.78) 5.4-17.00) 8.50-4.7) 22.80) . see Data Analysis section) for Survey years 99-00.41) 3.30) < LOD < LOD 4.4 (14.9) 95th 14.3 (12.8 (12.0 (7.670 (<LOD-1.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.29) < LOD < LOD < LOD < LOD 3.9-14.650-1.24-5. 0.0) 23.80-3.73) 7.9 (12.35 (6.3) 20.80-21.34 (6.0 (5.22 (6.80) 5.52 (6.20-18.10-10.34-3.70 (1.3) 10.580-2.670 (<LOD-1.10-4.9) 9.50) .9 (7.7 (10.00 (.S.70-5.80-6.3) 8.74) * * * * * 1.9) 10.15-6.7) 10.3) 22.0-19.92-17.4 (10.0-24.2 (9.80) .8-17.7) 16.90 (2.72) 2.1) 11.27) 9.00) 3.64) 10.04 (3.77-3.58 (1.42 (1.46-28.0 (14.8) 9.35) 4.90 (6.6-41.0 (15.680 (<LOD-1. and 03-04 are 0.50-5.90-9. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.66) 4.70-9.61-32.8-20.37) 2.0) 12.00-18.8) 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 1.5 (8.90-31.67) 4.70) 2.20-4.10-15.80-12.00-9.80-14. and 0.01 (2.7) 14.8-21.5 (9.910 (<LOD-2.3) 14.70-9. 01-02.29-4.6) 14.5-26.9-17.0) 13.12 (4.47-6.41-5.27 (3.90 (2.98-9.5 (8.34-10.88) 3.62-17.37 (3.81-6.82) 8.7-21.60) < LOD < LOD 2.6-19.30) 8.20-8.2) 14.8-20.50) 3.28 (7.11-6.6) 18.22) 8.90) 8.14 (6.30) < LOD < LOD .8 (12.39-13.6) 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 * * * 1.95-9.90 (5.00-4.70 (8.4) 7.90 (6.90) 4.89) 2.77-14.46-4.30) 3. < LOD means less than the limit of detection.90-15. respectively.20) 3.90 (2.17 (7.1 (10.90 (6.80 (2.86-10.6 (10.0) 18.50) 5.20) 3. which may vary for some chemicals by year and by individual sample.10 (<LOD-1.60 (5.80-4.63-14.790 (<LOD-1.60 (6.3 (9.

69-11.48 (2.78 (4.8 (8.73 (5.51-10.27-13.85-17.7 (8.2-30.S.9 (9.89-3.2) 8.950) .95) 3.00 (3.91) 3.72) 4.1 (19.75-3.86 (3.0 (13.6) 7.52-3.77 (2.25-9.2) 16.00 (5.3-34.99) 2.6) 95th 16.70-2.18) 2.8) 16.79-6.760 (<LOD-1.03 (2.01-5.29-2.8) 11.80) 3.43 (2.89) 5.9) 16.63 (6.27) * * * * * * * * 1.81 (7.30) 8.89-3.07) 2.0 (8.00 (2.64-11.5-17.03 (6.9) 19.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) 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 * * * .940) < LOD < LOD 1.33-10.9-17.42) 7.93 (6.4) 15.14 (2.7) 12.00 (7.34-18.4-16.4 (11.2-15.82-8.25 (4.55) 16.28) 6.15 (1.620 (<LOD-.58 (4.38-13.6) 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 * * * * * * .7-19.00) 2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.23-3.06 (<LOD-1.42-19.44-6.4) 7.7) 9.38 (1.78 (6.1 (13.0 (11.9 (9.92) 3.78-10.88 (1.973 (.05-3.6 (13.7) 15.42) 8.12 (7.590 (<LOD-.2 (9.2) 15.4) 6.30) 7.91-9.4-18.79-9.29) 3.72-4.6 (11.00 (<LOD-1.4) 16.77) 3.39-17.54 (7.7) 14.96-11.09-11.1) 13.71) < LOD < LOD 2.78) 4.51-7.5 (15.5) 10.94 (5.6) 14.3-15.7 (10.00) 8.16 (3.810 (<LOD-1.28 (1.8) 14.20-3.29 (2.89 (3.85-8.07) 2.97-4.47-9.99 (4.89-10.88-7.3 (7.1) 20.3) 6.37-5.2 (9.50-17.3) 8. Fourth National Report on Human Exposure to Environmental Chemicals 123 . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.61 (2.36 (2.4) 7.04) 9. population from the National Health and Nutrition Examination Survey.32) 2.38 (2.89-13.0 (10.5) 13.9 (9.94-14.89 (2.0) 14.07-3.93 (<LOD-2.4-15.97) < LOD .0-21.29 (5.3-17.16-14.690 (.2) 12.920 (<LOD-1.32-8.03) 3.11 (5.890-2.1 (8.5 (8.45) 6.27) 5.92 (5.6) 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 1.74-4.5 (11.96-10.30) 2.4) 7.67 (1.15) < LOD < LOD 75th 2.06) .02-4.75-3.27) < LOD .86-3.530-1.7 (11.11-3.74-19.41 (7.27) 1.50 (6.30-5.2) 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.19) 3.8 (10.2) 12.4) 9.0-19.7-23.54-5.2) 10.07 (5.34) < LOD < LOD < LOD < LOD 3.2) 12.6 (13.6 (10.55 (2.37) 3.12) < LOD < LOD 4.87 (3.54) 9.82-11.59-3.67 (7.63 (2.21-21.780-1.9-25.6-19.68) .28-12.6) 13.77 (2.1) 10.68-19.09-11.3) 9.53-8.93 (2.95 (2.95) 90th 8.21) * * * * * 1.71 (1.4-16.7) 14.6 (11.3) 12.3-17.83 (6.5) 22.68-4.910 (<LOD-1.83 (7.70-35.5 (9.45) 3.00 (<LOD-1.5) 8.6) 6.93-10.68-10.33) 3.6) 12.86) 9.7 (10.38 (.6 (12.2) 19.3-21.850 (<LOD-1.38) 1. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th .55) .5 (10.

380) .910 (.13) 2.95-5.340-.09.76-6. population from the National Health and Nutrition Examination Survey.26) .949) .89) 672 678 478 509 695 553 595 948 745 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.57 (2.700) .570 (.73 (1.570) * .80) 3.880 (.880) < LOD .30 (.89) 1.95) 2.68-5.04) 1.550 (.840 (.710 (.11-3.42-2.780 (.37-2.460-.91) 2.74-5.10) 1.592-.80) 2.780) .16) 2.730) .60-4.73 (2.459 (.910) 1.720-1.S.930 (.467 (.880) < LOD 75th . 124 Fourth National Report on Human Exposure to Environmental Chemicals .505 (.03) 1.30-3.680-1.40 (1.600 (<LOD-.50-2.48 (1.41-5.592) * 50th .280-.50 (1. 0.303-.690 (.560-.00-2.70 (1. respectively.750-1.34) 2.80) 2.31-3.31) 2.34) 2.23-3.46 (1.820 (.260 (<LOD-.15) 2.500 (<LOD-.46) 1.20-3.30) 4.455 (.930-1.32-1.22-2.00) 2.50) 1.63 (1.2.20) 3.160 (<LOD-.980) 1.10) 1.31) 95th 2.83) 2.960) .353-.33-2.690-1.09 (.47) 2. and 0.00 (1.04) .01) .20) 1.11-3.90-4.10-1.80) 3.45 (1.30) 1.740 (.20) 2.90) 2.201-.01-1.10) 1.60) 2.86) 3.39) 2. and 03-04 are 0.76 (1.760 (.30 (1.20 (1.600-1.50 (1.88) 1.800 (.45-4.80) 3.620-1.990-1.970) 1.46-3.29-2.75-2.690-.343 (.449 (.390-.597) * .54 (2.69-4.13) .89-6.657) * * .10-1. 01-02.90) 2.490 (<LOD-.35) 1.22-3.15) 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.87-3.65 (2.382-.457 (.570 (.950) 90th 1.38) 1.94 (3.350-.27 (3.98) .64 (1.398-.910-1.16-3.50-2.585) * * .380-.450 (<LOD-.80) 5.710 (.1.61 (1.549 (.240 (<LOD-.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 * .80 (2.00-4.680-1.930) < LOD .20) 1.10) 3.860) < LOD < LOD .618) * .22-3.47 (1.29) 1.390-.95 (2.16) 1.930) 1.96-5.440-.17) 1.89) .510 (.59-2.79) .20 (2.54-2.97 (2.60 (2.510 (<LOD-.592) * .54) .970) .17) 1.18 (.08 (2.78) .550 (. see Data Analysis section) for Survey years 99-00.810) .05-3.59-6.75 (2.960-1.45 (1.20 (1.710) .55 (3.20-2.79) .380-.749 (.30) 4.50 (1.740 (.20-1.30 (.18 (1.86 (1.830 (.388-.20) 3.05-2.570 (<LOD-.98-3. < LOD means less than the limit of detection.30-1.740-.600-.700) . which may vary for some chemicals by year and by individual sample.27 (2.70 (1.94 (2.90 (1.60) 3.21) 3.584) .820 (.960) 1.570-1.580-.750) 1.70-7.98 (2.30 (.01-3.20) 2.57 (1.30) 2.31-3.00) 1.32) 3.46 (2.720-1.20 (1.83) .36-4.22 (1.359-.70 (1.14-1.20-2.78) Sample size 1949 2519 1905 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * .30-3.26 (2.453 (.94) .58 (1.77-2.78) 952 1187 907 997 1332 998 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * .960) .83 (2.90) 3.540 (.720 (.780 (.14 (1.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Diethylthiophosphate (DETP) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.40 (1.940) < LOD .96-3.22-8.80 (1.590-.77 (1.74) 3.17-4.49) .83 (2.960 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.759) * .32 (1.650-.336-.350-. interval) Selected percentiles ( 95% confidence interval) Total * .740-1.850) < LOD .690) .49) 2.08 (2.19-1.73-5.48 (2.50 (1.580-1.70-2.587) * * .210 (<LOD-.670) .425 (.83) 1.50 (1.25-1.790 (.570 (<LOD-.45 (2.41 (2.400) .

930-1.990-1.380-.73-3.94) .07) 1.58-6.910) < LOD .92-8.820) 1.11-2.840) 1.75 (1.305 (.57 (1.42-6.81) 2.57-4.09) .61 (3.460) .61-3.640 (.790 (.77 (3.700 (.32) 2.510 (.590) * 50th .250 (<LOD-.08-2.412-.640 (.71 (1.66 (2.830) 90th 1.33 (1.55-3.73 (2.690) < LOD < LOD .45 (2.760) .10) 2. Fourth National Report on Human Exposure to Environmental Chemicals 125 .16-2.03-2.590-1.285-.688) * .57 (3.560 (.69 (1.17) 2.920) .540-.44-2.470) .88) .234 (.52 (1.500-. population from the National Health and Nutrition Examination Survey.370-.08-3.43 (1.710 (.42-8.377-.560-.510-.49-4.32) 1.29-4.270-.460 (.300-.390-1.06-2. interval) Selected percentiles ( 95% confidence interval) Total * .444-.17) 2.14 (2.560-.20-7.38-3.08) 1.700 (.750 (.390) .940-1.16-1.700 (.20-2.900) 1.60) .88 (1.480) .597) * .38 (1.71) .08 (2.97) 2.400) .07-2.61-3.22) .67) 1.850) 1.41 (.348-.99) 1.79) 1.380) .180 (<LOD-.22-3.08-2.740) < LOD 1.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Diethylthiophosphate (DETP) (creatinine corrected) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.790) .23) 2.720-1.22) 1.440-1.97 (1.05) < LOD .05-2.550) .80) 2.07 (.77-3.75 (2.60 (1.23) 1.67 (1.32) 5.52) 3.64 (2.470 (<LOD-.448 (.800-1.72 (2.980-1.39 (1.02-6.23) 2.03-1.72) Sample size 1949 2518 1903 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * .330 (<LOD-.535 (.31-1.591 (.670 (.710 (.65) 2.250 (<LOD-.800) < LOD .06) 4.00-1.58) 3.310-.49 (1.39) 2.08-3.25-3.99) 2.368) * .66) .79 (1.720 (.43) 2.393 (.270-.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 * .490 (.67-3.950-2.270 (<LOD-.460-1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.253-.04-1.22-3.550-.82 (2.330-.00-3.22) 4.880) 1.550-1.350) .47 (1.97 (1.08-2.310 (<LOD-.403) .70 (3.89 (1.61) 2.07) 5.28 (1.739) * .19 (1.509 (.64 (2.310 (<LOD-.400-1.76) 1.710 (.742) * * .47-4.S.840) .75) 6.30) 3.75-3.34 (1.750 (.630) * .280 (<LOD-.870 (.680 (.30-2.230 (<LOD-.38 (2.50) 1.11) 1.660-.02-3.32-1.840) 1.98) 952 1187 906 997 1331 997 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * .70 (2.820) .05 (1.47 (1.372 (.43) 1.580 (.07-3.07) 1.136-.22 (2.760) < LOD 75th .77-4.62 (1.33) .69 (3.07) 1.515) * * .590 (.645) .32 (.42) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.00 (3.92) 3.580-.72-4.320-.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.16) 1.05) 1.43) 2.08-3.97) 1.60) 1.08) 2.60 (2.58 (1.24) 4.640 (.318-.300 (<LOD-.44) 2.480-1.08-3.471-.62 (2.67 (1.04-5.84 (2.520 (.23) 3.71) 2.55 (1.550-.95) 1.92 (1.320-.520-.50 (1.08 (.18-2.730) .78) 3.57-2.05-4.72) 1.89-3.485) * * .13 (1.530 (.91 (1.45 (1.02-3.87 (2.453 (.42 (.447 (.11 (.67) .20) 1.53) .82) 2.90) 2.22-2.830 (.870) .23 (.04) 95th 2.740) .580) .72 (1.98) 1.17-2.380-1.36) 3.552 (.84-6.335-.510 (.63 (1.

respectively.00 (.79-2.8) 952 1187 946 996 1331 1019 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.52 (4.8 (26.66-5.57-2.1 (25.8-24.1) 95th 48.3 (12.41) 1.0) 3.70 (7.0-43.3 (12.3) 38.76 (2.0) 8.86-3.80) .0) 32. which may vary for some chemicals by year and by individual sample.0) 16.70-6.4 (10.20) 1.9 (19.92) * 2.0 (17.0-53.70) 1.7-41.5-27.10 (7.0) 13.70 (1.81-2.23-2.S.8) 41.79 (1.1-19.0-110) 34.7) 47.06) * 2.40) < LOD 1.18) 14.18) 20.41 (1.1 (11.0) 16.9) 17.1-47.0 (38.59 (1.11) 2.1) 38.830-3.6-27.82 (1.44) 3.0 (40.67 (1.2-62.3) 26.9 (10.0-53.9) 18.9-21.13 (1.79 (2.2-27.17-2.27-6.44) Selected percentiles ( 95% confidence interval) Total * 2.40-16. and 0.05) * 2.610 (<LOD-1.2 (12.5) 30.1 (25.40-4.3) 28.53) 1.2-27.41) 5.8) 32.42) 1.0-49.53 (1.70) 1.0 (11.96) 5.0 (38.2-80.4) 19.36-2.0) 33.0 (33.81-3.0) 18.830-4.48-2.8 (22.0) 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 2.21 (1.48) 5.0-260) 34.30) 4.83 (3.98) * 2.45) 2.06 (1.0-41.0) 28.0-47.99 (2.4.0 (6.4) 38.7 (28.0 (38.80) 90th 38.71) 5.0) 17.690-3.70 (.9 (23.0 (20.4 (19.3) 33.10-13.86 (1.80-18.0) 5.0 (8.0-41.07-5.61 (1.88) 1.2) 31.13 (1.1-25.19) 2.0-39.0) 20.29) 2.35-6.13) 12.46-6.3 (14.00-24.40) < LOD 2.85) * 2.0) 3.660-2.32 (2.29-4.0-29.5-74.0-52. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.70 (1.10 (1.0 (38.20-4.46 (.3 (24.48-2.2 (19. interval) 1.1) 140 (46.8) 39.50-20.10) 39.9) 38.59 (1.54 (3.8 (12.54 (1.10) .0 (21.0) 19.77) 38.2-47.0 (7.2-39.1 (22.10 (1.50-17.00 (.44-7.0 (13.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.7) 20.41) 1.58) 16.21 (3.0-69.50-5.0) 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. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.95 (5.65 (4.1-46.1 (10.90) 11.9 (27.83 (1. 0.40) 50th 2.30 (.9) 48.44) 2.0) 3.41-4.5.6 (11.0) 6.97) 6.0) 20.18.60 (2.94 (1.1-40.7 (12.23) 9.53) 40.0) 15.1) 18.0 (19.0-58.2-33.0) 28.91 (4.80-2.8-21.10-4.1 (26.75-14.26) 75th 11.16) 2.04-8.0-31.78 (1.16) * 1.11 (4.12) 1.0 (38.3) 31. and 03-04 are 0.0 (8.1) 38.77 (1.05) 1.90 (1.6-22.14) 5.2) 16.64-3.5-45.76 (2.4 (15.80) < LOD 1.6) 52.0 (38.5 (24.50 (2.0 (25.50-7.29-9.3 (23.0-92.70-17.0) 42.58-2.6 (15. see Data Analysis section) for Survey years 99-00.90-8.0) 45.31-6.80) 1.02 (2. population from the National Health and Nutrition Examination Survey.92-5.63-6.85 (1.0) 15.18) 6.74-2.88) 3.4-22.12 (3.4-76.19-2.33 (5.20 (2.470 (<LOD-1.93-3.0) 4.5-40.6 (26.71 (4.83-2.2-26.530-4.0-62. < LOD means less than the limit of detection.5-20.78) 9.600-2.6 (9.0-62.6-54.0-230) 35.0) 3.30-14.0) 4.21 (4.0 (32.71-2.26 (.0 (8.0-110) 42.6-45.46-2.04 (<LOD-2.70) 5.30) 11.8) 62.50-2.60) < LOD 1.0) 30.64-8.53) * 2.45) 2.98 (1.0-50.7-22.3 (10.83-2.04) 3.05-3.09 (4.7 (12.0 (37.10 (1.0) 31.5) 69.8 (12.8) 671 678 498 509 695 579 595 947 757 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.0-41.0 (24.25-3.72 (1.0-58.0 (38. 126 Fourth National Report on Human Exposure to Environmental Chemicals .0) 17.0 (26.87-7.61-2.0-39.0 (20.69) 2.57-2.9 (19.9-51.1-20.0) 4.23-2. 01-02.49-2.43-7.10 (1.90 (1.

00) 1.9-41.94) 19.6 (7.7 (11.33-5.27 (6.69-5.6-49.94) 1.25-3.06) 75th 9.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.59-2.95 (2.1-60. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.22-3.75 (1.22-2.3 (20.47-17.30) 28.4 (9.9-36.1) 27.4 (25.83) .5 (17.60) 4.35 (2.4 (12.4-71.97 (1.00 (4.45-1.9 (39.1) 25.16 (1.0) 48.62 (2.08) 1.9 (10.96) 2.61-2.76-2.0 (25.7-47.4) 12.1 (12.3) 28.23) < LOD 2.40 (5.95-16.3 (10.3-42.7-109) 22.47 (1.0 (32.3 (10.0 (23.57 (6.6 (27.99-4.33) 1.2) 36.60 (.6) 11.39 (1.7 (24.82 (2.91-2.0 (17.1-22.1) 27.6) 3.19) 5.3 (9.46-22.4) 12.860 (<LOD-1.2 (15.2) 13.2) 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.7-43.8) 11.5 (8.03-2.19 (1.9-52.72) 2.7) 30.45 (1.27) 50th 2.9-37.0-118) 29.1) 36.0) 3.5 (6.16 (1.28 (1.07-2.7) 23.2 (9.8-37.12 (1.40 (2. interval) 1.1) 15.27) 10.0) 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 1.40-4.7-19.35) .4 (21.44) 9.70-4.1) 13.11-2.888-1.9 (26. Fourth National Report on Human Exposure to Environmental Chemicals 127 .14-8.59-15.28) 1.23) 37.67-16.61 (1.08 (1.0 (14.57) 4.93) 5.07) 9.48) 1.1 (39.50 (2.19-14.1 (33.68) 47.6) 23.6-38.8 (7.9 (19.0) 10.46-5.83 (.6) 3.36-13.06) 1.95) 90th 32.00) 6.56) 1.870-3.0) 47.3-19.0) 25.06) 1.55 (2.43-2.68 (1.24 (1.0) 13.14 (.51) .890-4.21 (4.6) 112 (40.5) 70.36) 10.680-4.63-5.2-47.90 (.7) 26.7) 15.7-20.5-36.8-43.51) < LOD 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.29-5.3) 13.86) * 2.02) * 1.75 (1.7-38.20) Selected percentiles ( 95% confidence interval) Total * 1.41 (2.71 (1.1-63.6 (11.40-7.58-2.8) 15.2) 471 575 310 664 821 715 813 1121 937 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 1.26-4.7) 61.22 (2.4) 14.09 (5.52-4.7 (18.2) 4.870-3.22 (.38 (3.11) < LOD 1.2-38.5 (34.79 (2.7-37.00-16.0) 30.9 (13.4 (5.53) 1.47 (3.9) 24.18-1.4-21.4 (11.67 (1.7) 66.5 (15.0 (19.88 (1.94-20.19) 5.2-34.43-12.17) 2.88 (4.2-28.80 (1.70 (1.62) 4.56 (2.2 (21.02 (.50-5.4) 3.54-15.1) 25.7 (10.37-2.9) 24.1) 52.86) * 3.20-5.6) 7.03) 1.38-5.96-16.6-32.3 (8.4-39.6) 19.2 (22.16-2.71) 8.2 (16.66 (1.930 (<LOD-1.5-43.750 (<LOD-1.37 (1.5) 27.9) 54.66) 8.7 (18.9-18.2 (8.2) 41.59-2.16 (1.9) 12.18) * 2.91 (6.58-17.6-51.0 (39.67 (1.33) < LOD 1.2) 33.0 (6.5-97.07-2.71-2.899-2.33) 2.43) * 2.1) 13.1 (50.88 (4.9-95.1) 17.67-3.1 (25.27-3.4 (25.34) * 1.870-3.4-34.80-8.66 (1.38-1.95-16.32 (3.82) 1.5 (13.31) 2.3-22.75-6.5 (15.S.8) 23.8) 3.52 (1.54-2.4-67.7) 95th 51.8-45.0-70.75) * 1.2) Sample size 1948 2517 1962 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 2.0-71.9) 3.1 (34.84-13.48 (4.32-3.46) 1.36 (4.0-40.17-3.9 (7.9) 3.35) 1.46-6.88 (1.7) 34.2-70.8) 32.02) 1.18) 3.5-190) 30.12) 3.15 (.06-1.69-18.26-2.79-17.3-27.8-34.670-1.2) 13.5 (41.4 (19.64 (1.23-1. population from the National Health and Nutrition Examination Survey.0 (23.6 (24.19-6.61-22.8-26.8) 31.01 (.38) 5.

310 (.380-.140-.730-.050-.150 (<LOD-.130) .130-.36) .32) .650) .290 (<LOD-.171) * * .730) .1.160) .990) .560 (.830) .630 (.330-.770 (.13) .30) .140-.550) .S.610 (.690-1.190 (.080 (<LOD-.320-.15) .130) .360-.540 (<LOD-.100 (.610-.320 (.210 (.640) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.660 (.640-1.780) < LOD 1.410-1. 0.130-.084-.10) .870 (.990) .470 (.700-1.680 (.640) .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 * * * * * * .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 .410) < LOD < LOD < LOD < LOD .610 (.370-.290) < LOD < LOD < LOD < LOD 90th .110-.180) .090 (<LOD-. < LOD means less than the limit of detection.099-.120 (<LOD-.680) .850) < LOD .160) .410-.430-.162) * * * * * .400-.850 (.170-.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.090 (<LOD-.900 (.360-.650-1.20) .840) . and 03-04 are 0.290) < LOD < LOD < LOD < LOD Non-Hispanic whites Limit of detection (LOD.090 (<LOD-.300-1.230-.310) < LOD < LOD < LOD < LOD .40) .190 (.830 (.530-.12 (.080 (<LOD-.140) . which may vary for some chemicals by year and by individual sample. see Data Analysis section) for Survey years 99-00.090 (<LOD-.380-.290) < LOD < LOD < LOD < LOD .440-1.450 (.870 (.630 (.940 (.090 (<LOD-.42) .610-1.220 (<LOD-.870 (.230) .740) < LOD .930 (.260 (.120-. respectively. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.390) < LOD < LOD .03) .430 (.30) .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 * * * * * * * * * .640 (.190 (.130-.120-.410-.540) .470-1.540) 672 678 498 509 694 579 595 947 757 Non-Hispanic blacks .350) .460 (.300-.560 (.10 (.870 (.830) < LOD .700-1.570) .310) < LOD < LOD < LOD < LOD .700-1.00) .650-1.450 (.240 (<LOD-.30) .210 (.840) .870 (.090 (<LOD-. and 0.830 (.720-1.130 (.680-1.860) .720 (.700-1.42) .450 (.650 (.10) .720) .600 (.10) .220 (.160-. 01-02.990 (.390 (.770) < LOD 95th .350) < LOD < LOD < LOD < LOD .460-.870) < LOD .05.490 (.650) .150) .510-1.760) < LOD .270 (.60) 1.1. 128 Fourth National Report on Human Exposure to Environmental Chemicals . population from the National Health and Nutrition Examination Survey.310-.370-.540) .117 (.820 (.860-1.680-1.820 (. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th 75th .200) < LOD < LOD .140-.380-.420-.850 (.620 (.310 (.58) .280) < LOD < LOD < LOD < LOD .

600-1.710-1.510-.260) .220) < LOD < LOD < LOD < LOD .400 (<LOD-.190 (.780 (.360-.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.640-1.940) .800-1.940) .720 (.360-.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 (.500 (<LOD-.410-.14) 1.990) .740 (.470 (<LOD-.86) .440-1.230-.03 (.190-.890 (.260-.380 (.570 (.380-.600) .12) < LOD .070 (<LOD-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.140-.780) < LOD 1.19 (.580 (.730) .850 (.24) .100-.660-1.62) 1.310) < LOD < LOD < LOD < LOD Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.S.570-.161) * * .43) .880 (.180-.120) .320 (<LOD-.670 (.410) .730) .070 (<LOD-.01 (.700-1.110) .580) .650) < LOD .38) 1. Fourth National Report on Human Exposure to Environmental Chemicals 129 .200 (.720 (.78) .310) < LOD < LOD < LOD < LOD .490-1.58) 1.057-.360 (.060-.210 (.66) 1.02) .084-.070 (<LOD-.650-1.170 (.080) .170) < LOD < LOD .440 (.050 (<LOD-.111) * * * * * .230 (<LOD-.24 (.540 (.330-.380-. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th 75th .29 (.880-1.380-. population from the National Health and Nutrition Examination Survey.870) .140) .140-.03 (.070 (<LOD-.700 (.02-1.140-.580-1.080 (.700 (.410) < LOD < LOD .560 (.00) < LOD .570-1.220 (.970) .150-.140-.100 (<LOD-.090 (.860-2.580 (.67) .460 (.730) .09) .550 (.170 (.500) .400) .330-.110) .190 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.450) .280) < LOD < LOD < LOD < LOD .250-.750) < LOD 95th .03 (.290) < LOD < LOD < LOD < LOD 90th .370 (<LOD-.230) < LOD < LOD < LOD < LOD .200 (.730 (.700) .670-1.140-.86) .270 (.120) .550 (.810 (.36 (1.116 (.090 (<LOD-.080 (<LOD-.03) .110) .540 (.450 (.500-1.240-.110-.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 * * * * * * .860 (.390-.380-1.760) .520-.610-1.510) Sample size 1949 2515 1962 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * .20) 1.110) .330 (.360) < LOD < LOD < LOD < LOD .860 (.740) < LOD 1.990) .300-.410 (.60) .670 (.960) .410 (.300-.520) 672 678 497 509 693 578 595 947 756 Non-Hispanic blacks .580) < LOD .270) < LOD < LOD < LOD < LOD .540) .390-.340-.330-.410-.300 (.

170-1.53) 20.750-2.15) 14.46 (1.0 (4.50) 2.0 (6.800) 17.94-3.49 (1.30) 95th 19.80 (4.07 (3.10-3.380-.48) 13.0) 7.40 (1.850) 16.0 (5.45 (2.40-20.0) 4. see Data Analysis section) for Survey years 99-00.0 (17.0 (17.600 (.49 (1.40 (1.70-30.0-38.6) 5.00 (1.110 (<LOD-.30 (1.870) < LOD < LOD .250 (<LOD-.210-1.11) .0 (3.0 (17.85-3.62) 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 * * * * * * .28) .76 (1.42) .20-4.07) 1.0) 5.55-8.31-10.0 (5.35) 5.08.40) 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.880) 5.S.30-3.30-6.53 (2.14) 2.52 (1.610 (.43-4.80) < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 4.330 (<LOD-1.1.47 (3.12-1.35-10.21) 3.94 (1.48 (2.800-4.510-.690 (.0) 5.750-1.770 (<LOD-1.32 (1.0) 4.0) 4.10 (3.730 (.0) 5.31) .0) 2. 130 Fourth National Report on Human Exposure to Environmental Chemicals .0) 5.0 (13.05 (3.350-.40-4.37) .70-3.42) 2.20) < LOD < LOD < LOD < LOD < LOD 1.49) 17. respectively.29-10.30 (2.30-7.63) 32.99) 11.10 (3. 0.83-3.0-40.640 (.70-7.39 (2.6) 672 678 498 509 695 552 595 947 752 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.0-39.18) 1.770) 2.83) 2.0 (7.1.90-9.67 (1.900 (.32-9.88-3.07-3.16) Sample size 1949 2518 1930 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .0) 2.0) 2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.0) 2.740 (. and 0.800) 90th 13. which may vary for some chemicals by year and by individual sample.35) 11.190-1. population from the National Health and Nutrition Examination Survey.10-3.00-17.0) 3.87) 5.20-17.74 (3. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th 2.63 (3. and 03-04 are 0.00-17.90-28.890 (.51 (2.620-1.425-1.50) .00) .830 (.28-9.67 (2.01) 5.90) .580 (.90 (2.0 (17.0-44.0) 2.70-50.40-8.0-40.12) * * * * * * * * .97) 20.28) 1.20 (1.20-4.0 (4.55-4.00) .0) 4.3) 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 * * * * * * * * * .30 (.90-37.94-8.53-7.86) 4.590 (.24-7.90) .11 (1.910) 2.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.480-.0) 2.10-9.60) .61 (1.51-8.38-3.62-8.40) 2.21-3.96 (1.52) 5.67) .260-.23-6.0-38.0) 2. < LOD means less than the limit of detection.07-3.640 (.080-1.26 (2.14) .90-20.0 (17.0 (5.0 (5.0 (16.03 (.59-5.83-3.13 (3.15) 19.350-.07 (1.14-5.720) 2.39) .691 (.370-.52 (1.840 (.07 (3.30) .05-3.82-4.960 (<LOD-1.10 (.97) 20.00 (.40-7.74) 5.840 (<LOD-1.960 (.60) 1.0 (5. 01-02.360-1.87) 12.30 (1.70) 2.11) 13.90 (1.36-3.20 (1.30 (1.99) 19.00) 1.66) 4.90) .68) 2.05 (2.70-17.840-3.99 (1.33 (4.400-1.36-3.65) 1.0-38.610) < LOD < LOD < LOD < LOD < LOD 2.

59 (1.18) 1.21-3.97) .5) 2.340-.51-44.0 (9.240-.80) 3.57) 1.670 (.7 (6.700) 6.1 (7.25-9.47) 5.25-38.6) 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 * * * * * * * * * .92 (2.580) 1.53) .65 (2.71 (2.90-6.86) .7) 4.5) 2.370) < LOD < LOD < LOD < LOD < LOD 1.5-40.370-1.37) 4.14 (1.1 (5.55) 21.02-4.9 (11.41) 18.650) 90th 10.40 (.360 (.630-1.580-1.940-4.31) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.88 (2.540-1.960 (.96-8.780-4. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th 1.03) 2.390-.71 (.22-27.18) * * * * * * * * .04 (1.55) 21.430) 1.2 (8.3) 2.25 (1.7) 6.8) 4.770) .830 (.4 (4.580 (.91-4.32-6.77 (.53) 27.38 (2.430 (<LOD-.28-6.61) 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 .24) 3.800-2.8) 1.50) .8-33.0 (4.450 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.03) 16.11-5.5) 7.1) 2.40-12.5 (11.96) 2.850-3.540 (.56) .62 (1.27 (2.40-2.44-11.13 (2.84) 9.67 (2.15) 9.52 (.50 (4.33 (3.320-1.600 (<LOD-1.14-6.748 (.740-1.190-1.4) 2.29 (4.8 (20.29-4.1) 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 * * * * * * .88-3.44) .22) 2.0) 4.82-11.310-.340-.79 (.620-3.590) 2.50 (2.31-7.96-25.36 (.650 (.890 (.05) .89 (2.970-3.80 (.730-3.04-16.3) 3.10-3.01 (1.07-21.500 (.474-1.67) 1.48 (4.30 (4.790 (.41 (4.260-.7) 5.370 (.67-6.60) < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 4.830-3.40) 1. Fourth National Report on Human Exposure to Environmental Chemicals 131 .31-18.00-19.270 (<LOD-.10 (2.06 (.02) .4-34.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.790) 11.33-3.67) 2.43) .91) 2.83 (4.12-4.820) .150 (<LOD-.55 (3.9) 6.11) .700) < LOD < LOD < LOD < LOD < LOD 1.10) 2.S.02 (.260-.62-17.930) .8) 7.07 (2.7 (12.12 (4.33-4.7) 3.560 (.47) .69) 2.18) 95th 21.57-40.66-47.86 (3.35 (.860-2.48-7.57) 8.51-4.98 (4.69-7.75) 5.64) 30.31) .250 (<LOD-.340-.8) 2.47-10.47-10.85 (1.56 (1.50) 11.710 (<LOD-1.64-4.08) .83-11.17) 5.17 (1.74 (2.48-42.09-3. population from the National Health and Nutrition Examination Survey.00) .57 (.5 (9.340 (.49-2.5 (8.73 (4.8) 7.33 (1.02 (1.88) 17.85-3.8) 2.690-5.23-7.45 (1.330-1.81-17.580) 16.33-5.60 (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.39) 20.820 (.840-3.9) 5.470 (.32) 9.270-.88 (.56) 2.2-38.660) < LOD < LOD .

Correlation of urinary pesticide metabolite excretion with estimated dermal contact in the course of occupational exposure to Guthion. Daniell W. Environ Res 2001. Richardson RJ. Giordani B. Occup Environ Med 2003. Garabrant DH. Neurophysiological function in farm workers exposed to organophosphate pesticides. Centers for Disease Control and Prevention (CDC). and neuropsychological study of sheep farmers and dippers exposed to organophosphate pesticides. Leffingwell JT. Davis SW. The effect of the 14-day agricultural restricted entry interval on azinphosmethyl exposures in a group of apple thinners in Washington State. J Expo Anal Environ Epidemiol 2005. Berent S. Young AD. Garrison RP. Castorina R.111(3):377382. Novelli MT. Heudorf U.32(5):487-496. Peterson JC. Biologic monitoring of exposure to organophosphorus pesticides in 195 Italian children. Reprod Toxicol 1998a. Fenske R.14(6):869-889. Seta N. accidental. Bozzi N. Surveillance of occupational. Harnly ME. 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338(8761):223-227. Washington (DC): U. Scand J Work Environ Health 1998. Chronic central nervous system effects of acute organophosphate pesticide intoxication. EPA). Rodnitzky RL. McConnell R. Chronic neurological sequelae to organophosphate pesticide poisoning. 1991. Terry AV Jr.113(4):504-508. Occup Environ Med 2001. Pilkington A.php?record_id=2126&page=1.S. et al. Saieva C. Heaton RK. Robson MG. Scherer J. U. Occupational exposure to organophosphate pesticides: a neurobehavioral study.epa. Fourth National Report on Human Exposure to Environmental Chemicals 133 . Pedersen L. Lasarev M. 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. 1/12/09 Peiris-John RJ. Savage EP.20(2):115-22. Schenker M.30(2):98-103. Bull Environ Contam Toxicol 1994.12(2):134-141. Kidd M. Dinoff TM. J Occup Environ Med 2002.nap. Available at URL: http://books. et al. EPA.68(3):209-227 Maizlish N. Nell V. Santana J. Neurotoxicity among pesticide applicators exposed to organophosphates. Rosenstock L. Hansen S. Office of Prevention Pesticides and Toxic Substances. Rothlein J. The presence of dialkylphosphates in fresh fruit juices: implication for organophosphorus pesticide exposure and risk assessments.26(2):199-209.332(1-3):71-80. Caltabiano LM. O’Malley M.84(5):731-736. Chronic neurological sequelae of acute organophosphate pesticide poisoning.38(4):546-563. Smit LA. Effects of chronic. Johnson C. Arch Environ Health 1975. Daniell WE. Visuthismajarn P. 1993 [online]. Effects of occupational exposure to organophosphate pesticides on nerve and neuromuscular function. and spatial learning in monkeys and rats. Berry H. Wickremasinghe AR. Steenland K. Thompson ML. and cholinesterase status of date dusters and harvesters in California. Petchuay C. Muniz J. Am J Ind Med 1987. Occup Environ Med 1995. Weerasekera G. Available at URL: http://www. May. Effects of long-term organophosphate exposures on neurological symptoms. Bravo R. Malathion deposition. van der Hoek W. Spurgeon A. Am J Public Health 1994. 2004. Chrislip D. Calvert IA. London L. Stokes L. Buchanan D.2000 and 2001 market estimates. vibration sense and tremor among South African farm workers.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Krieger RI. et al. Ruberu DK. Rohlman D.43(1):38-45. Buccafusco JJ. et al. Seiber J. Tumino R. Pesticides in the Diets of Infants and Children. Claypoole K. Stephens R. Aprea C. Association between in utero organophosphate pesticide exposure and abnormal reflexes in neonates. Eskenazi B.44(4):352-357. Keifer M. low-level organophosphate exposure on delayed recall. Prendergast MA. Jenkins B. Environ Health Perspect 2005. Keefe TJ.24(1):18-29. Marshall E. Arch Environ Contam Toxicol 2000. Monitoring of urinary alkyl phosphates in pestcontrol operators exposed to various organophosphorus insecticides. The Pesticide Health Effects Study Group. Stark A. Environmental Protection Agency (U. Gillham R. Irish RM. Beach J. Neuropsychological effects of long-term exposure to organophosphates in sheep dip.edu/ openbook. National Academy of Sciences. Lancet. 4/7/09 Young JG. Jamal GA. Frasca G. S. Gladstone EA. Rothlein J. Barr DB. Weisskopf C. Lasarev M.S. Neurotoxicology 2005. Muniz J. Samuels S. Organophosphate pesticide exposure and neurobehavioral performance in agricultural and non-agricultural Hispanic workers. Lambert WE.345(8958):11351139. McCauley L. Variation in organophosphate pesticide metabolites in urine of children living in agricultural communities.12(2):153-172. Biological monitoring of organophosphate pesticides in preschool children in an agricultural community in Thailand. Twenty-four-hour urinary excretion of ten pesticide metabolites in healthy adults in two different areas of Italy (Florence and Ragusa).58(11):702710. Environ Health Perspect 2006. discrimination. Takamiya K. Vitayavirasak B. Int J Occup Environ Health 2006. Washington (DC). Bradman A.52(2):190-195.114(5):691-696. Lewis JA. gov/oppbead1/pestsales/01pestsales/market_estimates2001. Narang A.pdf. Masala G. metabolite clearance. Mounce LM. Sci Total Environ 2004. Burcar PJ. Ames RG. Lancet 1995.52(10):648-653. Hore P. low-level exposure to the organophosphate diazinon. Pesticide industry sales and usage . National Research Council (NRC). Lu C. Arch Environ Health 1988. Russo J. Levy LS. Salvini S. Phillips J. Myers JE. et al. A behavioral evaluation of pest control workers with short-term. J Toxicol Environ Health A 2005. Neurotoxicol Teratol 1998.

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

50 (1.0) 12. Fourth National Report on Human Exposure to Environmental Chemicals 135 .61-7. Inhalational and dermal routes of exposure are important in pesticide formulators and applicators.43-2.40-26.10 (3.60 (5.40-10.53 (1.30) 5. Approximately 21-24 million pounds per year were used domestically from 1987-1998. 1999.25) 1.90-7.80-8.67 (2.2) 972 1183 1022 1326 99-00 01-02 99-00 01-02 99-00 01-02 1.80 (7.31-2.3 (10. For instance.0) 18.50-8. USGS.60-4.04-10.91 (1.0) 10.47) 1.38 (3.30 (2.70-11.72) 2.10 (4.60) 5.13-3.30-12.66-4.70-17.5.37) 5. Chlorpyrifos is very toxic to fish and aquatic invertebrates and shows modest degrees of bioconcentration. staying bound to soil particles.68-2.Organophosphorus Insecticides: Specific Metabolites Chlorpyrifos CAS No.91) 16. Chlorpyrifos is a broad spectrum organophosphorus insecticide that has been widely used to control insects on food crops such as corn. Chlorpyrifos is degraded in agricultural soils with a half-life of several months.0) 14.70 (1.80) 2.8) 9.70) 1.80) 4.90 (1.51 (1.3) 8.0) 12.60-3.21) 3.29-1.59) 2.92 (1.0) 12. chlorpyrifos and TCPy were detected in all indoor air and dust samples (Morgan et al.05) 1.5) 7.00) 1. It also has been applied directly on animals to kill mites.1-16.40-2.84) 1.50-2.67 (2.89 (2.19 (1.63 (1.0 (10. 2002).44-5.99-4.77-15. pre.40 (6.30 (4.60 (2.50 (2.80) 1.40-13. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.80) 12.9 (7.71 (2.30-11.77) 1.EPA.0 (7.27 (7.03) 1.59-2.20) 10.19-3.29) 90th 7.20 (2.31-2.90-2.62-2.40) 2. Survey Geometric mean (95% conf. 5598-13-0 General Information The chemical 3. 2921-88-2 Chlorpyrifos-methyl CAS No.02) 1.09 (3.0) 8.90 (1.47-11.43-2.79-2.50 (2.0) 10. Exposure can also result from contact with contaminated surfaces.80 (1.6) 7.0-28.9 (9.8) 10.97) 7.30) 4. chlorpyrifos was no longer registered for indoor residential uses in the United States.10 (5.57 (2.S.30-1.6-trichloro-2-pyridinol (TCPy) is a metabolite of chlorpyrifos and chlorpyrifos-methyl.30-5.32) 2.04-10.2 (10.5 (8.50-2.52-2.0) 12.51) 1.90) 3..0) 12.47-13.7) 8.28) 2. and sprayed to kill mosquitoes.9) 697 660 521 701 602 947 Limit of detection (LOD.13 (1.76 (1.60-3. although some tolerances for specific food crops have been reduced in the past to avoid exceeding recommended intake limits for total dietary intake in special groups (U.20-11.10-17.4 (8. dermal.97) 2. 2002).71 (1.45 (1.03) 99-00 01-02 99-00 01-02 99-00 01-02 2.02 (1.20-4.S.97) 2.4 (10.7) 9.50-5.68 (7. air.20) 4.0 (7. population from the National Health and Nutrition Examination Survey. Estimated intakes from diet and water have not exceeded recommended intake limits.90 (3.15 (1.83) 1.60-2.80-10.76 (1.EPA.4 and 0.47-9.00-8.3 (11.78 (7.90 (2.70-15.96) 3.30-2.6-Trichloro-2-pyridinol Metabolite of Chlorpyrifos and Chlorpyrifos-methyl Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.47 (4.02 (7.44 (3.00-24. and is infrequently detected in ground water (IPCS.000 pounds are used per year.0 (9.36 (4. 2007).72-4.50 (1.32-1.51-2. Chlorpyrifos is not well absorbed through the skin but dermal exposure can be significant when other routes of exposure are low.09 (2. but can be detected in streams receiving runoff from application sites.and post-construction structural applications for termite control were to be phased out by 2005 (U.89-2.39-2.34) 1.50-14.0) 6.0) 9.8-15.7-23.0) 7.71 (6.4) 481 573 681 823 832 1113 99-00 01-02 99-00 01-02 1.37 (1.0 (7.39) 4.64) 3. 2005).55-5.81-2. interval) 1. applied to structures to kill termites. After 2001.67 (1.26) 7. Approximately 80.0) 8.0 (7.22) 2.1) 5.S. and on plants for days to several weeks.50 (2.9 (10.30 (2.70 (1.20) 2.20-14.70-16.28-3.20 (4.40 (5.05-5.40 (5.66-15.90 (6.20-3.10 (1.35) 1.46-2. in 142 urban homes and preschools in North Carolina.61 (1.30) 4.4 (9.10) 2.90) 7.0 (13.16) 2.0) 15.97-7.10) 6.14) Selected percentiles ( 95% confidence interval) Sample 95th 10.9) 11.90-8. and dust.98-15.87-6.5.0 (7. The general population may be exposed to chlorpyrifos via oral.22 (1. Chlorpyrifos-methyl is an organophosphorus insecticide also used in agriculture and not registered for residential use.17 (1.40) 9.5-24.01) 1.20-2.97) 4.3 (8.0) 11.44-2.20) 2.52-12.95 (4.95) 7.61) 75th 3.0) 10.35) 2.00) 2.50-4.63 (2.50-4.3) 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 1.74-9.4-15.60 (4.70-5.77 (1.24-3.90-4.63 (8.7) 13.9-18.94 (4.00) 3. Chlorpyrifos is Urinary 3.37 (4.74 (1.86) 4.20-16.4. It has low leachability.25) 3.77-6. and inhalation routes.24-1.30-9.88 (1.

97-3.97 (3.66) 1.22-6.88-8.41 (1.21-1.5) 5.88-10. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”). weakness.49-2.31) 1.27-7.24-4.66-11.46 (2.92-2.06 (1. 2005.Organophosphorus Insecticides: Specific Metabolites rapidly absorbed following ingestion.09 (1.72) 1.19) 3.50 (4. chronic exposure to chlorpyrifos may be associated with slight alterations in some components of neurophysiologic testing (Steenland et al.23-1.83-2.12-1.26-14.06-4.46 (1. the detection of TCPy in a person’s urine may reflect exposure to the environmental degradates. Ricceri et al.93 (2.60-3.47-2.44 (5.83) 1.91 (4.73 (1.05-4.87-3.44 (5.0) 6.01) 1. Thus.24-5.3) 9.91) 2.99) 1.63 (4.30-4.88) 6.08) 6.88 (1.75) 6.05-3.85 (2.38) 3.62-7. TCPy is more persistent in the environment than chlorpyrifos itself (U.95 (1.85) 4.6) 10.24) 5.25-11.64 (1.7) 697 660 521 700 602 947 136 Fourth National Report on Human Exposure to Environmental Chemicals .93) 5.01) 3.47 (1. Once absorbed. Overt cholinergic toxicity from chlorpyrifos has been described following suicidal ingestion and unintentional high level occupational exposure.22 (6.20-1.25-1.52 (5.19-1.35) 1.00-8.22 (4.63-2.56-2..2 (7.1-38.54) 5.28) 2.25-12.80-11.85) 1. 2006b).51 (1.36) 1.35-1. 1984).82 (3.64-2.6) 9.91) 1.39 (2.01) 3. Howard et al.53-5.EPA. and producing acute symptoms such as nausea.48 (2.62) 1.80-6.58 (1.71 (1..56 (4.24 (1.27-1.21-6.17-4.60 (1.88 (1.02) 7.24-1.57-2.74) 1.86 (1.42 (5. In pesticide applicators.79-13.0) 12.94-12.75 (1.1 (7.14-8...53 (2.8) 972 1183 1022 1325 99-00 01-02 99-00 01-02 99-00 01-02 1.93 (1. Human health effects from chlorpyrifos or chlorpyrifosmethyl at low environmental doses or at biomonitored levels from low environmental exposures are unknown.82 (2.58-5.16) 6.68) 6.76 (2.86 (3.92 (1.40) 1.80-4.09-2. 2000).39) 6.91-13.65-11.76 (3.S.91 (3.91) 1. resulting in excess acetylcholine at nerve terminals.33) 2.34-1.97 (2.43-10.91) 10.98 (6.07) 1.65-15.35) 2.49 (1.39 (4.33 (.29 (3.33 (5.77) 1.86 (1.5.00-13.98 (7.42 (6. paralysis.91-4.4) 4.68) 1..47 (5. Chlorpyrifos and chlorpyrifos-methyl both demonstrate moderate acute toxicity in animal studies. and seizures.1-21. cholinergic effects. 2006a.56 (1. Betancourt et al.78 (1.12-3. The metabolite TCPy does not inhibit acetylcholinesterase enzymes.97) 3.5 (6. phosphorothioates such as chlorpyrifos are metabolically activated to the “oxon” form which has greater toxicity than the parent insecticide.05-1.69 (1.16 (4. ubiquitous lowlevel environmental exposures in humans would not be expected to result in inhibition of cholinesterase activity.19-2.95 (3.1 (10.70-4. 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.49-2.2) 6.. and behavior may occur at systemically nontoxic doses or at doses of chlorpyrifos that do not result in cholinergic signs (Aldridge et al.89) 4.31-1. These organophosphorus insecticides share a mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system. and other metabolites.71) 3. 2006..00) 1.44-6.14) 1.3) 8.31-4.07) 5.88-8.3) 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 1.30-1.6-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.45 (1.54 (2.58) 1.56) 2.11 (2..39-1. population from the National Health and Nutrition Examination Survey.66 (1.0) 10.49-2. Metabolic hydrolysis leads to the formation of TCPy.44 (1.33-7.80) 3.82-4.62) 90th 5.37 (1. Chlorpyrifos is eliminated from the body primarily in the urine with a half-life of approximately 27 hours (Nolan et al.8) 9. 2005. interval) 1.11-9.63 (5.85) Selected percentiles ( 95% confidence interval) Sample 95th 8.33 (1.0) 481 573 681 822 832 1113 99-00 01-02 99-00 01-02 1.05-8.S. Slotkin et al.59-2. In addition to being a metabolite of chlorpyrifos and chlorpyrifos-methyl in the body.92) 3.9 (12. Recent in vitro and in vivo animal studies suggest that effects on neuronal morphogenesis.93) 2.55) 1.85 (3.81 (3. vomiting.01) 99-00 01-02 99-00 01-02 99-00 01-02 3.99-8.11) 7.11 (2.42-2.90-9.3) 8.05) 3.58) 5.57) 9.83-11.57) 2.02 (5.09-3. Based on animal data and human cholinesterase monitoring during occupational exposure.43 (4.88-9.0) 16.03) 1.55 (1.7) 7.45-1.3 (7.44 (1.12) 1.85-4.47 (1.94-14.55 (4. TCPy can also occur in the environment from the breakdown of the parent compounds.24-24.84-6.09-1.28) 2.96) 3.58 (1. 2005.56) 5.82) 8.57-2.93 (4.20 (2.48 (1.72) 2. Survey Geometric mean (95% conf. 2002).32) 1. neurotransmission.00 (7.19) 6.. Urinary 3. 2006.24) 75th 2.15 (4.72-2.59) 3. Roy et al.22) 1.44 (6.64-7.81) 2.940-1.06 (5.23) 14.58 (4.97) 3.17-4.

the weighted population mean of TCPy measurements was approximately three times higher (Adgate.113(8):1027-1031.5. Burgess SC. Of 482 pregnant women living in an agricultural community. Freeman NC. Koch et al. suggesting changing low-level exposure and variance in collection timing with respect to exposure (Meeker et al. U.. Berent S..109(6):583-590.. In a probability-based sample of 102 Minnesota children aged 3-13 years. but levels were roughly four to six times higher than the geometric means in the U. Occup Environ Med 2006. 1995) and were similar to levels reported in studies of healthy adults in Germany (Koch et al.. 2007). (1999) reported mean urinary TCPy levels in a sample of Maryland adults that were about three times higher than adults in the U.S. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Biomonitoring Information Urinary TCPy levels reflect recent exposure. Estimation of dose or intake based on the urinary excretion of TCPy indicates that environmental doses are generally below recommended limits (Hore et al. 2005). Finding a measurable amount of TCPy in urine does not mean that the level will result in an adverse health effect.6-trichloro-2-pyridinol in the Italian population—validation of analytical method and preliminary results (multicentric study). 2004). Aprea C.63(3):218220. 1992.gov/toxpro2. subsamples of NHANES 1999-2000 and 2001-2002 (CDC.EPA. Environ Health Perspect 2001.html and from U.. et al. 2001) than the corresponding values reported for the group aged 6-11 years from the NHANES 1999-2000 subsample (CDC. 2001). Meyer A. 2005). Lotti A. 2006) and episodically many times higher for pesticide applicators than median levels from NHANES 1999-2000 (CDC. 2004).e. 2005. Additional information about external exposure (i. Fourth National Report on Human Exposure to Environmental Chemicals 137 . Perera et al. urinary TCPy levels in children were reported not to have increased (Hore et al. Curwin et al. urinary TCPy levels averaged about sixfold higher than those in the NHANES 1999-2000 subsample (Mandel et al. Whyatt et al. 2005). Following crack-and-crevice application of chlorpyrifos in their homes. Albers JW. J AOAC Int 1999. the geometric mean urinary TCPy levels were similar in parents and children.Reference values of urinary 3. Eberly LE. Environ Health Perspect 2005. Barisano A. 2001) and Italy (Aprea et al.S. Chlorpyrifos is not considered to be mutagenic or carcinogenic (NTP.gov/pesticides/.. Barr DB. Slotkin TA. In Minnesota and South Carolina farmers who used chlorpyrifos.. Burns CJ. 2005).92(2):500-506.. EPA at: http://www.. representative subsample of NHANES 19992000 (CDC. Lioy PJ. Urinary levels of TCPy have been found to be hundredsfold higher for chlorpyrifos manufacturing workers (Burns et al. 2005) appear roughly similar to values reported for a nonrandom subsample of NHANES III (1988-1994) participants (Hill et al. 2005. Betancourt AM.. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample.atsdr. 2000). Seidler FJ.Organophosphorus Insecticides: Specific Metabolites 2004.. Some reproductive and teratogenic effects in animal testing were only observed at high doses of chlorpyrifos that caused overt maternal toxicity. MacIntosh et al..S. Giordani B..epa. Other small studies of environmentally-exposed persons have shown a high frequency of detecting low levels of TCPy. 2005. 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. References Adgate JL. but not chlorpyrifos.. Replacing conventional diets with organic diets in 23 children led to about a fourfold decrease in urinary levels of chlorpyrifos. 2002). population (CDC. 2005). Clayton CA. Chlorpyrifos levels in house dust and hand rinses did not correlate with levels of TCPy in urine (Lioy et al. Betta A. Garabrant D. Alterations in central nervous system serotonergic and dopaminergic synaptic activity in adulthood after prenatal or neonatal chlorpyrifos exposure. Catenacci G. Effect of developmental exposure to chlorpyrifos on the expression of neurotrophin growth factors and cell-specific markers in neonatal rat brain. Levels of TCPy in the U.S.S.cdc. median urinary levels on the conventional diet were several fold higher than those in the NHANES 1999-2000 subsample (Lu et al. In Iowa farm families using several different pesticides. Chlorpyrifos exposure and biological monitoring among manufacturing workers.82(2):305-312. 76% had detectable levels of TCPy and levels were similar to those reported for NHANES 1999-2000 (Eskenazi et al. Magnaghi S. Measurements of urinary TCPy in single spot urine collections show variability over time in environmentally exposed individuals and are poorly correlated between collections. Haidar S. 2006).. Aldridge JE. et al. Toxicol Sci 2006. environmental levels) and health effects is available from ATSDR at: http://www. CDC. 2005).. 2003. Carr RL. et al. 1999).

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Freeman N.114(10):1542-1546. Scand J Work Environ Health 2005.6-trichloro-2-pyridinol.org/documents/jmpr/jmpmono/ v99pr03. Hines CJ. Chlorpyrifos exerts opposing effects on axonal and dendritic growth in primary neuronal cultures. Heederik D. Dick RB. Gregg M. 4/7/09 Koch HM. Hill RH Jr. Chapman P. Lorenzini P. Tsai WY. Toxicol Appl Pharmacol 2005. Curwin BD.9(5):494-501. Bruun D. Harley K. Jones PA. Int J Hyg Environ Health 2001. Venerosi A. Kinney P. mothers and fathers living in farm and non-farm households in Iowa. et al. et al. Hardt J. Freshour NL. Third National Report on Human Exposure to Environmental Chemicals. Bennett DH.cfm?objectid=6F5E95EB-F1F6-975E7C20F4211536F46F. Fortuna S. Environmental Health Criteria 198. Urinary pesticide concentrations among children. House dust levels of selected insecticides and a herbicide measured by the EL and LWW samplers and comparisons to hand rinses and urine metabolites. Ozkaynak H.73:8-15. Bailey SL. Shealy DB.5. Robertson GL. Comparative developmental neurotoxicity of organophosphate insecticides: effects on brain development are separable from systemic toxicity. Developmental neurotoxicity of organophosphorous pesticides: fetal and neonatal exposure to chlorpyrifos alters sex specific behaviors at adulthood in mice.71:99108. et al.114(2):260-263.155(1):71-80. gov/ntpweb/index. Rauh V.nih. Levin ED. et al. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population. Quantitative morphological assessment reveals neuronal and glial deficits in hippocampus after a brief subtoxic exposure to chlorpyrifos in neonatal rats. Seidler FJ. Seidler FJ. Ryan PB. J Expo Anal Environ Epidemiol 1999. et al. Lu C. Bravo R. Striley C. Lein PJ. Slotkin TA. Yang D. Fenske RA. Meeker JD. Zhang J. Camann D. et al. Hammerstrom KA. Chlorpyrifos accumulation patterns for child-accessible surfaces and objects and urinary metabolite excretion by children for 2 weeks after crack-and-crevice application. Gurunathan S. chlorpyrifos. Slotkin TA. J Expo Anal Environ Epidemiol 2005. Robson M. Environ Health Perspect 2003. Available at URL: http://ntp. Baker BA.S.31 Suppl 1:98-104. Saunders JH. Croghan CW. J Expo Anal Environ Epidemiol 2005. A longitudinal investigation of selected pesticide metabolites in urine. Environ Health Perspect 2000. et al. Honeycutt R. Acquavella JF. Freeman N.113(2):211-219. et al. et al. Needham LL. Howell RJ. Eskenazi B.111(2):201-205.6-trichloro 2-pyridinol in their everyday environments. J Expo Anal Environ Epidemiol 2000. Chuang JC. Temporal variability of urinary levels of nonpersistent insecticides in adult men. Available at URL: http://www. Roy TS. Reid TM. et al. Biomonitoring for farm families in the farm family exposure study. Bravo R.114(5):746-751.112(10):1116-1124. Bradman A. Wartenberg D. Pesticide residues in urine of adults living in the United States: reference range concentrations. Jett DA. Ryan L. Edwards RD. Interim registration eligibility decision for chlorpyrifos. Kromhout H. Sharma V. Hore P.51(1):53-65.207(2):112-124. Levin ED. Chrislip DW. Barr DB.niehs. Alexander BH.htm.10(4):327-340.108(4):293-300.93(1):105-113. Toxicol Appl Pharmacol 1984. Chlorpyrifos: pharmacokinetics in human volunteers. Lioy PJ. Head SL. International Programme on Chemical Safety-INCHEM (IPCS). Jewell NP. MacIntosh DL. Environmental Protection Agency (U. 2921-882. Slotkin TA.204(2-3):175-180. Ryde IT. Environ Health Perspect 2004. 4/7/09 Perera FP. U. EPA). Atlanta (GA). Ricceri L. Barr D.15(3):271-281. Toxicol Sci 2006. Bucelli R. Hein MJ. Baker S. Chlorpyrifos. Effects of transplacental exposure to environmental pollution on birth outcomes in a multiethnic population. Environ Res 1995. Biological monitoring of exposure of the general population to the organophosphorus pesticides chlorpyrifos and chlorpyrifos-methyl by determination of their specific metabolite 3. Environ Health Perspect 2006. 1992. Nolan RJ. Morgan MK. Weltzien E. Adgate JL. Sheldon LS. Pellizzari E. Toepel K. Barr DB. Irish R. February 5. Capone F. Environ Health Perspect 2005.

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

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

* Not calculated: proportion of results below limit of detection was too high to provide a valid result.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.200 (<LOD-. Urinary 3-Chloro-7-hydroxy-4-methyl-2H-chromen-2-one/ol (creatinine corrected) Metabolite of Coumaphos Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.S.670 (<LOD-1.380 (<LOD-. see Data Analysis section) for Survey year 01-02 is 0. Survey Geometric mean (95% conf.560) < LOD 659 700 920 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. population from the National Health and Nutrition Examination Survey.270) < LOD 659 701 920 Limit of detection (LOD. Fourth National Report on Human Exposure to Environmental Chemicals 141 . interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2480 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2481 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .200 (<LOD-. Survey Geometric mean (95% conf. population from the National Health and Nutrition Examination Survey.2. < LOD means less than the limit of detection.S.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 . 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.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 .

U. Olsson AO. 2005. EPA). Sadowski MA. Atlanta (GA).pdf. September 2000.S.gov/oppsrrd1/ REDs/0018tred. Nguyen JV. Eigenberg DA. Reprod Toxicol 1998.S. Barr DB. Environmental Protection Agency (U.12(6):619-645.epa. Comparative organophosphate-induced effects observed in adult and neonatal Sprague-Dawley rats during the conduct of multigeneration toxicity studies. Reregistration eligibility decision (RED) addendum and FPQA tolerance reassessment progress report: Coumaphos. 1/14/09 142 Fourth National Report on Human Exposure to Environmental Chemicals . Freshwater KJ.Organophosphorus Insecticides: Specific Metabolites References Astroff AB. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine. Anal Bioanal Chem 2003.376(6):808-815. Available at URL: http://www. Centers for Disease Control and Prevention (CDC). EPA 738-R-00-010. Third National Report on Human Exposure to Environmental Chemicals.

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

. in the 2001-2002 subsample (CDC.76 (<LOD-3. Additional information about external exposure (i. Human health effects from diazinon at low environmental doses or at biomonitored levels from low environmental exposures are unknown. weakness. paralysis.48) < LOD < LOD 644 678 484 699 554 956 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. In animals.atsdr. 1986. Diazinon has moderate acute toxicity in animal studies. most of the measurements of 2-isopropyl-4-methyl6-hydroxypyrimidine in urine were below the limit of detection.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. Olsson et al.45 and 1. Thus.72 (<LOD-4. Survey Geometric mean (95% conf. and producing acute symptoms such as nausea. environmental levels) and health effects is available from ATSDR at: http://www. or reproductive toxicant (IPCS.. Seifert and Pewnim. In two nonrandom samples of United States adults and children. 2-isopropyl-4-methyl-6-hydroxypyrimidine was detectable in 57% and 43% of the 130 and 140 participants.S.gov/toxpro2. subsamples of NHANES 1999-2000 and 20012002. The U. Intoxications in humans from intentional overdose. 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. teratogen. respectively (Baker et al. Diazinon is not considered to be a mutagen. EPA at: http://www. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 144 Fourth National Report on Human Exposure to Environmental Chemicals . interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1842 2534 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2.EPA considers diazinon unlikely to be carcinogenic in humans. Biomonitoring Information Urinary levels of 2-isopropyl-4-methyl-6hydroxypyrimidine reflect recent exposure.Organophosphorus Insecticides: Specific Metabolites from dialkyl phosphate metabolite excretion (Garfitt et al..cdc. There has been only limited study of diazinon at systemically non-toxic doses that do not result in cholinergic signs (Anthony et al. At high doses..S. respectively. agricultural. 1998)..S. In addition to being a human metabolite of diazinon. diazinon does not accumulate in tissues (IPCS. resulting in excess acetylcholine at nerve terminals. and indoor applications have been documented.49 μg/L. 2-isopropyl-4-methyl-6-hydroxypyrimidine can also occur in the environment from the breakdown of the parent compound. population from the National Health and Nutrition Examination Survey. animal carcinogen. the detection of 2-isopropyl4-methyl-6-hydroxypyrimidine in a person’s urine may reflect exposure to the environmental degradate.S. 1992).epa. although the 95th percentiles for children 6-11 years old and for non-Hispanic blacks were 1. and seizures. 2000.gov/pesticides/. cholinergic effects. diazinon and other organophosphorus insecticides share a mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system. In the U.e. 2003). 1986 Rajendra et al. 2002). 1998). vomiting.html and from U..

Pesticides in the Nation’s Streams and Ground Water. Biological monitoring of exposure to organophosphorus insecticides in a group of horticultural greenhouse workers. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Effects of chronic intake of diazinon on blood and brain monoamines and amino acids. Fenske RA. Environmental Health Criteria 198. urinary 2-isopropyl-4-methyl-6hydroxypyrimidine was detected in less than 14% of multiple samples collected during varied diets (Lu et al. Available at URL: http://www. Pewnim T.S. urinary 2-isopropyl-4-methyl-6-hydroxypyrimidine levels were below the limit of detection (Bouchard et al. Barr DB.inchem. May 2004. Carrier G. Banister EW. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine. Bravo R.44(11):2243-2250. Cocker J. Bouchard M. revised February 15. Atlanta (GA). The Quality of Our Nation’s Waters. Anal Bioanal Chem 2003. Irish R.9(2):117-131. In 23 children. 1/14/09 U. Jones K. Drug Chem Toxicol 1986. Quantification of selected pesticide metabolites in human urine using isotope dilution high-performance liquid chromatography/ tandem mass spectrometry. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. Dumas P. Nguyen JV. Environ Health Perspect 2003.usgs. 4/7/09 Lu C. Redmon JB. Brunet RC.37(4):501-507. 6/1/09 Fourth National Report on Human Exposure to Environmental Chemicals 145 . March 2006. Barr DB. Bull Environ Contam Toxicol 1986. Diazinon. EPA 738-R-04-006.50(5):505-515.pdf. Exposure to the organophosphate diazinon: data from a human volunteer study with oral and dermal doses. References Anthony J.S. In 54 Canadian greenhouse workers. Environ Health Perspect 2006.376(6):808-815. EPA). Study for Future Families Research Group. 1998. Biochem Pharmacol 1992.gov/ oppsrrd1/REDs/diazinon_ired. Noisel N. 2005.org/documents/ehc/ehc/ehc198. Interim reregistration eligibility decision (IRED. International Programme on Chemical Safety-INCHEM (IPCS). Garfitt SJ. Rajendra W.S. Alteration of mice L-tryptophan metabolism by the organophosphorous acid triester diazinon.111(12):1478-1484.10(6 Pt 2):789-798. et al. Swan SH. Banister E. J Expo Anal Environ Epidemiol 2000. Available at URL: http://pubs. Diazinon. Needham LL. Liu F. Barr DB. Seifert J. (2003) found that 2-isopropyl4-methyl-6-hydroxypyrimidine was detectable in 96% and 58% of the subjects. Oloffs PC.134(1-3):105-113. 2006).. Sadowski MA. Baker SE. Mason HJ. 2006). Swan et al.epa. Olsson AO. Environmental Protection Agency (U. Available at URL: http://www. U. Effect of sublethal levels of diazinon: histopathology of liver. Driskell WJ. In a small number of men visiting fertility clinics in Missouri and Minnesota. Drobnis EZ. 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. 1992-2001. 2007 [online]. Toxicol Lett 2002. Toepel K. Geological Survey (USGS). Third National Report on Human Exposure to Environmental Chemicals..htm. Centers for Disease Control and Prevention (CDC).Organophosphorus Insecticides: Specific Metabolites 2005).gov/circ/2005/1291/. Kruse RL. Oloffs PC. Semen quality in relation to biomarkers of pesticide exposure. Beeson MD.114(2):260-263. Barr DB. Ann Occup Hyg 2006. 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.

shrubs. 2007). population from the National Health and Nutrition Examination Survey.S. phosphorothioates such as malathion are metabolically activated to the “oxon” forms which have greater toxicity than the parent insecticide. which is an organophosphorus insecticide that is used on a wide variety of agricultural crops.EPA. 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. Human health effects from malathion at low environmental doses or at biomonitored levels from low environmental exposures are unknown. vomiting. cholinergic effects. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 1920 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 50th < LOD < LOD 75th < LOD 90th * 99-00 99-00 99-00 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2. malathion and other organophosphorus insecticides share a common mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system.80 (<LOD-5. 2000). Malathion is rapidly eliminated from the body within 12-24 hours (Bouchard et al. Once they are absorbed. malathion has low acute toxicity. It is registered for use in public health mosquito control. When malathion is used on food or feed crops. and other metabolites. or oral routes (U. Malathion is slowly absorbed through the skin.EPA. Survey Geometric mean (95% conf. malathion dicarboxylic acid. and seizures. Limited general population exposure occurs through the diet. usually only a small fraction of the crop is treated. 121-75-5 General Information Malathion dicarboxylic acid is a metabolite of malathion. gardens. Metabolism of malathion leads to the formation of malathion monocarboxylic acid. Pesticide applicators and agricultural workers can have higher exposures via dermal. It has a short halflife in soils and water and is not considered persistent in the environment. paralysis. 2006). and in government programs such as the USDA’s Boll Weevil Eradication Program.5%) to kill body lice. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”). malathion dicarboxylic acid can also occur in the environment from the breakdown of the parent compound. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Malathion is also used medically in lotion form (0.S. 2003). as well as lawns. In addition to being a metabolite of malathion. < LOD means less than the limit of detection. inhalational. see Data Analysis section) for Survey year 99-00 is 2. the detection of malathion dicarboxylic acid in a person’s urine may also reflect exposure to the environmental degradate. in fruit fly control. Compared with other organophosphorus insecticides. but is more rapidly and efficiently absorbed via ingestion. It is highly toxic to aquatic invertebrates and rare fish kills have been reported from wide area applications onto surface waters and runoff into waters. which may vary for some chemicals by year and by individual sample.. About 31-35% of oral doses of malathion are excreted in the urine as malathion monocarboxylic acid (Krieger and Dinoff. weakness. and plants. Estimated intakes for the general population have not exceeded recommended intake limits. It is moderately to highly toxic to fish. ornamental trees. 146 Fourth National Report on Human Exposure to Environmental Chemicals .64. 2006). Most of the estimated 15 million pounds used annually are applied to cotton (U. Malathion is infrequently detected in groundwater sampling (USGS. depending on the species. resulting in excess acetylcholine at nerve terminals. and producing acute symptoms such as nausea.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.Organophosphorus Insecticides: Specific Metabolites Malathion CAS No. Thus. At high doses.S.

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

pdf. MacIntosh DL. Eskenazi B.gov/circ/2005/1291/.74(2):following table of contents. 2007 [online]. Lu C. Available at URL: http://www.Organophosphorus Insecticides: Specific Metabolites References Adgate JL. Environ Health Perspect 2001. Bravo R. Environ Health Perspect 2004. Irish R. 2005.132(4):794-795. O’Neill JP. Quintana PJ. Erratum in: Toxicol Sci 2003 Aug. Am J Epidemiol 1990. Hooper K. Centers for Disease Control and Prevention (CDC). Third National Report on Human Exposure to Environmental Chemicals. Environ Mol Mutagen 1993. Am J Public Health 1987. Increased frequency of specific genomic deletions resulting from in vitro malathion exposure. Reproductive outcome in women exposed to malathion. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population. Jewell NP. International Programme on Chemical Safety-INCHEM (IPCS). Environmental Protection Agency (U.73(1):182-94.epa. Kedan G. Malathion (addendum).gov/oppsrrd1/REDs/ malathion_red. Mutat Res 2002. Available at URL: http://pubs. Nicklas JA. and cholinesterase status of date dusters and harvesters in California. Environ Health Perspect 2006. 6/1/09 U.514(1-2):223231. Cancer Res 1996. Available at URL: http://www.112(10):1116-1124.38(4):546-553.usgs.109(6):583-590. Barr DB. 4/7/09 Kissel JC. July 2006. Eberly LE. Krieger RI. Kizer KW: Exposure to aerial malathion application and the occurrence of congenital anomalies and low birthweight. U. Needham LL. Fenske RA.77:1009-1010. Jaloszynski P. Barr DB. Gosselin NH. Trzeciak A. A longitudinal investigation of selected pesticide metabolites in urine. Malathion deposition. Ryan PB. J Expo Anal Environ Epidemiol 1999. Genetic toxicity of malathion: a review. Rappaport E. Petitti D. EPA). Lu C.22(1):7-17. Clayton CA. Bouchard M. Toepel K. March 2006. revised February 15. et al.114(2):260-263. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides.org/documents/jmpr/jmpmono/v2003pr06.inchem. Dinoff TM. Pluth JM. Pesticides in the Nation’s Streams and Ground Water. Prasad SB.445(2):275-283. Reregistration eligibility decision (RED) Malathion.S. Pesticides residues in food: 2003 FAO/WHO Meeting on Pesticide Residues. Brunet RC. metabolite clearance. et al.9(5):494-501.15(2):164-171. 6/1/09 148 Fourth National Report on Human Exposure to Environmental Chemicals . Thomas D. Hertz-Picciotto I.56(10):2393-2399. htm. Curl CL. Grether JK. Sharma GD. Genotoxic effects of malathion: an organophosphorus insecticide using three mammalian bioassays in vivo. Szyfter K. Barr DB. Mutat Res 1999. EPA 738-R06-030. Geological Survey (USGS). J Expo Anal Environ Epidemiol 2005. Griffith W.S. In vitro studies on the genotoxicity of the organophosphorus insecticide malathion and its two analogues. Giri S. Carrier G. Blasiak J. Toxicol Sci 2003 May. The Quality of Our Nation’s Waters. Neutra R. Samuel O. 1992-2001. Flessel P. Albertini RJ. Freeman NC. Atlanta (GA). Giri A. Barr DB. Arch Environ Contam Toxicol 2000. Harley K. Lioy PJ. Swan SH. Hammerstrom KA. Bradman A. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample. Goldhaber M. Comparison of organophosphorus pesticide metabolite levels in single and multiple daily urine samples collected from preschool children in Washington State.S. A toxicokinetic model of malathion and its metabolites as a tool to assess human exposure and risk through measurements of urinary biomarkers. et al. Harris JA. Weltzien E. Dumoulin MJ.

00) 3.90-11. 56-38-2 General Information Para-nitrophenol is a metabolite of the insecticides methyl parathion.30-3.90-9.70-3.70-6.22-3.61) < LOD 1.S. first registered in 1948.0) 3.20-5.50 (2.71 (2.28-4.41-4. Metabolism of ethyl or methyl parathion leads to the formation of paranitrophenol. 2007). < LOD means less than the limit of detection.850) < LOD .. methyl parathion was rapidly absorbed after ingestion.10 (<LOD-6. Both are toxic to birds.37-2. and to a lesser extent. and of the chemical nitrobenzene. Ethyl parathion.50) 1.57) 1. 2000).92) 5.70 (<LOD-3.910) < LOD < LOD < LOD 1.20 (<LOD-2.45) 5.50-9.50-14.45 (1.60) 1.37-4.09-1.10 (3.60-24.50 (2.58) 3.0) 3. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. pulmonary.49 (1. which may vary for some chemicals by year and by individual sample. Many previous registered agricultural uses of methyl parathion have been cancelled (U.70 (2.40 (1.80) 2.61) < LOD 1. population from the National Health and Nutrition Examination Survey.71) 971 1164 1018 1313 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .70 (2..770 (.48) 90th 2.16) < LOD 1.0 (3.700 (<LOD-.69 (2.40) 1.71 (3.40) 4.. phosphorothioates such as methyl and ethyl parathion are metabolically activated to the “oxon” forms which have greater toxicity than the parent insecticides.46 (3.50) 3. In animal studies.80 (1.28 (1. Given its limited use.00 (2.15-3. more slowly absorbed through the skin.910) < LOD < LOD .67 (1.30 (2.34 (3. but by 2003. and oral routes can occur in pesticide and agricultural workers (Muttray et al.44) 2.02-6.27) 2.990-1. Once absorbed. peak domestic use was as high as 5-6 million pounds per year. on cereal grains.40) 2.24) 479 565 680 813 830 1099 99-00 01-02 99-00 01-02 * * * * < LOD . interval) Selected percentiles ( 95% confidence interval) Sample 95th 5.20) 5.74) 5. Methyl parathion use is highly restricted.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 1.36-1. Survey Geometric mean (95% conf.10-1. Morgan et al.790 (<LOD-. O-ethyl-O-(4-nitrophenyl) phenylphosphonothioate.EPA.32-1.32-1.40-4.50 (1. 2006). was once a restricted-use insecticide with limited applications on certain agricultural crops. It had been applied to cotton. the potential for human exposure to either ethyl or methyl parathion through the diet or drinking water is low.40-3.18-3.28 (1. Methyl parathion has low water solubility.298-00-0 Ethyl Parathion CAS No.0) 3.70) 2.S.0) 2.940 (<LOD-2.20 (2.01) 695 660 518 679 603 941 Limit of detection (LOD.Organophosphorus Insecticides: Specific Metabolites Methyl Parathion CAS No.80 (2. 2003).10) 22. and Nitrobenzene Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.91-3.0) 3.69) 4.80 (2.50) 3.92-2.1. Fourth National Report on Human Exposure to Environmental Chemicals 149 .40-4.860 (<LOD-1.02) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD . binds tightly to soils resulting in low leachability. 2002.60-19.70-6. Methyl Parathion. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Urinary para-Nitrophenol Metabolite of Ethyl Parathion.730 (<LOD-.50 (1.30 (1. ethyl parathion.50 (1.37) 2.12) < LOD < LOD 1.10 (3.910) < LOD . In the 1990s. with limited applications in agriculture. and aquatic invertebrates.60-5.00 (2.8 and 0.47) 2.70) 2.21 (2.60-36.01-4.19 (.13-1.32-3.60 (4. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.66 (2. and has a short half-life in soils and on plants.57-4.S. Ethyl and methyl parathion are infrequently detected in groundwater sampling (USGS.30-16.50) 2.72 (3.0) 3.01) 4.33 (1. Increased risk of exposure via dermal. all registered uses were voluntarily cancelled (U.30-5. and eliminated rapidly from the body after absorption (Kramer et al.70-6.300-.33) 2.62 (1. Estimated intakes from diet and drinking water have been below recommended limits.10-11.70 (2.05) 4.70-3. 1977).67) < LOD 1.32 (1. Methyl parathion is not registered for residential use in the United States.50 (1.EPA.85 (2.79) 4.10) 4.70 (3.11-4.70) 2. fish.90 (1.37-4.89 (2.0) 4.21-1.26 (1.11) 2.

89 (2. para-nitrophenol can also occur in the environment from the breakdown of the parent these organophosphorus pesticides and from nitrobenzene. and seizures..84) 3.94-4. vomiting.43) 4. Methyl Parathion. 2005.00 (1. Jaga and Dharmani.13) 4.57-2.96 (1.33) 479 565 680 812 830 1099 99-00 01-02 99-00 01-02 * * * * < LOD .97-10.08 (1.940 (<LOD-1.72-2.EPA considers methyl parathion unlikely to be carcinogenic to humans.39 (1. methyl parathion.78) 2.70) 3. In addition to being a metabolite of methyl and ethyl parathion.20 (3.05) 4.9) 1.44-3.690-1. 150 Fourth National Report on Human Exposure to Environmental Chemicals . IARC does not consider ethyl parathion and methyl parathion classifiable as human carcinogens. 1995).cdc. 1995. Lores et al.25 (2.880 (. 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.33-3.88) 1. WHO. Parathion and methyl parathion have high acute toxicity in animal testing. and other organophosphorus insecticides share a common mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system.57) 6. gov/pesticides/.530) < LOD < LOD < LOD .09) 2.79) 1.930 (.10) 90th 2.30-1.59 (1.4 (3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.80 (1. and other metabolites.850-1.78-2.97 (2. At high animal doses of methyl parathion.79 (1.08) < LOD . 2004).78 (2.86 (2.440 (<LOD-.950) < LOD ..01 (2.07) 2.04) 1.78-2.60) 2. but lists ethyl parathion as a possible human carcinogen. resulting in excess acetylcholine at nerve terminals.10 (1.98-7. gov/toxpro2.31-3.2) 2. weakness. environmental levels) and health effects is available from ATSDR at: http://www.01-3.310-.07 (1. EPA at: http://www.540) < LOD .93 (2.15-10.30) 3.S.71 (1.800-1.26) 17. Slotkin et al.500) < LOD < LOD .01 (. Karanth and Pope et al.11) 1. 1978. Overt cholinergic toxicity and death from methyl and ethyl parathion have been described following suicidal ingestion.870) < LOD .20) .29) 2. teratogenic. Human health effects from parathion or ethyl parathion at low environmental doses or at biomonitored levels from low environmental exposures are unknown.48-4.95) 1.29 (2.73 (1.60 (1. Survey Geometric mean (95% conf.71) 1. cholinergic effects..33-6. Zurich et al. U. and producing acute symptoms such as nausea.60-2. ethyl parathion.41-2.67 (3.31) < LOD .970 (. 2006. and Nitrobenzene Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.680 (<LOD-1.08-3.04 (2.720-1. 1991).720 (<LOD-.21-21.97 (<LOD-4.00) 2.80 (1.e.S.3) 2. 2003.15) 3.83 (1.1) 2.Organophosphorus Insecticides: Specific Metabolites Metabolites”).730-1.17) . 2006.21) 1.56-2.840 (.55 (<LOD-3. interval) Selected percentiles ( 95% confidence interval) Sample 95th 4. In large doses.33-3.25) 1.16-4.430 (.82 (2.790-. 1990.44-3.atsdr.88 (1. 2004).14-3.77-7.91) 1.980 (.00 (1.35-3.26 (1.87 (1.7) 3. does not inhibit acetylcholinesterase enzymes.29) 1.20) 3.94-47..55) 2. retinal atrophy and sciatic nerve degeneration have also been observed (IPCS.S.91 (1.17-4.39) 1.. Urinary para-Nitrophenol (creatinine corrected) Metabolite of Ethyl Parathion.html and from U.13-12.2) 2.830-1.57-7.90 (1.. the detection of para-nitrophenol in a person’s urine may also reflect exposure to the environmental degradate. paranitrophenol. The metabolite. or generally to have reproductive toxicity at doses below those causing acetylcholinesterase inhibition in most animal studies (IPCS.11-4.37-1.23) 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 .45) 695 660 518 678 603 941 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.03) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD . Additional information about external exposure (i.640) < LOD < LOD 1. and unintentional acute or chronic high-level occupational exposure (Hill et al.23) 1.epa.76-14..400 (<LOD-.96 (1. Thus.67-2. Orsorio et al.930 (.35-3. accidental exposure.89 (2.790-1.06) 971 1164 1018 1312 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .82) < LOD . population from the National Health and Nutrition Examination Survey. Methyl parathion is not considered genotoxic..92 (2.370 (<LOD-.38-3.61) 4. paralysis.970 (.

Environ Res 1995.inchem. 2005). Pathak S. Lewalter J.33(5):270-276. McClure PC. Turner WE.. Pope C. Leng G.. et al..org/documents/jmpr/jmpmono/v95pr14. In a study of workers who handle parathion. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population.215(3):182-190. 2002). 4/7/09 Jaga K. Available at URL: http:// www. Role of individual susceptibility in risk assessment of pesticides. 2002. 2005). 2005. Hryhorczuk DO. J Expo Anal Environ Epidemiol 2005. Chicago area methyl parathion response. Dharmani C. 1999). and levels were similar or slightly lower that those in a small convenience sample of the U. J Anal Toxicol 1990.110 Suppl 6:1075-1078. Giordano G. Comparison of organophosphorus pesticide metabolite levels in single and multiple daily urine samples collected from preschool children in Washington State. Urinary excretion of paranitrophenol and alkyl phosphates following ingestion of methyl or ethyl parathion by human subjects. et al. CDC. Shealy DB. Slach EF. Hill RH Jr. Measurement of p-nitrophenol in the urine of residents whose homes were contaminated with methyl parathion. Weltzien E. Arch Environ Contam Toxicol 1977. Runkle KD. Bradman A.112(10):1116-1124.110 Suppl 6:1085-1091. Alley CC. Guizzetti M. Hill RH Jr. Neurotoxicol Teratol 2003. Kramer RE. Barr DB. Pesticide workers may have much higher levels following pesticide applications. Gregg M. Cline RE. oral or dermal administration. Environ Health Perspect 2002. Lu C. end-of-shift urinary para-nitrophenol levels ranged from 190 to 410 µg/ gram of creatinine (Leng and Lewalter. Pesticide residues in urine of adults living in the United States: reference range concentrations.Organophosphorus Insecticides: Specific Metabolites Biomonitoring Information Urinary levels of para-nitrophenol reflect recent exposure. Head SL. Parathion-Methyl (addendum). 2005. Environ Health Perspect 2004. Occup Environ Med 1999. International Programme on Chemical Safety-INCHEM (IPCS). 2005. Moomey CM. a range of values several hundred times higher than levels found in the U. and many residents were symptomatic (Barr et al. Arch Environ Health 1978. population (Olsson et al. McCann et al.71:99108.15(2):164-171. References Barr DB.S. Lin LI. Harley K. Organophosphorus pesticide poisonings in humans: determination of residues and metabolites in tissues and urine. Jewell NP. ACGIH recommends a BEI of 0. Effect of organophosphorus insecticides and their metabolites on astroglial cell proliferation. Morgan DP. Ashley DL. Rubin et al. Moseman RF. Centers for Disease Control and Prevention (CDC). 2004).5 mg (500 µg)/g creatinine for workers at the end of shift.. Methyl parathion: an organophosphate insecticide not quite forgotten. Wellman SE. Rockhold RW. J Biomed Sci 2002.. et al. Baker RC. 1995. et al.. Head SL.14(4):213-216. Baker S. Environ Health Perspect 2002. Barr DB. Laboratory investigation of a poisoning epidemic in Sierra Leone.htm. Kissel JC.9:311-320. Bailey SL. Hill et al.56(7):449553. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 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. Baker SE. DiPietro E. 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. general population (CDC. 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.25(5):599-606.21(1):5767. Kedan G. Atlanta (GA). Griffith W. Costa LG.S.. Needham LL. 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. Karanth S. Lores EM. Toxicology 2005. 2002. 2003) and in 482 pregnant females from an agricultural region of California (Eskenazi et al. Barr DB.6(2-3):159-173. Third National Report on Human Exposure to Environmental Chemicals. Fourth National Report on Human Exposure to Environmental Chemicals 151 . Finding a measurable amount of para-nitrophenol in urine does not mean that the level will result in an adverse health effect. Clark JM. Barr JR. Hetzler HL. Curl CL. 1995). McCann KG. Age-related effects of chlorpyrifos and parathion on acetylcholine synthesis in rat striatum. Bradway DE. Eskenazi B. Rev Environ Health 2006. et al. Pharmacokinetics of methyl parathion: a comparison following single intravenous.

Ryde IT. Sadowski MA. 0153. Rosenberg J. Involvement of glial cells in the neurotoxicity of parathion and chlorpyrifos.D. Available at URL: http://www.pdf. Hill RH Jr. 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. Toxicol Appl Pharmacol 2004.pdf. 1992-2001. U. et al. Pesticides in the Nation’s Streams and Ground Water.376(6):808-815. Assessment of human exposure and human health effects after indoor application of methyl parathion in Lorain County. Environmental Protection Agency (U. revised February 15. Case No. 1995-1996. Available at URL: http://www.S.usgs.04/106. Osorio AM.114(10):1542-1546.int/water_sanitation_health/dwq/chemicals/ methylparathion. EPA-738-FOO-009. EPA). Levin ED. September 2000. Kieszak S. Costa LG. May 2003. Nguyen JV. 1/14/09 U. Tate CA. Ohio. Slotkin TA. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine. Investigation of a fatality among parathion applicators in California. 6/1/09 World Health Organization (WHO). R. Mengle DC.Organophosphorus Insecticides: Specific Metabolites Muttray A. Barr DB. Methyl parathion in drinking water. Honegger P.gov/oppsrrd1/REDs/factsheets/0155fct. 5/19/09 Zurich MG. Schilter B. 2004. 2007 [online]. External and internal exposure of wine growers spraying methyl parathion. Toxicol Lett 2006. Ethyl parathion. Yacovac R. Jung D. Am J Ind Med 1991. Seidler FJ. Letzel S.E. WHO/SDE/WSH/03. Dunlop B. The Quality of Our Nation’s Waters. 152 Fourth National Report on Human Exposure to Environmental Chemicals . Backer G. Environ Health Perspect 2006. Olsson AO. Geological Survey (USGS). Environ Health Perspect 2002.gov/circ/2005/1291/.S. EPA).epa.20(4):533-546.162(2-3):219-224. 1/12/07 U. Rubin C.who.epa. gov/oppsrrd1/REDs/methylparathion_ired.110 Suppl 6:1047-1051. Interim reregistration eligibility decision (IRED) for Methyl Parathion. Anal Bioanal Chem 2003. Available at URL: http://pubs.S. Available at URL: http://www. March 2006. Facts.S. Ames RG. Monnet-Tschudi F.S. Hill G. Esteban E.201(2):97-104. Environmental Protection Agency (U. pdf.

The metabolite 2-(diethylamino)-6-methylpyrimidin-4-ol/one does not inhibit acetylcholinesterase enzymes. pirimiphos-methyl and other organophosphorus insecticides share a mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system. In the general population. teratogenic. 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. 29232-93-7 General Information The chemical 2-(diethylamino)-6-methylpyrimidin-4-ol/ one is a metabolite of the organophosphorus insecticide pirimiphos-methyl. weevils. 2006). and it is not considered persistent. fish. paralysis. It easily hydrolyzes in the environment to 2-(diethylamino)-6-methylpyrimidine and other breakdown products. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”). Estimated intakes from diet and water have not exceeded recommended intake limits (U. pirimiphos-methyl is rapidly absorbed and metabolized to 12 metabolites. Fourth National Report on Human Exposure to Environmental Chemicals 153 . Biomonitoring Information Urinary levels of 2-(diethylamino)-6-methylpyrimidin-4ol/one reflect recent exposure. Olsson et al. Once absorbed.S.gov/pesticides/.EPA. Finding a measurable amount of 2-(diethylamino)-6methylpyrimidin-4-ol/one in urine does not mean that the level will result in an adverse health effect. and moths on stored grain products such as corn. 1992. sorghum. In the U.47 μg/L for the total population (CDC. EPA at: http://www.epa. Metabolic hydrolysis leads to the formation of 2-(diethylamino)-6methylpyrimidin-4-ol/one. 2006). Thus. and producing acute symptoms such as nausea. 1992). subsample of NHANES 2001-2002.1% of the sampled population. and aquatic invertebrates.Organophosphorus Insecticides: Specific Metabolites Pirimiphos-methyl CAS No. 2-(diethylamino)-6-methylpyrimidin-4-ol/one can also occur in the environment. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. cholinergic effects. although the 95th percentile was characterized at 0. vomiting. occurrence of such toxicity is mitigated by its rapid degradation and its use in closed storage systems. Pirimiphos-methyl is not considered mutagenic. Human health effects from pirimiphos-methyl at low environmental doses or at biomonitored levels from low environmental exposures are unknown. In addition to being a human metabolite of pirimiphos-methyl in the body.S. U.S. Biomonitoring studies of 2-(diethylamino)-6-methylpyrimidin-4-ol/ one provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of pirimiphos-methyl than are found in the general population. 2003). 2005). In animal studies. In a nonrandom sample of 140 urine specimens obtained from adults and children in the United States. It has a lesser use as a cattle ear tag application to control flies.EPA. or reproductive toxicity (IPCS. which are mainly excreted in the urine (IPCS. Additional information about pesticides is available from U. or known to cause delayed neurotoxicity. and seed. At high doses. Pirimiphos-methyl is not registered for residential use in the United States. and seizures. Pirimiphosmethyl has low acute toxicity in animal studies. and other metabolites. which has limited applications for control of beetles. weakness.S. Though considered moderately-to-highly toxic in birds. (2003) detected 2-(diethylamino)6-methylpyrimidin-4-ol/one in 7. Toxic effects below doses that cause inhibition of acetylcholinesterase are unknown. phosphorothioates such as pirimiphos-methyl are metabolically activated to the “oxon” form which has greater toxicity than the parent insecticide. most of the urinary measurements of 2-(diethylamino)-6-methylpyrimidin-4-ol/one were below the limit of detection. the detection of 2-(diethylamino)-6-methylpyrimidin-4-ol/one may also reflect exposure to the environmental degradate.

670 (<LOD-1.780 (<LOD-1.430 (<LOD-. < LOD means less than the limit of detection.500 (.94) .880) 567 810 1104 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD .200-. which may vary for some chemicals by year and by individual sample.930) size 2481 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD .840) 669 687 929 Limit of detection (LOD.210-.27) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.840 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th .700-1.670) 567 810 1104 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD .00) 669 687 929 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.210-1.470 (.770) size 2481 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD .780 (<LOD-1. population from the National Health and Nutrition Examination Survey. see Data Analysis section) for Survey year 01-02 is 0. Survey Geometric mean (95% conf.410 (<LOD-1.250 (<LOD-.210 (<LOD-. 154 Fourth National Report on Human Exposure to Environmental Chemicals .31) .S.S.08) 1165 1316 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .55) .950) < LOD < LOD 1.07) . interval) Selected percentiles ( 95% confidence interval) Sample 95th .850 (.740-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.460) 1165 1316 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . population from the National Health and Nutrition Examination Survey.300-1.580-1.780 (.15) < LOD .21) < LOD .700-.610 (<LOD-1.680 (<LOD-.740 (.760 (<LOD-.2.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. Survey Geometric mean (95% conf.780 (. 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.64) .17 (.820) < LOD < LOD .

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

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

Yang J. Idel H. Moniz AC. tremor. 2003. In developing rodents. hypersensitivity. Estrogenicity of pyrethroid insecticide metabolites. Toxicol Appl Pharmacol 1991.251(3):855-859. Varoli FM. Wolff MS..8(1):197-202. Florio JC. bioallethrin and deltamethrin. Moniz et al.atsdr. Signs and symptoms of acute pyrethroid poisoning after massive ingestions include agitation. Assessing estrogenic activity of pyrethroid insecticides using in vitro combination assays. Available from URL: http://www. Garey J. Levsen K. Eriksson and Fredriksson. Song L. Behavioral and endocrine changes induced by perinatal fenvalerate exposure in female rats.Pyrethroid Pesticides and other ion channels may also explain some pyrethroid effects. dopaminergic.23(6):665-673. Shaw IC. Human doseexcretion studies with the pyrethroid insecticide cyfluthrin: urinary metabolite profile following inhalation. Idel H. Int J Hyg Environ Health 2002. Eriksson P.. Leng A. Lemonica IP. Yamada T. Wang SL.gov/pesticides/ and from ATSDR at: http://www.50(2):245-255. et al. Fredriksson A.. salivation. paresthesias) reported in agricultural workers from 1996 to 2002 (Spencer and O’Malley. 2000.. Ose K. 2005).35(2 Pt 1):227-237. neurochemical changes in cholinergic. Seth PK. 2006. Soderlund et al. fenvalerate. 1999. 2003. Kamita Y. Berger-Preiss E. et al. Abell AD. Go et al. Wieseler B. and striatal dopamine levels in male and female rats. J Environ Monit 2006. Go V. Ranft U. Toxicol Appl Pharmacol 2006. Salzgeber SA. Neurosci Lett 2001. Guillot TS. Xenobiotica 1997. Bernardi MM. Wolff MS. Neurotoxicol Teratol 2001.. Chen JH.. Cruz-Casallas PE.300(3):161-165.gov/toxpro2. cdc. Spinosa HS. Bernardi MM. Zhao RC. Hu JY. IARC considers deltamethrin and permethrin as not classifiable as to their human carcinogenicity. Thomson BM.. Richardson JR.html. Kang IH.8(1):18-21. choreoathetosis. et al. 2003. McCarthy AR. Kuhn KH. Effects of prenatal exposure to deltamethrin on forced swimming behavior.27(4):609-614. Kim TS. References Agency for Toxic Substances and Disease Registry (ATSDR). Neurotoxic effects of two different pyrethroids.205(6):459-472.cdc. Miller GW. and seizures (ATSDR.S. Shukla Y.1/15/09 Aziz MH.. Bull Environ Contam Toxicol 1999. Caudle WM.. Generally. Regul Toxicol Pharmacol 2002. Sunami O.gov/toxprofiles/ tp155. Lee SJ. 2002. Kim et al. 2006). Transient dermal paresthesias have been reported among pesticide applicators after direct contact with certain types of pyrethroid pesticides. Lazarini CA. J Reprod Dev 2004. and catecholaminergic pathways and behavioral changes have been demonstrated at subacute and subchronic doses for some pyrethroid pesticides (Aziz et al. Elwan et al. Neurodevelopmental consequences of gestational exposure (GD14-GD20) to low dose deltamethrin in rats. Concomitant exposure to organophosphorus insecticides may increase pyrethroid toxicity by slowing metabolic clearance of the pyrethroid. the pyrethroids are not considered genotoxic in in vitro testing or carcinogenic in animal testing (WHO. et al. Kim IY. cyfluthrin was the most frequent pyrethroid associated with symptomatic effects (irritant respiratory and dermal effects. Sugiri D..108(1):78-85.html.. Toxicokinetics of pyrethroids in humans: consequences for biological monitoring. Estrogenic potential of certain pyrethroid compounds in the MCF-7 human breast carcinoma cell line. 2004. 1991. Shafer. Kim HS. Kuhn K. Adhami VM. Leng G. WHO. The pyrethroids in general use are not considered teratogenic or to have significant reproductive toxicity (ATSDR. Garey and Wolff.. EPA at: http://www.27(12):1273-1283. In California. Kunimatsu T. Estrogenic and antiprogestagenic activities of pyrethroid insecticides. epa. 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. Leng G. Lack of (anti-) androgenic or estrogenic effects of three pyrethroids (esfenvalerate. Elwan MA. Biochem Biophys Res Commun 1998. 2002). Hu et al. 2006.atsdr. 1998. Okuno Y. on immature and adult mice: changes in behavioral and muscarinic receptor variables. motor activity. Pauluhn J. Lazarini et al.62:101-108. Garey J. 2002). 2003. Agrawal AK. 2005). 2001. Shin JH. Ray et al. Fourth National Report on Human Exposure to Environmental Chemicals 157 . though a few pyrethroid pesticides and some metabolites have shown weak or inconsistent estrogenic effects on standardized assays (ATSDR. Kunimatsu et al. 2005). [Effects of fenvalerate on reproductive and endocrine systems of male rats] Zhonghua Nan Ke Xue 2002. Indoor pyrethroid exposure in homes with woollen textile floor coverings.107(3):173-177. Leng G. 2001. Human cases of systemic poisoning are rare and usually result from accidental exposure or intentional ingestion of pyrethroid insecticides.211(3):188-197. Lewalter J. Pyrethroid pesticide-induced alterations in dopamine transporter function. McCarthy et al. and permethrin) in the Hershberger and uterotrophic assays. 2005). Pogo BG. Neurotoxicol Teratol 2005. Additional information about pesticides is available from U. Toxicological profile for pyrethrins and pyrethroids. September 2003.

S.S. Developmental neurotoxicity of pyrethroid insecticides: critical review and future research needs.S. The metabolism of cypermethrin in man: differences in urinary metabolite profiles following oral and dermal administration. Soderlund DM. Sheets LP. O’Malley M. Available at URL: http://www. 1992–2001. Environ Health Perspect 2005. EPA). Permethrin Facts (Reregistration Eligibility Decision Fact Sheet).22(8):983-991. pdf. 5/26/09 U. June 2006b. Permethrin.38:95-101. Available at URL: http://whqlibdoc. Available at URL: http://www.int/hq/2005/WHO_ CDS_WHOPES_GCDPP_2005. 5/26/09 U. and therapy. 5/26/09 158 Fourth National Report on Human Exposure to Environmental Chemicals . et al. Available at URL: http://pubs. Mullin LS.epa. sumithrin synthetic pyrethroids for mosquito control. April 2002. Clark JM.gov/pesticides/ health/mosquitoes/pyrethroids4mosquitoes. Toxicology 2002. 5/26/09 Woollen BH. U. Laird WJ.htm.S. Environmental Protection Agency (U. Safety of pyrethroids for public health use. J Toxicol Clin Toxicol 2000.gov/ circ/2005/1291/.186:57-72.epa. Environmental Protection Agency (U. Mechanisms of pyrethroid neurotoxicity: implications for cumulative risk assessment.S. Pyrethroid illnesses in California. Environmental Protection Agency (U. resmethrin.S.pdf. Pyrethroid insecticides: poisoning syndromes. Sargent D.113(2):123-136. Piccirillo VJ. March 2006.171:3-59.who. Crofton KM.usgs. World Health Organization (WHO). Lesser JE. synergies.htm. Reregistration Eligibility Decision for Cypermethrin. Geological Survey (USGS). Pesticide and Evaluation Scheme. Spencer J.10. Revised February 25. Xenobiotica 1992.gov/oppsrrd1/REDs/cypermethrin_red. EPA). 2007. Available at URL: http://www. Marsh JR. Pesticides in the Nation’s Streams and Ground Water. Rev Environ Contam Toxicol 2006. Shafer TJ. Meyer DA. 19962002. EPA).gov/oppsrrd1/REDs/ factsheets/permethrin_fs. 5/26/09 U. Forshaw PJ.S.epa.Pyrethroid Pesticides Ray DE. 2005. June 2006a.

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

< LOD means less than the limit of detection.Pyrethroid Pesticides Urinary 4-Fluoro-3-phenoxybenzoic acid Metabolite of Cyfluthrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. population from the National Health and Nutrition Examination Survey. 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.S. which may vary for some chemicals by year and by individual sample. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 160 Fourth National Report on Human Exposure to Environmental Chemicals . Survey Geometric mean (95% conf. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.2.2 and 0.

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

162 Fourth National Report on Human Exposure to Environmental Chemicals . Barr DB. Angerer J. Ranft U. Centers for Disease Control and Prevention (CDC). Schulz C. Isotope dilution highperformance liquid chromatography-tandem mass spectrometry method for quantifying urinary metabolites of synthetic pyrethroid insecticides. Heudorf U.206(2):85-92. Olsson AO. Becker K.109(3):213-217. Idel H.77(1):67-72. Heudorf U. Angerer J. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides. Berger-Preiss E. Williams RL. Rev Environ Contam Toxicol 2006. Angerer J. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Int J Hyg Environ Health 2006. Human exposure to indoor residential cyfluthrin residues during a structured activity program. Krieger RI. O’Malley M. Spencer J. Bernard CE.209(3):293-299.46(3):281-288. Third National Report on Human Exposure to Environmental Chemicals. Ball M.13(2):112-119. Drexler H. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation.Pyrethroid Pesticides References Baker SE. Seiwert M. Environ Health Perspect 2001.209(3):221-233. Heudorf U. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine. Arch Environ Contam Toxicol 2004. Sugiri D. et al. Int J Hyg Environ Health 2006. Pyrethroid illnesses in California. 2005. Hoppe HW. 19962002. Leng G. J Expo Anal Environ Epidemiol 2003.186:57-72. Angerer J. Hadnagy W. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. Atlanta (GA). Int Arch Occup Environ Health 2004. Butte W. Kolossa-Gehring M. Int J Hyg Environ Health 2003.

220-.160 (<LOD-.Pyrethroid Pesticides Cyfluthrin the cis-metabolite is found in the urine.47 (.155-.310) .120-.600 (.670-1.690) .2-dimethylcyclopropane carboxylic acid is a metabolite formed from cis-permethrin. more of the trans-metabolite than Urinary cis-3-(2.210-.380-.250-.960 (.400-.240) .270 (.950-2.350) .2-Dichlorovinyl)-2. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.850 (.230) .790 (. The cis-isomer of permethrin has more potent insecticidal activity than transpermethrin. Fourth National Report on Human Exposure to Environmental Chemicals 163 . and trans-cyfluthrin.460 (. 1985.43) .770-1.600) .670 (.150 (.210) 90th .580-1.2-dimethylcyclopropane carboxylic acid that is formed in the environment from the degradation of these pesticides (George.880 (.2-dichlorovinyl)-2.S.870) 1.110-.140 (<LOD-.08) .24) 1.680 (..2-dichlorovinyl)-2.520) .68359-37-5 Cypermethrin Permethrin CAS No.530 (.2-dimethylcyclopropane carboxylic acid Metabolite of cis-Permethrin.28) 468 580 667 831 816 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .680-3.180 (.410) .610) .890 (. 1999).270 (. which may vary for some chemicals by year and by individual sample.220-.740-1.410) .2-dimethylcyclopropane carboxylic acid formed in the environment from the degradation of these pesticides (George. Kuhn et al.280 (.110-.50) .07 (.1 and 0. but can also reflect exposure to trans-3(2. the presence of trans-3-(2. trans-cypermethrin.250 (.340) .200-.330 (.2-dichlorovinyl)-2.10) 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 .280-.13 (. Biomonitoring Information Urinary levels of cis.700) .68) .610) .240) .220) .2-dichlorovinyl)2.300 (.140 (.380-.and trans-isomers.2-dichlorovinyl)- CAS No.570-. Survey Geometric mean (95% conf.340-. cis-permethrin.470-1.730 (. The presence of cis-3-(2.380-.110-. population from the National Health and Nutrition Examination Survey.110 (<LOD-. trans-permethrin.200) .68 (.180) .200-.630) .44 (.370-.200 (.28) 671 680 518 701 591 957 Limit of detection (LOD.370 (.120-.510 (.270-.740 (.120-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Generally.202 (.1.460-. transcypermethrin and trans-cyfluthrin.780) .15) .or trans-3-(2.790-1.790) .920) 1. cis-3-(2. Similarly.490-.570 (. Cyfluthrin.600-1.32) .650-1.580) 1.440 (.2dichlorovinyl)-2.200-.630-.2-dimethylcyclopropane carboxylic acid in urine not only reflects the metabolic transformation of any of the three pesticides.200) .730 (. cis-cypermethrin.820 (.68) .52645-53-1 General Information Several pyrethroid pesticides are formulated as a mixture of cis.80) .790-1.2-dimethylcyclopropane carboxylic acid is a metabolite formed from trans-permethrin.430-.270 (.680) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .630) . interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.380) .330) .420-.500 (.210) .120-.21) . but it can also reflect exposure to cis-3-(2.262) * * * < LOD < LOD .35) .460-1. In the body. Kuhn et al.710-1.220-.300-.510 (.2dichlorovinyl)-2.730 (.300-. 1999). ciscypermethrin and cis-cyfluthrin.670-1.630 (. 1985.710) .35) 1.260 (. < LOD means less than the limit of detection. and cis-Cypermethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.900 (.170 (.220-.160 (.890 (. The chemical trans-3(2.53) .200) < LOD < LOD < LOD .770) .08) 947 1193 1004 1346 99-00 01-02 99-00 01-02 99-00 01-02 * * .910-5. and ciscyfluthrin.54) ..740-2.380 (.160 (.740) 1.490-1.12 (. 52315-07-8 CAS No.300 (.640 (.490-1.340) .470 (.550) .500 (.670-2.490-.11) .510 (.77 (.2dimethylcyclopropane carboxylic acid in urine not only reflects the metabolic transformation of any of the three pesticides.

2-dichlorovinyl)-2.12-2.180 (. 2006.530 (.640) 1.170) < LOD < LOD < LOD .290) .470-1.270 (.430 (. Studies in Germany of 396 children and adolescents (Becker et al.550) .270) .200) .03) 1. post- Urinary cis-3-(2. 2003).750-1.590) .170 (..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 .11) 1.320) .67 (.600 (.830) .2dichlorovinyl)-2.350) . Lu et al.104-. 2005).410) .440-.2-dimethylcyclopropane carboxylic acid levels at the 95th percentile were about one-third of the 95th percentile in the NHANES 20012002 subsample (CDC.59 (1..250 (<LOD-.59) .2-dimethylcyclopropane carboxylic acid did not increase.Pyrethroid Pesticides 2.230-.11 (.370-.590 (..2-Dichlorovinyl)-2.810 (.440 (.540) .200 (.260 (. though the 95th percentile levels increased several fold after exposure to nearby pest control operations (Leng et al. Schettgen et al.270) . Cyfluthrin.220 (.and trans-3-(2.340) .680-1.2dichlorovinyl)-2.550-1.840 (.780) 1.220 (.260-.. 2006) and 1177 urban adults and children (Heudorf et al.800 (.640 (.890 (..S.530 (.130-. In these volunteers.11) 947 1193 1004 1345 99-00 01-02 99-00 01-02 99-00 01-02 * * .450-.510-1. 2004. In a study of volunteers.220) .190) .150-.450 (. 2005).430-1.270-.37) . 2001.33) .700) .138 (. Estimated daily pyrethroid intakes based on urinary levels in the German children were below the acceptable daily tolerances (Heudorf et al. 164 Fourth National Report on Human Exposure to Environmental Chemicals .300 (.500 (.260 (.680 (.230-.400-1.750 (. Survey Geometric mean (95% conf.390-.880) .380 (. In the same residents.2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of cis-Permethrin.380-. In a study of urban residents in Germany (Berger-Preiss et al.640-1..700) .840 (.290 (.160 (<LOD-.2-dimethylcyclopropane carboxylic acids in children were related to residential pesticide use and house dust levels (Becker et al. and cis-Cypermethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.080-.640-1.21) .260) .300) .520) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .290-. 2002). 2003).420 (.250-.190 (.440-.and trans-3(2. the levels at 24-72 hours were slightly less than the 95th percentile in the NHANES 2001-2002 subsample (CDC.540 (.300 (.540 (.260 (..370-. 2005) In a small group of indoor pest-control operators.2-dichlorovinyl)-2.200-.900 (.710-3.230 (.250-.550) . 2006). * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 2005).350 (.710 (.560) . 2006).430-.140-.200-.450-1. Urinary levels of the two chemicals in adults were similar to those in children in these studies (Heudorf et al.300-. the median and 95th percentile of urinary levels of cis-3-(2..59) .400 (.340) .180-.150-.690-1.210-..24) .560) 1.29 (. median urinary levels of trans-3-(2.33 (.920 (.550-1.700-2.11) .08) 468 580 667 830 816 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .890) . 2002).580-1.570) .380) .49) .250-. 2004). representative NHANES 2001-2002 subsample (CDC.170 (.S. 2005).250) .780 (.80) .2-dichlorovinyl)-2.440 (.250) 90th .640-. the levels at 24-72 hours were slightly less than the 95th percentile in the NHANES 2001-2002 subsample (CDC.680-1.360-1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.230-..340-.182) * * * < LOD < LOD .190) .2dimethylcyclopropane carboxylic acids at the 95th percentile that were similar or slightly less than the 95th percentiles in the U.67) .370-.240 (<LOD-.120 (. urinary trans-3-(2.2-dichlorovinyl)-2. Other studies have provided evidence that urinary levels of cis.2-dimethylcyclopropane carboxylic acid reflect recent exposure to either their parent pyrethroid pesticides or their environmental degradates.290) . 2006.12 (.2dimethylcyclopropane carboxylic acid at the 95th percentile were about half the 95th percentile in the NHANES 20012002 subsample (CDC.550 (.31) . These studies indicated that intake is mainly from the diet and that dermal absorption contributes little to intake (Heudorf et al.11) .2-dimethylcyclopropane carboxylic acid did not increase at 24-72 hours after exposure to nearby pest control operations (Leng et al.14) 671 680 518 700 591 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.280-.150-. 2001) showed urinary levels of cis.390 (.390-.580) .250) . urinary levels of cis-3-(2. population from the National Health and Nutrition Examination Survey.280 (..300) .320-.

460-.69) 1.2-Dichlorovinyl)-2.68-2.08-6.55-3.17-1.7) 2.66) 478 576 675 826 823 1123 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .89 (2.19 (3.700) .63) 1.01) 4.2-dimethylcyclopropane carboxylic acid in urine does not mean that the level causes an adverse health effect.27 (1. < LOD means less than the limit of detection.84 (1.08) 1.670) .62 (1. The maximum post-application urinary levels.410 (<LOD-.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 .400-.10) 2.20 (.810-1.850-1.26 (.39-5.23 (.670) .610) 1.03-1.11-1.680-1.69 (1.28 (2.860) .49-5.2-dimethylcyclopropane carboxylic acid (Hardt and Angerer.550 (. which may vary for some chemicals by year and by individual sample.520-.700-1.76-3.2-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.94 (1.23) 2.40 (1.2-dichlorovinyl)-2.970 (.59 (1.76-4.95) 3.410-.910-1.410-.63) 1.730) . trans-Cypermethrin. 2005).12-6.20 (.750) .54 (1.55-4.820) .4.08-4.500-. Survey Geometric mean (95% conf.14-6.90) 1.410 (<LOD-.77 (1.or trans-3-(2.49-3.55-5.660) 1.87 (1.14-2.60-4.920-1.20 (. 2005).910-1.14) 1. Biomonitoring studies on urinary levels of cisor trans-3-(2.580 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.490 (<LOD-.2-dimethylcyclopropane carboxylic acid Metabolite of Cyfluthrin. were up to 27 times higher than the 95th percentile for adults in the NHANES 2001-2002 subsample (CDC.520) .03-1.13) .17 (.42) 1.68) 1.19 (2.620) < LOD 2.22 (1.800-1.60) 1.95) 2.25-3. and trans-Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.490-1.56 (1.S.68-3.56) 2. population from the National Health and Nutrition Examination Survey.43) 2.77) 1.56 (1.54) 4.81) 2.97-11. 2003) were similar to the 95th percentiles for adults in the NHANES 2001-2002 subsample (CDC.780 (.530) .68) 1.16) 1.470 (<LOD-.Pyrethroid Pesticides application median urinary levels of summed cis.5) 2.64-4.39 (1.49-3. however.66) 691 680 518 690 595 954 Limit of detection (LOD.42 (2.840-1.37 (1.and trans-3-(2.58) 961 1184 1015 1341 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .60) .35) 1.500 (.09 (.50 (1.710 (. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.2-dichlorovinyl)-2.17 (.19) 1.440 (<LOD-.01 (1. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.56) 2.07 (1.830-1.11-2.07-3. Urinary trans-3-(2.470 (.560 (.91 (1.480-. Fourth National Report on Human Exposure to Environmental Chemicals 165 .4 and 0.77) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .48) 4.560 (.41 (1. Finding a measurable amount of cis.68) 2.570) 90th 1.66) .560 (.25 (1.400 (<LOD-.2dichlorovinyl)-2.28 (1.77) 2.41-14.460-.85) 4. interval) Selected percentiles ( 95% confidence interval) Sample 95th 3.500) .940 (.420 (<LOD-.760) .

670) .930-1.26 (1.88) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 1.970 (.00) 5.500-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.660) .15) 3. and trans-Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. 166 Fourth National Report on Human Exposure to Environmental Chemicals .00 (1.86 (2.22-1.02-1.900 (<LOD-1.15-3.740) .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 .22) 1.440-.57) 3.730) .22-2.880-1.11) 478 576 675 825 823 1123 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .42 (.36) 2.28) 2.540) .31 (.640) .700 (.570 (<LOD-.81 (2.800-1.700-.480-.60 (1.44) 2.45 (1.36 (1.19) .720-1.27-2.42) 1.29) 1.37 (1. Survey Geometric mean (95% conf.07-2.65 (2.15-3.720-1.57 (1.64 (1.33 (1.700 (.530 (.580) .56 (1.34-3.2-Dichlorovinyl)-2.80) 1.55 (2.750) .41) 1.570-.15) 2.07-1.580 (.55 (2.35) 1.780 (<LOD-.19) 961 1184 1015 1340 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .33-1.39) 1.760 (.60) 2.75 (1.12 (.00) 1.34-4.15 (1.91 (1.12-1.87-8.33-2.820-2.00) 1.91) 1.39 (1.68) 3.00-5.55 (2.27-2.74) 2.13) 1.07-3.47 (1.S.74) .47-2.880 (<LOD-1.60) 2.880 (.40-2.61) 1.56-2.19 (1.2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of Cyfluthrin.70 (.56-5.35 (1.770) < LOD 2.15-3.11) 691 680 518 689 595 954 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.31 (2.530 (<LOD-. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.65) 1.720 (<LOD-.31) 1.470-.89) 2.560 (.30-6.07) 2. population from the National Health and Nutrition Examination Survey.47-2.11) .410-.48 (1.16 (1.850-3.48-2.780) 90th 1.67 (2.20-2.610-.570 (.08 (.3) 2.87 (1.850) .87) 1.45-2.30-3.87-3.13) .91-11.98 (1.800-1.20 (1.87) 1. trans-Cypermethrin.470 (.520 (<LOD-.780) .07) 2.Pyrethroid Pesticides Urinary trans-3-(2.08 (.850) 1.

Centers for Disease Control and Prevention (CDC). Pyrethroid exposure of the general population-is this due to diet? Toxicol Lett 2002.134(1-3):141-145. Heudorf U. Idel H. Int J Hyg Environ Health 2002. Heudorf U. Sugiri D. Toxicokinetics of pyrethroids in humans: consequences for biological monitoring. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. Heudorf U. et al. Berger-Preiss E. Hardt J. Berger-Preiss E. Idel H. Bravo R.62:101-108. Angerer J. A longitudinal approach to assessing urban and suburban children’s exposure to pyrethroid pesticides. Angerer J. Int J Hyg Environ Health 2006. Levsen K.205(6):459-472.68(6):1160-1163. Schulz C. Leng G. Environ Health Perspect 2001. Butte W. Third National Report on Human Exposure to Environmental Chemicals. Pearson M. Sugiri D.209(3):293-299. Idel H. 2005. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides. Permethrin and its two metabolite residues in seven agricultural crops.114(9):14191423. Kuhn K. J AOAC 1985. George DA. Angerer J. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. Angerer J. Indoor pyrethroid exposure in homes with woollen textile floor coverings. Angerer J.209(3):221-233. Environ Health Perspect 2006. Schettgen T. Bartell S. Lu C. Int J Hyg Environ Health 2003. Atlanta (GA).109(3):213-217. Fourth National Report on Human Exposure to Environmental Chemicals 167 .206(2):85-92. Ranft U. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine. Drexler H. Wieseler B. Drexler H. Hadnagy W.77(1):67-72. Hoppe HW. Angerer J.Pyrethroid Pesticides References Becker K. Int J Hyg Environ Health 2006. Seiwert M. Int Arch Occup Environ Health 2004. Ball M. Ranft U. Leng G.76(7):492-498. Barr DB. Bull Environ Contam Toxicol 1999. Heudorf U. Int Arch Occup Environ Health 2003. Kolossa-Gehring M. Biological monitoring of workers after the application of insecticidal pyrethroids. Leng G.

Following residential spraying with deltamethrin for malaria protection in Mexico. 1990). 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. Finding a measurable amount of cis-3-(2. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Baker et al. 2006) and estimated daily intakes based on urinary levels in children were considered to be below acceptable daily intakes (Heudorf et al.2-dibromovinyl)2.2-dibromovinyl)-2.. 2005). 2006) and 1177 urban adults and children (Heudorf et al. in detection of cis-3-(2.S.2-dibromovinyl)-2. In the NHANES 2001-2002 subsample.39 µg/L.. 168 Fourth National Report on Human Exposure to Environmental Chemicals .2-dimethylcyclopropane carboxylic acid in the environment (IPCS. Biomonitoring Information Urinary levels of cis-3-(2. In an analysis of 217 urine specimens from a nonrandom sample of United States residents.2-dimethylcyclopropane carboxylic acid at the 95th percentile ranged slightly higher (0.2dimethylcyclopropane carboxylic acid reflect recent exposure to deltamethrin or its environmental degradate. deltamethrin has been used against mosquitoes that carry malaria.2-dimethylcyclopropane carboxylic acid were below the limit of detection (CDC. Thus. Studies in Germany of 396 children and adolescents (Becker et al. 2005).Pyrethroid Pesticides Deltamethrin CAS No.3-0. 2001. Urinary levels for adults and children in these studies were similar (Heudorf et al.2-dimethylcyclopropane carboxylic acid of 0.2-dibromovinyl)-2..2-dibromovinyl)-2.2-dibromovinyl)-2.2-dibromovinyl)-2..5 μg/L) than the detection limit (0. 2005). in some situations replacing the use of DDT. 52918-63-5 General Information Cis-3-(2.2-dimethylcyclopropane carboxylic acid in children increased at least 450-fold relative to the non-detectable background levels for several days and mean levels remained slightly above background levels 45 days after the spraying (Ortiz-Perez et al.2-dimethylcyclopropane carboxylic acid is a metabolite of the pyrethroid insecticide deltamethrin. Outside the U.2-dimethylcyclopropane carboxylic acid in the urine may reflect exposure to deltamethrin or to cis-3-(2. 2004). 2001) showed that urinary levels of cis-3-(2.1 μg/L) for the NHANES 2001-2002 subsample (CDC.2dimethylcyclopropane carboxylic acid formed in the environment. urinary levels of cis-3-(2.2-dimethylcyclopropane carboxylic acid in urine does not mean that the level will result in an adverse health effect.2-dibromovinyl)-2.2-dibromovinyl)-2. (2004) reported a geometric mean concentration of cis-3(2. Deltamethrin can degrade to cis-3(2.2-dibromovinyl)-2. The peak mean levels in these children were more than 800-fold higher than the detection limit in the 2001-2002 NHANES subsample... mean peak urinary levels of cis-3-(2.

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

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

Pyrethroid Pesticides References Becker K. Ball M.inchem. Angerer J. International Programme On Chemical Safety (IPCS). Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides. Torres-Dosal A. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Lopez-Guzman OD. Int J Hyg Environ Health 2006. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. Batres LE. Centers for Disease Control and Prevention (CDC). Environmental health assessment of deltamethrin in a malarious area of Mexico: environmental persistence. Butte W.209(3):221-233. 2005. Carranza C. Hoppe HW. Deltamethrin. Heudorf U. Heudorf U. Environ Health Perspect 2005. Schulz C. Kolossa-Gehring M. Angerer J. Int Arch Occup Environ Health 2004.org/documents/ehc/ehc/ ehc97.109(3):213-217. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine. toxicokinetics. 5/26/09 Ortiz-Perez MD. Drexler H. Grimaldo M. Environmental Health Criteria 97. Int J Hyg Environ Health 2006. Heudorf U. et al. Angerer J. [online] 1990.113(6):782-786. Available at URL: http://www. Angerer J.77(1):67-72. and genotoxicity in exposed children. Seiwert M. Fourth National Report on Human Exposure to Environmental Chemicals 171 . Environ Health Perspect 2001. et al. Third National Report on Human Exposure to Environmental Chemicals.209(3):293-299. Atlanta (GA).htm.

The mean peak levels in these children were 83-fold higher than the geometric mean for children in the NHANES 2001-2002 subsample (CDC. 2005). In one study of 145 urban residents in 80 private homes in Germany. 2006. CDC. 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. Becker 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. 2003. the presence of 3-phenoxybenzoic acid in urine not only reflects the metabolic transformation of any of the six pesticides listed above. 2005). 2005).. 2005. the postapplication median urinary levels of 3-phenoxybenzoic acid were 24-fold higher than those for adults in the NHANES 2001-2002 subsample (CDC. 2003). Urinary levels of 3-phenoxybenzoic acid in children were found to be related to residential pesticide 172 Fourth National Report on Human Exposure to Environmental Chemicals . Median levels of urinary 3-phenoxybenzoic acid were 67-fold higher in 307 pregnant New York City women who used indoor pesticides compared with the median levels for adults in the NHANES 2001-2002 subsample (Berkowitz et al. 39515-41-8 CAS No. Finding a measurable amount in urine does not mean that the level will result in an adverse health effect. A study of 396 German children (Becker et al. 2006). Fenpropathrin Permethrin CAS No. but can reflect direct exposure to 3-phenoxybenzoic acid formed in the environment from the degradation of these pesticides. In an analysis of 217 urine specimens from a nonrandom sample of United States residents. Thus. Baker et al. 2006) showed that urinary levels of 3-phenoxybenzoic acid at the 95th percentile were similar to levels at the 95th percentile for children in the U.. 2005). representative NHANES 2001-2002 subsample (CDC.. 2004). 2002. 52918-63-5 use and house dust levels (Lu et al. CDC. Following residential spraying with deltamethrin for malaria protection in Mexico. 68359-37-5 Cypermethrin Deltamethrin CAS No.S. CDC... Biomonitoring Information Urinary levels of 3-phenoxybenzoic acid reflect recent exposure to the parent pyrethroid pesticides. Hardt and Angerer. 2003.. In 57 volunteers entering areas previously spot-sprayed with various pyrethroid pesticides.Pyrethroid Pesticides Cyhalothrin CAS No.52315-07-8 CAS No. 2005). In the New York City study. 2005). a temporal variation in levels was observed and considered to correspond to seasonal spraying of pesticides. 2005.. Saieva et al. (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. In a small group of indoor pest-control operators.. 2005). 52645-53-1 Tralomethrin CAS No. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 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. 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. median urinary levels of 3-phenoxybenzoic acid were slightly less than median levels in the NHANES 2001-2002 subsample (Leng et al. A small sample of occupationally unexposed Italian residents had median levels of urinary 3-phenoxybenzoic acid that were about fourfold higher than for adults in the NHANES 2001-2002 subsample (CDC.

266-.560-1.990) .434) .273 (.43) 3.640 (.280 (.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 .32 (1.62-8.46) 2.48-2.8) 3.26) 2.51-6.200-.69) 3.560-.55 (1.1) 3.41-2.601) .41-3. Deltamethrin.1) 3.03 (3.32 (2.160-.04) .328 (.32-21.69 (1.78) 6.42-2.250 (.246-.595) .960 (.820) .12) .64) 697 680 524 701 603 957 Limit of detection (LOD.53) 1.417 (.311 (.260 (.50 (2.292 (.355) . Survey Geometric mean (95% conf.25-1.364) .45-5.62-6.190-.420) .52-4.300 (. interval) .76 (1.760 (.350-.850) . and Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.320) .295) .507 (.373) .325 (.190-.430-.450 (.23 (2.369) .45 (2.740 (.35) 2.14-6.830-2.27-11.210-.65 (1.180-.454 (.810) 1.314 (.830) 90th 1.72 (1.78 (1.41) 3.35) 1.530-.230 (.49 (1.60) .83-11.25-4.26-2.13 (.34-6.406) .33) .12 (.56-5.288-.16) 1.39) 2.650 (.315 (.620-1.510-.Pyrethroid Pesticides Urinary 3-Phenoxybenzoic acid Metabolite of Cypermethrin.230-.820) .53-3.71 (1.560-.26) 2.48-2.340) 1.1 and 0.27-2.16) 974 1193 1024 1346 99-00 01-02 99-00 01-02 99-00 01-02 .370) .260-.73) 1.29-1.63 (3.21 (2.30) 3.51-3.260 (.298 (.330) .940) 1.238-.240 (.271-.89-71.680 (.297 (.1.44) 5.710 (.730 (.314) .360) .33 (1.34 (2.586) .430-.320) .230-.428-.260 (.78) 1.740 (.387) .04-5.81 (1.93 (1.35 (1.33 (2.292-.600 (.265-.270 (.490-.200-.30 (1.300) .92-3.470-.780) 4.590-.230-.800) 1.05) .62) 5.1) 3.247-.49-2.321 (.52-5.270) . see Data Analysis section) for Survey years 99-00 and 01-02 are 0.28) 1.35) 2.05) 1.427) .54) 1.226-. population from the National Health and Nutrition Examination Survey.190-.700 (.227-.90) 1.79) 3.34) 8.390) .230 (.25 (2.440) .30 (.25 (2.336 (.35 (2.300 (.01 (1.700-1.353 (.550-.276-.290 (.384) .320) .277-.S.320 (.267 (.490) .18 (2.610) .710 (.345) Selected percentiles ( 95% confidence interval) Sample 95th 4.374) 99-00 01-02 99-00 01-02 99-00 01-02 .220-.340) 75th .200-.253-.288 (.240 (.750-1.13) .352-.18 (1.840-1.38 (2.320) .36) 1.02-6.65-2.250-.250 (.570-1.46) .233-.250 (.75 (1.850) .590 (.41 (1.16-1.63-3.750) .25-7.510-.16) 483 580 682 831 833 1128 99-00 01-02 99-00 01-02 .630) .38 (2.86 (1. Fourth National Report on Human Exposure to Environmental Chemicals 173 .160-.340) .520 (.12) 4.190-.570-.362) .210-.870 (.800 (.49-2.670 (.78) 1.330) .27-2.750) .530-.49 (1.300 (.

274-.35 (1.03-1.21 (1.190-.48 (1.90) 3.840-1.86 (1.72 (1.362 (.92) 483 580 682 830 833 1128 99-00 01-02 99-00 01-02 .490 (.67 (1.271-.264 (.250) .230-.32 (2.437) .550 (.323 (.04 (3.19) 974 1193 1024 1345 99-00 01-02 99-00 01-02 99-00 01-02 .39) 1.410-.74) 3.530-.229-.720 (.290) .63-3.380-.700-1.250 (.270-.00) 1.17-1.460-.510 (.240 (.00) 1.40 (1.275 (.160-.280 (.750-1.81 (1.272 (.43-64. Deltamethrin.17 (.202-.230-.73-4.0) 3.530-.450 (.216-.83 (1.410) .321-.19) 2.261-.401) .36-6.550 (.225-.210-.480 (.10 (2.240-.11 (.03 (.590-1.200-.43) 1.62) 1.316 (.357) .440-.640 (.220-.350 (.280) .590) .860-1.510 (.35-3.677) .40) 2.330) .150-.280) .730) .91 (2.329) .25-5.73) 1.224-.02 (2.440-.550 (.810) 1.309) .387) .670) 3.300-.510 (.238-. population from the National Health and Nutrition Examination Survey.88-5.53 (1.272) .960-1.13-1.220 (.37) 1. Survey Geometric mean (95% conf.43 (1.350) .95) 1.62) . and Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.52) 2.00) 5.650) .480-.11 (.41-4.60-4.490-.94 (1.540 (.51-7.610 (.253) .640 (.240 (.75-8.91-4.370-.670) .84 (1.330 (.22 (1.05-3.52 (1.200-.210 (.190-.590) .07-5.560 (.27) 1.63) 1.930) 1.210 (.372) .240-.227 (.240-.312 (.09) 3.09-2.310) .460-.49) 1.730) .311 (.500) .173-.280 (.580 (.19-6.720) 90th 1.270) .240 (.328) .290) .02-1.860 (.49) 3.590) .280-.440-.274 (.330) 1.423 (.190 (.S.930) .380 (.178-.534) .06-3.270 (.44 (1.16-4.91) 9.49-2.230) .250 (.335-.37 (1.44) 2.09 (.43 (2.88) 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 .60) 1.261 (.330) 75th .41) 1.280 (.270) .270 (.21-4.13 (.400-.54 (1.309 (.91) .278) .25-2.67) 1.580) .390-.299-.370 (.630) .25) 2.200-.07) 2.329) .290-. interval) .09-2.740) .378 (.300-.420-.35) 1.96 (1.240 (.320) .36 (1.55 (1.570) .304) Selected percentiles ( 95% confidence interval) Sample 95th 3.226-.61-2.Pyrethroid Pesticides Urinary 3-Phenoxybenzoic acid (creatinine corrected) Metabolite of Cypermethrin.365) 99-00 01-02 99-00 01-02 99-00 01-02 .13-1.490 (.80) 4.330) .446) .67 (1.246 (.49 (1.04 (.400) .55) 3.15-2.48) 697 680 524 700 603 957 174 Fourth National Report on Human Exposure to Environmental Chemicals .730-1.234 (.760) .19 (2.240-.64-5.35) .83) 1.200-.400-.860-1.

Ortiz-Perez MD. 2005. toxicokinetics. Exposure to indoor pesticides during pregnancy in a multiethnic. Leng G. Arch Environ Contam Toxicol 2004. Berger-Preiss E. Seiwert M. Biological monitoring of workers after the application of insecticidal pyrethroids. Centers for Disease Control and Prevention (CDC). Int J Hyg Environ Health 2006. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Idel H. Ranft U.114(9):14191423. Barr DB. Grimaldo M. Barr DB.46(3):281-288. Lopez-Guzman OD. Godbold J.76(7):492-498. Sugiri D.206(2):85-92. Hadnagy W. Environmental health assessment of deltamethrin in a malarious area of Mexico: environmental persistence. Int J Hyg Environ Health 2002. et al. Hoppe HW. Leng G. Angerer J. Carranza C. Idel H. Batres LE. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. Levsen K. Ball M.Pyrethroid Pesticides References Baker SE. Lu C. Environ Health Perspect 2006.111(1):79-84. Kolossa-Gehring M. Ranft U. Isotope dilution highperformance liquid chromatography-tandem mass spectrometry method for quantifying urinary metabolites of synthetic pyrethroid insecticides. Sugiri D. Third National Report on Human Exposure to Environmental Chemicals. and genotoxicity in exposed children. urban cohort. Int Arch Occup Environ Health 2003. Atlanta (GA).205(6):459-472. Pearson M. Olsson AO. Int J Hyg Environ Health 2003.209(3):221-233. Environ Health Perspect 2005. Fourth National Report on Human Exposure to Environmental Chemicals 175 . Berkowitz GS. Liu Z. Lapinski R. Obel J. Torres-Dosal A. Berger-Preiss E.113(6):782-786. Hardt J. Bartell S. Angerer J. Bravo R. Becker K. A longitudinal approach to assessing urban and suburban children’s exposure to pyrethroid pesticides. et al. Deych E. Indoor pyrethroid exposure in homes with woollen textile floor coverings. et al. Environ Health Perspect 2003.

510) .130-.200 (.390-.130-.170 (.250-. The absorption.470) .157) .115-. +3.390) .360 (.260) . 0.099 (.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 .280) .180) .310) .190-.350 (.350-. Two antimony compounds (sodium stibogluconate and antimony potassium tartrate) have been used as antiparasitic medications.240 (. and pewter.390 (.280-.112-.210) .330 (.137) .250) .230 (.300) . and refuse incinerators that process or release antimony.220) 95th .150-.130-.260 (. sheet and pipe metal.220 (.470) .350 (.180) .117-.350) .260 (.310 (.110-.290-.280-.400) .130-.330) .120) .250 (.320) 787 683 618 554 667 723 768 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.340) .109-.150) .230-.300 (.310 (.100 (. water.390) .197) .210 (.230-.090) 75th . and 03-04 are 0. castings.080) .134 (.190) .140-.150) 90th .190) .120-.146 (.310-. 7440-36-0 General Information Antimony is found in ores or other minerals.160 (.130) .180 (.070 (<LOD-.141-.160) .210-.410) .200-.130 (.128 (.200 (.570) .160) .360) .220-.120) .120 (.190 (.200-.230-.350) . see Data Analysis section) for Survey years 99-00.220) .190 (.190-.200) .260-.148-.230-.200 (.095 (.154) .240 (.250 (.161) .190) .120-.220-. 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.130) < LOD . coal-fired plants.114) .390-.S.280-.190 (. and glass.350-.190) .280) .108 (.140) .126-.390-. 176 Fourth National Report on Human Exposure to Environmental Chemicals .137) .170-.330-. interval) .260) .280) .240 (.170-.132 (. often combined with oxygen to form antimony trioxide or with sulfur to form stibnite.105 (.230 (. 0.143 (.260) .120 (.130 (.207) .093 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.120 (.110-.350) .150 (.095-.120-.120) .122 (.240 (.110-.320) Total .270) .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 .150) .154) .200) .600) .300-.120-.220-.190-.120-. Stibine is a metal hydride form of antimony used in the semiconductor industry. People are exposed to antimony primarily through food and.123 (.080) .360 (.120) .200-.100-.100) .130 (.320) .530) .310 (.460 (.290 (.210) .220 (.169 (. It is used in metal alloys.300-. which may vary for some chemicals by year and by individual sample.320-.360-.090 (<LOD-.04.160) .310) .080-.180-.176 (.370) .110 (.070 (<LOD-.260-.180-.320-.07.120 (.080 (<LOD-.140) .200 (. and excretion of antimony vary depending on its oxidation state.470 (.190-.120-.150) .130 (.460) .190 (.270) . and as a fire-retardant in textiles and plastics.350 (.130) .160) .150-.131-.350 (.140 (.210) .400 (. and +5.230 (.330 (.120-.300) .350-.180-. storage batteries. Antimony enters the environment from natural sources and from its use in industry.190 (.180 (.360) .200 (.136) * .240-.300-.210-.108-. and 0.117-. < LOD means less than the limit of detection.136-.290-.230) . solder.190-.154-.145 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.160-.135) * .184) .330-.180 (. from air and drinking water.230) . 01-02.098-.250-.400) .170 (.145) Selected percentiles ( 95% confidence interval) 50th .260 (.140) .400-.090-.230-.170-.240) .300 (.115) .220) .330) .130 (.490) .160 (. Antimony can exist in one of four valences in its various chemical and physical forms: -3.130-.170-.140 (.103) . Dermal contact with soil.Metals Antimony CAS No. or other substances containing antimony is another means of exposure.140) . fireworks. to a lesser extent. ammunition.270 (.400 (.156-.088-.340 (.150-.100-.110-.180-.220-.280 (.490 (.158 (. enamels.410) .250-.142 (.350) .090-.250-.210) .120-.440) .200) .130 (.128 (.134-.500) .460 (.280 (. ceramics.144) .390) .130-.140 (.180 (.190) .400) .320 (.150 (.160-.175 (.160-.430 (.310-.140 (.125 (.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 .220-.140) .410-.210 (.140) .280-.420) . It is also used in paints.280) .250 (.150-.210) .087-.320 (.130) .160-.120 (.440) .178) .170) .200 (.164-. distribution.130 (.180 (.110) .320-.400 (.330) .160) . metal bearings.430 (.320-.150-.270-.350 (.126 (.160) .370-.180 (.130 (.170-.330 (.310 (.560) . Workplace exposures can occur at smelters.079-.330) .100 (.710) .070-.460 (.390) .120-.200-.04. respectively.220-.230) .240 (.500) . population from the National Health and Nutrition Examination Survey.280-.200) .119-.119) .090 (.220) .300) .160 (.130-.180-.430 (.340 (.270 (.270 (.440 (.150 (.133) * .270 (.240-.132 (.

228-.192) .226 (.132) .278 (.069-.280 (.109 (.727) .114 (.333 (.181) .148-. 1953).277 (.S.429 (.099-.138-.147) .30) .400 (.075 (.194-.485) .146-. interval) .238) .080 (.250-.421) .112-. An elimination half-life of approximately 95 hours has been estimated after occupational exposures (Kentner et al.107-.111-.139 (.200-.109-.149) .076-.380 (.084) . 1988.149-. 1995).447 (.075 (.161) .430) .195 (. 1986).127) .146-.098-.148) * .136) .120 (.176-.444) .178-.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.225 (.124 (.140) .143) Selected percentiles ( 95% confidence interval) 50th .233-.193 (.239-.220) .333) .130) .112 (.250-.188) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.391) .107-.113-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. diarrhea.263 (. The toxicity of stibine after acute inhalational exposure is similar to that of arsine. and kidney have been demonstrated in high dose animal studies depending on the dose.135) .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 .417) .159-.294) Total .320-.200-.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 .086 (.126 (.085) .146) .209-.106-.115 (.071-.193) .200) .261) .068-.267-.242-.105-.300) .229-.741) .112 (.156-.111 (.317) .250-. 1973).153 (.364 (.228 (.333-. resulting in hemolysis with abdominal and back pain (Dernehl et al. 1958) and occupational exposures (Briegner et al.123) .248-.236 (..308-.278) .338) .115-.138-.191 (.068 (.173 (.320-.333) 1132 1334 1281 1144 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .171) .318-.151) .097-.131) .108 (.076-.107-. Workplace standards and recommendations for air exposure Urinary Antimony (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.122 (.132 (. Histopathologic inflammatory and degenerative changes in the lung.115-.163 (.222 (.480) . 1944).255-.213 (.131 (.173) .233 (.129 (.069-.357) .265 (.173-.185 (.Metals than for trivalent compounds (Elinder and Friberg.317) .338 (.230) 95th .267) . Pulmonary edema may occur in severe cases of inhalation exposure (Cordasco et al.199-.137 (.196 (.414) .164) .167 (.159-.164 (.263-.333 (.129 (.103-.138) * .192-.204-. abdominal pain.095-.143) 90th .126-.121 (.104-. Inorganic antimony salts irritate the mucous membranes..276 (.267 (.248) .310) .214) . Ming-Hsin et al.115 (.224 (.209) .444) .108-.173 (.300) .257) .086) 75th .320 (.250 (.124-. and gastrointestinal symptoms such as vomiting.268) .310 (.124-.100 (.153-.245) .253 (.146-.425) .250-.186) .098-.117-.152) .320) .131-.096-.172-.119 (.061-.099-.187) .147-.238 (.087) .298 (.120 (.095-.385 (.250 (. and route of exposure (Elinder and Friberg.129) .300 (.130) .471 (. Human health effects from antimony at low environmental doses or at biomonitored levels from low environmental exposures are unknown.417) .080 (<LOD-.150-.233) .150-.127 (.321) .118 (.280-.130) .189 (.124) .156 (.119-.371 (.391) .143) .135 (. myocardium.271-.205-.128-.318-.333-.176 (.116 (.208 (.227-.079 (<LOD-.338 (.195-.117-.185 (.179-.183) .135 (.127) .092-.116-.357-.118 (.144-.209) .228 (.500) .082) .207) .130 (.074 (.125 (. species.195-.178 (.143) .113) .266 (.115) .139 (.122 (.471) .259 (.078 (.313-.286 (.317) .160 (.115 (.121) ..113-.082) .145) . and eyes.125-.295 (.098) .102-.188-.185-.225) .200-.121 (.108-.198) .109 (. liver.281-.192 (.163 (.310) .103-.230-.120 (.333 (.167 (. 1954).164-.176 (. Fourth National Report on Human Exposure to Environmental Chemicals 177 .114 (.308) .373) .108-.255) .129) * .352) .315) .209 (.161) .154-.082 (<LOD-.104-.170 (.741 (.265-.133) .089) .135) .117-.203) . 1962).175 (.167-.182 (.162-.127) .135) .120 (.343 (.106-.272) .333-.077) .352 (. skin. Acute inhalation of antimony has been associated with irritation of the respiratory tract and impaired pulmonary function (Renes.152) .244-.126) .181) .364 (.247) .203) .208-.250) . population from the National Health and Nutrition Examination Survey.320 (.438) .288 (.081 (<LOD-.269 (.241-.102-. Acute antimony poisoning may cause a metallic taste..159-.134) .206-. and ulcers (Werrin.238) .253-.217 (.143 (.429) .092) .167 (. Dysrhythmias and T-wave changes on electrocardiogram have also been noted after both therapeutic (Berman.081) .241-.138 (..235-.211) .140) < LOD .127) . 1986).256 (.333-1.405) .148-.114 (.181) .123 (.119-.

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

Werrin M. Antimony poisoning in industry. 27:38-45. Trace metals in urine of United States residents: reference range concentrations. Renes LE.Metals in urine. Sampson EJ.76(1):53-59. and serum of Italian subjects. Ting BG. Chemical food poisoning. Pirkle JL.99-108. blood. Fourth National Report on Human Exposure to Environmental Chemicals 179 . Quarterly Bulletin of the Association of Food and Drug Officials 1962.95:89-105. Morrow JC. Sci Total Environ 1990. Paschal DC. Jackson RJ. Environ Res 1998. et al. Industrial Hygiene and Occupational Medicine 1953.

00 (6.8) 34.80) 6. trimethylarsine oxide.80-9.1) 1281 1276 03-04 03-04 03-04 9.0 (22. black.12 (6.6-35.4-65. semiconductors.0 (43.41 (7.5 (34.29 (8.90-14. 2005).9-34. Arsine (AsH3) is a reactive.6-141) 53.5) 41. Roxarsone and other organic arsenicals are anticoccidial agents added to poultry feed.4 (24. to a lesser extent.08 (5.3-15. Since the 1940s.000 metric tons annually.5-19. retaining walls.50-14.3-111) 78.4 (26.5 (40. and as homicidal poisons.2 (13. Although it is still widely used in the United States.02-8.66-8. and other metals. Arsenic is measurable in most soils. it is found in over 200 crystalline or mineral forms. and as a cosmetic to lighten complexion.57) Selected percentiles ( 95% confidence interval) 50th 7.6 (32.0-60.6) 11.7-83.84) 8.8) 7. Arsenic can combine with such non-carbon chemicals as sulfur and oxygen to form arsenides. copper arsenates. see Data Analysis section) for Survey year 03-04 is 0.8) 29. In the last century. the smelting of copper. to a lesser extent.6 (13. cacodylic acid. interval) 8. and produce.5) 95th 65.9 (8. were used as treatments for syphilis.4 (48. Also. Various forms of inorganic arsenic can occur in groundwater from natural sources or as a result of soil application or industrial waste. referred to as inorganic arsenic compounds. lead.Metals Arsenic CAS No.2-20.5) 66.0 (15. as alloy in metal bearings.8) 7.90) 75th 16. arsenic compounds.5-52.1) 15.9-62.84) 8.1-18.1) 7. and in lead-acid storage battery grids. psoriasis.10-7. ocean and fresh waters. 2001).1 (38.12-10.90-8. mostly for use in wood preservation (ATSDR.2-17.5-178) 46.9 (17.25-9.3) 10.3-19. 7440-38-2 General Information Arsenic is an element that is widely distributed in the earth’s surface in small amounts. Arsenic trioxide (As2O3. population from the National Health and Nutrition Examination Survey.4) 13. pesticides. cancers. General population exposure to inorganic arsenic can occur through consumption of drinking water and. a trivalent compound known as white arsenic) is a common natural and commercial form that can be released into the air during volcanic action. mental disorders.7 (11.90 (7.74. arsenic as elemental metalloids may be used in some ammunition.7) 90th 37.6) 618 722 1074 Limit of detection (LOD.5) 43.70-9.90) 16. grain. chromated copper arsenate (CCA) has been used to treat outdoor timbers and pressure-treated woods to prevent wood rot.5 (23. and. though in some locations arsenite may be prevalent (WHO.0-19. and foods.30) 17.13-8.3) 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. Gallium.30 (7.2-61. and arsenates (oxidation states of -3.6 (15.4 (31.1-40.7) 65. and play sets. meats.90-7.6 (9.0 (14.30 (6. solders. lead hydrogen arsenate. +3 and +5).55 (7. Arsenic and its compounds have had many uses in the past and present as medicines.10 (6.4) 60.2 (41. Groundwater Urinary Total Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.5 (36. Water sources contain mostly inorganic arsenate. 180 Fourth National Report on Human Exposure to Environmental Chemicals .8) 30. The United States no longer produces arsenic from mining but imports about 22.8-77.2 (51.20 (8.90 (7. CCA-treated wood has been restricted since 2003 and no longer can be used in residential applications such as decks.5 (14.40) 7.10-10.77) 6.70 (6.90-8. arsenites. and gray forms). or rarely as elemental metalloids (yellow.90 (5. from coal burning.5-41. Before the 20th century. such as arsenopyrite (FeAsS) and realgar (As4S4).4) 40.8) 33. Arsenic can also combine with organic substances in nature to form such organic arsenic compounds as arsenobetaine. Arsenic trioxide is approved to treat acute promyelocytic leukemia.00-9. sodium arsenite.S. In nature. alloys. Survey years 03-04 Geometric mean (95% conf.8-61.34-9. Various arsenic compounds were used in paint pigments and for tanning animal hides.4 (7.7) 24. arsenocholine.9-46.9) 21.90-11.70) 8.2-93.19-9. and indium arsenides are used in the semiconductor industry. particularly arsenic trioxide.0 (11.2) 46.97) 8. and monosodium methyl arsenate were used as pesticides but contemporary uses are restricted.8) 17.34-10.50 (8. aluminum. and arsenosugars.9) 68.27) 9.2 (12. gaseous hydride manufactured in small quantities for use in the semiconductor industry.80 (5.8 (48.7-95.1) 290 725 1542 03-04 03-04 9.10) 10.6-43.2) 15.1 (32.

7 (11. TMAO is also formed in the environment from microbiological action and is a metabolite of arsenic in certain mammals.81-9.66 (7.35) 7.7-34.. Children may have additional exposures from ingestion of contaminated soils (e.S.7) 95th 50.0-26.01) 7. organic arsenic can be converted back to methylated and inorganic arsenic.12-10.0) 42.8-62.. 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. have caused clinical arsenic poisoning.8-75.9-56.88 (5.93-8. dust. Survey years 03-04 Geometric mean (95% conf.44-11.96) 12.76 (6. 2001). Extremely high groundwater arsenic levels. Gamble et al. NRC.6 (17.30-9. 2006. Chowdhury et al. dose level.47 (7..47-6. shellfish. 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. Arsenate is reduced in the body to arsenite (oxidation state +3).8 (20.07-9. arsenic does not show biomagnification in the food chain (WHO. 2001).2) 40.50 (6. as observed in Bangladesh where millions of people have been exposed.1) 58.61 (7. The semiconductor dopants. mine tailings).8 (11.20-9.6-17. age. 2001).5) 290 725 1542 03-04 03-04 8.1) 24. Steinmaus et al.8-32. inorganic arsenic is widely distributed within the body. Inorganic arsenic and its metabolites have elimination half-lives of approximately 2–4 days (Lauwerys and Hoet. 2001). arsenocholine. and arsenosugars. but is poorly absorbed dermally (WHO.Metals sources of drinking water often have measurable arsenic and several regions of the United States have naturally higher arsenic levels than the U.2) 90th 30. and contact with CCA-preserved wood structures.0) 14.4-64. WHO. Arsenite is then oxidatively methylated to the monomethylarsonic acid (MMA) and dimethylarsinic acid (DMA) with subsequent excretion primarily in the urine (NRC.5-17.93-9.04 (5.99-9.10-16.33-10.88) 7.75 (5.32 (5.0 (17.4 (12.4 (11. with trivalent inorganic arsenic (arsenite) being more toxic than pentavalent inorganic arsenic (arsenate) (NRC.3-64.8 (21.64 (7. Inorganic arsenic is well absorbed from the gastrointestinal tract and absorbed to a lesser degree through inhalation.3-53. 2001).0) 1281 1276 03-04 03-04 03-04 8..8 (12. kelp.1) 8.2) 15.5 (9.58-10. EPA’s maximum contaminant level (Hughes. interval) 8. After absorption.7-18.0-38. 2007.9) 618 722 1074 Fourth National Report on Human Exposure to Environmental Chemicals 181 . 2001).18 (5.7-188) 27. 2003.g.0) 26. 2007. Smoking tobacco is also a source of inorganic arsenic.2-46..2-15.00 (6.4) 32.59) Selected percentiles ( 95% confidence interval) 50th 7.7 (9. and some other seafood can contain organic forms of arsenic including arsenobetaine.41) 6. 2001. In aquatic organisms.44) 6.7-35.4 (40. though some reduction may occur in the gut prior to absorption.0 (31. Direct exposure to DMA and MMA may result from use of the two pesticides. cacodylic acid and monosodium methyl arsenate.10-8. These organic forms of arsenic from seafood are absorbed and quickly excreted in the urine (WHO.86-17.28-7.1 (14. so exposure to the general population is extremely limited.3 (27.75) 13.5) 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 8.40) 8. Smelter workers can have significant inhalational exposures to airborne arsenic trioxide for which air standards have been established.1 (11.24 (7.2 (12.01) 11.7) 28..8) 27.13) 8.0-69. 2001).0-18.0) 33. population from the National Health and Nutrition Examination Survey.3) 6.5) 17.45) 5. Ingestion of arsenosugars in kelp and algae can also lead to the excretion of DMA.3-62.6 (35.51) 75th 14.0) 12. Though modest bioconcentration occurs in some aquatic life.9 (45.33 (6.9) 53.7 (25.38-10.3-41.4 (42.25-9. EPA.23-7. WHO.31 (6. 1988).25 (6.4 (26. arsenocholine is converted to arsenobetaine and also to small amounts of TMAO (Christakopoulos et al.S.6) 45. trimethylarsine oxide (TMAO).4) 54.4 (24. selenium. 2006.66-8.8) 22.47 (6.3 (24.3) 9.1) 6.1-36.04) 7.5-120) 40.8 (27. 2001).1) 7. In aquatic sediments.11 (5.66-8.06 (4.6 (10. Tseng.S. and folate status (Chen et al. gallium arsenide and indium arsenide. U. 2007.7-17. are used in enclosed ultraclean operations within the semiconductor industry. Fish. Inorganic forms of arsenic demonstrate high acute toxicity.9) 13. 2001.

60) 1.10 (<LOD-1.50) 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD 1. vomiting. 2007. 2007.20 (<LOD-1. 2001). noncirrhotic portal hypertension. arsenic trioxide) includes hemorrhagic gastritis with nausea. Chronic elevated arsenic intakes have been associated with diabetes. which can lead to dehydration and shock.20 (<LOD-1.10 (<LOD-1. With chronic exposure. 2001).. Studies of arsenic at levels typical of U. hematocytopenias. WHO. Chile). WHO.60) 1. drinking water have not been associated with increased cancer rates (Schoen et al..30) 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1.50) 1. 2001).Metals +3) shows greater toxicity than arsenite itself (Aposhian et al. Bredfeldt et al.. NRC. Chronic human intake of arsenic at less than acutely toxic doses. apoptosis. Taiwan. Chronic arsenic exposure in humans is considered to be a cause of skin.EPA has established drinking water. but additional or confirmatory research is needed (Kapaj et al. and endothelial injury (Kumagai and Sumi. fatty acid oxidation. lung.50) 621 725 1078 Limit of detection (LOD.. cell transformations. 2006..g..30) 1. Acutely.50) 2568 95th 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1. see Data Analysis section) for Survey year 03-04 is 1. 2004). The risk of lung cancer appears more pronounced when large environmental exposures start in childhood (Smith et al. interference in signal transduction pathways.10 (<LOD-1. The U.. 2000. 2001. hyperkeratosis.. 2006. Raml et al. Although arsenate is reduced in the body to arsenite. leading to a decrease in adenosine triphosphate energy production. including inhibition of numerous enzymes. Laboratory studies using inorganic arsenic have shown chromosomal aberrations.0. Survey years 03-04 Geometric mean (95% conf. and bladder cancer (IARC. 2001. 2001).80) 1. OSHA and ACGIH have established workplace standards and guidelines for arsenic exposure and monitoring.S.20 (<LOD-1. WHO. gluconeogenesis. increased oxidative stress.10 (<LOD-1. Such actions may lead to decreased energy production. The organic forms of arsenic occurring in seafood have little known toxicity. Cohen et al. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.. 2001). 2004). and by uncoupling oxidative phosphorylation (NRC. and altered gene expression. 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. Cardiac arrhythmias. Cellular glucose uptake. and hyperpigmentation of the skin (NRC.S. < LOD means less than the limit of detection. can cause peripheral sensorimotor neuropathies. 2006) or when exposure occurs in smokers (Chen et al.. including drinking water sources with elevated arsenic levels (e. hypertension.10 (<LOD-1. some of these effects may take years to develop. food residue. 182 Fourth National Report on Human Exposure to Environmental Chemicals . renal failure. and production of glutathione may be affected as well. cytotoxicity.. 2004.. Acute unintentional inhalation of arsine gas can produce hemolysis of red blood cells. hepatotoxicity.g. Bangladesh. arsenite will inhibit cellular pyruvate dehydrogenase by binding to the sulfhydryl groups of dihydrolipoamide. which may vary for some chemicals by year and by individual sample. it may have its own separate toxic action by substituting for phosphate in glycolysis and other pathways. respectively. WHO. and it also will inhibit succinate dehydrogenase. NRC. 2006) and newly discovered thioarsenic metabolites may also be as toxic (Naranmandura et al. 2006. and diarrhea. 2001). and childhood neurodevelopmental effects in observational human studies. population from the National Health and Nutrition Examination Survey.20 (<LOD-1. substitution in phosphate metabolism. and DNA repair inhibition (Cohen et al.S. U. peripheral vascular disease. Arsenic has many actions demonstrated in cellular studies.EPA. Acute toxicity resulting from the ingestion of large amounts of trivalent arsenic (e.S. 1998. 2007). and peripheral neuropathy may also occur with large doses or after surviving an acute overdose. 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.

. 1999). median urinary total arsenic levels in 4052 adults varied with seafood intake. 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. In a Nevada town where groundwater levels were naturally elevated. 2006). gov/toxpro2..cdc.41) 3. 2006). Meza et al.33 (<LOD-3. 1998.61 (<LOD-3. and the FDA has established a bottled drinking water standard... 2001). Pellizzari and Clayton. 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.. 2004. higher mean or median total urinary arsenic levels have been reported among people living in specific western areas of North America (Calderon et al. Shalat et al.. 2008. 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. Caldwell et al. environmental levels) and health effects is available from ATSDR at: http://www. and were about two-fold lower than those for the U..atsdr..75 (<LOD-2.... 2007..95) 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine..S. Pellizzari and Clayton. 1992. 2006. 2006). the median total urinary arsenic in about 200 people was approximately four times higher than that of the U.04 (<LOD-3. Compared with this Report.. had decreased since the prior 1990– 1992 survey. Survey years 03-04 Geometric mean (95% conf. 2004.18 (<LOD-3. 2001). In animal studies.89) 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2. Valenzuela et al.. IARC and NTP recognize inorganic arsenic and arsenic compounds as human carcinogens.S.e. 2001). Levels of total urinary arsenic in the U. 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.. population from the National Health and Nutrition Examination Survey.S. 2006. 2006)... 1999.00) 1. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th < LOD 90th < LOD Sample size 3. DMA produced bladder cancer in some chronic rat studies (Cohen et al. population (Rubin et al. Josyula et al.69 (<LOD-3. 1986).33 (<LOD-3.19) 3. Caldwell et al.50) 2568 95th 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2. 1999. Offergelt et al.. Daily variation in creatinine-corrected urinary arsenic is relatively small when intake is constant (Calderon et al.html. 2008). 2000). Though CCA-treated wood contains several thousand times more arsenic than untreated wood. WHO.18) 3.S. Shalat et al. Calderon et al. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 2007. though air levels of arsenic fume and dust are correlated with urinary arsenic levels at higher occupational inhalational exposures (Jakubowski et al.50) 1. but generally only at maternally toxic doses (WHO. Vahter et al.. Additional information about external exposure (i. In the German Environmental Survey III of 1998. 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. Consequently. Pellizzari and Clayton 2006). Fourth National Report on Human Exposure to Environmental Chemicals 183 .75 (<LOD-2.. 2005) and Urinary Arsenic (V) Acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. 2000. arsenic has been fetotoxic and teratogenic.Metals compounds.80 (<LOD-4.70) 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD 2. 2006.. urinary arsenic levels have been accepted as a good biomarker of dose (WHO. 2003. although urinary arsenic levels were not associated with CCA contact (Shalat et al.. population in NHANES 2003–2004 (Schulz et al. 2008).

Detectable levels of MMA reported in NHANES 2003–2004 were found only at the upper percentiles and. Total arsenic measured in the urine includes all species of inorganic and organic arsenic.30) 2.g. which may vary for some chemicals by year and by individual sample. population showed a higher contribution of arsenobetaine (Caldwell et al.4-35.5) 292 728 1548 03-04 03-04 1.S.3 (21.68) .. 2005.70 (3.3) 35.. 2005.1) 18..20) 3. a control population of 696 Tacoma residents had median urinary DMA levels similar to those for NHANES 2003–2004 (Kalman et al. Caldwell et al.80) 1. dermal keratosis.00-1. and arsenobetaine being the main contributors to the total urinary arsenic levels (Caldwell et al. median levels of urinary DMA were about 40-fold higher than the adult median reported in NHANES 2003– 2004.800) 1. vasospasm.00-12. When seafood intake is avoided. interval) 1.20) 7.0) 4. 2000.800 (.40-7. China.5 (26. arsenobetaine.20-3. MMA. with DMA.00) 3..05) < LOD .40) 5..6. Tseng et al. 2007).62) 2.4) 23.6 (25. Some noncancer effects of arsenic (e.00-6.6-44.800-1. 2008). In the residents of a Chilean town who consumed water with high levels of arsenic. arsenite. 4..2 (6.20-190) 31. population in the NHANES 2003–2004 subsample.9 (7. 2000.19 (. arsenobetaine and arsenocholine will greatly increase the level of total urinary arsenic and comprise the highest percentage of the total urinary arsenic level.70 (5.11-1.48-2.40-6.20 (2. 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.83) Selected percentiles ( 95% confidence interval) 50th 1.45 (1..600 (.80-5. 2008. see Data Analysis section) for Survey year 03-04 is 0.9-23. Caldwell et al. and urinary DMA represented about 67% of the total urinary arsenic (Hopenhayn-Rich et al.50) .00-4.74 (1.1) 45.28) 1.. DMA has been the predominant metabolite composing the majority of measurable inorganic-related arsenic in the urine (i.S. For residents of Inner Mongolia.8-50..3 (9. and peripheral neuropathy) have been associated with urinary levels as low as 50–100 μg/L in chronically exposed populations (ACGIH.90-7.30 (1.9 (6.50-6.80 (3.31-1.20 (4.70-21.6 (11.1-51. arsenocholine. and other factors such as nutrition.400-. and TMAO. Individually measurable species resulting from inorganic arsenic exposure are arsenate. Sun et al. Caldwell et al. Urinary Arsenobetaine Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.871-1.30 (2. After recent seafood ingestion.S. respectively.. Arsenate. 1990.9) 13. Also..70-21.800 (. Valenzuela et al. Caceres et al. 1. arsenite.1-94.80 (.2-38. and 0.5) 621 725 1078 Limit of detection (LOD. population from the National Health and Nutrition Examination Survey.4 (16.6. 184 Fourth National Report on Human Exposure to Environmental Chemicals . as evidenced by trace or nondetectable levels of arsenobetaine and arsenocholine in the urine.66 (1.4) 31. 2005.. 1985.10 (4.0) 29.60) 1. Measurable organic arsenic species in this Report are three biologically generated environmental forms. 1996.3) 1284 1284 03-04 03-04 03-04 1. Aposhian et al.500-1.e.8 (17.50) 90th 16.Metals other areas of the world (Ahsan et al.3-39. and TMAO were detected in only 7.90-29.20-25. These associations are stronger at higher urinary levels.60-3. Chowdhury et al. 2008).5) 32. 2001).5 (14. Survey years 03-04 Geometric mean (95% conf. Great Lakes region residents had median urinary DMA levels that were slightly less than median levels in NHANES 2003-2004 (Caldwell et al.7 (21. The higher percentiles of total urinary arsenic levels in the U. 2000.4. < LOD means less than the limit of detection..00 (1. and two methylated metabolic products.40) 75th 5.. methylation capacity..8-40.8 (12.. geometric mean levels were about 70-fold higher than for the U.37 (1.7) 13. In the late 1980s. 2001.3) 95th 35.7-22.30) 10.20 (.800-4.6) 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 * * 1.43-1.17-1.0 (27. 2008. DMA and MMA.20 (1.700-1.80 (4.3% of a representative sample of the U.10) 4.6 (13. DMA and MMA compose most (about 75%) of the total arsenic species measured in urine. population (Sun et al. when seafood organic arsenic is subtracted). Pellizzari and Clayton... 2008).900-1.. population (Ahsan et al.93) 1.8) 35. Levels of DMA and MMA increase in approximate proportion to the intake of inorganic arsenic.0 (26. 2003).8.0-23.7) 15.. 2008). arsenocholine. 2006). and duration of exposure are also considered important. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.S.50) .10) 8.00 (. 2007) with higher levels of arsenic in the drinking water. In most human studies.55 (1.29 (1.1-25.7 (13. Blom et al.700-1. WHO.2-35.5) 29.70) 6.S. in NHEXAS 1995–1996.900 (.20) 18.

40) 1.36) 2.83) 2. 2003. WHO.9-18.37-2.12) < LOD .43) 75th 5. 2008).55) 1. 1992. * Not calculated: proportion of results below limit of detection was too high to provide a valid result..78-5.938-1.612-1.6 (6.82) Selected percentiles ( 95% confidence interval) 50th 1.15-4.786-1.13-39.9 μg/L.7) 17.0) 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.67) 1.S.7) 9.15-1.88 (5.2 (13.5) 26.16 (.6-46.83) 8.. interval) 1.53 (.93 (1.65 (1.50-7.10 (.9 (25. population for the sum of inorganic related species was 18.47 (2.51-2.0 (9.0-36. 2001).47 (1. 2007).39-3. 2001).91) 90th 16. which is below the ACGIH BEI (Caldwell et al. population from the National Health and Nutrition Examination Survey.79 (1.901-2. Urinary Arsenobetaine (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.909-1.70) 5.531 (.62-6. The 95th percentile of the U.S.15-1.2 (12. Vahter et al.4 (24.21) 5.88) 2.18-1.30) 1.4-28. In recent years. Information about the biological exposure indices is provided here for comparison.29-14.6-32. these levels were much lower than those found in other studies where environmental exposures were highly elevated (Chowdhury et al. Offergelt et al.2 (4.959-1.44 (1.833-1..5 (18. 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.9) 14. Caldwell et al.3-24.9 (13.4-21.05) 1.6 (9.2 (12.4) 32.00 (1..80) . Finding a measurable amount of arsenic in urine does not mean that the level of arsenic causes an adverse health effect. 2006.3) 1284 1284 03-04 03-04 03-04 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. 1986. 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.40 (1.7) 30. 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.00 (3..1-36.9) 32.29 (4.3) 95th 29.82) 4.32-7.19-2.638) 1.50-15. 2008).877 (.3 (10.91 (4. Sun et al.64-29.6) 19.68 (1.25 (.1) 26.30-1.61-6.400-.4) 292 728 1548 03-04 03-04 1. Fourth National Report on Human Exposure to Environmental Chemicals 185 .78 (3..51) 5.8) 29. Survey years 03-04 Geometric mean (95% conf.73-6. 1998.5 (18.67) 4.58 (3. not to imply a safety level for general population exposure.80-153) 17.5-20.72) 12.54 (1.11 (.28) 1.76-27.5) 17. 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.81 (4.25-7.4-82... Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.05 (.4 (11.4) 13. 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.43) 14.6-29.1-18.Metals as with DMA.3 (10.45) 1.14 (1.

< LOD means less than the limit of detection. Survey years 03-04 Geometric mean (95% conf. Urinary Arsenocholine (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 0. population from the National Health and Nutrition Examination Survey. 186 Fourth National Report on Human Exposure to Environmental Chemicals . * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 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.S. population from the National Health and Nutrition Examination Survey.6. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th < LOD 90th < LOD 95th < LOD Sample size 2568 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.S. Survey years 03-04 Geometric mean (95% conf. which may vary for some chemicals by year and by individual sample.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.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 3.80) < LOD 621 725 1078 Limit of detection (LOD. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th < LOD 90th < LOD 95th < LOD Sample size 2568 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1.2.00) 1. Survey years 03-04 Geometric mean (95% conf.S.29) < LOD 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. < LOD means less than the limit of detection.Metals Urinary Arsenous (III) Acid 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.95 (<LOD-2.00 (<LOD-2.40 (<LOD-1. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th < LOD 90th < LOD 95th < LOD Sample size 2568 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1. population from the National Health and Nutrition Examination Survey. which may vary for some chemicals by year and by individual sample. see Data Analysis section) for Survey year 03-04 is 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.44) 2.20 (<LOD-1. Urinary Arsenous (III) Acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. Fourth National Report on Human Exposure to Environmental Chemicals 187 .70) < LOD 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2.00 (<LOD-3.08 (<LOD-4. population from the National Health and Nutrition Examination Survey.S.

90 (3.81 (5.6 (9.00-9.0) 9.82-5.34 (3.00) 4.78 (4.12-4.0) 95th 16.79 (3.0-17.0) 11.0 (8.69 (3.14) 3.45 (8.80-6.00-13.6) 292 728 1548 03-04 03-04 3.6-18.00 (5.8) 7.00-11. population from the National Health and Nutrition Examination Survey.00 (7.0 (10.00 (3.24) 3.33) 3.98) 4.32-10.95 (4.S.50 (4.70) 5.09 (7.00-22.34-4. interval) 3.00-3.0) 12.00) 9.37 (2.16 (2.84-18.73 (3.3 (8.74) 90th 9.55 (2.46 (4.86 (2.15) 4.00) 4.90) 2.60-3.0-16.57 (3.60-4.34) 3.05) 5.70-3.00) 6.5) 95th 13.94) 3.0 (10.00 (5.52) 3.33-4.00-10.82-9.00 (3.69-3.00-15.71-4.59 (6.00-15.0) 9.31) 4.00-5.0) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites Sample size 2568 03-04 03-04 03-04 4.8) 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 3.45) 3.12 (3.0-16.91) 75th 5.80-3.20-12.7-16.25 (4.0 (11.1-15.00-4.00-7.0 (12.03-6.60-6.90) 5.80-5.34 (3.49) 10.80) 7.0-17.10) 3.20-4.0 (9.20) 11.31-4.00 (5.44 (2.7.0) 621 725 1078 Limit of detection (LOD. population from the National Health and Nutrition Examination Survey.9 (7.92) 3.65-8.00 (4.00 (3.48 (2.9) 11. Survey years 03-04 Geometric mean (95% conf.0 (13.00) 3.78) 4.18 (6.00-11.0 (8.00-7.67) 9.16 (4.27-5.00-8.06) 5.00 (6.5) 12.3 (7.00 (6.0 (9.0 (9. interval) 3.17-4.Metals Urinary Dimethylarsinic Acid Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.00-7.71) 3.0) 17.42) 3.71 (3.32 (8.0-12.00-11.19) Selected percentiles ( 95% confidence interval) 50th 3.7) 12.00 (3.70 (3.11 (3.62) 4.0-19.16-11.34-4.60-7.71 (4.0 (14.S.85 (3.00 (5.1-18.70-12.45) 8.74 (2.1-22.44) 5.00) 6.27-2.0) 16.28) 2.7) 1284 1284 03-04 03-04 03-04 4.0) 13.24-4.9) 12.00 (5.03 (3.37 (3.22) 4.0 (12.65-6.80 (4.0 (10.00) 6.17 (2.00-4.39-3.61-11.00) 6.0) 11.97-3.6) 1284 1284 03-04 03-04 03-04 4.30 (7.00 (6.29-4.5 (11.11) 4.94-3.80) 2.00) 7.9) 5.0 (13.84-8. see Data Analysis section) for Survey year 03-04 is 1.7 (10.3 (8. Urinary Dimethylarsinic Acid (creatinine corrected) Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.00) 90th 11.73) 6.2) 10.08 (2.88 (4.00-7.00 (3.72 (4.82) 3.00-4.0) 17.4 (7.4) 621 725 1078 188 Fourth National Report on Human Exposure to Environmental Chemicals .48 (3.00-12.86-21.00) 75th 6.95-3.00) 3.69 (3.32 (4.05) 10.92-12.50-5.0) 13.0 (10.7) 13.95-6.00-3.49-4.00-4.9 (11.9) 13.50-15.00 (3.95-4.00) 5.0) 14.0) 292 728 1548 03-04 03-04 4.70-4.86-7. Survey years 03-04 Geometric mean (95% conf.1 (8.10) 6.05) 3.57-5.00-4.38 (3.27 (2.0-25.8) 7.00-15.69-6.0) 16.67) 8.0-18.00 (7.77 (3.00-4.14) Selected percentiles ( 95% confidence interval) 50th 3.13-4.0) 10.61-16.89 (3.00-12.30) 3.27 (3.17-6.0) 9.00) 12.

60) 2.54) 90th 2.70-2.45) 3.15-1.28 (1.53) Sample size 2567 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.30-2.30 (1.00) 1.50 (2.00 (<LOD-1. population from the National Health and Nutrition Examination Survey.00 (1.00-1.00-2.00) 1.50) 621 725 1077 Limit of detection (LOD.05-1.71-2. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th 1.88 (1.90) 2. < LOD means less than the limit of detection. population from the National Health and Nutrition Examination Survey.46-2.60) 1.18-1.90) 1.33 (1.985) 1.40) 1.75) 621 725 1077 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.84-3.53 (1.00) 2.20 (1.10 (1.00 (2.33 (1.00-2.80 (2.35-3.11-1.20 (1.10-1.60) 2.40-2. Urinary Monomethylarsonic Acid (creatinine corrected) Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.80 (1.30 (1.90 (1.40-2.30) 1.43-3.30) 2.50 (<LOD-1.40) 2.61-3.79) 2.88-2.86) 3.S.57) 95th 2.28 (1.20 (1.30 (1.52 (2.40) 1.61) 2.20 (1.80) 1.40-3.80) 1.60) 292 728 1547 03-04 03-04 * * < LOD < LOD 1.40-3.36) 1. which may vary for some chemicals by year and by individual sample.60 (2.58) 2.86) 2.50-2.73-2.10) 95th 2.853-1.20 (1. see Data Analysis section) for Survey year 03-04 is 0.18-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.34) 2.70-3.00) 1.80-2.60) 1283 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.50 (1.77) 1.30) 1.Metals Urinary Monomethylarsonic Acid Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.10 (<LOD-1.31 (1.80 (1.50) 1.90) 2.80 (1.46 (1.17) 2.900-1.86 (2. Survey years 03-04 Geometric mean (95% conf.40 (1.20 (1.10-1.00-4.37 (1.40 (2.10 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.85) 1.30) 90th 1.30-1.85) 2.00-1.00 (<LOD-1.90 (2.10) 2.10 (.22) 3.82-2. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th 1.14-1.07 (1.80 (1.60 (1.20-3.10 (.50 (1.62) 2.81) 1.07) 2.86 (2.70-2.96-2.9.30-1.20-1.16 (2.53-2.80) Sample size 2567 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.53) 1283 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.10-3.07-3.20) 2. Survey years 03-04 Geometric mean (95% conf.23) 1.22 (1.60-2.816 (<LOD-.53) 292 728 1547 03-04 03-04 * * < LOD < LOD 1. Fourth National Report on Human Exposure to Environmental Chemicals 189 .63 (<LOD-1.S.80-2.88 (1.00 (2.36 (1.93) .00) 2.70-2.70) 2.30 (2.31-3.70-2.82-2.

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

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43 (5. such as brazil nuts.95-6.59-11.72) 1.75) 2.35-1.30) 2.91 (2.41-3..61 (5.92) 2.20 (3.48 (6.34 (2.38 (1. fireworks. population from the National Health and Nutrition Examination Survey.8) 9.44 (1.60) 1.59) 3.10-5.35 (3.60-10.87-7.30) 8.30-1.90) 1. such as barium chloride.21-2.14-1.80 (1.90-13.50-6.70-8.49 (1.30) 4.65) 1.80-5. bricks.30) 5.30-2.03 (1.80 (2.87 (5. 0.35-4.36 (4.85) 1.87 (6.61 (1.36 (1.26-1.40) 3.32) 8.30 (1.88) 7.56 (6.40 (5.57-7.50) 2. 7440-39-3 Medically.80 (2.27 (1.76-7.21 (1.64-3.30) 5.54) 1.45) 7.24-1.41-1.80) 6.00) 6.48-4.62) 1.33 (1.35-1.20-1.51 (1. Barium salts have also been available as rodenticides.09 (1.50) 2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.85) 1.74-2. rubber.15 (6.15-11.62 (1.41) 1.44-5.76-3.50) 4.63 (2.78-2.11-1.66) Selected percentiles ( 95% confidence interval) 50th 1.50 (5.47) 4.20-5.52 (1.37-1.39-1.80 (1.60) 3.37 (4.40 (1.87) 7.65-5.80) 7.01-7.43 (1.52 (4.70) 5.02 (7.54-1.93-2.60-3.22-1.37-8.30 (5.76-2.37) 1.04-2.50 (1.90) 2.29-1.74-3.86-4. depilatories.27 (1.76 (3.12 (2.15) 5.86-5.60-6. respectively.60 (2.40) 7.50 (4.51) 1. are high in barium (Genter.62 (1.43) 2.20-1.21-8.90) 4.63 (1.99 (4.00 (2. were relatively well absorbed following inhalation (60-80% of a dose) or ingestion (11-32 % of a dose).40 (1.71-9.10) 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 1.22) 6.40) 7.56 (1.06-1.19-1.34 (1.00-8.1) 9.80 (1.43 (1.4) 9.65) 3.26) 2.17-1.50 (1.27) 2.60) 1.46-1.06-2.63) Total 1.50 (6.61 (1.96-2.54) 2.86) 6.56 (1.8) 5.46) 1.65) 1.40 (4.32-1.88) 4.73) 3.88 (5.91) 6.39) 1. Barium compounds are used by the oil and gas industries to make drilling muds.95 (4.10 (3.55-7.67) 6.11 (3.10 (4.91) 2.73 (5.55-3. it combines with other chemicals such as sulfur or carbon and oxygen.05% of the earth’s crust.25-11.S. and ceramics.05-2.4) 6.00-76.31 (2.62) 1.14-6.20-1.18 (6.99-5.38) 8.63) 1.73) 1.12 (2.70-2.80 (5.70) 7.49) 2.36-1.35 (2.98) 1.76) 1.44-2.73 (6.11 (2.47-1. glass.8 (6.38) 2.87-14.07 (2.24 (4.40 (1.50 (4.77-3.81-3.25 (1.82) 2.26) 5.30) 5.70 (5.90) 2. Urinary Barium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.56) 4.56 (2.90-9. barium sulfate and barium carbonate).32-7.93 (4.69 (1.90 (1.65-1.50-6.87-3.04-6.51) 7.54 (6.49) 11.40 (5.10) 5. Certain foods.16 (1.43) 6.73-5.15 (1.00) 4.53) 692 683 618 540 667 723 765 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.19) 2.65 (5.12.71 (2.63 (5.38 (1.50 (1.30-5.78) 1.70) 3.18) 3. whereas others are practically insoluble (e. soluble forms of barium. Workers employed by industries that make or use barium compounds can be exposed to barium dust.80-2.82-6.26-7. The general population can be exposed to low amounts of barium in air.00-3. In nature.54) 1.01 (4.70) 1.60) 4.74) 3.78-3.70-3.49) 8.39) 4.43) 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 1.80) 1.20 (4.50-1.88) 1.22-1.15-1.82) 1.81-2.15-1.20-6.61 (3.00) 1. barium sulfate is used as a contrast medium for taking radiographs of the gastrointestinal tract.18-1.24-1.49-9.20-8.85 (2.25-1.30-1.10 (2.28) 90th 5.70 (1.86 (4.71) 1.42 (1.11 (3.70-6.64) Sample size 2180 2690 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 2.20-8.30) 3.48-4.70) 4.31-2.30 (2.64 (1.g.20) 2.28-1.50-1.90-2. Ingested soluble barium General Information Elemental barium is a silver-white metal which comprises approximately 0.54-8.12.50 (4.50 (2.10-4.34 (1.86 (4.80-3.45 (1. water.90 (6.84) 5.Metals Barium CAS No.39 (1.29-5.36) 5.39 (1.29) 5.09 (2.48) 1.60-6.65-8.37) 5.53) 2.50 (1.70-2.35) 5.34) 2. and food.93-8.08-8. interval) 1.77) 1. and 03-04 are 0.30-2.00) 1.50 (3.50) 1. Some barium salts are freely soluble in water.20 (1.56) 1.30 (3.71) 95th 6.60-2.12) 6.68 (1. 01-02.51) 2.31.54-1.71) 2.90 (4.30-3.2) 6.20-8.57 (5.53) 1. and 0.10) 3. tiles.78) 1.47-1. Small amounts of barium can be released into the air during mining and other industrial processes.46) 1. Fourth National Report on Human Exposure to Environmental Chemicals 193 .30 (5.00 (1. In single dose animal studies.97 (1.14 (6.77 (3.40 (5.16) 5.9) 5.50 (1.63 (8.75-3.87-9.60 (1.94-6.20-1.4) 7.40-13.15 (2.57) 3.61-8.12) 7. 2001).70) 1.21 (1.35 (1.72) 4.36-1.53-5.08 (6. see Data Analysis section) for Survey years 99-00.81-2.61 (2.72) 75th 3.70-5.49-1.66 (4.80-7.54 (2.48) 1. Barium compounds are also used commercially in paint.12-1.49) 4.63) 1.

49 (1.27 (2.47 (5.22-1. diarrhea.32) 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.40 (1.23-2.35-1.48-5.72) 4.Metals was eliminated primarily in feces and to a lesser extent.28-11.56 (1.46-22.0) 5.81-7.00 (5.12) 2. paralysis.710-1.96) 4.84-5.78 (2.28) 5.891 (. 1989).24-1.81-6.42 (4.06) 2.47) 10.4) 5.82) 1.92 (4.45-1.43) 1.55 (5.77-5.02) .41 (1.02 (3.10-1.66 (1.76 (2.963 (.32) 2.53 (2.68-3.24 (5.48 (1. a benign condition that may occur among barite ore miners.21 (1.56 (1.28-6.99) 1. and cardiac dysrhythmias.8) 4.48-3.23-1.03) 3.75) 1.81-6.88 (6.38 (1.58-6. NTP. 2001).33) 1.31 (4.42) 1.35-3.54 (2. The health effects of exposure to barium compounds depend on the dose.62 (2.25-11.96 (4.25 (1.45) 1.32 (1.880-1.28-7.67-6.75) 1.26-1. in urine.33 (1.65 (5.26) 4.2) 6.86) 5.36 (3.74) 1.25) 4.60 (1.55 (1.3) 6.33) 6.92) 2.00 (2.80-6.38) 1.32 (2.20 (1.11) .64) 7. are not absorbed when administered.S.39-5.54) 1.03) 1.51 (1.96 (4.88 (2.04) 1.79-5.64 (1. Following intravenous injection in animals.65 (2.04 (2.29-1. Symptoms following acute high dose include perioral paresthesias.56-3.97 (5.10 (6.47) 1. 1985.36-2.70) 10.16 (1.2) 5.27) 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 .57-5.54) 2.62 (1.52) 2.29) 1.703-1.76) 2.45) 95th 6.0) 7.03-1.31-1.44-2.55-5.29-4.84-2.58) 4.00) 1.64) 7.33 (5.55 (4.90-2.37-1.37-2.02) 4.18 (1.36-1.60 (2.36 (1.49-1.74 (5.58 (2. 1986).24-1.921 (.58 (4.73-4.68-3.70) 1.28-1. Human health effects from barium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.64 (1.77) 1.85-5. population from the National Health and Nutrition Examination Survey.50) 1.46) 3. 1984.53-21.86-7.38 (1.75) 2..58) 75th 2.60 (1.832-1.11) .63-4.23-5.57-10.53) .01 (4.41) 5.47) 1. Toxicity from soluble barium salts is rare.13-3.37 (1.30) 2.39 (3.34-3.75) 2.29-3.49 (1.50) 297 368 290 621 762 725 1262 1559 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 1.39) 4. about 75 % of a dose of soluble barium was eliminated within 3 days (Reeves.45-1.00-1.19-1.00 (3. Chronic high doses in animals resulted in kidney damage (McCauley et al.24-6.76) 2.31) 5. interval) 1.57) 2.18 (1.48 (1.45-8.34-1.39 (2.40 (1.19-1.58) 1.87) 1. Insoluble barium salts.00) 4.31 (1.60 (5.62 (4.59) 1.55) .15-4.40 (1.52) 7.64 (1.76-3.24-11.39 (2.13-2.03-1.39-1.37 (1.00 (3.80) 4.54 (1.51 (1.71 (5.08-1.64 (1.76 (3.26-1.04) 5.29 (1.86 (2.91) 2.69 (5.52 (3.42) 1.52) 1.16-1.50) 2.39-1.56) Selected percentiles ( 95% confidence interval) 50th 1.08-2. Barium is not rated for human carcinogenicity.59-7.01 (5.68 (3.75-3.38 (4.59) 2.19-2. Wones et al.915 (. hypertension. Chronic accumulation of inhaled barium dust in the lung tissue may cause baritosis.73) 2.09) 6.96-6.03) 2.72 (2.05-1.41 (1.33-1.69-9.79) 1.06) .68 (3.68) 1.5) 1083 1334 1281 1097 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.26-4.40-1.97) 1.74) 1.00) 6. 1990).82) 1.31-1.38) 4.61) 2.51-3.72) 6.01) 1.57 (6.60) 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 2.28 (1.55 (1. and route of exposure.2 (3.52-10.45 (3. 1994.83) 2.76 (4.37) 2.46) 2.38-5.00) 4. but can occur after intentional or accidental ingestion of barium carbonate in rodenticides (Genter.49-1.27-3.36 (5.98 (2.59 (1.45 (1.30 (1.83) 3.45-6.33 (1.51) 4.44-2.46 (2.34-5.10-2.41 (2.38) 1.44 (1.19-1.38-1.48) 2. Barium blocks cellular efflux of potassium resulting in profound hypokalemia.56) 4.22-4..38 (4.34 (1.22-2.91-2.36-1. weakness.881 (.36 (3.35-1. chemical form.99 (4.50 (4.754-1.47) 4.59 (1.43-6.00-7.96) 7.29 (3.14-2.26-1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.33-4.29-4.46) 1.91 (3.38-7.91 (3.80) 3.777-1.24-3.77) Total 1.84) 2.76) 1. vomiting.61 (4.39 (2. Perry et al.55-6.48-1.51) 6.47-8. Urinary Barium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.77) 1.51) 4.24-6.89 (2.02-5.97-4.59) 1.73-2.26-1..63) 1.89) 90th 4.57-7.20-1.68) 3.27) 7.20-2.68 (2. water solubility.47 (2.32 (1.41) 4.52-4.0) 6.60 (2.16) 11.84 (3.96) 4.20-8.24 (3.3 (6.75-22.34) 1.4 (5.62) 2.29-7.50) 1.77) 1.36 (1.905 (.22-1.97 (4.10) 3.20) 4.51 (3.27-1.24) 3.70) 4. such as those used in medical radiographic procedures.39-10.11-2.96) 4.77) 5.31-1.48 (1.99 (2.10) 6.30 (1.97-3.49-1.

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

interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th < LOD < LOD < LOD 90th < LOD < LOD < LOD 95th < LOD < LOD < LOD Sample size 2465 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 . nuclear. less than one percent of the inhaled dose was slowly absorbed into the blood and eventually incorporated into the skeleton. are mined for commercial recovery of beryllium. 196 Fourth National Report on Human Exposure to Environmental Chemicals . soil. and refined beryllium is used in mirrors and special metal alloys for the automobile. and can be found in mineral rocks.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. 7440-41-7 General Information Pure beryllium is a hard gray metal.130 (<LOD-. Burning coal and oil can produce small amounts of beryllium dust that can be released into the air.13. computer. Beryllium compounds are commercially mined.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 . beryllium is used in instruments. A half-life of 450 Urinary Beryllium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. Exposure to beryllium occurs mostly in the workplace. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. bertrandite and beryl.S.13. population from the National Health and Nutrition Examination Survey.Metals Beryllium CAS No. near some hazardous waste sites. inhaled insoluble beryllium sulfate was retained in the lungs and nearby lymph nodes. or drinking water containing the metal.140 (<LOD-. see Data Analysis section) for Survey years 99-00. < LOD means less than the limit of detection. respectively. aircraft. which may vary for some chemicals by year and by individual sample. Two types of minerals. Low-level beryllium exposure in the general population can occur through breathing air. coal. eating food.130 (<LOD-. the lightest of all metals.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 . In studies of laboratory animals. 0. and dental bridges. and 03-04 are 0. x-ray machines. and from breathing tobacco smoke. electrical. In medicine. and volcanic dust. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. Beryllium is also used in the production of sports equipment such as golf clubs and bike frames. and machine-parts industries. 01-02. and 0.13.

Genetic factors modify individual sensitivity to beryllium and susceptibility to developing chronic beryllium disease (McCanlies et al. 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 . respectively. population from the National Health and Nutrition Examination Survey. IARC has classified beryllium as a human carcinogen. Air levels greater than 100 µg/m3 can result in erythema and edema of the lung mucosa. is a granulomatous interstitial lung disease that is caused by chronic beryllium inhalation and the resultant immunologic response. 2003. or berylliosis. NTP considers beryllium to be a known human carcinogen.Metals days has been calculated for beryllium elimination from the human skeleton (IPCS. including contact dermatitis and subcutaneous nodules.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. based upon excess lung and central nervous system cancers in studies of workers.333) < LOD < LOD < LOD < LOD 1227 1334 1281 1238 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . Human health effects from beryllium at low environmental doses or at biomonitored levels from low environmental exposures are unknown. EPA. 2002). and drinking water and environmental standards have been established by U. The effects of occupational exposure to beryllium depend on the concentration of beryllium in the inhaled air and the duration of air exposure. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.281 (<LOD-. Fourth National Report on Human Exposure to Environmental Chemicals 197 . * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Maier..S.231 (<LOD-. Skin exposure can result in delayed hypersensitivity reactions. 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. 1990).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 . S. Chronic beryllium disease. Workplace air standards and guidelines for external exposure have been established by OSHA and ACGIH.346 (<LOD-. which produces pneumonitis.

158:165-190. 1998). Costa R. Paschal DC. Sabbioni E. VI. Clin Chim Acta 2000.. et al. Andrew M. Pirkle JL. Available at URL: http://www. They reported urinary beryllium levels ranging from 0. Kriess K. Trace element reference values in tissues from inhabitants of the European community I. Hamilton et al. McCanlies EC.org/documents/ehc/ehc/ ehc106.23:827-839.1 μg/L). Finding a measurable amount of beryllium in urine does not mean that the level of beryllium causes an adverse health effect. Comparison of representative ranges based on U.e. Review of elements in blood. Given these results. Hamilton EI. Apostoli and Schaller (2001) stated that detection limits in earlier studies were inadequate to estimate nonoccupational exposures. population were generally undetectable in NHANES 1999-2000. Minoia et al. which approximate this Report’s limit of detection. (1994) noted that analytical methods used in several general population studies appeared to have limits of detection that were insufficiently low (i. Weston A. environmental levels) and health effects is available from ATSDR at: http://www. Clin Chest Med 2002. International Programme on Chemical Safety (IPCS). Genetic and exposure risks for chronic beryllium disease. Ting BG. Urinary beryllium--a suitable tool for assessing occupational and environmental beryllium exposure.74:162-166. 1990. plasma and urine and a critical evaluation of reference values for the United Kingdom population. Sampson EJ.76(1):53-59. Pozzoli L. and serum of Italian subjects. 20012002.Metals (i. 2000. 198 Fourth National Report on Human Exposure to Environmental Chemicals . Schaller KH. Sabbioni E. Trace metals in urine of United States residents: reference range concentrations... Am J Epidemiol 2003. Int Arch Occup Environ Health 2001. Sci Total Environ 1990. References Apostoli P. 3/27/08 Komaromy-Hiller G. Centers for Disease Control and Prevention (CDC). Element reference values in tissues from inhabitants of the European community. et al. A study of 46 elements in urine. Levels of beryllium in urine for the U.e. 1990.. less than 0. In other studies.gov/toxpro2.12 to 0.htm. Beryllium [online]. Apostoli P. it is likely that urinary beryllium levels in the U. Minoia C. blood. Environmental Health Criteria. 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. patient population and literature reference intervals for urinary trace elements. Morrow JC.inchem. and the 95th percentile for males in NHANES 2001-2002. 2001). Third National Report on Human Exposure to Environmental Chemicals. Ash KO. Jackson RJ.13 μg/L.S. Pietra R.15 μg/L in workers exposed at the recommended threshold limit value (Apostoli and Schaller. 106.. Paschal et al.cdc. and the fact that most NHANES participant levels were undetectable. Environ Res 1998.S. Howerton K.html. Biomonitoring Information Urinary beryllium levels represent recent and accumulated exposure.296(1-2):71-90.S.157:388-398. Sci Total Environ 1994. Atlanta (GA) 2005. and 2003-2004. urinary levels for general populations have been either undetectable or had different detection limits than in this Report (KomaromyHiller et al. population are lower than levels in workers. Maier L.atsdr. HLA-DPB1 and chronic beryllium disease: a HuGE review. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Van der Venne MT. Gallorini M.95:89-105. 0.

3. < LOD means less than the limit of detection.800-1.368-.400) .500-.600) .20-1.00 (. EPA.400 (.30) .50-1.400-.700-1.500 (.500 (.600 (.200 (.00 (.20-1.400 (.00 (.300-.900-1.412 (.50-1.300) . Cadmium also may be emitted into the air from zinc.400) .300-.00 (1.337) .600) .00-1.S.600) .289-. malleable.235 (.40 (1.300) .400) < LOD .00-1.10 (1.S.50 (1.304-.10) 1.S.300 (.400 (.304 (.500-.00 (.600 (. Other uses include pigment production.900 (.600) .452) . during refining of lead and copper from sulfide ore.600 (.300 (<LOD-.40-1.500) .300-.20) 95th 1.500-.30) 1.300) .300 (.300-.500 (.800) 1.800 (.367-.300) .00-1.500-.500) .300-.300-.500-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.20) .600-.400 (.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 .10) 1. and incineration of municipal waste materials.40 (1.00 (. bluish-white metal that is obtained chiefly as a by-product of processing zinccontaining ores (principally sphalerite. as zinc sulfide) and to a lesser extent. and 03-04 are 0.500) .200 (<LOD-.313 (.70) 1.40) 1. Blood Cadmium Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U.300 (.300-.296-.400) < LOD .10) 1.300-.600 (.800-1.216-.700-1.00-1.300) 75th .600 (.80 (1.600-.600 (.500-.400 (.600 (.50) 1.300-.500 (.00-1.275-.400 (.400 (.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-.300-.300 (.60-1.425 (.70) 2742 2268 2085 1842 2219 2292 2716 3806 3478 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.900-1.40 (1.400 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.500-.00 (.10 (1.400) < LOD < LOD < LOD .283 (.500-.70) 1.600-.300 (<LOD-.80) 1.600-1.400 (.400) .200-.20) 1.90) 1.10 (1. Important sources of airborne cadmium in the environment are burning fossil fuels such as coal or oil.470) * .400 (.400-.14.300-.20-1.300 (<LOD-.300-.50-1.400) .20-1.40 (1.40-1.40 (1. cadmium use has declined in response to environmental concerns (http:// minerals. Since 2001.60 (1.10 (1.500-.700) 1.20) 1.300-.60 (1.300 (.400) .300-.40) 1.378-.300 (.700) .20) 1.500-.400-.gov/minerals/pubs/commodity/cadmium).400 (.10) 1.600 (.30-1. The predominant commercial use of cadmium is in battery manufacturing.70) 3913 4339 4131 4057 4606 4241 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .400 (.600 (.500) . coatings and plating.30-1.200 (. and 0.800 (.400-.300 (.441) * .00 (.20) 1. population from the National Health and Nutrition Examination Survey.449) Selected percentiles ( 95% confidence interval) 50th .424) * .700-1.00 (.700) .30-1.400-.50-1.600) 1. 0.00 (.900-1.300-. 7440-43-9 General Information Cadmium is a soft.309-.40 (1.700 (. plastic stabilizers.600) .00-1.700) .500 (.900-1. 01-02.600) 90th 1.255) .200 (.50 (1.300) 1.427) * .700) .50) 1.300) .600) .60 (1.900-1. which may vary for some chemicals by year and by individual sample.300-.00-1.Metals Cadmium CAS No.378 (.426-.400-.300) .400 (.400 (.10 (1.300-.326 (.10) 1.300 (.300 (.10) 1.500 (. Fourth National Report on Human Exposure to Environmental Chemicals 199 .30) 1.400 (.700) . lead.398) < LOD < LOD < LOD < LOD < LOD < LOD .20 (.300 (.400-.usgs.900-1.20) 1.700) .362-.500 (. or copper smelters (U.20) .70) 1.300) .10) 1.420 (.300 (.300 (.300 (.344) .460) .900-1.200-.50 (1.400) .300) .500-.300) .400) .400-.400) < LOD .50 (1.500 (.300-.400-.600 (.300) .00) .500-.300-.30) 1.500) .60 (1.20) 1.60) 1.20) 1.376-. respectively.300) .200-.361-.403 (.421 (.386-.60) Total * .40 (1.400) . see Data Analysis section) for Survey years 99-00.800) .393 (.50) 1.300 (.30-1.80) 1.600 (.200) .10) 1.300-.500 (.300) .300 (<LOD-.70) 1.500) .304 (.800) .600) .500-.333 (.20-1.200) .266-. interval) .20-1.395 (.500-.10 (1.60) 1.200 (<LOD-.600) .00) .10 (1.900-1.20-1.600) .300-.403) .400) . U.300-.366) * * .400 (.00-1.331) .900-1.700) .900 (.60) 1.00 (.359-.600 (.400) . and nonferrous alloys.00 (1.468 (.200-.400 (.20 (1.900-1.500) .400) .200-.513) .500-.60 (1.382 (.30 (1.00-1.400-.500-.3.400) .30-1.500-.20) 1.300) .600 (.400) .700) .10 (.600 (.500-.400) .

20 (1.34) 1.633-1.204 (.393-.977) .167-.214-.222) .175 (. see Data Analysis section) for Survey years 99-00.886) .848 (.175 (.290-.30-1.229-.078 (.445 (.092 (.210 (.918-1.265) .107-.210) .700-.191-.366-.01 (.189-.28 (1. and 0.860) 1.354) .440 (.289-.57) 1.972 (.261-.19) 1.135-.980-1.200 (. About one-third to one half of the total body burden accumulates in the kidney tissues (Nordberg and Nordberg.610) .210 (.452 (.32 (1.220 (.15 (.539) .230) 75th . Urinary Cadmium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. 2003).22 (1.02-1.510-.15) . ingestion through food is the largest source of exposure.06.714-1.01) .196-.231) .221) .733-.141 (.171-. respectively.112-.763-.080 (.210 (. and various seeds.04 (.450 (.257) .26) size 2257 2690 2543 Total years 99-00 01-02 03-04 50th . The gastrointestinal absorption of dietary cadmium is about 5% in adult men and 10% or higher in women (Diamond et al.400-.270 (.199 (.28-1.233) .219 (.890-1.839 (. The kidney is a critical target and shows the earliest sign of cadmium toxicity.440-.190-. For nonsmokers who are not exposed to cadmium in the workplace. Cadmium in soil is absorbed by plants.322 (.381-.559 (.227 (.295) .101) .189) .200-.412) .067-.134) .440 (.507) .221 (.989-1.229) .327 (.25) 1.260 (. rice. copper) and protein.249) .806) .589 (.875) . drinking water is a source for cadmium intake.202-.220-.273 (.077 (.388-.109 (.700-.148-.181 (.233) .960 (.892 (.109-. calcium.173) . interval) .520-.623) .960) 1.810-1. 2004a.790 (.130 (.140 (.52 (1.230 (.170-.870) .510) .211 (.261-.470-.350 (.15) 1.519) .190-. Cadmium absorption may be increased with iron deficiency (Berglund et al.067-.169-.251) .17 (.41 (.192-. including many food crops such as cereal grains.336) .229) .366-.220) . an inducible metal binding protein.820) 1.200 (.980-1.817 (. population from the National Health and Nutrition Examination Survey.277 (.20 (1.980) .201 (. however.490) .235) .550 (.194-.200-.28) 1.170-.38) 1.S.818 (.210 (.74) 1.06) .090) . 2003).500) .48 (1.090) .519) .180 (.160) .302 (.237-.126) .285-.100-.880) .184-.09-1.551) .190-.06.255) .686-.940-1.263) .339) .135 (.260-.400-. To a lesser extent.220) Selected percentiles ( 95% confidence interval) Sample 95th 1.114-.209 (.20) 1.191 (. 1994). Cadmium is absorbed via inhalation and ingestion.232) . 2001). Renal tubular and glomerular damage.178-.255) .530) .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 .07-1.253-. potatoes.990) .260-.72) 1.362) .753-.247) .128 (.265 (. whose body burdens of cadmium can be approximately twice that of nonsmokers.580) .. a factor that may contribute to the higher absorption of cadmium by women (Diamond et al.394-. The estimated half-life of cadmium in the kidney is from one to four decades (ATSDR. 01-02..36) 1.423-.540) .360) .482) .193 (.115-.980) .241) .202 (.306 (. **All results are corrected for molybdenum oxide interference in the ICP-MS method.83) 1.150) .330-.262) .220-.270 (.06-1.280 (. Inhalation of cigarette smoke is a predominant source of exposure in smokers.596) .445 (.206) .366) .232 (.320) .980 (.06-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.13) .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 ..466 (.191-. wheat.17) .387) .313) .065-.110-.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.640) .12-1. Diamond et al.165-.120 (.17 (.430-.633 (.153-.607) .Metals 2000).** Survey Geometric mean (95% conf.255) .390-.456-.890 (.226) .25 (1.700-.741-1.157) .257-.492 (.060-.390-.680 (.300) .077 (.447 (.13-1.551 (.230) .490) 1.121 (.061 (<LOD-.476-.12 (.06.436-.390 (. Kikuchi et al.886-1.206 (.240) .216 (.430) .748-1.210 (.192-.24) 1. With chronic exposure.51 (1.817 (.730-..283 (.38) 1.300 (.207-.963-1. 2003)..47) 1.240-.239 (.281 (.766 (.310 (.150-.713) .10 (1.238) .498-.179-.38) .316 (.203 (.299) .500) 90th .480) .223 (.329 (.351-.148) ..481) .38) .545 (.249-.246) .219 (.919) . and 03-04 are 0.843-1.820-1.195-.177-.151-.081) .183-.198) .210) . 1999.705-.061-.20-1.170 (.22 (.426 (.01-1.855-1.13 (.892-1.279 (.813 (.493-.187 (.43) 1.462 (.326) .189-.82) 1.450 (.800 (.308) . cadmium accumulates in the liver and kidneys where it is bound to metallothionein.243-.433-.157-.04 (. 2003.455 (.203) .226) Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 * .160 (.858 (.530 (.372) .479) .836-1.087-.20 (1.820 (.160) .733) .458 (. Horiguchi et al.219 (. 200 Fourth National Report on Human Exposure to Environmental Chemicals .208-.790 (. 0. zinc.211-.800-.284) .17 (.717-.475 (.092) .193-.310) .160-.136) . individual values vary and are affected by factors such as dietary intake of essential nutrients (iron.234 (.03) .875 (.272-.282 (.238-.

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.206-. At lower environmental exposures.382) .234-.136-. **All results are corrected for molybdenum oxide interference in the ICP-MS method.227-.209) Selected percentiles ( 95% confidence interval) Sample 95th .098) .210 (.140-.204-.501 (.184) .813-.444-.078 (.085-.093 (.678-.507-.470) ..162 (.239-..343-.545) .156 (.02 (.181 (.647-.219 (.253) .** Survey Geometric mean (95% conf.208-.075 (<LOD-..191 (.795) 1.225) .412 (.090 (.097) .716-. 2003.198) .381-.182) . 2004b).084 (. most often a result of occupational exposure (Roels et al.158-.107) .551) .607) .100 (.210) . Staessen et al.423 (..197-.826-1.985 (.387-.137 (.308) .126 (.17) .234) .433-.207-.688-.00 (.740 (.247-.884) .434 (.166 (.719 (.630-.135) .176 (.229) .163 (.666-.07) .147-.631) .929) .909-1.729 (.622 (.096) .614) .189-.490 (. During the 1950’s and 1960’s.789 (. can result from high dose chronic exposure.211 (.215 (. Noonan et al.426-.432 (.757) .304-.154 (. 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.247-. 2002.391-.541) .252 (.157-.207) .221-.712 (.130-.159 (.173 (.783) .091 (..077-.173-.438) 90th .113-.377-.266-.16) . 2002.438-. two studies in Japan did not find an association between cadmium in urine and renal biomarkers (Ezaki et al.274) 1.156) .476) . interval) .148 (.154-.143-.123-.340) .184-.300-.331 (.727-.653) .784) .137-.191) .388-.263 (. 2000.08) 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.325 (.219 (.091) .123-.232) .690-.187) .38) .449) .268 (. Olsson et al.182) .101) .071 (.219) Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 * .316) .170-.067-..350) .157-.273 (.487 (.245 (.940-1.693 (.190 (. a condition known as “itaiitai” (“ouch-ouch”) affected postmenopausal women living in a cadmium-polluted region of Japan. 1999).178-.757 (.250) .830-1.075-.078-.261 (.242) .191-.998) .222-.364) .223) .382-.536 (.04) size 2257 2689 2543 Total years 99-00 01-02 03-04 50th .311) .084-.667) .156-.690 (.716) .850) .147 (.479 (.783 (.175-.150-.240) .591 (.293-.687-.906) .178) .874-1.833-1.329 (.940 (.559-.418-.278) .143-.238-. 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.194-.423-.181) .387 (.431) .691-.Metals manifested by irreversible proteinuria and progressive reduction in glomerular filtration rate.316 (.281) .210 (.171-.218) .226) 75th .280 (.270 (.. Fourth National Report on Human Exposure to Environmental Chemicals 201 .516-. 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.418) .086 (.538) .174-.221 (.617 (.917) .192) .094) .289) .232) .321) . population from the National Health and Nutrition Examination Survey.533) .06 (.267 (.917 (.289) .308 (.686 (.144-.335 (.850) .190 (.725-1.304) .199 (.440) .143) .839) .404 (.856) .09 (.176 (.202 (.253 (.500-.792 (.170 (.238) .818) .199-.261) .560-.678 (.085 (.292) ..205 (.234 (.263-.240) .645-.111-.136-.779 (.267 (.690-.235) .318 (.147-.414-.281) .08) .696-.962) .051-.919 (.283 (.131-.185) .140-.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 .175 (.414 (.161-. 1999).106) .518) .650-.185 (.208 (.184-.481 (.398-.865 (.. 2004).13) .979 (.338 (.806-1.168-.083-.941 (.168-. Jarup et al.07 (.233 (.05) 1.537-.177) .S.201-.826-1.769 (.931 (.247-.767) .336-.873 (.091 (.473 (.216-.415) .104) .876-1.224 (.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 .122 (.767 (.212 (.112) .181 (.813-1.063-.236-.663 (.255-.421 (.818) .484 (.00 (. 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. 2002.187-.446) .182) .104) .927-1.470) .256-.168 (.830) .708-1.181-.828) .472) .266) .352) .200 (.159 (.209) .261-.10) 1.16) 1.146-.288-. 1999).074-.288) .441-.827) .718 (.440) .282 (.296 (.220 (.297) .562-.754) . However.196 (.288 (.700 (.163) .404) . Horiguchi et al.175 (..12) 1.856 (.303) .225) .183 (.491-.241) .700) .228-.722-.950) .668-.531 (.183) . 1996.674-1.687 (.802 (.

Staessen et al. People who are occupationally exposed may have blood and urine cadmium levels that are higher than those of the general population. 2003.gov/ toxpro2.. Komaromy-Hiller et al. 2002... study subjects living near a former zinc smelter were similar to those from an unexposed community and to those in this Report (Noonan et al. pituitary gland and kidney tumors in animals and has been associated with lung cancer in humans in occupational epidemiologic studies. 2003. 2004. and drinking water and environmental standards have been established by U. blood cadmium was also slightly higher in Mexican Americans and participants 20 years and older (CDC.. 2003. maternal blood or maternal urine and birth weight (Nishijo et al. Ezaki et al. Biomonitoring studies on levels of cadmium provide physicians and public health officials Fourth National Report on Human Exposure to Environmental Chemicals . In postmenopausal women.. Ezaki et al. 2000). decreased bone density was correlated with mean urinary cadmium levels of approximately 1 mg/gram of creatinine (Staessen et al.26 and 3.. Small epidemiologic studies have noted an inverse relationship between cadmium in cord blood. 2002). not to imply a safety level for general population exposure. data (CDC. 2004). Staessen et al.. 2005.... Staessen et al.. EPA. 2003.. with peak values observed in the fifth to sixth decades (CDC. 2002). 1999). Wennberg et al.. For NHANES 19992000. Olsson et al. Creatinine-corrected urine cadmium values in U. Several studies of populations residing in areas with higher cadmium soil concentrations or with frank cadmium pollution have reported mean blood and urine cadmium levels considerably higher (as much as 10 times higher) than control groups or representative U. intermediate in former smokers and lower in never-smokers (Becker et al. 2005). Mannino et al. 2000. urinary cadmium reflects both cumulative exposure and the concentration of cadmium in the kidney... Biomonitoring Information Blood cadmium reflects both recent and cumulative exposures.1 mg/L (Alfven et al. 2006). 2002). CDC. Blood cadmium levels are about twice as high in smokers compared to nonsmokers (Becker et al. Surveys of populations not known to have increased cadmium exposure have reported similar urine and blood levels (Becker et al. Jarup et al. 2002... 2004. 2002).. Suwazono et al... Salpietro et al. Further research is needed to address the public health consequences of such exposure in the United States. Olsson et al. respectively.. 2004b). In the typical environmental exposure... 1988). Wilhelm et al. 2002.S.html. Women had higher blood and urine cadmium levels compared to men of similar ages.e. Becker et al.. Wennberg et al..atsdr.cdc. 2000. Information about external exposure (i. Finding a measurable amount of cadmium in blood or urine does not mean that the levels of cadmium cause an adverse health effect. In adults aged 60 years and older. 2006). In this Report the urinary and blood cadmium levels at the 95th and 90th percentiles. Horiguchi et al.. Acute and heavy exposure to airborne dusts and fumes. as may occur from welding cadmium-alloyed metals.46 mg/gram of creatinine) (Ezaki et al..... Workplace exposure to airborne cadmium particulates was associated with decreases in olfactory function (Mascagni et al. Jin et al. Olsson et al. 1996. has resulted in severe.. However.. 2003). Cadmium can produce lung... 2002. Chronic inhalation exposure to cadmium particulates was associated with changes in pulmonary function and chest radiographs that were consistent with emphysema (Davidson et al.. Becker et al. potentially fatal pneumonitis (Fernandez et al. Occupational standards are provided here for comparison only. 2005. 2000. Animal studies have demonstrated reproductive and teratogenic effects. 2004. Zhang et al. 2002. 2003.S. 2006.. Both IARC and NTP consider cadmium a human carcinogen. Workplace standards and guidelines for air exposure to cadmium have been established by OSHA and ACGIH. 2004. two studies of women in Japan with lower exposures found no correlation between renal tubular effect markers and blood or urine cadmium levels (geometric means were 1. 2002). Friedman et al. Subtle increases in markers of renal tubular effects have been associated with urine cadmium levels as low as approximately 1 mg/gram of creatinine (Akesson et al. 2003.. Blood and urine cadmium levels are typically higher 202 in cigarette smokers. Moriguchi et al.. 1996). Horiguchi et al.. respectively.. 2005.S. Waalkes (2003) provides an overview and summarizes potential mechanisms for carcinogenicity. 1999). 1999. 2005. 2002. 2002) and length at birth (Nishijo et al. 2006. 2004b. The 95th percentiles for cadmium levels in this Report were less than the OSHA standards for both blood cadmium (5 mg/L) and urine cadmium (3 mg/gram of creatinine). Jarup et al.. the risk of low bone mineral density increased by nearly three-fold when the blood cadmium exceeded 1. Noonan et al.. Becker et al. approached these values associated with subclinical changes in renal function and bone mineral density.Metals greater urine cadmium levels may have an increased risk for bone fracture and diminished bone mineral density (Alfven et al. environmental levels) and health effects is available from ATSDR at: http://www.

Clin Chim Acta 2000.gov/toxprofiles/tp5. Third National Report on Human Exposure to Environmental Chemicals. Nerbrand C. et al. Jin T. diabetes mellitus. Wang H. 4/8/09 Alfven T. Komaromy-Hiller G. 102:10581066. Centers for Disease Control and Prevention (CDC). Vahter M. Kumagai N. Chislovska NV. Costa R. Dietary exposure to cadmium at close to the current provisional tolerable weekly intake does not affect renal function among female Japanese farmers. Furuki K. Schulz C. Environ Res 2006. Moriguchi J. Sasaki S. Miyamoto K. Mascagni P. Okamoto S.59:497]. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Fatal chemical pneumonitis due to cadmium fumes. Atlanta (GA). Kaus S.46:372-374. Savage-Brown A. Hellstrom L. Pickering CA.102:83-89. Nermell B. Kundiev YT. Lukyanova EM. Toxicol Lett 2004. Seifert B. patient population and literature reference intervals for urinary trace elements. Urinary cadmium levels predict lower lung function in current and former smokers: data from the Third National Health and Nutrition Examination Survey. Nordberg G. Bernard A. Sasaki S.96:353-359. Horiguchi H. Jones RL. Schulz C. Seiwert M.cdc.95:20–31. iron deficiency. Jarup L. Hotz P. Taylor AJ.59:194-8. Krause C. Vahter M. Oguma E. Toxicol Appl Pharmacol 2004a. et al. Becker K. et al. Ezaki T. Toffoletto F. Ukai H.html. Machida M. Int J Hyg Environ Health 2002. Davison AG. Bo M. Palomar M. Fourth National Report on Human Exposure to Environmental Chemicals 203 . Lepom P. Int J Hyg Environ Health 2003.45:43-52. Ezaki T. Neurotoxicology 2003. Diamond GL.354:1508– 1513. et al.57:668-672. Occup Environ Med 2000. Kikuchi Y. Chiappino G.110:699-702. Lancet 1999. Howerton K.66(Pt A):2141-2164. Miyamoto K. Moriguchi J. Toxicological profile for cadmium update. Oguma E. Comparison of representative ranges based on U.1(8587):663-667. and dietary predictors of elevated blood cadmium levels in Ukranian children: Ukraine ELSPAC group. Buchet JP. Tsukahara T. Nomiyama T. Bregante G. Agency for Toxic Substances and Disease Registry (ATSDR). Fayers PM. Alfven T. Olfactory function in workers exposed to moderate airborne cadmium levels. Consonni D. Greves HM. possibly better than b2microglobulin. Available at URL: http://www. 1999 [online]. Carlsson MD.24:717-724. Akesson A. Lancet 1988. Furuki K. Fukui Y. Intestinal absorption of dietary cadmium in women depends on body iron stores and fiber intake. J Occup Health 2003. Stock AL. Ye T. Cadmium fume inhalation and emphysema. et al. Thayer WC. et al. et al. 196:114-123. Comprehensive study of the effects of age. References Akesson A.atsdr. Uptake of cadmium in meals from the digestive tract of young non-smoking Japanese female volunteers. Persson B. Fukui Y.296(1-2):71-90. Berglund M. Environ Health Perspect 2005. Grubb A. ShkiryakNizhnyk AZ. Serra J.148(1-2):11-20. Horiguchi H. Venables KM. Mannino DM. et al. et al. Lidfeldt J.13(11):1627-1631. Choudhury H. Friedman LS.000 women in the Japanese general population: a nationwide large-scale survey.76:186-196.S. Becker K. No clear-cut evidence for cadmium-induced renal tubular dysfunction among over 10. Cadmium and lead in blood in relation to low bone mineral density and tubular proteinuria. Seiwert M. Gadea E. Environ Res 2004b. Lison D. Bellerup P. a1-Microglobulin as a promising marker of cadmium-induced tubular dysfunction. Tsukahara T. population. Dekio F. Int Arch Occup Environ Health 2003. Machida M. et al. Pharmacokinetic/ pharmacodynamics (PK/PD) modeling of risks of kidney toxicity from exposure to cadmium: estimates of dietary risks in the U. Darbyshire J. et al. Takebayashi T. Jarup L. Mucha A. Ikeda Y. Elinder CG.205:297-308. Uemura T. Sanz P. Osteoporosis and renal dysfunction in a general population exposed to cadmium in China. Occup Med 1996. Kaus S. and cadmium burden on dietary cadmium absorption in cadmium-exposed female Japanese farmers. J Toxicol Environ Health 2003. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Ash KO. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Holguin F. Ikeda Y. environmental. Environ Health Perspect 1994. Renal effects of low-level environmental cadmium exposure: 5-year follow-up of a subcohort from the Cadmibel study. Zhu G. Thorax 2004. Lundh T.S. 206:15-24. Low level exposure to cadmium and early kidney damage: the OSCAR study [published erratum appears in Occup Environ Med 2002.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. Environ Health Perspect 2002. 2005. Environ Res 2004. Tubular and glomerular kidney effects in Swedish women with low environmental cadmium exposure. Lauwerys R. Anthropometric. Fernandez MA.

cadmium. Olsson IM. Okubo Y. Nakagawa H. Kobayashi E. lead. et al. or cadmium in controlling occupational and environmental risks of nephrotoxicity. Merlino MV. Cadmium carcinogenesis.3:26-41. Nakagawa H.30(5):395-399. Environmental exposure to cadmium.100:330-338. Usefulness of biomarkers of exposure to inorganic mercury. Tanebe K. Available at URL: www. Bensryd I. Cadmium in blood and urine – impact of sex. and mercury in the population of northern Sweden. Environ Health Perspect 2002. Staessen J. Sager PR. et al. Environ Res 2006. et al. Ren Fail 1999.110:1185-1190. Roels H. Noonan CW. Schwenk M. Revised 2000 [online]. Lauwerys R.39:2507-2515. Tanebe K. Buchet JP. Ginucchio G. Minciullo PL. Renal effects of cadmium exposure in cadmium nonpolluted areas in Japan.84 (Section A):4455. Japan.353:1140-1144. Kuznetsova T.21(3-4):251-262. age.59(1):22-25. J Environ Sci Health B 2004. Lijnen P. and former smoking – association of renal effects. et al. Public health implications of environmental exposure to cadmium and lead: an overview of epidemiological studies in Belgium. 2000. Friberg L. Environ Health Perspect 2002. Effects of maternal exposure to cadmium on pregnancy outcome and breast milk. Hoet P. Kido T. Wilhelm M. Fan YG. Kathman SJ. New York: Plenum Press. Wang JX. Emelianov D. Biological monitoring of toxic metals.epa. Nakagawa H. Honda R. Int J Hyg Environ Health 2006. Arch Environ Health. dietary intake. iron status. Gangemi S. Hazard Summary. 151-168. Tawara K. Suwazono Y. Zhu HD. Staessen JA. Nordberg GF. 2001. eds. Mueller PW.gov/ttn/atw/ hlthef/cadmium. 204 Fourth National Report on Human Exposure to Environmental Chemicals . Ottosson H.209:301305. Nordberg M. Lybarger JA.html. Lancet 1999. Zhang YL. et al. Thijs L. Honda R. Schultz C. 2004. et al. Nishijo M. Cadmium concentration in maternal and cord blood and infant birth weight: a study on healthy non-smoking women. Lundh T. Effects of exposure to low levels of environmental cadmium on renal biomarkers. Stelitano A. EPA). Lison D. J Perinat Med 2002. Revised and new reference values for arsenic. created 1992. Time trends in burdens of cadmium. Effect of environmental exposure to cadmium on pregnancy outcome and fetal growth: a study on healthy pregnant women in China. and risk of fractures: prospective population study.S. Gallmans G. In: Clarkson TW. lead. Campagna D. Lundh T. forearm bone density. Bruiglia S. Salpietro CD. J Cardiovasc Risk 1996. lead. Stegmayr B. pp. Vangronsveld J. Cadmium compounds. Toyama. Biological monitoring of cadmium. Environ Res 2000.110:151-155. Sarasua SM.59:394-397. Bergdahl IA. Occup Environ Med 2002. Wennberg M. United States Environmental Protection Agency (U. and mercury in blood or urine of children: Basis for validation of human biomonitoring data in environmental medicine. Relationship between newborn size and mother’s blood cadmium levels. Nogawa K. Nordberg GF. Jansson J-H. Saito S.Metals Nishijo M. Liu QF. Mutat Res 2003. 4/8/09 Waalkes MP. Skerfving S. Roels HA. Zhao YC.533(12):107-120. Oskarsson A. Roels HA.

6 (9.60-6.7) 10.99-11.54) 4.40 (4.8) 12.90) 5.37) 7.98 (7.82) 5.10-8.45-5.42) 6.16-6.87) 5.0-15.40-5.80-6. infrared lamps.20) 7.82-4. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.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 4.04) 7.53-11.81) 4.40-11.60 (8.01-8. and high-power gas-ion devices.70-5.90 (4.74) Selected percentiles ( 95% confidence interval) 50th 4.00-8.64) 5.9 (10. Urinary Cesium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.70 (5.7) 11.1 (9.81 (4.4 (9.90) 7.2-13.21 (4.4) 9.59) 7. and cardiac arrhythmia (ATSDR.62 (5.23-4.8 (10.95) 5.47-4.5-16.25) 4.64) 5.08) 7.03 (4. nausea.2) 11.2 (9.77 (4.49 (5.50-7.43 (5.7) 884 683 618 568 667 723 821 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. Fourth National Report on Human Exposure to Environmental Chemicals 205 .25-5.5 (10.2) 12.71-9.1) 10.80-10.20-5.0) 12.09) 5.36 (3.47-8.50 (6.33 (6.92-13.2 (9.8 (10.6 (9.35 (4.1) 9.3) 12.70 (8.91-8.77 (9.10 (8.8) 12.00-8.71-5.5-14.35-5.20 (6.77 (9.80 (8.60 (7.12-5.62) 4.1) 11.23) 9.03 (4. Human health effects from cesium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.5) 12.7 (9.0 (9.5-13. Inorganic cesium compounds are used in photomultiplier and vacuum tubes.99) 9.56-11.00-9. diarrhea.3-13.34 (4.27-5.88 (8.3 (8.62 (5.25 (3.35 (4.8) 12.10-9. although cesium was generally of low toxicity when given to animals. and 0.2-13.14.60-7.08 (7.59 (5.70) 7.9) Total 4.1) 9.40) 7.22 (4.94 (4.00) 6.94) 4.55 (4.9 (11.64 (4. For absorbed cesium salts. Little is known about the health effects of this metal.00) 7.97-7.90) 4.72) 4.68) 9.69-6.39-4.2-12.72-7.63) 6.3) 10.5) 10.64-10.60-5.14.7 (11.90-10. respectively.66 (7.84-5.8) 9.70) 5.60) 7. photographic emulsions.52-9.9 (11.8) 11.80 (8.90-12.64-5.6 (11.55 (7. semiconductors.86-12.40-5.83-4.20) 8.0 (10.81) 4.00-10.1-13.3) 10. Case investigations of ingestions of large doses of cesium chloride have reported decreased appetite.98 (7.29) 4. 0.S.27) 4. and 03-04 are 0. interval) 4.97 (7.74 (4.10 (6.12) 5.84 (4.43-8.1-12.45-8.60) 5. see Data Analysis section) for Survey years 99-00. population from the National Health and Nutrition Examination Survey.94 (4.81-14.05) 5.5) 9.4 (9.59-5.79 (4.7-14.53 (6.94-4.6) 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 4.80 (4.10 (8.4-13.12-11.08-5. the body half-life is estimated to be 70-109 days based on 137Cs exposures.32-5. Radioactive 137Cs has been used medically to treat cancer.70-8.40-5.49 (4. and clay.70 (8.7 (9.89-5.90-12.42) 7.97) 4.09-5.50 (4.7 (8.33-5.5 (8.05-5.84) 8.30-5.3 (8.83) 6.21) 90th 9.90) 9.84) 5.87-7.05-5.4) 11.90) 5. scintillation counters.71 (8.87 (4.80 (4.13 (5.15-8.4) 95th 11.4) 12.10 (6.07) 4.4 (10.0) 12.10-7.71-8.01) 7.99-6.7 (10.31-8.08 (6.20 (4.2.30-10.30 (6.7) 10.03-4.74-5.01-6.89) 5.59-5.8) 9.29 (4.8) 11.55-11.49) 4.76-6.1 (10.67 (4.50 (7.70) 5.07-11.91 (7.93 (4. Most human exposure to cesium occurs through the diet.26 (3.0) 11. Workplace guidelines for cesium hydroxide are available from ACGIH and NIOSH.9) 8.20-4.4) 10.1-12.44 (8.90 (6.40) 5.99) 7.20) 5.9 (10.32 (3.95-4.13 (8.12 (4.02 (4.38) 5.39) 7.9) 12.70 (9.16-6.05) 5.95 (3.6 (9.40-7.80-10.87 (4.10-5.0) 10.90-10.04 (4.26) 4.56 (4.90-8.64) 4.3-13.13-8.27 (7.89) 4.86 (7.7 (9. 01-02.00 (7.68 (7.9 (11.17) 4.71) 4.40-11.81) 9.37) 5. 7440-46-2 General Information Cesium is a silver-white metal that is found naturally in rock.42-7.9 (11.80 (4.60-12.73-5.80-10.7 (10.08-5.9) 11.96 (6.71 (4.4) 12.14 (4.13 (7.50) 9.63 (4.86-11.32) 4.26-11.34) 9.3) 10.1) 11.2-14.8 (11.6 (9.40) 5.8-13.60-6.60) 7.59-5.3-15.73-11.20-7.70 (6.00) 4.54-11.3) 9.7 (10.24) 4.99-11.61-6.36 (6.80) 7.Metals Cesium CAS No.70 (6.63-4.60-7.5-14.36) 3.3) 10. However.80 (8.61) 7.4) 10.6 (11.0) 11.7) 11.90-10. soil.40-5.30 (6.52) 7. cesium hydroxide is corrosive and irritating at high concentrations.22-4.84-9.17 (6.50 (4.17-6.50) 5.56 (4. 2004).20) 4.80-11. Whether cesium compounds are carcinogenic is unknown.26) 7.49) 75th 7.57-5.30) 7.00-4.80-13.97) 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 4.2-13.87 (4.46) 7.1 (11.33 (5.0-13.70 (4.20-8.6) 10.30) 5.0) 9.6) 11.0) 12.77-8.56) 5. and as polymerization catalysts.50 (4.

35-11.59-8.03) 5.S.3 (9.27) 4.17 (6.84-7.12) 3.26 (4.14-6.05-3.38) 10.64 (8.76-9.77) 4.3-15.35) 3.41-4.90-3.63-6.87 (5.61-3.20) 5.37) 4.85) 5.43) 8.2 (8.44 (8.74) 3.14-7.83-6.94 (5.27 (6. population results shown in this Report (Alimonti et al.78) 4.67 (6.77 (4.53 (4.22 (3.67) 5.04-11.91 (5.10) 7. Minoia et al.41-7.56) 4.87) Sample size 2464 2689 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 5.3 (8.74 (4.3) 1226 1334 1281 1238 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 3.57) 3.91) 5.90-8.98 (6.43 (8.33 (5.62-8.64) 9.75 (6. population from the National Health and Nutrition Examination Survey.29) 5.92 (5.78 (3.18 (7.91) 4.53) 6.89-4.2) 11.56) 3.95 (3.00-5.9 (9.59) 4.10 (3.7) 10.85) 4.95) 10.9 (10.07-4.5) 7.95-6.06 (3.65-4.56-10.34 (5.83-7.63 (7.00-5.20-8.12-6.35 (3.73 (3.11 (5.88-10.S.48) 7.55) 4.58 (6.82) 7.70) 7.75 (7.74) 75th 5.13) 7.0) Total 4.16-8.82-4.09) 8.50 (5.08) 3..00) 6.08) 4.46-4.22-11.38-7.84-9.31-6.43 (4.16) 5.6) 6.9) 10.14 (6.41) 9. Komaromy-Hiller et al.18) 8.58 (4.53) 3.30 (4.66-6.96-4.50) 8.91) 5. 2005.76-6.27 (6.26 (3.39) 5.08 (5.04-5.77-5.77 (7.80) 6.74-11.50) 4.44 (4.4) 10.60 (3.50 (7.28) 8.30) 10. 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.15 (7.98 (7.26-6.75-11.65-3.00-8.S.0 (7.22) 6.42 (5.37-3.95) 4.08) 4.21-3.42 (4.46) 6.96 (4.31-4.05) 3.65 (6.95-12.45 (4.79) 6.09 (4.61 (7.72-5.27-6.30 (3.2 (8.17-4.46-8.96-4.19-3.51 (7.0) 7.10 (5.13-9.98) 5.84-11.25) Selected percentiles ( 95% confidence interval) 50th 4.13-9.58) 3.47 (7.70) 6.96) 4.71 (7.99 (3.50 (6.47) 7.19-6.68) 3.43 (4.3) 11.1) 11.17) 4.44-5.5 (9.05-4.14) 4.45-6.94) 7.84-9.98) 5.3) 9. Urinary Cesium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.44-9.64-6.07) 8.38 (3.28 (5.31 (4.60-10.43-11.35 (4.24-10.88-4.39 (5.41) 4.58) 8..16-5.03-5.5) 9.56 (4.84-7.52-5.44) 3.97-4.93-7.27-4.40) 7.30 (7.02 (5.08 (3.54 (3.77 (6.47) 6.46 (8. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. interval) 4.02-4.63) 6.2) 340 368 290 718 762 725 1406 1559 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 3.09) 4.68-11.72 (4.7) 10.63 (6.36-10.60) 3.18-7.83) 8.62) 5.63-6.81 (4.73-4.33-8.90-8.40) 6.50-5.36-6.24 (3.20-4.54 (4.33-3.04) 5.8) 10.31 (4.07) 8.67 (5.30-4.56) 4.8) 5.47) 6.05) 6.71) 6.17) 9.5) 9.08-3.05 (4. (2000) found urinary cesium levels that were slightly lower than those reported for the U.72) 4.41 (5.90 (7.53 (6.91 (5.60-20.21-4.21 (2.42-4.33 (5.47) 4.60 (5.64) 4.48-6.03-6.39) 8.15-4.8 (9.78) 4.18-6. Using clinically submitted specimens..93-9.97) 8.55 (3. Two small studies of European populations reported urinary cesium levels similar to U.06) 5.58-5.99-9.16-8.05-3.29-3.28 (4.38 (3.15) 95th 8.41 (4.01-8.50) 4.43 (3.12 (3.91-7.11 (5.04) 6.55-5.08 (6.78 (3.95) 8.70 (7.92) 3.00-4.51 (4. Urinary cesium levels were similar in a group of forest fire fighters and residents living near the fire area (Wolfe et al.51 (4.46 (7.51 (3.87-4.99) 4.14-4.10 (3.20-4.20-4.85-4.06 (5.95 (5.00-9.54 (5.10-4.81 (4. population.42-6. 1990).13 (3.64) 5.35-7.96) 4.08-7.50) 4.6 (9.28) 7.51) 4.49) 3. Finding a measurable amount of cesium in the urine does not mean that the levels of cesium cause an adverse health effect.00 (8.7-12.23 (7.99-4.87) 5.25) 4.66 (6.06) 4.48) 90th 7.41 (8.3 (10. and were also roughly similar to those in this Report.47 (4.6 (9.91-9.29-3.63 (4. 2004).14) 4.36-3.24-4.79) 4.86 (4.29) 4.91-6.29) 4.00-10.74 (5.07 (5.30) 10. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.03) 6.8) 6.38-12.51 (3.54 (4.68) 6.42-4.43-6.68 (4.15-11.21-5.66 (5.97-5.79) 9.66 (5.79-5.Metals Biomonitoring Information Urinary cesium levels reflect recent exposure.79 (5.30-4.64 (4.27 (8.40-5.68) 4.99-9.0) 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 .

cdc. Apostoli P. Pozzoli L. Rapid Commun Mass Spectrom 2005. blood. Pietra R. Mott JA. Sewell CM. Spezia S.S. Toxicological profile for cesium. Forte G. Centers for Disease Control and Prevention (CDC). Uncertainty of inductively coupled plasma mass spectrometry based measurements: An application to the analysis of urinary barium. antimony and tungsten. and serum of Italian subjects. Sabbioni E. Voorhees RE. Sci Total Environ 1990. Howerton K. Comparison of representative ranges based on U. 4/8/09 Alimonti A.14:120-128. Ash KO. Fourth National Report on Human Exposure to Environmental Chemicals 207 . Third National Report on Human Exposure to Environmental Chemicals.2004 [online]. Gallorini M. Available at URL: http://www.gov/toxprofiles/tp157.95:89-105. Minoia C. cesium. patient population and literature reference intervals for urinary trace elements. Wolfe MI. Ronchi P. 2000. J Expo Anal Environ Epidemiol 2004. Trace element reference values in tissues from inhabitants of the European community I. et al. Wood CM. et al. Gatti A. Komaromy-Hiller G. Costa R. Clin Chim Acta 2000.296(1-2):71-90. New Mexico.19:3131-3138. Paschal D. Mincione G. Atlanta (GA) 2005.html.Metals References Agency for Toxic Substances and Disease Registry (ATSDR). Assessment of urinary metals following exposure to a large vegetative fire.atsdr. A study of 46 elements in urine. et al.

300-.930-1.800-.360-.570 (.20 (1. Cobalt compounds are used as catalysts in producing oil and gas.450) .67) 1.07.700) .520 (.499 (. It is also a component of porcelain enamel applied to steel bathroom fixtures.463-.430 (.750 (.330 (.850-1. and 03-04 are 0.50 (1.900) .434 (.340-.810) .340-. and soil.410 (.16 (.920-1.430 (.340) .81) 1.26-2.270-.285 (.570) .380 (.32-2.424) .410) .590) .490-.670-.890) .23) .450-.820 (.850) .530 (.394) . and magnetic recording media.520-.580 (.750 (.17-1.07.540-.379 (.550) 90th .480 (.47) 1. 0.259-.09) .430-.320 (.710) .75 (1.520-.870-1.377-. shiny.390) .590 (.410-.313) .01 (.17 (.630 (.740 (.620) .01-2. varnishes.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 .890) 95th 1.393-.670 (.359 (.560 (.750-.470) .480-.348-.830-1.710 (.398) .03) 1.290-.47 (1.316-.350 (.369 (.348-. steel-belted radial tires.00) .630 (.610-.370-.820 (.680) .820 (.13) 1.360-.454 (.900-1. and fertilizers.47) 1.900-1. blue-colored pigments.294 (.32) 1.12) 1.02-1.22-1.730) 1. and inks.310 (.610 (.334) .414) .65) 1.14) .350-.44) 1.32 (1.370-.05) 1.940-1.670-.03) .431) .380-.520) .860 (.06-1.581) .469-.390-.39) 1.420 (.05 (.620-.16) 1.270-.50) 1.850-1.583) .460 (.371 (.399) .07 (.370 (.410 (.520 (.14-1.500 (.372) .520 (.01 (.410 (.16-1.800-.291-.339 (. Cobalt occurs naturally in airborne dust.465) .373-.36) 1.03-1.386) .32 (1.29 (1.430) .92) 1.16) 1.930 (.630-.600) .460) .800) .950-1.810) .460-.570) .390 (. large appliances.81) 1.690 (.540-.543) .S.333-.01-1.400-.450) . Cobalt compounds are also used in manufacturing battery electrodes.08-1.416) .04 (.380 (.950 (.03) 1.940 (.37-1.480 (.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 .03 (.374 (.960-1.52 (1.520-.519 (.670 (.620-.490-.350-. see Data Analysis section) for Survey years 99-00.430 (.890-1.48) 1.280-. automobile airbags.420) .28 (1.390 (.930) .890-1.540-.640) . The cobalt used in U.53) 1.07-1.460) .Metals Cobalt CAS No.04-1.350-.435 (. population from the National Health and Nutrition Examination Survey.379 (.405-.373) .21) 1.487) .880-1.850) 1.600 (.980-1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.660) .25-1.640) . industry is imported or obtained by recycling scrap metal that contains cobalt.590-. 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.73) 1.740-. 208 Fourth National Report on Human Exposure to Environmental Chemicals .750 (.355-.310-.650-.06 (.610) .550-.07-1.12) 1.550 (.308-.26) 1.319) .47 (1.33 (1. and 0.15-1.470 (.515 (.06 (.900) .410-.270-.660) .530) .352 (.760) .04) 1.950 (.790 (. and kitchenware.790) .790-. seawater.428-.461 (.23-2.S.24 (1.650 (.375 (.410 (.331-.26-1.870 (.418 (.42) 1.380 (.16 (1.680 (.420) .580 (.16-1.523) .450-.580 (.680 (.417) .22 (1.60 (1.920) 1.03 (.540-.680) .24 (.46 (1.427-. Medical uses include joint and dental prostheses and radioactive cobalt in cancer chemotherapy.350) 75th .28-2.09 (. respectively.940-1.370) .15 (1.26) Total .710) 1.980) .564) .520-.338-.410 (.540) 1.343) Sample size 2465 2690 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .450) . 01-02.360-.810-.460 (. diamond-polishing wheels.870 (.500) .496) .740-.364-.570-.17 (1.380-.48) 1.510) 1.502) .28 (1.08) .68 (1. 7440-48-4 General Information Cobalt is a magnetic element that occurs in nature either as a steel-gray.404) .520 (.327-.32) 1.431) .99) 1.343 (.760 (.950) . Among its many uses are manufacturing superalloys used in gas turbines in aircraft engines. hard metal or in combination with other elements.59 (1.370-.330) .410) .398 (.640) .700) .17 (1.333-.900) .16 (1.570-.770) .316 (.08.19) .09 (. Cobalt is used as a drying agent in paints.910-1.430) .04-1.04-1.367 (.336-.419) Selected percentiles ( 95% confidence interval) 50th . It is emitted into the environment from burning coal and oil and car and truck exhaust.600-.450) .440-.690-. hard metal (alloys of cobalt and tungsten carbide).300 (.64) 1.410-.305-.670 (.520) .45 (1.460) .650 (.26) 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.301 (.890-1.530-.452 (.340 (.390 (.690-.22) 1.840) .950-1.330-.880 (.340) . Usual human exposure is from food sources.33-1. interval) .590-.660-.28 (1.388-. and in synthesizing polyester and other materials.610) .56) 1.05 (.620-.

529 (.644 (.898 (.598 (.361 (.433) .352) .425) .457) .830 (.562) .932-1.335 (.826-1.475 (..487-.905) .847) .365) .393-.574-.393 (.792 (.29 (1.917) .282-.293 (.333-.595) . A portion of cobalt retained for long periods is concentrated in the liver.352 (.963-1..850 (.429) 1.277-.872 (.10) Total .378-.348) .313-.419) .317 (. using hard metal cutting tools. interval) .257-.328 (.361 (.548 (.83) 1.728 (.428-.50 (1. an essential human nutrient.10 (.302-.479-.476-.740-1.259 (.500-.488) .388 (.275-.838 (.439) .409) . 1979).362 (.33) .469-.937 (.408 (. Exposure in the workplace may come from electroplating.435 (.30 (1.256-.523 (.04 (. 2003).542 (.02 (.387) .301-.753) 1.324) .343 (.554 (.16 (1.879-1.756 (.552 (.471 (.278 (.319-.421) .861-1.313-.57) 1.06 (. A nutritional requirement for cobalt other than that contained within dietary cobalamin has not been established.543) .760-1.513 (.560-. Lung retention of relatively insoluble cobalt compounds such as cobalt oxide may be prolonged.301) . but with a minor fraction (10-15 %) exhibiting a half-life of several years (Mosconi et al.388 (. 1994.33) 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 .291 (.271 (.36) 1.11-1.952 (.17) .753-.248-.384) .976 (.298 (.304-.29) .736-.391 (.00 (.703-.533 (.50) 1.457 (.561) .522) .297-.03-1.821-3.04-1.00) .467-.280-.689 (.337) .513) .842) .963) .534-.738 (.434-.462) .09) 1.582-.861 (.306) 75th .337 (.304) .983) .54) 1.694) .368) .15 (.955) .848 (.662) .. 1972). population from the National Health and Nutrition Examination Survey. Once absorbed and distributed in the body.378-.313-.324-.250) .331-.378 (. in the feces.313-.829-1.983-1.550-.707) . Workplace standards and guidelines for external air exposure to cobalt and several of its compounds have been established by OSHA and ACGIH.781-1.708) .333-.426 (.326-.28) 1.35) .362-.Metals fabricated from cobalt alloys (Lhotka et al.647) .290 (.50) 1.804) 1.554 (.471-.290 (.634-.455 (.609) .938) .757-1.444 (.342-.611) .289) .259-.900-1.785) .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 .353-.297) .296) ..333 (.329 (.372) . 1994).442-.438) .630-.833-1.16 (.382-.990-1.562) .635 (.392 (.547 (.237-.683-. and to a lesser extent.10) .632-.73) 1.990) .376 (.500 (.327 (.23 (1.257 (.468) .563-.00 (.272-.537 (.391) Selected percentiles ( 95% confidence interval) 50th .479) .55) .60) 1..435-.523 (.487-.821 (.585) .27) 1.344-.360) .463-.03 (.781) 95th 1.500-. Smith et al.362) .12 (.268 (.616-.728) .314 (.25 (.774 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. Urinary Cobalt (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.35) 1. cobalt is excreted predominantly in the urine.975 (.938-1. with pulmonary clearance half-lives of from one to two years (Hedge et al.599) .505) .400 (.323) .673-.608 (.750-.316 (.591 (.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 .895-1.378-. refining or processing alloys.704-.310) .630-.667-1.243-.667-1.16 (.407) .279) .691 (.481) 90th .669) .33) 1.11-1.361-.960 (.638-1.S. or using diamond-polishing wheels that contain cobalt metal.963) .36) 1.829) .290 (.407 (.278-.234 (.929) .850-1.417 (.352 (.327-.895-1. Recent inhalation exposure to soluble cobalt compounds can be monitored by measuring cobalt in urine or blood (Lison et al.508-.10-1.282 (.247 (.449) .00 (.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 .273 (.949) .600-.611) .353 (.29 (1.471-.365-.334) .792-1.404-.. 1972).355) .396) .457-.723 (.963-1.248-.425-.381) .857-1.733-1.313 (.452-.700 (.275-.27) 1.49) 1.14 (.19) .251-.00) .513-.300) .534 (.12-1.25 (.402 (.503-.515 (.844 (.368 (.593) . respectively.449-.744) 1.417) .328) .15) 1.911-1.296-.281) .313-. Elimination reflects a multi-compartmental model dominated by compartments with half-lives on the order of several hours to a week. Human studies with 60Co administered as soluble cobalt chloride have reported oral absorption ranging from approximately 1 to 25 % (Smith et al.594) .396) . Cobalt is absorbed by oral and pulmonary routes.328 (.851 (.346 (.615) .29) 1.00 (.349) .581) .309) .495 (.333-.964 (.380-.343-.679-.786-.824 (. Cobalt constitutes 4% by weight of vitamin B-12 (cobalamin).279 (.303-.215-.737 (.358 (.640) .239-.738 (.329-.29 (1.294-.955) .286) .274-.16) .363) .394) .700 (.00-1.727 (.461) .606 (.361-.339-.386 (.750) .626-.777-.306 (.660-.369 (.24) .60) 1.368) .259) .44 (.

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

Edmonds CJ.51(7):447450. Hoet P. Industrial Chemical Exposure: Guidelines for Biological Monitoring.34:620-626. Linna A. oxides. Absorption and retention of cobalt in man by whole-body counting. Fujimura N. De Boeck M. Weyher I. Steffan I. Health Phys 1979. Co-sensitivity between cobalt and other transition metals. Am J Epidemiol 1998. Kato M.58(10):631-634. DeSantis V. Metal-on-metal versus polyethylene in hip arthroplasty: a randomized clinical trial. Sci Total Environ 1997. Goto S.45:246-247. et al.150(1-3):167-171. Occup Environ Med 2001. Unwin P. Sci Total Environ 1994. Robinson C. Four-year study of cobalt and chromium blood levels in patients managed with two different metal-on-metal total hip replacements.48:172-173.150:177-183. Hammon E.88(4):443448. Cobalt-specific T lymphocytes in synovial tissue after an allergic reaction to cobalt alloy joint prosthesis. McMinn DJ. Br J Ind Med 1993. Lisi P. Lison D. The release of metals from metal-onmetal surface arthroplasty of the hip. Am J Ind Med 2003. et al. Swennen B.150. salt. Cannon SR. Ziaee H. Goto S. McCalden RW. 3rd ed.148:241-248. Int Arch Occup Environ Health 1997. Zhuber K. Pradhan C. Barnaby CF. Cobalt and antimony: genotoxicity and carcinogenicity. Gross RT. and hard metal dust. Ghat IS. J Bone Joint Surg Br 2005. Molders J. Outcome of occupational asthma due to cobalt hypersensitivity. Buchet JP. Oksa P. Schaller KH. Angerer J.533:135-152.50(9):835-842. Fourth National Report on Human Exposure to Environmental Chemicals 211 . Biological monitoring of cobalt exposure based on cobalt concentrations in blood and urine.44:124-132. et al. Vitali MT. Daniel J. Diepgen TL. Radulescu M.28(5):1121-1128. Chess DG. Boca Raton (FL): Lewis Publishers. Sabbioni E. Lauwerys R. Falcone G. Uitti J. Leghissa P. Meier R. 2001. Swennen B. Occupationallyinduced “isolated cobalt sensitization. Bunn HF.” Contact Dermatitis 2001. Kirsch-Volders M. Lung cancer risk in hard-metal workers. Lasfargues G. Iavicoli I.Metals effects of cobalt. Stanescu D. The effect of the diameter of metal-on-metal bearings on systemic exposure to cobalt and chromium. Sabbioni E. Szekeres T. Dunstan E.20(1):25-31. J Bone Joint Surg Br 2006. Palmroos P. Meyer zum Buschenfelde K-H. A report of two cases from mineral assay laboratories and a review of the literature. Dickel H. J Rheumatol 2001. Kusaka Y. Bacis M. Kuska Y. Lison D. Hypothyroidism and thyroid hyperplasia in patients treated with cobalt JAMA 1955. Kriss JP. Respiratory health of cobalt production workers. White MA.21(2):189-195. Lhotka C. Iversen BS. Wild P. Ichikawa Y.242:1412-1415. Contact Dermatitis 2003. Schank M. Rorabeck CH. Occupational asthma from cobalt sensitivity in workers exposed to hard metal dust. Trace element reference values in tissues from inhabitants of the European Union. Cresti R. J Orthop Res 2003. Clin Orthop Relat Res 2003.69(3):193-200. J Trace Elem Med Biol 2006.95:29-37. Christensen JM. Linnainmaa M. Chest 1989. Peltier A. Regulation of the erythropoietin gene: evidence that the oxygen sensor is a heme protein. Urinary cobalt as a measure of exposure in the wet sharpening of hard metal and satellite blades.36:732-734. et al. Salvatori S. Moulin JJ. Roto P.157:117121.406:282-296. Carnes WH. Thomassen H. Mutat Res 2003. Zobelein P. Romazini S. Metal ion levels after metal-on-metal proximal femoral replacements: a 30-year follow-up. Mosconi G. Thakker DM. Goldberg MA. Sabbioni E. Tilley S. 1985. Lauwerys RB. Zweymuller K. Zedda S. Hedge AG. Blunn G.(1-3):133-139. Smith T. Buchet JP. Science 1988. Epidemiological survey of workers exposed to cobalt oxides. Kiilunen M. and cobalt metals. cobalt salts. et al. Kristiansen J. Jarvis JQ. Bozec C. Int Arch Occup Environ Health. Health Phys 1972. Pisati G. Shirakawa T. J Occup Med 1992. Hoher T. Cobalt excretion in urine: results of a study on workers producing diamond grinding tools and on a control group. Bourne RB. Salama A. Sci Total Environ 1994. Exposure assessment in the hard metal manufacturing industry with special regard to tungsten and its compounds. Cobalt cardiomyopathy. MacDonald SJ. Thabe H.216:253-270. HoffmannB.87(5):628-631.204:147-160. Laippala P.55(4):269-276. Sanghrajka AP. Sci Total Environ 1998. a study of 13 elements in blood and urine of a United Kingdom population. Arch Intern Med 1990. Toxic trace element reference levels in blood and urine: influence of gender and lifestyle factors. Kraus T. Dunning SP. X. Biological monitoring of workers exposed to cobalt metal. Occup Environ Med 1994. et al. Lison D. Weber A. Lauwerys R.22:359367. Alessandrelli M. Schramel P. Cleland D. Heki S. Long-term clearance of inhaled 60Co.

lead was added to gasoline and residential paints and used in soldering the seams of food cans.40-2.20-3. 7439-92-1 General Information Elemental lead is a soft.00 (3.80 (1.30-1.60-1.04-1.10-3.30 (1.90-6.40 (5.10-3.80 (2.50-5.70 (1.30-1.70) 3.20 (3.00 (1.40-3.70-3. adult lead exposures tend to be limited to Blood Lead Geometric mean and selected percentiles of blood concentrations (in µg/dL) for the U.19 (1.10 (4.40) 2.899-.80-2.37 (1.83 (1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.70 (2.60 (3.60 (1.50 (2.70) 4.90) 1.25 (1.20) 3.40 (1.52-1.40-3.43) 1.20-1.10-4. and 0.20 (1.80-3.70-5.20-3.20-4.00 (2. the main source of lead exposure for the general U. interval) 1.60) 2.20) 5.70 (2.70-6.14-1.50-3.900-1.40-1.60) 1.36) 1.60-2.48) 1.90 (3.50 (1. Lead has a variety of uses in manufacturing: storage batteries.30) 1.30) 2.60 (2.50-4.50 (3.40-5.40) 2.70-1.40) 3.69) 1.51) 1.30 (1.50 (2.02) 1.60) 3.90-2.80) 1.70) 1.90 (3.40) Total 1.50) 1.66) 1.90) 2.32-1.30 (1.70) 4.80 (1. see Data Analysis section) for Survey years 99-00.60 (1.00) 2.40-6.90 (2.50-2.00 (5.20) 2.90) 3.87) 1. Elemental lead can be combined with other elements to form inorganic and organic compounds.10-2.80) 2.90-4.986) .50-2.10 (3.00) 2.10-2.30 (2. and for radiation shielding.10) 4.90) 2.43-1.40-1.90 (1.40-1.70) 4.00-1.31) 1.60) 5.72) Selected percentiles ( 95% confidence interval) 50th 1. In the past.90) 1.60 (3.70) 3.60) 3.62 (1.37-1.00) 5.80 (1.90) 3.10) 2.40) 5.80 (3.00-6.30) 5. leaded glass.80 (5.10) 1.23 (1.10) 1.40) 2. Lead was used in plumbing for centuries and may still be present. antique-molded or cast ornaments.00) .30 (4.00) 1.62-1.80 (5.10 (1.20) 4.60 (2.60-4.60 (1.96-2.75 (1.3.45-1. solders.40) 4.80-3.50 (1.30 (2.20 (3.00) 1.50 (4. bronze).90 (2. malleable. metal alloys (e.20) .878-1.00) 3. population was aerosolized lead emitted from combustion engines that used leaded gasoline.20) 3.40-6.50 (1.50 (1.10 (2.20 (2.10-4.30) 2.90-4.80) 1.90) 2.60) 5.90) 2.25 (1.00) 1.00-5.30 (1.00) 6.10) 1.10-2.80 (2. Lead is most often mined from ores or recycled from scrap metal or batteries.14-1.69 (1.946 (.43 (1.70 (3.00) 2.90-4. 0.62) 1.25) 1.70 (3.50-6.30-4.30 (4.50) 1.30 (2.70) 1.91) 1.50) 3.30 (2.52 (1.39) 1.20-6.32-1.10-3.43 (1.75) 1.50) 5.90-4.45 (1.90) 1. 212 Fourth National Report on Human Exposure to Environmental Chemicals .70-2.80) 1.40-3.60) 4.80-3.60-1. Aerosolized lead is either inhaled or ingested after it is deposited on surfaces and food crops.50-1.80-4.55-1.70 (2.36-1.50) 4. Before the 1980’s. Since lead has been eliminated from gasoline.50-3.60) 1.40-2.10) 3.00) 1.20-1.60 (2.40-1.50 (4.20) 3.10-6.37 (1.50 (3.00 (4.80) 1.80-5.10 (1.50-1.40-1.30-2.50 (2.80 (1.40) 1.70) 1.30 (2.40 (2.50-5. 01-02.00) 1.3.00) 4.g.70-4.00-4.20-3.50 (2.60) 2.10-2.00) 4.70) 1.60 (4.81) 1.40) 2.30-5.20 (3.01 (1.40 (3.70-2.43) 1.52-1.70 (1.20) 3.20 (1.90-2.60 (1.80) 2.70 (1.60) 1.00-1.10 (1. brass.86) 1.50-1.80) 2.78 (1.40 (2.10-3.75-2.34-1.51 (1.90 (3.80 (1.60-3.70-1.89) 1.00-2.12-1.80) 3.50) 7.10-1.75-1.30-1.55 (1.60) 3.90 (4.20 (3.80 (2.50) 75th 2.30) 2742 2268 2085 1842 2219 2293 2716 3806 3478 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.30-2.60) 2.60) 2.60 (1.50) 1.50) 4.00) 3.77 (1.60 (2.60) 2.87 (1.60) 4.53) 1. respectively.50) 2.93-2.80 (1.90-2.30-2.00 (4. ammunition.66 (1.40) 1.10) 2.56 (1.17) .30) 2.20 (3.60) 3.800-1.50-1.60-2. dense.60) 4.20) 4.20-2.60) 4.50) 1.20-2.00 (6.60) 1.69 (1.20-3.80 (4.69) 1.30 (3. ceramic glazes.60 (1.60-1.00 (1.70) 2.S.70-1.60 (3.90) 2.20 (1.10) 3.22 (1.10-2.60) 1.S.50-1.40) 1.10-1.09) 1.70 (5.40-2.Metals Lead CAS No.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 1.70) 4.40 (4.00-4.90) 5.30-1.39-1.90 (3.70 (1.30 (2.90-2.40 (1.50) 2.80-3.40 (1.20 (3.80-4.10) 3.10 (2.90 (1.50-2.55-1.60 (3.20 (3.90 (3.50-4.71-1.40 (1.80 (4.10 (2.942 (.14-1.80) 2.00) 2.20 (2.68-1.30 (2.80-4. plastics.70-2.65 (1.60) 723 898 911 905 1044 856 2135 2231 2081 4207 4772 4525 6-11 years 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 2.46 (1.30) 95th 5.20) 1.60 (1.70) 3.30 (4.60-1.36-1.50 (2.900 (.70) 1.28.900 (.30-2.50-2.95) 1.30-6.20) 90th 3.80) 1.10-8.20 (4. and 03-04 are 0.10) 5.90-3. blue-gray metal that occurs naturally in soils and rocks.30-1.50) 5.50) Sample size 7970 8945 8373 Age group 1-5 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 2.60-6.40-1.60 (2.30-1.60 (2.60-4.10-1.40-4.10-2.20 (1.00-4.20 (1.10-6. such as lead phosphate and tetraethyl lead. population from the National Health and Nutrition Examination Survey.49-1.

20 (1.10 (.18-1.688 (.60-1.60 (1.70) 1.480-.700 (.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 .30-5.766 (.90-2.820-1.730 (.30 (3.40) 1.10-3.671-.960-1.729-.600) . Fourth National Report on Human Exposure to Environmental Chemicals 213 .40 (2.66 (2.595-.41) 2.90-3.745-. 0.833 (.32 (1.900) .570-.600 (.785) .955-1.642 (.70 (1.30) 1.636 (.560-..33.573 (.80) 2.940 (.1.60-2.40) 2.33-2.700-.753 (.70 (2.00-2.90 (2.00 (2.90) 2.915-1.700-.625-.86 (1.30 (1.718) . bullet fragments retained in human tissue.641-.30) 2.708-.30-1.900 (.30 (2. pewter utensils and drinking vessels.30) 2.30-1.20) .800) .20) .50 (1.80-2. respectively.S.86-2.30-3.822-1.10 (. interval) .680) .661-.960 (.23) .589-.700) 1.10 (.40 (1.20) .700-.700 (.600-.700-1.50) 2.920 (.31 (1. stained glass framing.800 (.11) 2.10 (1.650) 1.628) 1.40) 2.52-1.29) 2.506-.923 (.06) .80 (2. lead-containing folk remedies and cosmetics.60) 2.23-4.40 (1.70-2.59) 1.701) .935) 1.12) 90th 2.637-. absorbed lead is bound to erythrocytes and then is distributed initially to multiple soft tissues and eventually into bone.773) .50 (2.00 (1.00) 2.31-3.990) 1.700) .80) 1.20) .70) 3.00-1.640-.800 (.540 (.70-3. However.700-.00 (1.625 (.10-5.03-2.20-1.10-1. and 0.535-. lead-contaminated dust in indoor firing ranges.660) .91) 2.90) 1.10) .800 (.900) .931) .40 (1.80) 2.78-2.62-4.580-.73 (1.40) 2.900) .40) 2.10-1.40) 1.591 (.90 (2.800-1.620) 1. battery and radiator manufacturing) and recreational sources.564 (.78-2.40) 1.21 (2.833-1.40 (1.600-.90-2.556-.800-1.00) 2.04) 2.90-2.04 (.49 (1.50) 1.00) 1.579-.40-3.800-.00 (1. 2007.30) 1. lead-based painted surfaces undergoing renovation or demolition.70) 1.10-1.70) 3.30) 1.82 (2.960-1. 01-02.40 (1.690) 75th 1.80) 3.572-.840 (.80-2.27) 1.900-1.89) 2.800) .579-.600) .04) .590 (. 1991).20) 1.710-1.900) .80 (1.50-2.00) .10) 2. and contact with soil.90-3.674) 1. Absorption of ingested lead can be as much as five times greater in children than adults and even greater when intakes of dietary minerals are deficient.19 (1.20 (1.620 (.70 (2. Less common sources of incidental or unique lead exposure are numerous: lead-glazed ceramic pottery.40-5.900-1. CDC.60-3.749) .700 (.13) .09) 1.86) 1.02) 1.90 (1. and 03-04 are 0.50 (1.970-1.862) .70 (2.677 (.900 (. dust. or water contaminated by mining or smelting operations.800) .40) 3.07 (.00-1.00-2.50) 1.731 (.14-1.51) 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.80 (1.80) 2. or after soluble lead compounds are ingested.60 (1.20-2.20) 1.800) .03 (1.630 (.86) 95th 2.00-1.35 (.00 (.700-.850 (.857) .60 (1.80) 1.600 (.10) .910-.80-3.10-3.97) 4.20 (1.757-.60-2.900-1.605) .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 1.50) 1.59-2.604 (.90-2.78-2.70) 1. Lead is absorbed into the body after fine lead particulates or fumes are inhaled. Approximately half of the absorbed lead may be incorporated into bone.20 (1.04-2.695 (.80) 1.50 (2.20) 1.62) Total .848 (.700 (.986) .40-1.90-4. population from the National Health and Nutrition Examination Survey.540-.00 (1.553-.900) .90 (1.30) 1.610 (.44-2.90 (2. imported children’s trinkets and toys.680-.64) 2.800) .60-3.558 (.66 (2.659 (.680-.50 (2.613) ..02 (.795 (.90 (1.50) 2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. the primary source of exposure in children is from deteriorated lead-based paint and the resulting dust and soil contamination (Manton et al.10-1.900 (.10-3.20 (2.810-1.07-1.941) .g.616) .60 (1.40) 1.40-1.30) 2.30-2. Children may also be exposed to lead brought into the home on the work clothes of adults whose work involves lead.10 (1.10-1.70 (2.33 (2.52 (1.828) Selected percentiles ( 95% confidence interval) 50th .00-2.80) 2.14 (1.20-2.Metals occupational (e. Small amounts of environmental lead also may result from burning fossil fuels (ATSDR.790 (.808 (.691-.40 (2.14 (1.29 (2.700 (.10 (1.11 (1.752 (.17 (1.82 (1.04 (.00) .20 (1.700 (.13-3.815 (.20-1.72) 1.60 (2.10 (1.10) 2.990) 2.818) .40 (2.900) .600-.40-1.20 (2.80) 2.50-3.10) 1.600-. older plumbing systems with leaded pipes or lead soldered connections.40-2.651) .24-1. 2000).738) .75) 4.40) 1.30) 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 1.50-1.600-.20 (2.526-.20 (3.52-1.80) 3. which is the site of approximately Urinary Lead Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.00) .50-2.40 (2.70) 2.27 (1.75) 3.90) 2.500-.710-.800 (.1.30-1.920 (.800-.640 (.20 (1. In the blood. see Data Analysis section) for Survey years 99-00.40-1.30) .30) 1.30-1.900-1.50-2.90) 2.50) 3.20-1.22) 1.00) .

The skeleton acts as a storage depot.64 (1.603-. Staessen et al.667) .404 (. CDC.33) 2.702) .11-1. seizures.592-.765) .31) 1.962 (.22-2.383-.718) .97-18.06 (1.43-1.82) 1.66) 2.708 (.940 (.659-.731-.33-1.668-.18 (1.15-2. For instance.594-.677) .73) 2. 1995).09) 1. 1993).00 (1.68 (1.02-1.11 (.461) .404-.914-1.31 (1.800-.03) 1.18) .588-.61) 1.655) .375 (.97 (1.20) .975-1.03) 2.64) 2.612-. Approximately 70% of lead excretion occurs via the urine. interval) .11 (1.79 (1.71 (1. Lead can cross the placenta and enter the developing fetal brain.89-2.742) Selected percentiles ( 95% confidence interval) 50th .94-2.14 (1.977) 1.15) 1.71-2.63) 1.17-1.508) .990 (.75 (2.10) 884 682 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites 214 Fourth National Report on Human Exposure to Environmental Chemicals .77) 2.696 (.03-2.S.25-1.11) 1.380-.03 (.342-.648 (.08) .36-2.644 (.701 (. and iron.641 (.0) 3.753) .66 (1.61) 3.46 (1.15-2.997-1.436) .469 (.07) .12-1.702-.933) .97) 1.85 (1.19-5.09-1.09-1.37-1.18) 2.900 (.55 (1.938-1.638 (. scant amounts are lost through sweat.707 (.882-1.571-.623 (.01 (.645-. BLLs and associated toxic effects differ in children and adults. BLLs near 10 µg/dL can affect blood pressure in adults and neurodevelopment in children (Bellinger.559-.15) 1.933-1.47 (2.510-.00 (1..662) Sample size 2465 2689 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.00) .763) .89-5.667-.38 (2. and through binding to ion channels and regulatory proteins.561-.44) 1. Additional mechanisms include generating reactive oxygen species and altering gene expression (ATSDR.53) 1.682) .828) .914 (.62-3. abdominal pain.98) 2.88) 2.43 (2.698) .988 (.98-2.742) .50-2.31 (1.88-2.83) 1.03) . population from the National Health and Nutrition Examination Survey.50-1.06) 1.08-2.601-.18) 1.535) .722 (.721 (.657) 1.22-1.34-1.65-2.914 (.06 (.66 (1.14) 1.03 (.56-2.718) 1.988-1. 2003.04) 2.862-.681-.43) 1.63) 4.11 (.72) .51) 1.693 (.79) 1.31 (2.635 (.86 (1.51 (1.652 (.70 (1.734) .61) 1.29 (1.618 (.677-.710) .569 (.920-1.92) 2.50) 1.41 (1. The toxic effects of lead result from its interference with the physiologic actions of calcium. 1995.52 (1.571-.712 (.85-2.781-1. based on prospective population studies.851) .43) 2.608-.78 (2.686) .26) 2.50-2.810 (.85) 1.676) .33) 1.10 (.681-.56 (1.56-3.08) .979 (.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 .47) 1.551-.639 (.79) 2.43 (1.07-1.607-.69 (1.41) . through the inhibition of certain enzymes.62-2.492-.853-1. Lead is cleared from the blood and soft tissues with a half-life of 1 to 2 months and more slowly from the skeleton.677 (.40-1.639) .10) 1.22) .946-1.606-.37-1.05 (1.670) 1.46 (2.917-1. Schwartz.579-.587-.720 (. with a half-life of years to decades.26) Total .709 (.655) 75th 1.703) .41-1. and nails (Leggett.622 (. with lesser amounts eliminated via the feces.88 (1.981-1.739) .701) .88) 1.75-2.529-. 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.898) .47 (1.645-.23 (1.404 (.603-.828-1.615 (.62) 2.838) .790) .11) .97) 1.774 (.746) .00 (.400) .639 (.593 (.64) 95th 2.621 (. In 1991.683-.33 (1.19) 1.938 (.992-1.28-1.35) 2. Large amounts of lead in the body can cause anemia.25-1. 1991.17 (.957-1.605-.72-2. zinc.98 (1.625 (.496 (.. and paralysis.18) 1. 1996).03 (1.992-1.85-2.758) .03 (.963-1.39-1.870 (.05-1.05-1.679) 1.03) 1.44 (1.655-.20) .22) 1.588-.52) 1.649 (.603 (. encephalopathy.00 (1.796-1.926 (.639 (.594-.658 (.56) 3.671 (.45 (1.88) 2.654) .06) .55 (1.876-1.667-.841-1.31) 1.02) 1.688) .608 (.755 (.679-.720 (.05 (.22) 1.73-2. hair.28) 2.633 (.01) .53-1.74 (1.59-3.44 (1.617-.49 (1.03) 2.700-.38 (2.38 (2.62-1.632 (.48 (1.61) 1.918 (.87) 1.61) 1.50 (1.28) .03) .725) .604-.64-2.04-3. 2004.. Equilibrated blood lead levels (BLLs) after chronic intake are associated with certain toxic effects. O’Flaherty.94 (1.460-.50-2.673) .10 (1.78-4.09-1.20-3.730) 1. kidney injury.725) .586-.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 .812-1.893) .644) .971 (.67-4.432 (.793-1.615 (.65 (1.541-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.702) .609 (.72-2.07 (.887 (.24 (1.58) 1.11 (1. and approximately 40 to 70% of lead in blood comes from the skeleton in environmentally exposed adults (Smith et al.15-3.428) . 1993. Nash et al.722 (.623 (.83 (2.698) . 2007).27 (1.96 (1.408-.03) 90th 1.Metals 90% of the body lead burden in most adults.583-.918-1.

environmental levels) and health effects is available from ATSDR at: http://www. Many animal studies have established the multiple neurotoxic effects of lead (ATSDR. Data submitted through state public health programs from 2006 showed that 1. Overall. Surveillance data reported by U. 1995) and associations between increased bone lead concentrations and blood pressure (Hu et al. 2002a). Schwartz et al. 1995. A general population survey of adults Germany in 1998 reported a geometric mean blood lead concentration of 3. Borja-Aburto et al. approximately 11. and low family income (CDC. 1996.. 2005b). respectively. 1987. 2005b. when the geometric mean BLL was 2.Metals µg/dL or higher as the level of concern in children. lead in women may be associated with hypertension during pregnancy.S... reduce sperm count. though there is greater individual variation in urine lead than in blood and greater potential for contamination. with overt encephalopathy. including minority race or ethnicity. Jones et al (2009) showed that the prevalence of BLLs of 10 µg/dL or greater decreased from 8. However.4% in NHANES 1999-2004. 2003). higher than 100-200 µg/dL)..... 2000). Lanphear et al. 2006).. Bellinger 2005. 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. the national prevalence rate for adults with BLLs 25 mg/dL or higher was 7.6% in NHANES 1988-1991 to 1.. Telisman et al. particularly in the skeleton.6%) were lower than those from NHANES 1991-1994.g. Pirkle et al. Recent studies have suggested that neurodevelopmental effects may occur at BLLs lower than 10 µg/dL (Canfield et al. 1996. Information about external exposure (i. IARC considers inorganic lead compounds probable human carcinogens. seizures. 1991. residing in housing built before the 1950’s..atsdr. Muntner et al.4% of children had BLLs of 10µg/dL or higher (CDC. For example. Staessen et al.0 µg/dL in females (Soldin et al.000 adults. High dose occupational lead exposure. and peripheral neuropathy generally occurring at much higher levels (e. subtle or nonspecific neurocognitive effects have been reported at BLLs as low as 20-30 µg/dL (Mantere et al. CDC. which is an 84% decline. 1984. 2000)..9 µg/dL) and percentage of children with BLLs greater than 10 µg/dL (1. 2002. 2007). Schwartz. 2001). 2002). Jones et al.. Workplace standards and guidelines for lead exposure and monitoring have been established by OSHA and ACGIH. A general population survey of adults in Italy tested in 2000 found BLLs slightly more than double those reported for U.21% of approximately 3.. adults in the 1999-2000 NHANES sample.gov/toxpro2.gov/nceh/lead/surv/database/State_ Confirmed_byYear_1997_to_2006. usually with BLLs greater than 40 mg/dL.. 1999). Korrick et al. premature delivery. At low environmental exposures..07 µg/dL (Becker et al. 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. 2003.75 µg/dL in U. NTP considers lead and its compounds reasonably anticipated to be human carcinogens.3 million children tested had BLLs of 10 mg/dL or higher (http://www. 2006). both the geometric mean (1. Payton et al.S.cdc. 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. Biomonitoring Information Blood lead measurement is the preferred method of evaluating lead exposure and its human health effects.. BLLs greater than 10 µg/dL continue to be more prevalent among children with known risk factors.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. the prevalence rate has declined annually since 1994 (CDC. 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. urban residence. may alter sperm morphology.5 per 100.S. The U. 2003. Urine levels may reflect recently absorbed lead. 1999). adult residents.. and spontaneous abortion (Baghurst et al.S. adults in the 19992000 NHANES sample (Apostoli et al. 2005a).7 µg/dL and 4..S. More recently.S.cdc. 1998). In NHANES 1999-2002 in children 1-5 years old. 2009).. adult population has similar or slightly lower BLLs than adults in other developed nations (CDC. and decrease fertility (Alexander et al. 2003. almost double the geometric mean of 1. 1994). Temporal declines in children’s BLLs have been found in other developed countries (Wilhelm et al. Fourth National Report on Human Exposure to Environmental Chemicals 215 . A decrease in BLLs is evident also in adult NHANES results reported over past decades (CDC.. 1996. In occupationally exposed adults.xls).e.html..2 µg/dL in males and 3. the geometric mean BLL was 3.. and organic lead compounds not classifiable with respect to human carcinogenicity. Both drinking water and ambient air standards for lead have been established by the U. Low level environmental lead exposure may be associated with small decrements in renal function (Kim et al. BLLs reflect both recent intake and equilibration with stored lead in other tissues. EPA..

Lanphear BP.54(20):513-516. 2005b. Robertson EF. Bellinger D.123:e376-e385.287:1-11. MMWR Morb Mortal Wkly Rep 2005a. The relationship of bone and blood lead to hypertension.cdc. Hänninen H. Neurotoxicol 1987. Cognitive deficits with blood lead concentrations < 10 µg/dL in US children and adolescents. Borja-Aburto VH. Vimpani FB. Weiss ST. Atlanta (GA). Hu H. Lead. Neurodevelopmental effects of postnatal lead exposure at very low levels.348:15171526. IARC Monogr Eval Carcinog Risks Hum 2006. MMWR Morb Mortal Wkly Rep 2006. 1999-2002. Jones RL.gov/toxprofiles/tp13. Semen quality of men employed at a lead smelter.150(6):590-597. Blood lead levels—United States. Inorganic and Organic Lead Compounds. Pirkle JL. Available from URL: http://www.275(15):1171-1176. Public Health Rep 2000.89:330-335. et al. Hu H. Roberts RR.87:1-471.cdc. Managing Elevated Blood Lead Levels Among Young Children. Cory-Slechta DA. gov/mmwr/preview/mmwrhtml/mm5420a5. Luukkonen R.101(7):598-616. Birth Defects Research (Part A). Jusko TA. Trends in blood lead levels and blood lead testing among US children aged 1 to 5 yeas. Krause C. Cox C. Auinger P. Jacobson JL. References Agency for Toxic Substances and Disease Registry (ATSDR). et al. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Rotnitzky A. Aro A. Available at URL: http://www.55(32):876-879. Hunter DJ. Preventing Lead Poisoning in Young Children. Vupputyuri S.10:43-50. Kuehnemann TJ. Kim R. Lead and hypertension in a sample of middle-aged women. Hernberg S. doi:10. Hu H. Adult blood lead epidemiology and surveillance—United States. Farias P. Environ Health Perspect 1993. Ronchi L. Apostoli P. CDC. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population.82:60-80. Canfield RL. Kaufman JD. N Engl J Med 2003. Meyer PA. Atlanta (GA). Intellectual impairment in children with blood lead concentrations below 10 µg/dL. Korrick S. 4/14/09 Centers for Disease Control and Prevention (CDC).8(3):395-401. Teratogen update: lead and pregnancy. Homa DM. Blood lead reference values: the results of an Italian polycentric study. 4/14/09 Alexander BH. Pediatrics 2009. 2003-2004.cdc. Third National Report on Human Exposure to Environmental Chemicals. Bellinger D. Speizer FE. Bavazzano P. Pediatrics 2004. Sparrow D. Available at URL: http://www.53:411-416.275:1177-1181.cdc.cdc.htm.205:297-308. JAMA 1996.htm. Environ Res 2000. Atlanta. 4/14/09 Centers for Disease Control and Prevention (CDC).1542/peds:2007-3608. Blood lead and chronic kidney disease in the general United States population: 216 Fourth National Report on Human Exposure to Environmental Chemicals . 2005. Henderson CR. Ganzi A. Rios C. Batuman V. Hertz-Picciotto I. et al. van Netten C. Reese YR. Lanphear BP. Dietrich K. Muntner P. 1991 [online]. 2002 [online].atsdr. 4/14/09 Centers for Disease Control and Prevention (CDC). Brody DJ. Recommendations from the Advisory Committee on Childhood Lead Poisoning Prevention.gov/mmwr/preview/mmwrhtml/ mm5532a2.26:359-371. Acquisition and retention of lead by young children. A longitudinal study of low-level lead exposure and impairment of renal function: the Normative Aging Study. Ewers TG. McMichael AJ. Am J Public Health 1999. 4/14/09 Centers for Disease Control and Prevention (CDC). Sci Total Environ 2002. et al.gov/nceh/lead/ CaseManagement/caseManage_main.gov/nceh/lead/publications/ books/plpyc/contents. Centers for Disease Control and Prevention (CDC). Ga. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Wager C.html.113(4):1016-1022.115:521-529. Korrick SA. Coresh J. Stanek KL. Toxicological profile for lead. Chiodo LM. Cox C. Occup Environ Med 1996.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. Seiwert M. Checkoway H.htm. Neurotoxicol Teratol 2004. Lepom P. Neri A.htm. A prospective follow-up study on psychological effects in workers exposed to low levels of lead. Payton M. Leggett RW. Jacobson SW. The Port Pirie cohort study: lead effects on pregnancy outcome and early childhood development. Caldwell KL. Rojas LM. Muller CH. et al. JAMA 1996. Mantere P. Available at URL: http://www. 1988-2004. Kaus S. Manton WI. Aug 2007 [online]. Schulz C. Wigg NR. Angle CR. Am J Epidemiol 1999. Blood lead levels measured prospectively and risk of spontaneous abortion. Becker K. Age-specific kinetic model of lead metal in humans.73:409-420. Scand J Work Environ Health 1984. Int J Hyg Environ Health 2002. Baj A. Weiss ST. Blanco J. Sparrow D. Rotnitzky A. Available at URL: http://www. Baghurst PA.

and mercury in blood or urine of children: basis for validation of human biomonitoring data in environmental medicine. Kinetics of lead disposition in humans. Association of blood lead.104(1):60-66. 50:31-37. Schulz D. population to lead: 1991-1994. Int J Hyg Environ Health 2006. Lee BK.S. Flegal AR. Staessen JA. Hwang KY. O’Flaherty EJ. and copper in men. lead. et al. Lauwerys RR. and hypertension in perimenopausal and postmenopausal women. Lustberg M. Gunter EW. Cvitkovic P. Gavella M. Kaufmann RB. Smith DR. Osterloh JD.140:821-829. Soldin OP. Nash D. Toxicol Appl Pharmacol 1993.327:109-113. Environ Health Perspect 1998. Lee SS. dimercaptosuccinic acidchelatable lead. Use of endogenous.289(12):1523-1531. Environ Health Perspect 1996. Low-level lead exposure and renal function in the Normative Aging Study. Brody DJ. Schwenk M. Stewar WF. Sherwin R. Pizent A. IV. Physiologically based models for bone-seeking elements. Revised and new reference values for arsenic. blood pressure. Kaufmann R. Kidney Int 2003.106:745-750. Lee GS. zinc. and tibia lead with neurobehavioral test scores in South Korean lead workers. Rubin R. Wilhelm M. Pirkle JL. cadmium. Roels H. Hickman T. et al. Hu H. Schwartz BS. Arch Environ Health 1995. J Hum Hypertens 1995. Sparrow D. Blood lead concentrations in children: new ranges. Jurasovic J. Environ Health Perspect 2000. Semen quality and reproductive endocrine function in relation to biomarkers of lead. Blood lead. Schwartz J. Am J Epidemiol 1994. Telisman S. Weiss ST. Fourth National Report on Human Exposure to Environmental Chemicals 217 .209:301305. Hanak B.153(5):453464.9:303-327. Paschal DC. Amery A. Soldin SJ.Metals results from NHANES III. Rocic B. Exposure of the U. Low-level lead exposure and blood pressure. stable lead isotopes to determine release of lead from the skeleton. Payton M. blood pressure and cardiovascular disease in men. JAMA 2003. Lead. Am J Epidemiol 2001. cadmium.108(1):45-53.63:1044-1050. Magder L.118:16-29. Clin Chim Acta 2003.

12) .800 (..285-.00 (2.30) 1.800 (.00 (2.20-3.40-2..900) 1.60) 1.900) .700-.418-. In addition.600 (. 1999 .10) .500 (.60) 1. 1994. Imported folk and alternative medicines occasionally are contaminated with inorganic mercury. have often required public health intervention (Zeitz et al.00) 3.979 (..70 (1. to form inorganic mercury compounds or salts..S.80) 1.40-1.484) .877 (. inorganic.50) 5.50-2.30 (1.50) 4. and mining and smelting.90) 90th 3. interval) . 1998. sulfur. thermometers.60 (1.00-1.00 (2.00) . such as chlorine (e. The kinetics of the different forms of mercury vary considerably.g. Atmospheric elemental mercury can be deposited on land and water.20-4. IARC.30) 3.600) 1.50-1.50) 2.80) 3.800-1.50-3.10-3.419 (.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 .655-. thimerosal.490 (.00-5.563 (. sphygmomanometers and barometers. an organic form of mercury.40-2. merbromin).70 (4. Hursh et al.00 (.700-.S. electrical lamps.80 (1.2.g. Inorganic mercury exists in two oxidative states (mercurous and mercuric) that combine with other elements.70) 911 856 2081 4525 03-04 03-04 .70-2.700) . Woods et al.40-1.20 (2.00 (1.30) 5. which can bioaccumulate in aquatic and terrestrial food chains. Poorly absorbed from the gastrointestinal tract.30) 3. Inorganic mercury compounds such as mercuric oxide are used in producing batteries and pigments and in synthesizing many organic chemicals.400 (.30-6.70 (1. Kingman et al. Elemental mercury is a shiny.700-.90-3..40 (3.60-2. elemental mercury is absorbed mainly by inhaling volatilized vapor.900) 75th 1..20-4. 218 Fourth National Report on Human Exposure to Environmental Chemicals .776 (. elemental mercury is used in rituals practiced in some Latin American and Caribbean communities.400-.00 (.70 (3..800-1. Also. it is oxidized in Total Blood Mercury—2003-2004 Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U.300 (. Other major uses include electrical equipment (e. and dental amalgam.800-1. Elemental mercury is released into the air from the combustion of fossil fuels (primarily coal).80) 4.400-.500 (. which create an episodic potential for volatization and inhalation of mercury vapor. water can be contaminated by the direct release of elemental and inorganic mercury from industrial discharges.30) 4132 4241 03-04 03-04 03-04 . thermostats and switches).797 (.700) .472-.90 (1.60-6.40 (4.00) 1.40-3.00) 4.900) 1. Elemental mercury is used to produce chlorine gas and caustic soda for industrial applications.. and is distributed to most tissues.60 (2.60-3.714-.927) .800-1.672) .700-.Metals Mercury CAS No.90) 95th 4. constitutes the main source of dietary mercury exposure in the general population.20) 2.02) . Metabolism of mercury by microorganisms in aquatic sediments creates methyl mercury. population from the National Health and Nutrition Examination Survey. 1993).00 (.90) 3. phenylmercuric acetate) or topical antiseptics (e.700 (. 7439-97-6 General Information Mercury is a naturally occurring metal that has elemental (metallic).300-.372) .781 (. may contain inorganic mercury. 1980. synthetic organomercury compounds were once used in pharmaceutical applications. and mercury compounds are still used as preservatives (e.80 (1. The ingestion of methyl mercury.800 (.30 (2.753-1.40) 1.00) 1. predominantly from fish and other seafood.g.30) 1. Some cosmetic skin creams from countries other than the U.363-.40 (4.30-4.00 (.574) . see Data Analysis section) for Survey year 03-04 is 0. 2002).814 (. silver-white liquid (quicksilver) obtained predominantly from the refining of mercuric sulfide in cinnabar ore.903) Selected percentiles ( 95% confidence interval) 50th .500) . Inhalation of elemental mercury volatilized from dental amalgam is a major source of mercury exposure in the general population (Halbach.60) 2085 2293 3478 Limit of detection (LOD.919) . Apart from methyl mercury.40) 3.800 (.80 (1.700-.40 (3.900 (. mercuric chloride).900) 1.90 (1.50) 1. with the highest concentrations occurring in the kidneys (Barregard et al.80 (3.500-.90 (4. or oxygen. After elemental mercury is absorbed.60 (1.g.703-.30-5.860-1.886) .689-.326 (.60-6.30-2.300) . and organic forms. Accidental spills of elemental mercury.800-1. Survey years 03-04 Geometric mean (95% conf. solid-waste incineration.60-5.. 2007).500-.

.900 (.700 (.374) .300) . 2003).500-.10 (1.40-2..30-2.500-.10) . Jonsson et al.20) 1.20-3.10 (.200-. The slow-phase half-life may be several weeks longer in persons with chronic occupational exposure (Sallsten et al.50) 95th 2.820 (. 1995. Smith et al.297-.500-.329 (.307 (.70 (1.300) .30-11.10) ..800 (.00-3.700 (.50-12.40) 1. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.738-...70-3.300 (. Less than 15% of inorganic mercury is absorbed from the human gastrointestinal tract (Rahola et al.00 (2. 1994.600) . and peak urine levels can lag behind peak blood levels by days to a few weeks (Barregard et al.. interval) Selected percentiles (95% confidence interval) 50th .541-.900-1.70-5.30) 1. excretion of mercury occurs predominantly through the kidney (Sandborgh-Englund et al.60) 1. 1992.944 (.800-1.600 (.60 (2.377 (.30 (.10 (1.200-.02 (.90) 3.90) 90th 1.00-6.600) .20 (2.60) 1.00 (2. with most elimination occurring through in the feces (Sherlock et al.90 (4.268-.3) 4.50) 1. 2004.7) 4. Suzuki et al.40-2.10 (..30-4.700-. Miettinen et al. 1990).90) 2.14.900 (.697-. Smith and Farris.80-3.475) .940) Race/ethnicity (females.50) 3.200-.0) 4.90) 2. thereafter.00) 1.50) 1.00 (2.80 (1.50) 2. for both acute and chronic exposures.500-.700-1. a measure of accumulated dose (Cernichiari et al.60 (1. The half-life of inorganic mercury in blood is similar to the slow-phase half-life of mercury after inhalation of elemental mercury.400-.60) 2.800 (.60 (1.. 1991.06 (. 1973).90 (4.30) 3. National Health and Nutrition Examination Survey.30-4.700 (.70) 4. 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. 1975.35 (1. 1984.Metals the tissues to mercurous and mercuric inorganic forms.700) 2.200 (. 1993). 1994) and then undergoes slow dealkylation to inorganic mercury.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 .500 (. 1969.377) .800) 1. 1999-2002.70 (1.20 (.800) .265-..200-.300) . 1992).10-3.14 and 0..70-6.. and a useful marker of exposure in epidemiologic studies (Grandjean et al.10 (5. The fraction of methyl mercury absorbed from the gastrointestinal tract is about 95% (Aberg et al. Geometric mean Survey years (95% conf.10) 1.90 (1.269-.726-1. Myers et al.500 (.70) 1.900-1.317 (.S. 2005).824) 1.200 (.60 (1.40 (1.27) . population.300) . and the newborn’s levels decline gradually over several weeks (Bjornberg et al. 1971)..00) 4. urinary mercury levels decline with a half-life of approximately 1-3 months (Roels et al.300 (.70) 4.00-1..700 (.80 (3.90 (3. Fourth National Report on Human Exposure to Environmental Chemicals 219 .20-3..299-.73) 1.30 (1..300) .30-5.300 (.30-6. Sandborgh-Englund et al.00) 6.00) 1.256-.70-3. Methyl mercury is incorporated into growing hair.. Methyl mercury enters the brain and other tissues (Vahter et al.20-11. 1994).00-2.23) .500-.200-.30-6.70-5.871-1.30-3. 1993).60 (3.825-1.10 (1.30-6. 1996).833 (.60 (3.20) .800-1. 1992 and 1999.50-2..30 (1..300) .343 (. 2003).700-.01) .395) .00) 2.800) .500-1. Vimy et al.667 (.50-3.90 (1.00) 7.40) 2. 1998).70 (1.10 (3..80) 579 527 370 436 588 806 Limit of detection (LOD.00 (1.407) . After exposure to elemental mercury..664-1. Human pharmacokinetic studies indicate that methyl mercury declines in blood and the whole body with a half-life of approximately 50 days.90) 5.800-1.80) 1. 1998). Excretion occurs by renal and fecal routes.40) 5.20-3.300 (.00) .900 (. 16-49 years) Mexican Americans Non-hispanic blacks Non-hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .318 (. McDowell et al.00-2.00 (3. Inorganic mercury and methyl mercury are distributed into human breast milk in relatively low concentrations. 1996.50 (2.20-2.. Vahter et al. 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.800) 1..700-1. Lesser penetration of inorganic mercury occurs through the bloodbrain barrier than occurs with either elemental or methyl mercury (Hattula and Rahola.40-1.00-2.800) 75th . Mercury levels in the cord blood are higher than in the mother’s blood (Stern and Smith.30) 1.919) .50 (1.20) . Transplacental transport of methyl mercury and elemental mercury has been demonstrated in animals (Kajiwara et al.06-1.369) 1.10-1.800 (.40 (1.29) .200-. 1999).60) 3.30 (1.

The constellation of findings may include anorexia.. High-level prenatal exposure may result in a constellation of developmental deficits that includes mental retardation. 1996). insomnia.500-. 2002.600 (. 2005).600 (. 2000. 1995. fatigue.600 (. and pinkish discoloration of the hands and feet (Tunnessen et al..600 (. Although recent investigations have suggested a possible link between chronic ingestion of methyl mercury and an increased risk for cardiovascular disease.700-.. Oskarsson et al. overt signs and symptoms of chronic inhalation may include tremor.600) . the existence of a causal relation is unresolved (Chan and Egeland.600 (.800) 4015 4132 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD . gingivitis. sensory impairments. Drexler and Schaller. 220 Fourth National Report on Human Exposure to Environmental Chemicals .600) . 2003).600 (. Sakamoto et al.500 (<LOD-.500-.. and neurocognitive and behavioral disturbances. Smith et al. Sakamoto et al. Workplace standards for inorganic mercury exposure have been established by OSHA and ACGIH.600 (. and cerebral palsy (NRC. pain in the extremities.700 (. Salonen et al. 2000. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 1998..800) .500-.800) 792 842 2060 4453 03-04 03-04 * * < LOD < LOD < LOD < LOD .600) . Large amounts may cause irritant or corrosive effects on the gastrointestinal tract (Sanchez-Sicilia et al.Metals may be more efficient for inorganic mercury (Grandjean et al. 2004.. Stern 2005. Inorganic mercury exposure usually occurs by ingestion. 2004). 1995. and a drinking water Inorganic Blood Mercury Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U. 1993). 2004.600-. ataxia.. see Data Analysis section) for Survey year 03-04 is 0.500 (.600) .600) . 2006.. cerebellar ataxia. 1983). maculopapular rash.500-. 2000). interval) Selected percentiles ( 95% confidence interval) Sample 95th .600-.700-.. Rice. In recent epidemiologic studies.600-. 2006.500 (.500-. irritability. typically after a latent period of weeks to months. the most prominent effect is on the kidneys where mercury accumulates and may lead to renal tubular necrosis.. Survey Geometric mean (95% conf. Acute.700 (. hearing impairment. which may vary for some chemicals by year and by individual sample.600-. DeRouen et al.700-. Factor-Litvak et al.600) ... Overt poisoning from methyl mercury primarily affects the central nervous system.600) .700 (. Bellinger et al..600 (. causing parasthesias..42. 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.500-.600) . Mercury levels in breast milk also decline in the weeks after birth (Bjornberg et al.. Smith et al.700) 2007 2240 3406 Limit of detection (LOD.500-. 1951. dysarthria.500 (<LOD-. limb deformities. Acrodynia is a sporadic and predominantly pediatric syndrome historically associated with calomel (mercuric oxide) in teething powders and occasionally other inorganic forms of mercury. and progressive constriction of the visual fields..500-. 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. < LOD means less than the limit of detection. high-dose exposure to elemental mercury vapor may cause severe pneumonitis. Vupputuri et al.S. hypertension.700) ..500) ..800) . 1963). 1970. Rissanen et al. dysarthria. and sleep disturbance (Bidstrup et al.700) size 8147 Total Age group 1-5 years 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th 90th .700 (. Once absorbed. Low-level exposure from dental amalgams has not been associated with neurologic effects in children or adults (Bates et al. depression. particularly irritability. anorexia. 2005. population from the National Health and Nutrition Examination Survey. 1987).600) * 03-04 03-04 03-04 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .600) .700 (.500-. short-term memory loss. Occupational exposure to elemental mercury vapor has been associated with subclinical effects on biomarkers of renal dysfunction (Cardenas et al. At levels below those that cause acute lung injury. 2004). altered physical growth.700 (.

28) 1.Metals standard for inorganic mercury has been established by U. et al. total blood mercury increased with age.254 (. average age 9.24 (2.67-3. These distinctions can help interpret mercury blood levels in people.350-.770-1.65) 1.430 (.14-2.16 (1. 2009).01 (.549) .78 µg/L for adults and 0.360 (. EPA. EPA at: http://www.55 µg/L.358 (.e. aged 18 to 69 years.. However.76-3.39-3.447 (.495 (. A cohort of 1127 U.. Total blood mercury levels increase with greater fish consumption (Dewailly et al. environmental levels) and health effects is available from the U.610-1.530) .408) . 2000)..24) 1. Urinary Mercury—2003-2004 Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.96 (1.9 years).870-1. 1998).700-1.330-.97) 2.88) 287 722 1529 03-04 03-04 .cdc. (2000) studied 1216 blood donors in the Czech Republic (896 men and 320 women.534) .66) 3.340-.430 (.840-1.480) 75th 1.60-2. From 1996 through 1998. Information about external exposure (i.07 (.200 (.840) 1.54 (2.78-2. 2003).09 (2.440 (.S.213-. During the same survey periods.20 (1.96 (1. 2001.280-. the developing fetus may be the most susceptible to the effects of ongoing methyl mercury exposure (NRC.442-. see Data Analysis section) for Survey year 03-04 is 0.405-.S. the total blood mercury concentration is due mostly to the dietary intake of organic forms. population from the National Health and Nutrition Examination Survey. 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.epa.460) . slightly higher total blood mercury levels were found in U.12 (. Sanzo et al.. interval) .08 (1. These men had no occupational exposure to mercury but previously had received dental amalgams at military facilities (Kingman et al. Among the three racial/ethnic groups. Urine mercury levels increase as more occlusal surfaces of teeth are filled with mercury-containing amalgams (Becker et al.433 (. Benes et al.00) 1.33 (2. In Germany the geometric mean for blood mercury was 0.05) 1. Fourth National Report on Human Exposure to Environmental Chemicals 221 .61) 1. 2002).. 1997.30) 3. 2009).930-1. Kingman et al.76-4.420 (.S.370) .330-.31) 2.250) .410-.23) 2..03-4.413-.16 (.290-.890 (.400 (.14.89) 3. average age 33 years.S.99-6.480 (.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 .14) 90th 2. Grandjean et al.580) . Survey years 03-04 Geometric mean (95% conf.555) .68 (2. 758 children.960 (.31) 1266 1272 03-04 03-04 03-04 .58 µg/L for 4645 adults.77-2. 2004.88 (1. and increased slightly in non-Hispanic white children (Caldwell.60 (1. IARC considers methylmercury to be a possible human carcinogen and elemental and inorganic mercury to be unclassifiable with regard to human carcinogenicity.S. total blood mercury levels declined slightly in non-Hispanic black and Mexican American children.19 (1.63-2. and the age-related changes differed across the groups (Caldwell et al.67-2.940 (.406-.396-. Schober et al. range 40 years to 78 years) had an average total blood mercury concentration of 2.700 (.330-. although non-Hispanic black females had higher levels than non-Hispanic white or Mexican American females.460 (.34-3.18) 2. 1998). In NHANES 19992002.05) 3. who participated in a 1998 representative population survey (Becker et al. Over the NHANES 1999-2006 survey periods.570) .. 2001.08 (1.atsdr.416 (.19 (2..492) Selected percentiles ( 95% confidence interval) 50th .840-1.420 (. military veterans (mean age 52.463) .93 (1.52) 2.60) 619 713 1066 Limit of detection (LOD.382-.509) .313-.29) 1.520) .. Biomonitoring Information In the general population.8 years. Clinically observable signs of ataxia and paresthesias may occur when blood mercury levels increase to approximately 100 µg/L after methyl mercury poisoning.23) . Mahaffey et al. 1995.85-2.441 (.88-3.90) 2.42) 95th 3..00 (.160-. particularly methyl mercury.304) . total blood mercury geometric mean levels in females aged 16-49 years did not change..509) .46) 3.46 µg/L for children.76-3.13-2.870-1.530-.gov/mercury and from ATSDR at: http:// www. 2006).330 (.430) .26 (1. 2003).360-.360-. Urinary mercury consists mostly of inorganic mercury (Cianciola et al. adult women in several ethnic subgroups (Hightower et al. the median concentration of blood mercury was 0..476 (.gov/toxprofiles...530) .

.12-3.909 (.280-. Survey years 03-04 Geometric mean (95% conf.455) .28 (. 2006).06 (.486) Selected percentiles ( 95% confidence interval) 50th ..S.485 (.64-2.566) . 2002) adult population surveys were similar to those in a U.385-.990) .56) 1266 1271 03-04 03-04 03-04 . DeRouen et al.11) 2.275) .00 (. ACGIH recommends that the blood levels due to inorganic mercury exposure in workers not exceed 15 µg/L. 2009).297 (.652) .246-.88-2..31 (1.77 (2.86) 95th 2.384 (.343 (...970 (.545 (.587 (. 1992).391) .225-. 1998).417) .40-1.630) .964-1.54 (2.522-.46-2.00) 90th 1. Urine mercury and the number of dental amalgams were correlated.208-.875-1.18-1.21) 1. Recent studies in children with dental amalgams and urinary levels less than 5 µg/g of creatinine did not have changes in cognitive-behavioral testing when followed for 5-7 years (Bellinger et al.88 (1.44) 1. 1988. reversible increase in urinary N-acetyl-glucosaminidase.400-.07) 1.61) 1.347) .508 (. and on average.588) . military veterans with dental amalgams. The ACGIH (2007) currently recommends that urinary inorganic mercury in workers not exceed 35 µg/g of creatinine.368) .362 (.06 (.537) .30) 1. Levels in U.13 (1. et al. Biomonitoring data will also help scientists plan and conduct research on exposure and health effects..23-2. An expert-panel report recently prepared for the U.09) 1. et al.78-4.32-2.714-1..76 (1. a biomarker of perturbation in renal tubular function.476 (.464 (.51-2.616) . women of childbearing age have generally been much lower than these levels (CDC..309-.79 (1.365 (.404-.687) .62 (1.463 (. Langworth et al.35 (1.00) 286 722 1529 03-04 03-04 .90) 618 713 1066 222 Fourth National Report on Human Exposure to Environmental Chemicals .39) 1. the urine mercury increased by approximately 0.40 (1. Urinary Mercury (creatinine corrected)—2003-2004 Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.443 (.480) . 2006.265-.535) 1.447-.276 (.455-.532 (.619-.01) 2.30) 2.800-1.525 (. population from the National Health and Nutrition Examination Survey.41-2.67 (1.S.87) 2.400) .S.32 (1.498) 75th . among workers with urinary mercury concentrations of 25-35 µg/L or greater (Barregard et al.969-1. 2002). representative sample of women aged 1649 years reported in NHANES 1999-2006 (Caldwell. 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.1 µg/L.25 (.65 (1.63) 1. 2003). and Italian (Apostoli et al.16) 1.13-2.472-. Blood mercury levels of women and children in NHANES 19992006 were also below levels established as occupational exposure guidelines (Caldwell. Information about the biological exposure indices is provided here for comparison.67 (1.S..391-. Urinary mercury levels in recent German (Becker et al. not to imply a safety level for general population exposure.784) 1.306 (.376-.79) 1.04-3. 2005).696 (. 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..11-2.03) 2.196-.599) .447 (.301-.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 .307-.289) .11) 1.Metals 2000).365 (.333-.255 (.358) .455-. In the study of U. Czech (Benes et al.620-.392-. mean urinary mercury was 3.S.768 (.785-1. interval) .87 (1. 2009).667-1.88-2.1 µg/L for each surface with a dental amalgam (Kingman et al.217 (.

600 (.35) .92) 4.25) 2.81 (3.500-.516 (.99) 1.51 (3.05 (3.502-.97) 2.631-.658 (.99-2.966) .24-1.569-.38) 4.54) 595 531 381 442 594 826 Limit of detection (LOD.831) .15 (2.51) .77) 2.710 (. interval) Selected percentiles (95% confidence interval) 50th . 16-49 years) 99-00 01-02 .65) 1. 1999-2002 Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for females aged 16 to 49 years in the U.699) 1. 1999-2002 Geometric mean and selected percentiles of urine concentrations (in µg/L) for females aged 16 to 49 years in the U.61) 1.89 (2. interval) Selected percentiles (95% confidence interval) Survey years 50th .710 (.32-3.45-2.37) 1.68) 3.69 (1.560-.664) .508-.79) 3.657 (.03-2.14) 3. Geometric mean (95% conf.47) 1.809) .31-1.740 (.540 (.07) 1.42-3.91-7.426-.15-1.810) .28 (1.95 (2.16-5.21-3.723 (.97) 2.592 (. 1999-2002.99 (3.18 (3.790) .68-3.930) .55) 90th 3.580 (.27 (1.41-6.656-.07-2.92) 2.59-5.892) .45 (1.04-10.721 (.13-4.84 (2.85-3.22-3.39) Sample size 1748 1960 Age group (females) 16-49 years Race/ethnicity (females.833) .772 (.55-3.30 (1. population.522 (.97 (1.13 (2.526-.691) .774) .56 (1.76) 2.09-1.61-6.03 (.53-3.62 (3.14 and 0.50-4.610-.23-1.94) 1.846) .520-.615 (.606 (.72) 1.85) 4.76 (1.48 (2.622-.616-.81-6.62 (4. National Health and Nutrition Examination Survey. Geometric mean Survey years (95% conf.30 (2.32) 2.00 (2.909-1.636-.91 (2.44) 3. Urinary Mercury (creatinine corrected)−Females Aged 16-49 Years Old.79) 1.S.685 (.724 (.45-3.84 (2.97) 2.596 (.580-.37 (1.686) . population.62 (1.50 (2.42) 90th 2.16) 5.92) 3.824) .475-.742-1.S.710) 1.579-.98 (5.83-3.10-2.24) 6.832-1.09-1.27 (2.77) 1.39-3.420-.850-1.520-.719 (.05 (2.870) .00 (3.03 (.14.582-.56) 3.665) Mexican Americans Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .45) 95th 3.31 (1.76-5.410-.07-5.560 (.41 (1.709) 75th 1.450-.27-1.35 (1.30-2.46) 3.706 (.21 (2.68 (3.17) 95th 5.639 (. 16-49 years) 99-00 01-02 .540-.650 (.670) 75th 1.637) .53) 595 531 381 442 594 826 Fourth National Report on Human Exposure to Environmental Chemicals 223 .56) 4.655 (.70 (2.00) 2.69-3.501-.41 (1.50 (1.43-1.06 (.650 (.45) 2. 1999-2002.63) Sample size 1748 1960 Age group (females) 16-49 years Race/ethnicity (females.52) 3.18) 3.387-.23-1.620 (.22 (.Metals Urinary Mercury−Females Aged 16-49 Years Old.664) Mexican Americans Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 . see Data Analysis section) for Survey years 99-00 and 01-02 are 0.665) .806) .99 (2.46-4.565 (.30 (2.04-1.87-4.14-2.910) .650) 1.624-.578-.41 (2.557-.65-4. National Health and Nutrition Examination Survey.632 (.553-.14-1.760 (.45) 2.799) .605-.03) 1.831) .744) 1.10-4.32 (1.47) 1.21 (1.57-4.3) 5.709) .46 (1.42) 2.

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The kinetics of intravenously administered methyl mercury in man. Daniels JL. Most B. Longnecker MP.111(12):1465-1470.40:413-419. et al. Patil LS. The contribution of dental amalgam to urinary mercury excretion in children. et al.115(10):1527-1531. Smith JC. Tunnessen WW. Turner MD. Effects of occupational exposure to elemental mercury on short term memory. 1993-1998. Aguinagalde FX. Am Ind Hyg Assoc J 1970.128(2):25125-25126. Public health consequences of mercury spills: hazardous substances emergency events surveillance system.258(4 Pt 2):R939-945.289(13):1667-1674. et al. Whittle K. Sandler DP. Azpiri MA. Mottet NK. Burbacher T. Environ Health Perspect 2007. Bernardo MF. Langolf GD. Dorronsoro M. Imai H. Suzuki T. Hum Toxicol 1984. Bolger PM.Metals Sanzo JM.48(4):221229. Vimy MJ. Farris FF. Lorscheider FL. Woods JS. McDowell M. Newton G. An assessment of the cord blood: maternal blood methyl mercury ratio: implications for risk assessment. Matsuo N. Fisher HL. Osterloh J.124:221-229. Arch Environ Health 1993. Environ Res 2005. Estimation and validation of mercury intake associated with fish consumption in an EPIC cohort of Spain. Mooney TF. Hislop D. Sherlock J. Baser M. Methyl mercury pharmacokinetics in man: a reevaluation. The hair-organ relationship in mercury concentration in contemporary Japanese. Smith JC. Blood mercury levels in US children and women of childbearing age. Public Health Nutr 2001.79:786789. Environ Health Perspect 2002. Effects of exposure to mercury in the manufacture of chlorine. Hongo T. Amurrio A. Br J Ind Med 1983. Goldberg J. Pediatrics 1987. McMahon KJ. Sinks TH. Nakazawa M. Am J Physiol 1990. Acrodynia: exposure to mercury from fluorescent light bulbs. Zeitz P. Vorwald AJ. 1999-2000. Amiano P. Maternal-fetal distribution of mercury (203Hg) released from dental amalgam fillings. Leitao JG.31:687-700.37:245-252.97(2):195-200. Jones RL. JAMA 2003. Environ Health Perspect 2003. Leroux BG. Topping G. Toxicol Appl Pharmacol 1996. Smith PJ. Vupputuri S. 226 Fourth National Report on Human Exposure to Environmental Chemicals . Vahter M. Hall LL.98(1):133-142. Toxicol Appl Pharmacol 1994. Shen DD. Toxicol Appl Pharmacol 1994. Smith RG. Environ Res 2005. Lind B. Takahashi Y. Kaye WE. Guo S. Stern AH. Speciation of mercury in the primate blood and brain following long-term exposure to methyl mercury. DeRouen TA.4(5):981-988. Schober SE. A review of the studies of the cardiovascular health effects of methylmercury with consideration of their suitability for risk assessment.2:117-131. Yoshinaga J.110:129-132. Stern AH. Elevation of mercury in human blood from controlled ingestion of methyl mercury in fish. Smith AE. Blood mercury level and blood pressure among US women: results from the National Health and Nutrition Examination Survey 1999-2000. Friberg L. Allen PV. Orr MF. Martin MD.

hard metal widely used to add strength and hardness and retard corrosion in metal alloys.3-47.8 (85.3 (55.5-65.7-47.2-37.0) 60. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.9-82. and xanthine oxidase (Kisker et al.0-71.7 (51. 0.S.6) 71.2-79.7 (58.3 (53.5 (41.6) 71.7-122) 93.0 (43. Excretion occurs predominantly via the kidneys.7-60.9 (40.6 (55.9 (44. Molybdenum is a nutritionally essential trace element that enters the body primarily from dietary sources.7-73.0-38.2 (83.2-91.0-85.9) 34. 1997).6-96.7) 78.0) 54.6) 93.2) 79.1) 126 (106-147) 109 (94. 01-02.6 (73.9 (37.3-75.2-53.0) 39.2) 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. inks.3) 37.6-42.5-66.2 (61.2-70. urinary excretion over six days CAS No.7) 78.2 (56.4 (79.9 (73.4) 42.1-55.4) 56.1-52.5 (41. and paints.5 (48.8-49.1) 59.7-51.0-62.0 (41.1) 57.7-41. hydrogenation catalysts.6) 53.3 (64.2-42.2) 40.4) 76. aldehyde dehydrogenase.2 (49.2) 37.3 (37.1 (38. The recommended dietary allowance for adult men and women is 45 µg/day (IOM.5 (43.6) 121 (103-139) 133 (113-155) 121 (106-143) 153 (126-188) 132 (121-147) 117 (109-129) 135 (119-154) 117 (108-129) 107 (99.2) 53. Molybdenum occurs in natural waters and may be present in concentrations of several hundred micrograms per liter or higher in ground and surface water near mining operations Urinary Molybdenum Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.7 (45.1-51.6-62.7 (73.8) 75.8.4 (48.3-91.0 (81.5.6 (40.4-61.8) 39.6 (40.8-108) 87.3 (79.6) 51.7 (37.5-91.9-83.7) 46.5) 60.9) 67.1 (91.5 (49.5 (74.8) 44.4-52.8) 46.7-50.9-85. More recently.5-46.6 (43.7-92.5) 47.8 (67.6 (55. semiconductor and battery industries have begun to use molybdenum.0-56. and 03-04 are 0. 2001)..9-56.7-105) 69.5) 44.3) 90th 135 (125-146) 124 (117-130) 111 (105-118) 95th 180 (154-216) 165 (145-176) 138 (133-146) Total 45.5-68.0) 55. and the average dietary daily intake of molybdenum is approximately 100 µg/day (IOM.9 (52.4) 52.1 (71. molybdenum is a cofactor for three enzyme classes— sulfite oxidase.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 47.5-52.4-75.3) 85.6-46.8-106) 88.7) 57.3 (84.1-59.1 (34.8) 40.8 (42. and 1.1) 46. lubricants.4) 49.3 (46.0) 97. 2001. chemical reagents in hospital laboratories.1-44. Fourth National Report on Human Exposure to Environmental Chemicals 227 .7) 51.3 (47.7-84.2 (40.9-55.0) 62.7 (44.9-55.0 (76.2 (38.7) 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) 60.8-90.6) Selected percentiles ( 95% confidence interval) 50th 50.0 (46.3 (38.3 (73.9) 62. 1996).3) 41.8 (82.0-101) 82.5-124) 108 (92.5 (37.7) 77.7 (50.0-110) 90.7) 86.2-59.2) 41.5 (81.0 (42.1-48.3) 83.1-52.3) 54.7 (71.6-58.8.0-77.3-44.6-55.4) 41.2-59.8) 48.9 (32.0) 45.1) 82.9 (78.1-63.7) 75th 84.5-52.0-100) 63. At a daily oral molybdenum dose of 24 µg.5) 80.0-65.4-82.7) 45.6-111) 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 52.6-72.7-39.0) 84.4 (72.8-46.4 (48.0 (48. 7439-98-7 General Information Elemental molybdenum is a silver-white.9 (33.5) 85. WHO.6 (52.2 (55.9 (34.4 (34.3 (55.0 (42.Metals Molybdenum or ore deposits.3) 47.8-94.7-96.3 (71.7-68.2 (69. and in pigments for ceramics.2) 48.6-82.1-88. interval) 45.2 (49.1) 35.4) 45.3-115) 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. In humans.7-91.2) 150 (128-187) 130 (120-141) 119 (112-130) 119 (105-138) 115 (104-128) 101 (97.5-41.4 (80.3) 65.2 (63. Compounds of molybdenum are also used as corrosion inhibitors.2) 52.5) 80. population from the National Health and Nutrition Examination survey.7 (36.0-53. which exert homeostatic regulation over molybdenum balance.9-109) 97.5 (67. respectively. Gastrointestinal absorption of molybdenum averages 8893% for dietary intakes of 22-1490 µg/day. see Data Analysis section) for survey years 99-00.

5) 63.7) 62.8 (57.0) 53.6) 39.3) 40.2) 37.9 (64. Levels of molybdenum Urinary Molybdenum (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.3 (71.2-40.5 (79.5) 90th 108 (97.5 (40.5 (39.5 (39.0) 38.2 (37.5 (38.9 (39.5 (34.2 (36. dust and other fine particles produced during refining or shaping of molybdenum or molybdenumcontaining alloys are inhalational pathways of exposure.2-47. 1995).0) 39.0-120) 85.1 (54.2-80.3 (71.0-46.0-41.1-34.3 (37.1-67.5 (35.2) 38.03 mg/kg/day in humans (IOM. 2001).6) 43.3-52.4) 44.6) 39.1 (42.6-63.S.3-68.9) 41.9-41..2 (69.9-42.2 (52.1 (39.3) 44.6 (42.9-61.6 (36.2) 43.8-47.1-100) 86.9 (49.5-46.1 (40.5 (35.7-52.6-41.7 (66.7 (77.9-45.6-78.4 (55.2 (50.7-38.6 (38.3) 61.2) 55.4) 116 (101-126) 104 (88.2) 37.3 (58. respectively.0-56.1-43.0 (58.Metals was 18% of the ingested dose.8-118) 81.9 (64.4-66.0) 95th 144 (125-171) 130 (120-149) 120 (107-135) Total 42.3 (53.4 (67.2) 39.5) 60..7-62.4-118) 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 .2-121) 107 (92.6-45.2 (40.0) 72.4 (53.4 (59.5 (78.6-88.3-102) 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 40.4) 60.2 (33.5-35.7) 75th 63.3-59.8-84.9-45.9 (73.1) 101 (83.2 (40.6) 48. but available epidemiologic data are scant.2 (73.5-50.1 (44. 1999). and molybdenum has not been systematically evaluated for carcinogenicity by IARC.5-48.3 (55.7) 41.4) 122 (107-133) 109 (99.8) 39.2) 39.4-120) 101 (84.2-96.1) 43.2-41.0) 88.5-62.8-66.5) 71.6-61.2) 58.5-99.1-112) 78.8) 79. of the ingested dose (Turnlund et al.9 (39.9-40.1 (38.4-76. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. Molybdenum is generally considered to be of low human toxicity.7-120) 87.9) 40.5) 73.1-38.8) 38.6-76.2-65.4 (37. at daily oral doses of 95 µg and 428 µg. In industry.1) 65. and urinary levels reflect intake from all sources.3) 41.4-41.9) 31.0 (74.7) 112 (95.1-81.4 (56.3 (36.1 (30.5) 72.2 (43.5-92.9) 44.0-46.4) 77.5 (83.6-61.9-87.5 (80.3-45.0) 33.1-40.5 (37. 1993). urinary excretion over six days rose to 50% and 67%. Based on studies finding adverse reproductive effects in rats and mice. population from the National Health and Nutrition Examination survey.9-71.4-42.1-41.0-103) 103 (90.8) 62.6 (36.8-52.3-46. EPA.2) 42.8 (56. Chronic exposure to very high levels may result in higher serum uric acid levels and a gout-like illness (Koval’skiy et al.3) 37.4-185) 106 (94.1) 56.3-115) 98.7 (75.5-70.3) 43.5-119) 90.5 (50. U.9-96.0) 36.5 (65.5-45.9 mg/kg/day and established a tolerable upper intake level of 0.1 (37.5 (65.7 (30.4-39..6 (59. 1997).3) 57.6 (71.7) 115 (93.8-46.8 (37.6-63.3-44.1 (38.5 (54.S.8-65.0-133) 119 (88.8-47.8) 38.3) 56.7) 53.3-43.1) 37.4) 58.0) 62.9-68.9 (35.9 (40. Biomonitoring Information Molybdenum is an essential element for health. One case-control study suggested a possible link between occupational exposure to molybdenum and lung cancer (Droste et al.5 (41.9-117) 57.3-141) 109 (81.4 (78.4) 89.6) Selected percentiles ( 95% confidence interval) 50th 41.8 (90.0) 39.7-43.8) 61.1-39.5 (40.1 (33.4) 47.7) 57.3) 64. A long term inhalation bioassay of molybdenum trioxide in mice yielded “some evidence” of carcinogenicity (NTP.2-49.1-127) 90.0 (35.7-137) 129 (109-155) 112 (97.8) 37.5 (36.1-45.7-100) 77. the Panel on Micronutrients of the Institute of Medicine identified a no observed adverse effect level (NOAEL) of 0.4) 61.9-118) 91.2) 42.1-109) 89.8) 45.0 (80.2-103) 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 42.6 (57.7) 45.5-44.7) 42. 1961.2-96.3 (83.4-107) 85.4 (40.6) 36.9) 92.9) 173 (130-243) 159 (129-170) 132 (107-158) 85.5) 214 (154-1040) 185 (165-219) 160 (129-257) 112 (78.5-97.3 (36.8-67.3-56.4 (44.1) 40.9 (79.1) 37.7-93.5-69. interval) 43.1-39.7-44.5 (37. Human health effects from molybdenum at low environmental doses or at biomonitored levels from low environmental exposures are unknown.0-38.2 (40.8) 71.3 (51.4) 48.1-43.1-79.5 (41.9 (36.8 (36.1 (82.0) 44.7-40.3) Sample size 2257 2689 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 85.9) 79.4-106) 85.2 (57.5-60. and clinical or epidemiologic evidence of adverse effects is limited.3 (37.8-42.2-46.8 (75.4) 40.1 (49.5 (59.

White and Sabbioni. 4/14/09 Iversen BS. iodine. Sci Total Environ 1998. Available at URL: http://books. Dietary reference intakes for vitamin A. Available at URL: http://www. Institute of Medicine (IOM).gov/index. 4/14/09 White MA. Environmental Protection Agency (U. Schleyerbach U.S. 1996. cfm?objectid=070A72C6-E9C1-AE67-4BFAB97AD0F427E8.nap. Food and Nutrition Board. chromium. Third National Report on Human Exposure to Environmental Chemicals. pp. Sabbioni E. Schaub J. TR-462.niehs. Ann Rev Biochem 1997. Standing Committee on the Scientific Evaluation of Dietary Reference Intakes. Trace element reference values in tissues from inhabitants of the European Union. Inductively coupled plasma mass spectrometric determination of molybdenum in urine from a Danish population. (DC): National Academy Press. Schindelin H. National Toxicology Program (NTP). pp. Koval’skiy GA. EPA). et al. 56:322-327. 16:1313-1319. Menne C.htm. Ronchi A. population were well characterized in NHANES 1999-2000 and 2001-2002 (CDC. 420-441. Am J Clin Nutr 1995.. arsenic. Vermeire PA. Urinary molybdenum concentrations in infants may be slightly lower than those in other age groups (Sievers et al. 2001.216:253-270. 2001). and retention studied with stable isotopes in young men at five intakes of dietary molybdenum. Molybdenum absorption. Molybdenum.S. van Sprundel MP. vitamin K. Changes of purine metabolism in man and animals under conditions of molybdenum biogeochemical provinces. Zhurnal Obshchey Biologii 1961. iron. Aprea C. Inductively coupled plasma mass spectrometric determination of molybdenum in urine. and zinc: a report of the Panel on Micronutrients. Peiffer GL.. excretion. 4/14/09 Sievers E. Molybdenum-cofactorcontaining enzymes: structure and mechanism. Weyler JJ. molybdenum. 2002. J Trace Elem Med Biol 2001. Occup Environ Med 1999. Yarovaya GA. Turci R. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 1998. boron.nih. Kristiansen J.. U. these levels were comparable to those reported for adults in smaller European population surveys (Iversen et al. Fourth National Report on Human Exposure to Environmental Chemicals 229 . References Centers for Disease Control and Prevention (CDC). Kisker C. Washington. Rees DC. 2005). Rapid Comm Mass Spectrom 2002. manganese. copper. 1998). Van Meerbeeck JP. silicon.Metals in urine for the U. Molybdenum in infancy: methodical investigation of urinary excretion. In: Trace elements in human nutrition and health. Minoia et al. 1313-27-5) in F344 Rats and B6C3F1 Mice (inhalation studies) 1997 [online]. Keyes WR. Sciarra G. Geneva: WHO. Minoia C. Toxicology and carcinogenesis studies of molybdenum trioxide (CAS No. A study of 13 elements in blood and urine of a United Kingdom population. 2005. World Health Organization (WHO). 144-154.gov/iris/ subst/0425.15(2-3):149-154. X. Finding a measurable amount of molybdenum in the urine does not mean that the level of molybdenum causes an adverse health effect. White MA. Sabbioni E. vanadium.S. Gatti A. Droste JHJ. Shmavonyan DM. Christensen JM. nickel. Atlanta (GA). edu/openbook. Analyst 1998.php?record_id=10026&page=420.22(3):179-191. Molybdenum 1993 [online]. 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.66:233-267. Turnlund JR. Available at URL: http://ntp.62(4):790-796. Occupational risk factors of lung cancer: a hospital based case-control study.123(1):81-85.epa.

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

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

Int Arch Occup Environ Health 1997. Schierl R. Occup Environ Med 1998.inchem. 2003. Neuendorf J. and in blood and urine in the United Kingdom. Parrot JL. ruthenium. 289-380. Fries HG.123(3):451-454. Br J Pharmacol 1969. Raab W. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population.70(3):205-208. 3/31/08 Moore W Jr. population were below the limit of detection (0. Blanks R. Biomonitoring of traffic police officers exposed to airborne platinum. Nickel. Environmental Health Criteria 125. palladium. Several studies have shown that background concentrations in general populations were usually less than 0. Allergy and histamine release due to some platinum salts. Int J Hyg Environ Health 2004. 1991 [online]. 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. eds. Hysell D. et al. 206:15-24.76(1):5-10. Ruff F: Histamine release by sodium cholorplatinate. and platinum.04 µg/L) in this Report. Turfeld M. Farago ME. and gold excretion of patients after insertion of noble-metal dental alloys. Duneman L:Long-term urinary platinum. Rommelt H. Schulz C. 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. International Journal of Hygiene and Environmental Health 2003. Biological monitoring of hospital pharmacy personnel occupationally exposed to cytostatic drugs: urinary excretion and cytogenetic studies. Czerczak S. Pethran A. Wilhelm M. Influences on human internal exposure to environmental platinum.. Pethran et al. Environ Res 1975a. Finding a measurable amount of platinum in the urine does not mean that the level of platinum causes an adverse health effect. 1998).56(3):283-286. Levels of platinum in urine for the U.4(1):27-36.19:685-691. Kavanagh P. Bocca B.htm. Herr CE. Alimonti A. Stilianakis NI.inchem. Arch Environ Health:1969. Kuster W. Ewers U. Nowak D. Urinary platinum levels associated with dental gold alloys. Kulka U. 2003. Biomarkers 1999. J Expo Anal Environ Epidemiol 2003. Angerer J. Seiwert M.. rhodium. Saindelle A. Arch Environ Health 2001. osmium. pp. Moore W Jr. 2004. Fruhmann G.. Environ Health Perspect 1975b.S.207(1):69-73. Grimm CH.13(1):24-30. et al. Kaus S. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Platinum-industry and precious-metal workers had urinary concentrations about one-thousand times higher than general populations (Schierl et al. Urinary excretion of platinum from platinum-industry workers. One study found that traffic-control officers had no greater urinary platinum concentrations than office-based control subjects (Iavicoli et al. Schierl R. References Becker K. Schierl R.. Platinum concentrations in urban road dust and soil. International Programme on Chemical Safety (IPCS)... 1997. In: Bingham E... Crocker W. Carelli G.35:313-321. Gold-platinum dental restorations were correlated with increased urinary platinum concentrations. 2001). Patty’s Toxicology. Saindelle A. Herr et al. Part 1: monitoring of urinary concentrations. palladium. Boos KS.org/documents/ehc/ehc/ ehc125. et al. Petrucci F. Schierl. Thornton I.61(7):636-9. Seifert B. Jankofsky M. Powell CH.10:63-71. et al. 2003). Iavicoli I.. Pethran A. Schierl R.9:152-158. Begerow J. Schierl et al..01 µg/L (Becker et al. Ruff F: Platinum and platinosis. Gromiec JP. Wilhelm et al..005 µg/L (Iavicoli et al. 2000. Revised and new reference values for some trace elements in blood and urine for human biomonitoring in environmental medicine. Platinum. New York: John Wiley & Sons. Hall L. Ensslin AS. van de Weyer C. Kazantzis G. Gieler U. Available at URL: http://www. 1998). which elevate urinary platinum by five to twelve-fold (Begerow et al. Occup Environ Med 2004. Analyst 1998. 2004) or less than 0. Senofonte O. Schulz C. 5th ed. Stara J: Biological fate of a single administration of 191Pt in rats following different routes of exposure.Metals the International Programme on Chemical Safety at http:// www. 1999. Hysell D. Hebert R. Herr et al. Kelly J. Hauff K. Int Arch Occup Environ Health 2003. Uptake of antineoplastic agents in pharmacy and hospital personnel. 232 Fourth National Report on Human Exposure to Environmental Chemicals . Campbell K. Cohrssen B.org/documents/ehc/ehc/ehc125. 2004). Biomonitoring Information Urinary platinum levels reflect recent exposure. 2003.htm. Huber R.55(2):138-140. Stara J: Preliminary studies on the toxicity and metabolism of palladium and platinum.

220) .500 (.155 (.470) .360-.360-.400 (.480) .145 (.135-.290 (.158) .340) .420) .170 (.500) .690) . 7440-28-0 General Information Elemental thallium is a blue-white metal found in small amounts in soil and in sulfide-based minerals.240-.180-.145-.370 (.270 (.330-.160-.430 (.450 (.190 (.400-.160-.159 (.400) .410-.250-.150-.150-.290 (.400) .490) .330-.500) .137-. thallium is produced in a fine particulate form that can be absorbed through inhalation or ingestion.190 (.146 (.200 (.550 (. see Data Analysis section) for Survey years 99-00.196) . Human health effects from thallium at low environmental CAS No.134-.480) .270-.160 (.370 (.200-.390 (.190 (.190-.160 (.280) .410-.200 (.220) .400-.185 (.240) .250-.180) .172 (.390) .280-.250 (.470) .250-.390) .330-.173) .310 (.218) .200-. Thallium disappears from the blood with a half-life of several days.420) .400 (.270 (.390) .240-.170-.330) .360-.200) .210 (.390-.370-. It is still used in relatively small amounts in pharmaceutical and electronics manufacturing.159 (.230) .167-.191 (.200 (.159 (.380 (.330-.470 (.400 (.400) .510) .177) .450 (.220-.230-.290 (.350-.200-. respectively.200) .270 (.173) .230) .250-.350-.270-.260 (.179-.440 (.217 (.145-.290 (. 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.590) .330) .270) . Elimination from the body tissues occurs slowly through urine and feces (Blanchardon et al.148-.440) .260-.450 (.520) .220 (.450 (.02.320-.370) .280 (.310) .250-.340-.410 (.220 (.470) .167-.340 (.170-.630) .370 (.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 .400-.410-.320 (.200) . however.360 (.172 (.450 (.370-. it has not been specifically mined or refined in the United States since 1984.420 (.290-.187-.350-.480) .410 (.156) .390-. population from the National Health and Nutrition Examination Survey.330) .410) .440) .450 (.184 (.220 (.02.180 (.162-.490) . 0.420) . Thallium exposure occurs primarily from industrial processes such as coal-burning and smelting.239) .190 (.430 (.340-.410 (.230-.350 (.390 (.250-.150-.156-.202 (.150-.510) 1200 1313 1281 1213 1340 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .200 (.350-.188) .460-.360) . In addition.290) 90th .167 (.170) .420) .133-.420) .400-.310 (.202 (.197-. the latter being the current major industrial consumer of thallium in this country. representing distribution into other tissues.250 (.280) .440 (.510 (.330-.340-.390) .150-.400 (.350 (.230 (.640) .176 (.400) 95th .172) .147-.250-.340-.460) 861 675 618 561 657 723 801 1114 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.410 (.420-.500) .160 (.460) .590) .225) .560) .192) Selected percentiles ( 95% confidence interval) 50th .170-.270 (.144 (.202) .320) .400 (.470 (.350-.300 (.270) .300) .147-.240-.420) .02.360-.240) .460 (.250) . In the past.290) .520 (.520) .350) .S.490) .370-.480) .380-.215) .201 (.170) .220 (.180-.200 (.200 (.370 (.157-. 01-02.180 (.480) .450) .260-.370) .165 (.170) .200-.370 (. From these and other sources.290-.180 (.270 (.220 (.310 (.170 (.410 (. Fourth National Report on Human Exposure to Environmental Chemicals 233 .300) .320) .380) .170 (.400) .280) .380-.430) .220) .183) .440-.420-.330-.200) .430-.310-.290) .181-.410-.160-.220) .173-.160 (.260 (.370 (.300 (.230) .410 (.170-.320) .340) .178) ..400-.490 (. In the United States.154-.149 (.450 (.420) .190 (.183) .360 (.520) .280 (.180) 75th .150-. thallium readily crosses the placenta and also distributes into breast milk.280 (.153-.200) .430 (.240) .300 (.220) .430) .350-.170-.260) .171 (.196) .440 (. and 03-04 are 0.140-. and 0.243) .360-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.330) .197 (. thallium was obtained as a by-product of smelting other metals.490) Total .360 (.290) .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 .175) .206) . interval) .450 (.420-.430-.170-.300-.160 (.160-.260-.190 (.420-.450 (.390-.370 (.280-.260-.440 (.410-.147-.182-.360 (.163) .410-.210) .290 (.330-.156) .440) .180-.250-.210 (.390-.350) .217) .220) . 2005).370-.210-.230) .180-.300) .201 (.185-.230-.290 (.170-.290) .218) .200) .260 (.430-.270-.160-.300) .260-.Metals Thallium depilatory cosmetics.430 (.380 (.

198) .317) .264 (.200-.293) .282 (.237-.129-.286 (.214) .204 (.229-.281-.323 (.197-.278) .153) .348) .338-.198-.atsdr.226) .148-. 1992) Workplace air standards and guidelines for external exposure are established by OSHA and ACGIH.254-.462) .196-.152) .369) Total .260-.368 (.321) . Thallium produces toxicity by replacing intracellular potassium in the body.145 (.156 (.263-.244 (.289) .153-.348 (.S. Relatively high-dose intentional or accidental ingestion can result in gastrointestinal symptoms followed by multiorgan failure.369 (.222) 90th .211 (.254 (.226-.343 (.222-.349 (.144-.155) .148 (.194 (. IARC and NTP consider the evidence for the carcinogenicity of thallium as inadequate or unclassifiable.297) .300) .282-.214 (. and polyneuropathy.361 (.156) .171) .141-.153-.143 (.346-.189) .208-.172) .173 (.269) .224 (.192 (.458 (.192-.307 (.176) .191-.255 (.297 (.197) .214) .378 (.176) .173) .177) .258 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.164) .161 (.250) .161) .138 (.286-.167) .156 (.248) .208) .293 (.205 (.238) .gov/toxpro2.219) .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 .286 (.125-.194 (.137-.313-.456) .155 (.159) .377) .267-.215) .283 (.149 (.299-.287-.356) .128 (.162) .287 (.198-.389) .157-.230) .328 (.167) .271-.168 (..366) .178 (.304) .350) .222) .333 (.333-.300-.213 (.170) .153 (.157) .312 (.278 (.161 (.211 (.280-.304) .217-.600) .356-.184-.159 (.223 (. respectively. EPA.259) .151) .304 (.325-.173) Selected percentiles ( 95% confidence interval) 50th . Information about external exposure (i.155-.171-.233) .162-.389) .167-.375 (.265-.210 (.154 (.164) .200-.365) .318-.122-.313-.300) .231) .207-.235 (.214 (.148 (.326-.160) .286) .200) .321 (.162 (.238-.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 .306-.304) . and death.274-. population from the National Health and Nutrition Examination Survey.366 (.162) .272-.280) .149-.231-.271-.235-.131-.221) .286-.333 (.146-.207) .350 (.184-.200 (. (ATSDR.135-.148-.html. Levels of thallium in urine for the U.306 (.342) . Severe accidental thallium poisonings from ingesting of rat poisons that contained water-soluble thallium salt have occurred.304) 95th .241) .160 (. although additional mechanisms of action are possible.153-.151-.158) Sample size 2413 2652 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .156 (.169) .140 (.236) .333-.348-.152) .313 (.215-.187-.166 (. Biomonitoring Information Urinary thallium levels reflect recent exposure.148-.147-.330-.157 (.147-.170-.176) .149) .153 (.146 (.387) .214-.412 (.424 (.469) .402) .cdc.313 (.333) .462) .133-.402) .158 (.422) .292 (.215 (.243) .383) .338 (.317 (.278) .216 (.171) .188 (.145-.191-.200-.146-.208-.204) .169 (.156 (.181) .246-.152) .362) .377) .300 (.167 (.240) .389-.167-.278-.297 (. interval) .227 (.273 (.140-.223) .154 (.S.221) . environmental levels) and health effects is available from ATSDR at: http://www.250-.329) .319) .424) .153 (.143) .256 (.180) .272 (.532) .e.383 (.458) .233 (.180-.182 (.364) .134-.162) .258-.217) .218 (.324) .184-.203-.269 (.221 (.370 (.143-.145) .143-.387) .271-.S.147-.333-.176) . 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.291-.222 (.146-.260 (.160-.179) .244-. Chronic high-level exposures have been associated with weight loss.202 (.266-.278 (.337-.146) .301-. Peripheral neuropathy and alopecia are well-documented effects of acute and chronic exposures.222 (.343 (.206 (.158-.149-.148-.167 (.167 (.286 (.273-.169-.143 (.135-.135-.162-. neurologic injury.198-.207 (.170) .364) .144-.153 (.185 (.160) .271-.364 (.136 (.166 (.346) .340-.328-.217-.154 (.154 (.133 (.237) .307) .278) .317 (.250-.364 (.286 (.142-.155-.234-.Metals doses or at biomonitored levels from low environmental exposures are unknown.145-.412 (.327) .142 (.306-.150) .153) .146 (.196 (.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 .153 (.167 (.159-.128-.278-.192-.400-. arthralgias.160) 75th .289) .229) .333) .150) .179-.146) . and a drinking water standard has been established by U.142 (.119-.140 (.273-.161) .380 (.212) .

Martin J-C. 1980. Urinary concentrations of 100 μg/L in asymptomatic workers (500 times higher than median levels in the U. Pozzoli L. Gallorini M. Atlanta (GA). Schaller et al. Int Arch Occup Environ Health 1980. Ting BG.113(1):47-53. Buhlmeyer G. 1990.1 mg/m3 (Marcus.. Soddemann H. and serum of Italian subjects. Environ Res 1998. Radiat Prot Dosim. et al. Paschal DC. Schmidt M. Ewers U. Fourth National Report on Human Exposure to Environmental Chemicals 235 .216:253-270.cdc. X. Valentin H. Challeton-de Vathaire C.. Raithel HJ. Int Arch Occup Environ Health 1981.atsdr. Schaller KH. Apostoli P. Available at URL: http://www.47(3):223-231. Sci Total Environ 1998. 1981. 1998. Long term retention and excretion of 201Tl in a patient after myocardial perfusion imaging. et al.35(1):4-9. Intake and health effects of thallium among a population living in the vicinity of a cement plant emitting thallium-containing dust. Paschal et al. with concentrations ranging up to 76. Kramer U. 1985). Toxicological profile for thallium. 2005) and are shown with results from NHANES 2003-2004 in this Report. Brockhaus et al. Sabbioni E. 1992 [online]. Seventy-eight percent of the urine specimens in that study contained greater than 1 μg/L. population) are thought to correspond to workplace exposures at the threshold limit value of 0. White MA. 2005. A study of 13 elements in blood and urine of a United Kingdom population. 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. Brockhaus A. et al.76(1):53-59. Sampson EJ. Third National Report on Human Exposure to Environmental Chemicals. Sabbioni E.Metals (CDC. (1981) studied 1. Minoia et al. Nearby residents were exposed by eating garden plants that had been contaminated by the thallium. Minoia C. Manke G. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. References Agency for Toxic Substances and Disease Registry (ATSDR). Wiegand H. Marcus RL. blood. Trace element reference values in tissues from inhabitants of the European Union. Jackson RJ.. 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. Cassot G. Trace metals in urine of United States residents: reference range concentrations.5 μg/L.. Trace element reference values in tissues from inhabitants of the European community I.95:89-105. J Soc Occup Med 1985. Celier D. Investigation of a working population exposed to thallium. Boisson P. A study of 46 elements in urine. Centers for Disease Control and Prevention. 2005. 7/15/09 Blanchardon E. Pirkle JL. Pietra R.S.html.265 people living near a thallium-emitting cement plant in Germany.48(4):375-389. These urine levels are generally comparable to levels observed in earlier studies of general populations (Brockhaus et al. Sci Total Environ 1990. Investigations of thallium-exposed workers in cement factories. Dolger R. Morrow JC. White and Sabbioni.gov/toxprofiles/tp54. Finding a measurable amount of thallium in urine does not mean that the level of thallium causes an adverse health effect. 1998).

140-.066-.071 (.170-.270-.830) .180-.300 (.096 (.122) . Although workers occupationally exposed to tungsten carbide may develop serious lung disease (“hard metal disease”).110 (.100) . filaments for incandescent lamps.090) .170) .050-.210 (.140 (.135) .400 (.097-.220) .00) .100) .090-.120) .150 (.390) .180-.Metals Tungsten CAS No.220) .091) .151) .130) .290) .290-.170) .090 (.140-.500) .230) .160 (.450-.170 (.810) .069-.109) .530 (.320 (.087) .620) .250) .090-.310-.420-.110) .150 (. their illness may stem from exposure to cobalt mixed with tungsten carbide rather than to tungsten alone.240-.260 (.086 (.126) .210 (. 236 Fourth National Report on Human Exposure to Environmental Chemicals .04.420-.320-.180) .084) . Occupational exposure is from dusts released during grinding or drilling of hard metals.260-.090-.250) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.116) .064-.090 (.073-.060-.150-.310 (.160 (.490 (.060-.065 (.360 (. 0.520) .090-.790) .160 (.093 (.120-.250-.300 (.190 (.630) .280 (.080) 75th .370 (.270 (.105 (.101 (.450 (.190-.087-.104) .300) 95th .080-.04.120) .060 (.650) .250) .120-.340) .110-.550) .110 (.490) .070-.310-.120-.120) .800) .130-.430 (.520) .260-.082) .056-.350 (.510 (.340-.137 (.070) .210 (.060 (.470) .090 (.560 (. Tungsten is used mainly for producing hard metals. and 0.150 (.074-.090-.160-.310) .270 (.180) .100 (.470 (.460) .100-.090-.120-. and for producing ferrotungsten.082 (.060 (.110 (.180-.060-.560) .240 (.069) .100) .460 (.093) .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 .380-.470-.160 (.111-.190) . and it has not been classified with respect to its carcinogenicity by either IARC or NTP.260-.080 (.210-.060 (.310-.132) .100 (.350) .050-.290-.110 (.330-.130) .250) .260 (.220-.470 (.120) .090-.070-.270-.082 (.340-.370 (.158 (.270-. mainly as scheelite (CaWO4). Most background environmental exposures to tungsten are from the soluble forms such as tungstate salts that may occur in drinking water.180) .370) . Tungsten compounds are used as lubricating agents.S.062 (.110 (.060-.130 (.550) .320-.570 (.120-. Evidence is lacking for the carcinogenicity of tungsten.400) .250) .100) .430-.500 (.560) .073) .080-. which are used in rock drills and metal-cutting tools.130-.190-.280 (.070-.092) .100 (.140 (.390 (.460 (.530 (.180) .080 (.280-.480) Total .520) .360 (.430 (.133) .082-.770 (.113 (.110-.230-.380) .058-.260) .560) .230-.065-.080 (.110) .290-.100) Selected percentiles ( 95% confidence interval) 50th . see Data Analysis section) for Survey years 99-00.093-.220) .430) .080) .073 (.360 (.250-.068) .380 (.640 (.090) . 7440-33-7 General Information Tungsten is a steel-gray to tin-white metal that occurs naturally in the earth’s crust.160-.360-.380 (.430-.081 (. Little information is available on the toxicity of tungsten.190-.220 (.200-.092 (.210 (.073-.310-.500 (.140 (.123-.380-.080) .130-.070) .160) .470) .180 (.071-. Urinary Tungsten Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.530 (.400 (.204) .070) . respectively. and 03-04 are 0. and as catalysts in the petroleum industry.400-.120) .230-.070 (.120) . 01-02.110-.060 (.096-.300-.113 (. Human health effects from tungsten at low environmental doses or at biomonitored levels from low environmental exposures are unknown.570 (.180 (.230-.370 (.620) .210) .130) .200) .320) .330) .360-.170) .590) .076 (.170 (.670) .060-.370-.190-.060 (.360) .440) .190 (.410-.410 (.078-.120 (.113 (.580) .370-.230 (.550 (.400 (.270-.800) .160) .350) .090) .070-. population from the National Health and Nutrition Examination Survey.290 (.084-.095-.050-.080) .050-.53) .550) .300 (.090-.460) .620 (.070 (.200 (.070 (.084 (.113 (.210 (.170) .250) .160 (.140) 90th .950) .077-.690) .150) .130-.460 (.080 (.160-.430 (.380-.095-.160-.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 .350-1. interval) .120-.380-.180-.100-.04.330-.076 (.100) .350) .560) .330 (.510-.130) .105) .092 (.510-1.080-.088 (.400 (.300) .140 (.101-.290) .100 (.088) .330) .230) .070-.130) .310-.090) .130 (.107 (.320 (. which is used in the steel industry.340-.062 (.080 (.060-.270 (.410) 790 680 618 562 649 723 802 1117 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.056-.070) .100-. bronzes in pigments.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 .

091) .500) .061-.122-.139 (.145 (.333-.198-.083 (.341 (. 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.071) .245-.201 (.144-.057-.060 (.083) .084 (.200-.057-.333) .100) .158) .133) 90th .119-.105 (.250 (.270 (. measure urinary tungsten.105 (. population.385 (.150-.200-.081 (.360 (.216 (.497 (. Biomonitoring Information median urinary levels were as much as 15-fold higher than median levels in the U.169 (.107-.197) .414) .164 (.331-.237-.287) .133) .279 (.667 (.300 (.188-.124-.222) .285) .125) .224) .302-.094-.375) .197 (.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 .121 (.333 (.179-.065 (.098-.370) 320 363 290 679 744 725 1339 1544 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .063 (.301) . Patients with medically-inserted tungsten found at increased levels in drinking water.253-.131-.218 (.340 (.148) .065 (.054-.054-. and 2003-2004 (Paschal et al.091 (. Workers involved in grinding operations that released tungsten metal into the air had elevated urinary levels that Levels of urinary tungsten reflect recent exposure.086) .130 (.074) .484 (.148 (.061-.138 (.078 (.203-.079) .061-.158) .823) .258-.439 (.216-.139) .28) .072-.136 (.087) .082) .431) .085 (. Nicolaou et al.138 (.154) .211 (.216-.086-.267-.199 (.104-.108) .184 (.167) .116-.138) .605) .279 (.215) .139-.426) .079) .078 (.167-.080-.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 .158 (.122 (.143 (.158) .197-.199 (.108-.072 (.109 (.333) .077) .084) .067 (.069 (.214) .431) .059-. population (CDC.176-.136-.064-.253 (.347 (.073 (.439 (.S.240-.096) .095) Selected percentiles ( 95% confidence interval) 50th .077-.117 (.098 (.170-.217-.265 (.071 (.739) .634 (.055-.125 (.092) .126-.079 (..344-.089) .064-.075 (.233-.205-.364 (.168 (.412 (.436-1.056-.294 (.209-.068-.059-.063 (.065-.S.359 (.880) .153) .069-.301) .459) .667) .074) 75th .410-.284) .144 (.136-.080 (.169) .146 (.075-.208-.106 (.237) .174) .078) .093) .150-.090-. A study of 14 unexposed adults yielded values that were similar to the 95th percentiles in this Report.439) Total .070 (. similar to those in this Report (Schramel et al.146 (.091) .315-.(Kraus et al.084) .354-. 2003.272-.082) .065-. population in the NHANES 1999-2000 slightly higher values than those found in NHANES 1999.056-.S.426) .071 (.124 (.082 (. A were more than 900 times higher than the overall geometric nonrandom subsample from NHANES III demonstrated mean of the U.075) .167-.062 (.079) . interval) .339 (.329 (.216-.083) .053-.120) .094) .090-.215 (.180-.317 (.078) .069 (.176-.214-.098-.063-.222-.071 (.074-.300-.354) .085) .353 (. Using neutron activation analysis to 2000.300-.077-.152-. 1997).091 (.358) .157) .187) .582) .049-.146) .261-.293 (.255 (.100) .554) .098-. 2001).727) .063-.333 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.300) .063-.258 (.073 (.088) .077) .275 (.339 (.079 (.155-.383 (.116 (.308) .267) .161) .121-.109-.453) .099-.317-.482 (.231 (..083 (.484) .279 (.439) 1160 1306 1281 1178 1345 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .359 (.308) . 1998).065-.431) .111 (.286-.465) .091) .198) . 2001-2002.555 (.085-.120) .079) .066 (.065) .250 (.206-.059 (.084 (. or exposure that a control group of non-metal workers had mean levels differences.086) .231-.237) .095-.072-.150 (.063-.068 (.797) .153-.253) 95th .392) .080-.299 (.088) . population from the National Health and Nutrition Examination Survey.091) .059-.329-.154) . In whereas the tungsten-worker group had mean urine levels a Nevada community where tungsten was measured and 35 times higher.306) .074 (.538) .103-.317) .381) . (1987) found possibly due to methodologic.333 (.094) .283) .081 (.116) .060-.174 (.326) .060-.167) .073 (.465) .067-.083-.133) .078-.089 (.075-.098) ..250-.179-.130-.379 (.075) .302-.201) .081-.186 (.117) .136-.070 (.086) .143-.071) .067 (.119 (.Metals Workplace air standards for external exposure have been established by ACGIH and recommended by NIOSH.073 (.165) .386) .071-.452-.301) .255-.081) .197) . 2005).066 (.122-.217-.075 (.071) .181 (.080 (.436) .333 (.058-.278-.100 (.216 (.353 (.151 (.333-.074-.093-.087 (.190) .255 (.136-.462) .

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

021-.038 (.018) .046 (.007 (.064 (. and 234U.009-. 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. including nuclear weapons.008-.056) .008 (.013-.008-.011) .054-.016-.046) .018 (.026-.037 (.007-.007-.007 (.009) .016) .026 (.049) .033 (.030 (. population from the National Health and Nutrition Examination Survey.011) .013) .027-.014 (.011) .018-.050) .026 (.007-. and as an aid in electron microscopy and photography.021) .008 (.031 (.028 (.012-.007 (.007-.158) .011-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.036 (.007-. It usually occurs as an oxide and is extracted from ores containing less than 1% natural uranium.010) * .009-.046 (.008 (.023 (. 7440-61-1 General Information Uranium is a silver-white metal that is extremely dense and weakly radioactive.020) .006 (.043) . milling.007-.017-.009 (.012) .013 (.006-.039) .013 (.006-.021) .005-.063) . human exposure occurs primarily by inhaling dust and other small particles.022-.035) .009-.031 (.051) .046 (.017-.006 (.019-. Thus.009 (.015 (.008 (.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 .017-.041 (.023-.017 (.020-.007) 75th .009) .036-.066) .006-.006-.007) .030 (.027) .030-.007 (.012 (.015 (.009-.018) .023-.021) .028 (.031 (.009 (.015-.007-.007 (.009) .006-. DU has been used by the military in armor-piercing ammunition and as a component of protective armor for tanks.017-.007-.036) .009-.010-.007-.72%).008 (.005-.007 (.005-.013) 90th .028-.023 (.009-.010) .036-.042) .009) .023-.008 (.010) .008) .016-.007 (.048) .013 (.007) .009) .041 (.010 (.046-.022) .027-.027) .013 (.034-.020) .037) .012) . 0.007-.012-.008 (.035-.015 (.009) * .023-.011) .042 (.012-.039-.007-.012 (.065) .011) .019-. Variable concentrations of uranium occur naturally in drinking water sources.019-. respectively.030 (.012 (.040) .009) .012-. in some ceramics.014 (.034-.009) .008) .008 (.009 (.009) .006-.023) .010) .006 (.017) .016) .010 (.008-.010) .010 (.007-.027 (.040-.009) .027) .034) .020-.010) .022 (.004.035) . the primary exposure sources for nonoccupationally exposed persons are dietary (especially root vegetables) and drinking water.018) .008-.044 (.067) .006-.036) 883 683 618 568 667 722 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.008 (.010-.036 (.031 (.054) .010 (.088) .008 (.020-.008-.021 (.006-.008 (.026) 95th . 235U (about 0.008) 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 .024-.009) .024 (.010-.032 (.011-.022-.009 (.024-.005.006-.016) .007-.040 (.047 (.040) .010) . nuclear fuel.006 (.062) .026-.009 (.114 (.050) .049) .012 (.015 (.017) .037) Total .011) .026 (.008 (.011) .007 (.012-.015) .029-.013 (. 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.065) .021-.007 (.008 (.045) .007-.011 (.006-.006-.033-.008 (.010) * .007) .037) .014 (.012 (.008-.010) .017) . Since the 1990’s.022-.019-.004.017-.007 (.127) .007) .007 (.052 (.008) .008 (.037-.055 (.027-.046 (.005-.011-.031-.008-.033) .036) .060 (.013-.008) .006-.010 (.029 (.S.008 (.021 (.017) .053) .013 (.011 (.039) .028 (. Natural uranium is a mixture of three isotopes: 238 U (greater than 99%).040 (.027 (.013-.028-.024-.026) .011-.017) .007-.056) .009) .009 (.279) .021 (.020-.007-.009-.007-.010-. interval) . and 03-04 are 0.008-.027) .009) .026) .033 (.014 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.038) .007) .018) .012) .016) .009) Selected percentiles ( 95% confidence interval) 50th .011-.012 (.010) .007-.031 (.016 (.009-.072) .010-.009 (.012) .053 (.069) .016) .009 (.067) .023) .011-.073) .009-.009) .030) .037) .027 (.018 (.008 (.020-.012-. see Data Analysis section) for Survey years 99-00.009-.027 (.016-.016) .025-. and 0. or processing.048 (.008) .011-.045) .014 (.023 (.Metals Uranium CAS No.019 (.014 (.006-.015) .009 (.010-.023) . 01-02.005-.020 (.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 .040-.017-. Fourth National Report on Human Exposure to Environmental Chemicals 239 .054) .017 (.029-. In workplaces that involve uranium mining.043 (.013 (. Uranium has many commercial uses.

009 (.007 (.022-.017-.006) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.018-.010-.007-.012) .026 (.146) .026) .020-.034-.011) * .009) .024 (.027 (.020 (.015 (.007 (.017 (.025 (.013) .034 (.016) .010 (.007 (.019-.014 (.042-..056) .039) .029) .012) .007 (.011 (.006-.025-.029) . 2005).015 (.024) .027) .016 (.067) .004-.006-.007-.013) .007-.007-. 240 Fourth National Report on Human Exposure to Environmental Chemicals .025 (.040 (.016) .008) .009 (.007 (.034 (.006 (.008) .020-.009-.011-.061) .006-.012 (.015) .014-.039) .017 (.005 (.007) .019) .033 (.006-.010-.021 (.033 (.008) .010-.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 .029) .027-. Human health effects from uranium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.031 (.080) .008-.025-.007) .011-.008) .012 (.009) .010) .S.034) .006-.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.013 (.059 (.016) .027 (.005-.058) .028) .006-.013) .042) . the half-life of insoluble uranium in the lungs is several years (Durakovic et al.027-.005-.013 (.1%-6% of an ingested dose may be absorbed.006-.007-.005 (.034 (.053) . Radiation risks from exposure to natural uranium are very low.008) 75th .044) .010 (.014) .007 (.Metals impact.030-.006-.009) .022 (. which can occur occasionally from high occupational exposure.006-.048) .021 (.026-.050 (.015) .027-.035 (.077) .011) .010) .010 (.006-. which represents distribution and excretion.022-.039) .034 (.017-.016) .014-.006-. where limited absorption occurs (less than 5%).005 (.010) .005-. interval) .048) .100 (.006-.008) . 1992). In cases of retained DU shrapnel.010) * .005-.011-.009) .015 (.008 (.008 (.006) . After long term or repeated exposure.004-.006) .037 (.007 (.026 (.029 (.020 (.013-.019 (.010-.047) .017-.009-.024-.010 (.024 (.008) .005-.007 (.006 (.028 (.007 (.014 (. Depending upon the specific compound and solubility.035 (.006-.032) .016) .013 (. 0.016-.006 (.024-.009) .020-.010-.010 (.006-.018 (.011-. liver.030 (.016) .030) .033 (.011-.009) .008) .021 (.028 (.007-.019-.007 (.039) Total .024) .009) .018-.018) .063) .051) .007-.006 (.016-.007 (.013 (.009 (.033 (.007 (.030 (.009-.007 (.051) .028-.006-.020) .006) .005 (.013 (.015-.007 (.028) .016) .009) .006-.017) .034-. kidneys.023-.007 (. After exposure to soluble uranium salts.009) .024-.022 (.270) .020 (.008-.007 (. 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. Soluble forms of uranium salts are poorly absorbed in the gastrointestinal tract.034 (.006-.045 (.012) .006-.009) Selected percentiles ( 95% confidence interval) 50th .022-.017) .006-.031-.015-.020-.010) .008) .006-.007) .051 (.011-.054) .019-.030) .009) .010-.007-.017) .014) 90th .024) .029 (.015-. population from the National Health and Nutrition Examination Survey. Uranium is eliminated in feces and urine.024) .007 (.011 (.006 (.008-.011-.027 (.008) .015-.074) .015 (.015-.043 (.026 (.013 (..009 (. After inhalation.005-.024 (.007 (.030-.053) .009) .008-.021 (.018-.006 (.022) .012 (.019 (.008 (.012 (.030 (.010-.016-. Health effects from uranium exposure result from chemical toxicity to the kidney.010) . about 50% of the absorbed dose is eliminated in the urine within the first 24 hours.025-.058) .010-.027) .027-.012 (.009-.051) .008) .009-..012 (.013 (. with much slower elimination from bone.012 (.008 (.029) .011-.032) .008 (.007 (.019) .008 (.005-. and bones can accumulate uranium with the largest amounts being stored in bones (Li et al.041) .012-.041) 1227 1334 1280 1237 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .007-. the shrapnel acts as a source of chronic.006) .008) .022 (.011-. the initial half-life of uranium is about 15 days (Bhattacharyya et al.006-.008 (. 2003).021-.013 (. low level exposure.008 (.014) . Inhaled uranium-containing particles are retained in the lungs.019 (.007 (.028) .006-.009-.008-.015) .006-.029 (.014) .017-.013 (.008 (.019-.011) .009) * .012-.009 (.007 (.014-.010-.010-.019-.025-.007-.015) .008-.028) .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 .024) .021) .033) .025) 95th .010-.016) .016-.006-.011) .010) .008 (.042) .018-.050) .013 (.018-.050) .

during. Sci Total Environ 1991.55 μg/L (median 0. 2000). Komaromy-Hiller et al. Durakovic A.162 μg/L) (Orloff et al.. In a much larger study of 446 Gulf War veterans who were concerned about past exposure to DU.. population. 1994.65 μg/L). 2002. McDiarmid M. Finding a measurable amount of uranium in urine does not mean that the level of uranium causes an adverse health effect. Boyd P. 2006). 2003..168(8):600-605. Determination of the isotopic composition of uranium in urine by inductively coupled plasma mass spectrometry. urinary levels of uranium were as high as 9. Urinary uranium measurements in 103 Canadian military personnel showed mean urinary levels slightly less than geometric mean in this Report (Ough et al. Biomonitoring studies on levels of uranium provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of uranium than are found in the general population. 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.atsdr. soldiers who had been injured and had embedded DU shrapnel for as long as eight years. IARC and NTP have no ratings for uranium human carcinogenicity.. Byrne AR. although slightly increased during and after deployment. Recent studies of veterans have been conducted to examine concerns about DU exposure during military conflicts. Pullat VR.62:562-566. Dietz LA. Drinking water and other environmental standards have been established by U. (Kurttio et al. Hamilton et al. Health Phys 1992.066 μg/g creatinine (Gwiazda et al.. Third National Report on Human Exposure to Environmental Chemicals. 28 soldiers who may have been exposed to DU by inhalation. Thomas RG.1996.011 μg/L (McDiarmid et al.html. 2006). in that the levels were below their respective detection limits (Byrne et al.110 to 45 μg/L (Ejnik et al.... EPA. Stradling GN. had a mean urinary uranium concentration of 0. Hamilton MM. 2005.. Muggenburg BA. with emphasis on quality control. McDiarmid et al. Vol. Benedik L. 2000). In 17 U.. and 2003-2004 (Dang et al. Eighty-five percent of those levels were above the 95th percentile of the NHANES 1999-2000 population. respectively. Tolmachev et al. Centers for Disease Control and Prevention (CDC). Metivier H. Information about external exposure (i.Metals injury associated with elevated urinary uranium levels (Kurttio et al. A previous nonrandom subsample from NHANES III (n = 499) (Ting et al. Kent (England): Nuclear Technology Publishing. References Bhattacharyya MH. 1-49. 1991. eds. Pillai KC. Biomonitoring Information Levels of urinary uranium reflect recent and accumulated exposure. or wound contamination. Nuclear Regulatory Commission (NRC) has set an action level of 15 μg/L urinary uranium to protect people who are occupationally exposed (U. Fourth National Report on Human Exposure to Environmental Chemicals 241 .078 μg/L (ranging up to 5.S.1992. 2001-2002.. Karpas et al. NRC.e. 2002). 2004).107:143-157. Mil Med 2003. In: Gerber GB. 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.78:143-146. (May et al. 1978). but in whom no shrapnel was embedded. A cohort of 46 U. Squibb K. Dang HS. In a study of 105 persons exposed to natural uranium in well water. Carmichael AJ.S.61 μg/g creatinine. et al. the geometric mean urinary uranium concentration was 0.. Radiation protection dosimetry. Six workers in a depleted uranium program showed concentrations of 0. Health Phys 2000. 1999) and other small populations have shown urinary concentrations that are similar to those in NHANES 1999-2000. the median urinary concentration was 0. Horan P. Breitenstein BD.S. Determining the normal concentration of uranium in urine and application of the data to its biokinetics. soldiers evaluated before. and no consistent effects on multiple endpoints of kidney function were found. urine and hair of exposed and non-exposed persons determined by radiochemical neutron activation analysis. Uranium content of blood.. 41 (1).S. ingestion. Guidebook for the treatment of accidental internal radionuclide contamination of workers.. Volf V. In two studies of a Finnish population with high natural uranium concentrations in their drinking water.S. Older studies have demonstrated urinary uranium concentrations that are consistent with levels in the U. Ejnik JW.cdc. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 2004). Workplace air standards and guidelines for external exposure to soluble and insoluble uranium compounds have been established by OSHA and ACGIH..gov/ toxpro2. 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. 2004). Zimmerman I. The U. pp. 2004). Atlanta (GA). 2006). 2006)... 2006. 1992.S. the median urinary uranium concentration was 2.. In the same study. environmental levels) and health effects is available from ATSDR at: http://www. Galletti.

McDiarmid M. Int Arch Occup Environ Health 2006. Engelhardt SM. Gwiazda RH. Smith D. An examination of uranium levels in Canadian forces personnel who served in the Gulf War and Kosovo. Comparison of representative ranges based on U. Saha H. D’Annibale L. Harmionen A.94:319-326. Radiat Environ Biophys 2005.158:165-190. Auvinen A. patient population and literature reference intervals for urinary trace elements. Roth P. Inductively coupled plasma mass spectrometry as a simple. Orloff KG. Tolmachev S. Oeh U. Washington (DC): NRC. Jarrett JM. Environ Res 2004. Karpas Z. Health Phys 2002. Clin Chim Acta 2000. Hancock RG. Costa R. Environ Res 1999. July 1978. Kuwabara J.S. Katorza E. Health Phys 2004. Oberbroekling KJ.67(8-10):697-714.81:45-51. Noguchi H. Makelainen I. Gucer P. Auvinen A. Saha H. Human exposure to uranium in groundwater. Ejnik J.86:12-18. et al. Wilson PD.S.S. Salonen L. Paschal DC. Am J Kidney Dis 2006.71(6):879-85. Biologic monitoring for urinary uranium in Gulf War I veterans. plasma and urine and a critical evaluation of reference values for the United Kingdom population. Ough EA. Kurttio P. Bennett LG.S. U. Cordero S. Military deployment human exposure assessment: urine total and isotopic uranium sampling results. VI. J Toxicol Environ Health A 2004. McDiarmid MA. Kidney toxicity of ingested uranium from drinking water. and inexpensive method for determination of uranium in urine and fresh water: comparison with LIF.296(1-2):71-90. McDiarmid MA. Sabbioni E. Pirkle JL. Heller J.Metals Galletti M. Komaromy-Hiller G. Metcalf S. et al.110(4):337-342. Kurttio P. Karpas Z. Salonen L. U. Health Phys 2003. Lorber A. rapid. Roiz J. Detection of depleted uranium in urine of veterans from the 1991 Gulf War. Marino R.91(2):144-153. Biokinetic modeling of uranium in man after injection and ingestion. Sci Total Environ 1994. Mistry K. Van der Venne MT.87:51-56. concentration and daily excretion of uranium in urine of Japanese.44:29-40. Biological monitoring and surveillance results of Gulf War I veterans exposed to depleted uranium. Hamilton EI. 242 Fourth National Report on Human Exposure to Environmental Chemicals . Halicz L. Lewis BM. Marko R. et al. Renal effects of uranium in drinking water. Hollriegl V. Nuclear Regulatory Commission (U. Nuclear Regulatory Commission (NRC) Guide 8. Ting BG. Pinto V. Andrews WS. Squibb K. Li WB.22–Bioassay at uranium mills.82(4): 527-532. Uranium daily intake and urinary excretion: a preliminary study in Italy.79(1):11-21. May LM. et al. Oliver M. Komulainen H. Uranium and thorium in urine of United States residents: reference range concentrations. Shelly T. Kalinsky V. Englehardt SA. Paretzke HG. Element reference values in tissues from inhabitants of the European community. Charp P. Ash KO. Jackson RJ. Kane R. Howerton K.47(6):972-982. et al. Scott K. Wahl W. Cremisini C. Squibb K. et al.85:228-235. Sampson EJ. NRC). Pekkanen J. Environ Health Perspect 2002. Review of elements in blood. Health Phys 1996. Health Phys 2004. Health Phys 2006.

00-5.16) 3.87-3.20) 3.0) 9.19 (3.40-6.0-17.50 (8.09) 3.05.90) 5.00-6.70-3.20-12.90-9.70 (3.20-4. see Data Analysis section) for Survey years 01-02 and 03-04 are 0.. and limited applications in pharmaceutics.0) 13.60) 5.40 (3.62 (3.0-29.93-4.20) 4.00) 4.S. 2001-2002 performed on surplus samples (variable unavailable of NHANES website) Fourth National Report on Human Exposure to Environmental Chemicals 243 .0) 8. 2002).0) 14.56) 3.90) 6.50-4.50-3.0) 9. milk.0 (12.50) 3.10 (2.40 (5.50 (3. 2005).00) 5.0) 13.30 (5.0-18.51 (3. population from the National Health and Nutrition Examination Survey.5 hours and has a small estimated volume of distribution (Crump and Gibbs.44-4.0) 12.80) 3.0) 11.10) 5.79 (2.0) 13.80) 12.66) 3.84) 14.11) 4.22-5.93-3.0) 374 314 828 721 1618 1487 01-02 03-04 01-02 03-04 4.0) 13.00) 7.0) 1335 1229 1485 1293 01-02 03-04 01-02 03-04 01-02 03-04 4.0) 13.10 (6.0 (11.40) 2.0) 708 617 681 652 1228 1092 Limit of detection (LOD.90-11.10 (6.80 (7.g.30-17.30 (2.40-13.0 (11.10-11.50) 6.90-11. Animal and human studies have shown that perchlorate can inhibit thyroid hormone production (NAS.30) 6. Other manufactured uses include fireworks.40-4.19-4.0) 13.0-19.47-4.46) 3.40) 4.80-4.54 (3.10 (7.80 (6.0-17.93 (4.0-20.0) 13. or ammonium salt.0 (11.0 (9.60-7.0) 15.0-17.80 (3.10) 5.40 (4.90-10.10) 3.90 (5. Large doses of perchlorate have been used as a medicine to treat hyperthyroidism and to diagnose disorders related to thyroid or iodine metabolism.80-12. and electroplating. lettuce) can be the main sources of intake for humans (FDA.60-6.76 (3.70-5.40 (3.40-7.0 (11.75 (3.50-4.03) 3.00) 3.90-3.40 (5.0) 10.40) 90th 10. EPA’s Contaminant Candidate List (CCL) for drinking water in 1998 following discoveries of its presence in drinking water supplies throughout the southwestern United States (U.0) 9.05 and 0. matches.40) 3.39-4.10-11.0) 19.Perchlorate Perchlorate (Urbansky.70-6.40) 3.67-5..35 (3.45-4.80-15.60 (7.88) 3.51 (3.70-12.0-17.0) 14.30-7.70 (3.20) 7.49-3.0 (11. laboratory analysis.0 (11.07-4.40) 3.30) 6.50-7.22 (2. Perchlorate has been characterized as a mobile and persistent ground and surface water contaminant.20 (8.EPA.60 (4.40 (4.40) 6.20 (2.70-7.10) 3.81-16. 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. 1998). potassium.20 (7.60) 3.0) 15.0 (8.01 (2.20 (5.12) 3. Drinking water.0) 9.70 (3.74-3.20 (2.20-11.90-6.68) 4.10 (5.0-15.50 (5. It is normally found and produced as the anion of a sodium.80) 7.0) 8. 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. interval) 3.20 (6.40-4.18-3. certain catalytic metals.80-8.90-9.90 (4.20 (4.0 (11.0) 95th 14.65) 3.0) 10.32 (3.50-11.0) 10.20-4.70-11.70) 3.38) 5.29-3. In addition.80-4.0 (8.96 (3.70-3.08-3.0 (11. 7601-90-3 General Information Perchlorate is an inorganic chemical containing one chlorine and four oxygen atoms.0-17.0 (9.0 (8.0) 9.02 (3.S.60 (4.0-18.30 (2.50) 11.50) 5.0 (9.0) 11.89-3.0 (9.81) Selected percentiles ( 95% confidence interval) 50th 3. Survey years 01-02 03-04 Geometric mean (95% conf.0) 16.21 (2.90 (2.0 (13.0 (12. small amounts of perchlorate can form naturally in the atmosphere (Dasgupta et al.0 (8.0-15.00-6.30-7. Perchlorate is excreted unchanged from the human body with an estimated elimination half-life of about 7.0-23.55) Sample size 2820 2522 01-02 03-04 01-02 03-04 01-02 03-04 4.0-14.0 (8. 2007).80 (3.31) 2.0 (12. and reducing agents.11) 3. Perchlorate was added to the U.10-4. leather tanning.10) 12.0) 11.0 (11.S.0 (11.05 (2. Perchlorate is stable under most environmental and physiological conditions.0 (9.90 (5.40 (5. 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 (4.30-19.90 (3.60) 8. and certain plants with high water content (e.0) 13.0) 14.90-12.0 (9.50) 5. but has strong oxidant properties in the presence of concentrated acids.20-3.90-3.80-6.10-12.10-7.0-18.00) 3. fabric dyeing.0 (9.0) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites 3.30 (5. 2005).30-6.0 (10.0 (12.70-9.90 (5.75-3.40 (8.80) 75th 6.26 (2.76) 4.0-17.40-5.0) 9.40-11.

Li et al.30) 75th 5.90-11.60) 3.81-3.93-5.33 (7..60 (3.S.51 (3. 2007).29-6. levels.00 (2. medications). However.44) 3.40) 17.30) 3.30-5.32) 5.87) 7.4 (8. Steinmaus et al.30) 90th 9. dietary iodine intake.0) 6.87) 2.26) 4.00-3. 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.80) Selected percentiles ( 95% confidence interval) 50th 3. gender.10) 6.12-2.40 (4.6) 20. 2005).83 (5.84) 2.50 (6.90-15.0 (8.42 (3.25) 5.0) 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 .90-2.20-3.0) 9.0 (11.39-4.20 (4.10-7. 1999.71 (5.90-9.10-3.4 (11.39 (3.73) 3.30-10.21 (2.64) 5.70 (4.05 (4.25) 5. Many factors may be important in consideration of perchlorate action on the thyroid: dose.37-13.50) 2.12 (6.60) 10.20) 3.3-14.41-9.3) 11.S.5) 8.30 (5.90) 5. Follicular cell thyroid tumors would Urinary Perchlorate (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.80 (4.1-14.00) 3.6) 12.14 (2.30-5.70-5. although iodine intake was higher than U.0 (11. congenital hypothyroidism is a condition for which nearly all newborn blood is screened.S.0-44.00 (4. 2005).09 (7.1 (11.60-3. population from the National Health and Nutrition Examination Survey.97-5.60-11.35) 3.61-10.00 (6.39) 2.6-17. urinary perchlorate at environmental exposure levels were inversely associated with thyroxine levels and positively associated with levels of thyroid stimulating hormone (Blount et al.61 (5.0) 12. and the presence of other substances known to affect thyroid function (e.22 (2.S.61-5.74) 7.0) 13.60-8.53 (2.86) 4.90 (7..0) 13. 2002.40-10.30 (6.00) 9.0-14.56-3. Though it produces follicular cell thyroid tumors in animal studies at goitrogenic doses.40) 5..37 (4.44-6.90 (2.33-6.0) 7. 2005.19-10.20-9.45) 3.50-3.22-4.70) 2.87-3. NAS.80 (7.0 (9.40 (3.20-3. nitrate.34-3.0) 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 3.70 (2.60-11.S.0 (9. 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.20 (7.93-8. Short term human studies of the effect of perchlorate on RUI have been used for risk estimation (Greer et al.96) 2. but without effects on serum levels of thyroid stimulating hormone or thyroxine (Braverman et al.50) 9.0) 10.26 (3.03 (2..0) 12.20 (6.67) 5.40 (3. 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.19-6.0-17.89 (2.10 (6. Survey years 01-02 03-04 Geometric mean (95% conf.47) 2.10 (2.24 (4.35 (4..50) 5.50-5.66) 3.3) 12.10 (4.04-3.0-14.7 (11.95 (2.90 (4.10 (4.30 (3.70-15.0) 1335 1220 1483 1284 01-02 03-04 01-02 03-04 01-02 03-04 3.S.20 (3.51-4. 2006.4-16.18-3.70-3.24-2. During gestation and infancy.93) 3.90-20. 2000).75) 3.72 (3.2) 8.70) 10.20 (2.25) 5..60-6. suggesting its tumorgenic effect is a result of a chronic increase in thyroid stimulating hormone indirectly resulting from iodine uptake inhibition.0) 14.35 (2. menopausal status.60-5.99-3.3) 8.90 (2.22-4. In the U.10) 13.0) 12.4) 13.08 (3. levels and sufficient in most participants (Tellez et al.36 (8.08) 3.90-3.0 (10.70 (2. up to 68% RUI has been demonstrated.80-3.43) 6.00-11. U.76-3.50 (3.46-13.04-3. 2002.80-3. Greer et al.60-8.70-4.54 (2.07 (2. age.89-3.87 (5.54 (3. 2005).82 (5.99 (5.98) 3.50) 95th 12..0) 374 313 827 715 1617 1476 01-02 03-04 01-02 03-04 3.10 (1.20-10.1) 8.10) 4.22-6. Lamm and Doemland.20) 8. 2001.09) 3.59) 3.0 (11.45-2. women with urinary levels of iodine less than 100 micrograms per day.93-5.46-4.93-7.1-13..80 (7.0-19.64-3.2) 8.4) 8.8 (11..77 (3..15-12. perchlorate is negative in most genotoxic assays (U.40 (7.5 (13.33-12.41) Sample size 2818 2504 01-02 03-04 01-02 03-04 01-02 03-04 5.EPA. Also.3 (10.0 (9.4 (11.1 (8. thiocyanate.1-22.60-5.50) 2. chronicity of exposure.S.0) 4.46 (3.87 (7.00) 4.16-3. it is known that maternal and congenital hypothyroidism adversely effects neurological development and decreases learning capability.0 (8.1-16.50) 6. 2003.4 (10.56 (3.58) 2.91) 4.76 (3.EPA.00-2.Perchlorate inhibition (RUI). interval) 3. 2002).29) 2.20-4.g.02-4. in a representative sample of U. Lawrence et al.30) 5.02) 3.60) 8. 2005.25 (3.0) 9.52-9.52 (8.10) 3.60-15.40) 3.50-9.0) 12.

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.S. Compared to a previous study of pregnant women in three Chilean communities with varying perchlorate levels in the drinking water. et al. Impact of smoking and thiocyanate on perchlorate and thyroid hormone associations in the 2001-2002 national health and nutrition examination survey. Magnani B. Urinary perchlorate and thyroid hormone levels in adolescent and adult men and women living in the United States. Gibbs JP.S. Li FX. population. epa. The effect of perchlorate. Greer SE. Dyke JV.htm. Biomonitoring Information Urinary perchlorate levels reflect recent exposure. Jackson WA. Pino S. Richman K. Thyroid 2000. CFSAN/Office of Plant & Dairy Foods..113(11):A732. Food and Drug Administration (FDA). National Research Council of the National Academies.110(9):927-937. Daaboul JJ. Doemland M. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Pleus RC. The levels seen in NHANES 20032004 show a similar pattern to NHANES 2001-2002.10(8):659-663. Pirkle JL. J Occup Environ Med 2000. Crump KS.gov/Food/FoodSafety/ FoodContaminantsAdulteration/ChemicalContaminants/ Perchlorate/ucm077653. He X. Perchlorate Exposure of the US Population. When these NHANES 2001-2002 urinary levels of perchlorate are used to calculate daily oral intakes for the U. Braverman LE. Osterloh JD. Li Z. most of the population is considered to be below the U. Thyroid 2001. Environ Sci Technol 2006.S. Long-term environmental exposure to perchlorate through drinking water and thyroid function during Fourth National Report on Human Exposure to Environmental Chemicals 245 . Landingham CB. Lamm S. Erratum in: J Occup Environ Med 2004. Crump KS.Perchlorate be unlikely to occur without overt perturbation of thyroid homeostasis. Cross M. Blount et al. Valentin-Blasini L. The effect of short-term low-dose perchlorate on various aspects of thyroid function. Blount BC.17(4):400-407. Steinmaus C. Caldwell KL. Sesser DE.gov/safewater/ccl/perchlorate/perchlorate.115(9):1333-1338. et al. Miller MD. Abarca CR. Benchmark calculations for perchlorate from three human cohorts. 2001-2002. Chacon PM.114(12):1865-1871.90(2):700-706. Additional information about exposure and health effects is available from the U. Tellez RT. Byrd D. Health Implications of Perchlorate Ingestion. Barnard JC.atsdr.. J Clin Endocrinol Metab 2005.EPA at: http://www. J Occup Environ Med 2003.41(5):409-411. Braverman LE. Valentin-Blasini L. newborn thyroid function. Braverman LE. et al. Lawrence JE. Deyhle GM. et al. Environ Health Perspect 2005.40(21):6608-6614. Lau EC. 2005). Environ Health Perspect 2002. and environmental perchlorate exposure among residents of a Southern California community. 6/2/09 Greer MA. Goodman G. May 2007. National Academy of Sciences (NAS). 2007). J Expo Sci Environ Epidemiol 2007.gov/toxpro2. Dasgupta PK.113(8):10011008. Rutherford GW. Howd R. Mauldin JP. Kirk AB. Lamm SH. Low dose perchlorate (3 mg daily) and thyroid function.html. Lamm SH. Washington (DC): National Academy Press. Environ Health Perspect 2006. Primary congenital hypothyroidism. 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. Perchlorate in the United States. Pirkle JL. (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.42(2):200-205.45(10):1116-1127.. References Blount BC.fda. Page Last Updated: 05/28/2009. thiocyanate.46(5):509. 2005). Buffler PA. 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. Preliminary Estimation of Perchlorate Dietary Exposure Based on FDA 2004/2005 Exploratory Data. Lamm SH.11(3):295. Environ Health Perspect 2007. Lawrence J. Osterloh JD. Available at URL: http://www. Finding a measurable amount of perchlorate in urine does not mean that the level of perchlorate causes an adverse health effect. Analysis of relative source contributions to the food chain. Skeels MR. and nitrate on thyroid function in workers exposed to perchlorate long-term. Has perchlorate in drinking water increased the rate of congenital hypothyroidism? J Occup Environ Med 1999. Also. Neonatal thyroxine level and perchlorate in drinking water. 2005. Health effects assessment for environmental perchlorate contamination: the dose response for inhibition of thyroidal radioiodine uptake in humans. Kelsh MA.html and from ATSDR at: http://www. EPA reference dose (Blount et al. Erratum in: Environ Health Perspect 2005. Blount BC.cdc. Pino S.

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

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

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

Roughly similar levels of PFCs in serum have also been measured previously in other samples of the U. the median PFCs values tend to be roughly similar in these age categories (Olsen et al.S. < LOD means less than the limit of detection.800 (. 2003.400 (<LOD-.. 2003).600-2. see Data Analysis section) for Survey year 03-04 is 0.80) 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 .. reproductive.00) .800 (. or increased cancer rates (Alexander et al. Harada et al..900 (.400-. 2007a. population.S..400) . Cook et al.300 (<LOD-. PFOS.00) .S... 2004).400 (<LOD-. However. PFOS. Olsen et al.. Due to marked intergender differences in the elimination of PFOA in rats and substantial differences in the half-life of PFOA in rats.. Fei et al.300 (<LOD-. Fourth National Report on Human Exposure to Environmental Chemicals 249 .400-1. 2003. and other PFCs have not been classified as to human carcinogenicity by IARC or NTP.700 (. developmental and teratogenic effects were demonstrated in offspring.50) . 1999. Twelve different PFCs were measured in the sera of NHANES 2003-2004 participants. 2007a. Olsen et al. development in offspring was stunted and hypothyroxinemia was observed. In comparing three separate reports on adults. thyroidal).800 (.400-1. 2007b. 2007. Slightly higher levels of PFOS and PFOA in males than females have been noted in several other studies (Calafat et al.400-1.400-1. 2003a). Effects on serum liver enzymes in limited observational studies of human occupational exposures are unclear. 2004. 2003a).80) 640 1454 03-04 03-04 * * < LOD < LOD . 1992.600 (.300-1. EPA. interval) Selected percentiles ( 95% confidence interval) Sample 95th . and humans.500-1. EPA.10) . 2005)..500-3. perfluorohexanesulfonate (PFHxS). At high but non-toxic maternal doses of PFOS.10) * 03-04 03-04 * * < LOD < LOD < LOD . 2003a. and no substantial age trends were seen within adults ages 20-69 (Olsen et al. 2005).900 (. the potential to estimate risks to humans from animal doses is uncertain.40) .800) 1.Perfluorochemicals and testicular tumors in high dose animal testing (Biegel et al.400 (<LOD-. 2003a. animal and human serum PFOA levels have been compared: serum levels associated with toxic effects in animals are 66-11.800 (. 2007b). Two recent cross-sectional human studies observed a negative correlation of birth weight with serum levels of PFOA (Apelberg et al.... 2001. hepatotoxicity.500) .700) . 2004).500) .500) .500-. 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.10) ..500) 90th . Thibodeaux et al.. Serum Perfluorodecanoic acid (PFDeA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U. 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. Lau et al.500 (<LOD-1.. Kennedy et al.500-1.00 (. Olsen et al.10 (. PFOA.500 (.500 (.500) ..600 (.00) .. U.108 times higher than background serum levels in humans (Butenoff et al. Late gestational exposure to PFOS in animal studies has also demonstrated early neonatal lethality.900 (. 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.. and changes in thyroid hormone concentrations (Grasty et al. 2003a. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. U.S. elderly and children.80) 485 538 962 Limit of detection (LOD.500-1.300 (<LOD-. PFOA..400-. 2003).500-1. 2007). 2003).400-1. monkeys. 2004b).800) 1. 2004a. and there was no clear evidence of excess all-cause or diseasespecific mortality. At doses causing maternal toxicity. 2004. In such studies. population from the National Health and Nutrition Examination Survey. 2003. possibly related to lung immaturity (Lau et al. A study of workers chronically exposed to primarily PFOA showed no biochemical evidence of hepatotoxicity or hormonal changes (adrenal..3..600 (. Animal studies of PFOS have demonstrated weight loss. Biomonitoring Information Serum levels of PFCs (particularly PFOA and PFOS) tend to reflect cumulative exposure over several years.20) . Survey Geometric mean (95% conf. which may vary for some chemicals by year and by individual sample.20) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD .

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

which may vary for some chemicals by year and by individual sample.400 (<LOD-.Perfluorochemicals Serum Perfluorododecanoic acid (PFDoA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U. population from the National Health and Nutrition Examination Survey. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.400 (<LOD-.400 (.600) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .S. Survey Geometric mean (95% conf.600) < LOD .500) 485 538 962 Limit of detection (LOD.500) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th < LOD 90th * 03-04 03-04 * * < LOD < LOD < LOD < LOD . < LOD means less than the limit of detection.900) < LOD .500-.300-.300 (<LOD-. Fourth National Report on Human Exposure to Environmental Chemicals 251 . interval) Selected percentiles ( 95% confidence interval) Sample 95th .S.900) < LOD 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD .500 (<LOD-. see Data Analysis section) for Survey year 03-04 is 1. see Data Analysis section) for Survey year 03-04 is 0.0. < LOD means less than the limit of detection. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th < LOD 90th * 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 485 538 962 Limit of detection (LOD. which may vary for some chemicals by year and by individual sample. population from the National Health and Nutrition Examination Survey. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Serum Perfluoroheptanoic acid (PFHpA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.600 (. Survey Geometric mean (95% conf.3.400) .300 (<LOD-.

30 (6.966 (.70-2.20 (1.56-1.60-8.963 (.10-5. Survey Geometric mean (95% conf.09 (.30 (3.40 (1.60 (1.80-2.20) 03-04 03-04 2.10 (1.50 (6.10 (. interval) 1.90) 90th 5.77-2.80) 1.50 (1.80-4.00) 2.30) 3.80-3.0) 1053 1041 03-04 03-04 03-04 1.44 (2.30 (2.10) 1.80 (1.900 (.60-2.900-1.90 (4.50 (6.40 (2.10) 8.90 (1.900 (.80 (1.72 (1.60-4.40) 4.90) 3.40 (1.60) 9.600-.20) 1.50-6.90 (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 1.12) .90) 8. population from the National Health and Nutrition Examination Survey.00-8.721-1.40-1.30-2.08) 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 1.90 (1.50 (1.861 (.00-1.10) 6.90-2.20-1.87-2.54) .10) 75th 1.80) 3. 252 Fourth National Report on Human Exposure to Environmental Chemicals .60) 3.16) Selected percentiles ( 95% confidence interval) Sample 95th 8.70-2.86 (1.00-1.00-7.00-6.834-1.0) 8.10) 75th 3.900-1.Perfluorochemicals Serum Perfluorohexane sulfonic acid (PFHxS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.30) 3.70) 13.60 (6.60) 1.50-10.30) 3.70) 1.697-1.40) 2.700 (.20-2.20 (6. Serum Perfluorononanoic acid (PFNA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.809) 1.10) 4.20 (1.20-3.70) 2.30 (1.826-1.20) 1.900-1.3.60-4.30-12.80-7.30 (2.50-6.93 (1.50 (1.70) 1.40 (1.60 (1.80-3.984 (.04) .30-9.90 (1.50) 6.90-10.62-2.00 (5.6) 7.80-6.70) 2.80-4.912-1.900-1.816-1.S.00 (.900-1.26) 2.40 (1.30 (7.72) 1.20-1.852 (.10-9. interval) .00) 1.90 (1.60-2.40) 640 1454 03-04 03-04 1.30 (1.00 (.1.40) 1.60-3.70) 3.17 (1.10 (.92 (1.91) 2.60-3.10) 5.00 (1.60-7.689 (.80-8.03) 1.80) 5.50 (4.27) 1.00 (1.50) 2.60-2.900-1.30 (1.73-2.30-6. population from the National Health and Nutrition Examination Survey.90) 1.90 (2.00) 1.10 (4.50 (1.80-4.90-19.00 (1. Survey Geometric mean (95% conf.20-1.20) .60 (1.90) 1.700-1.800 (.10) 1.5) 8.80-12.20) 485 538 962 Limit of detection (LOD.51) 1.00 (2.20 (6.900) 1.800-1.10) 6.05-2.70-10.40-3.00 (1.50-3.30) 03-04 03-04 .20-1.14) Selected percentiles ( 95% confidence interval) Sample 95th 3.20 (1.40) 640 1454 03-04 03-04 2.70-6.10-9.80-7.80) 90th 2.30 (1.20) 2. see Data Analysis section) for Survey year 03-04 is 0.60) 2.80 (4.40) .5) 5. see Data Analysis section) for Survey year 03-04 is 0.70-7.30) .14 (.40) 1.50 (4.42 (1.10 (4.50) 2.17-1.10) 4.10 (.3 (9.80-8.70 (2.70-5.10) 1053 1041 03-04 03-04 03-04 .50 (2.S.835-1.00) 3.40-1.1) 485 538 962 Limit of detection (LOD.586-.20 (1.67-2.01 (1.90) 1.16) .80) 4.70 (1.

9-23.3-22.2 (21.70) 3.0-70.30-6.8-78.20 (4.3) 41.00) 3.5 (28.50 (4.7-69.9-38.5) 32.8 (45.9 (17.0) 90th 41.99-3.30 (5. population from the National Health and Nutrition Examination Survey.20) 5.89 (3.4 (23.30-5.4) 56.70) 4. Survey Geometric mean (95% conf.Perfluorochemicals Serum Perfluorooctanoic acid (PFOA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.5) 57.0 (20.90 (5.4 (19.85-4.4 (19.91) 3.0) 485 538 962 Limit of detection (LOD.1 (19.6 (19.07-4.8-22.2) 30.9) 27.2 (16.70-10.00 (3.6-50. population from the National Health and Nutrition Examination Survey.70 (5.20) 5.27) Selected percentiles ( 95% confidence interval) Sample 95th 9.2 (28.50 (3.5-21.47-4.60 (7.0) 21.70-7.80) 8.9) 22.60-13.00 (5.6-45.0) 36.7 (7.1-52.20-5.4-42.8-22.2-22.30) 6.20) 7.2 (18.2) 30.70-5.00 (5.30-3.21-3.5) 18.4-25. interval) 20.95 (3.4.80-9.8-35.20) 7.79) 4.6) 35.1.6) 42.40) 90th 7. interval) 3.0-16.7-23.10) 5.5-62.90-4.1) 57.70 (3.60 (6.3) 42.6) 62.0) 21.67-4.30 (3.60) 8.10-3.82) 4.7-33.3-61.10 (3.8) 46.90) 6.70-9.6 (35.1 (24.8-30.11 (2.5) 7.60 (3.5) 19.40-6. see Data Analysis section) for Survey year 03-04 is 0.90 (7.90 (7.53) 3.30 (3.30-8.4) 75th 30.7 (35.9 (19.80-12.6) 7.5) 8.50-4.20-4.80 (6.7 (35. Serum Perfluorooctane sulfonic acid (PFOS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.18 (3.1) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 4.7-49.9 (13.8 (34.40-17.6-24.9) 22.9 (22.0) 03-04 03-04 19.7 (43.80 (7.50) 4.7 (19.60-14.40 (6.60 (4.6 (44.84-3.7-53.30) 7.60) 03-04 03-04 3.6) 21.9-19.3 (28.3 (35.35) 3.4-17.8) 27.70-7.70) 6.7 (13.2 (19.40-14.3 (17.96 (3.40) 5.1) 15.4) 640 1454 03-04 03-04 23.60 (6.8-81.80 (6.5 (28.27) 4.47 (4.6) 1053 1041 03-04 03-04 03-04 3.1-33.3) Selected percentiles ( 95% confidence interval) Sample 95th 54.10 (3.8-22. see Data Analysis section) for Survey year 03-04 is 0.1-35.1-36.90-4.50-6.20) 4.7-30.4) 21.2) 45.0 (27.3) 485 538 962 Limit of detection (LOD.90 (7.80 (5.37 (2.40 (4.8) 32.5) 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 21.30-11.3 (35.40) 3.40) 75th 5.4) 20.S.20) 10. Survey Geometric mean (95% conf.60 (5.6 (42. Fourth National Report on Human Exposure to Environmental Chemicals 253 .5-23.20-9.90-12.1 (23.50-13.0-20.60-6.4 (17.5) 9.6) 9.1-25.5) 1053 1041 03-04 03-04 03-04 14.60-9.5-33.8 (37.3) 28.0) 23.2 (27.2) 640 1454 03-04 03-04 4.50) 7.3 (44.2-57.0) 43.7) 39.9) 9.4 (28.40-6.7 (43.S.6) 18.20 (4.80-4.1-24.40-10.70 (5.65-4.10 (6.0-66.

300 (.300 (.300 (.300-.300) .500) .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-.200 (<LOD-.S.300) * 03-04 03-04 * * < LOD < LOD < LOD < LOD .300 (.500) .300 (.200-.400) 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD .500) < LOD 485 538 962 Limit of detection (LOD.200-.300 (.2.500) .300 (. 254 Fourth National Report on Human Exposure to Environmental Chemicals .400 (<LOD-.300 (.500) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD . population from the National Health and Nutrition Examination Survey.300 (.4.300-.200-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.300 (.S.200-.Perfluorochemicals Serum Perfluorooctane sulfonamide (PFOSA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U. Survey Geometric mean (95% conf.200-. see Data Analysis section) for Survey year 03-04 is 0.200-. see Data Analysis section) for Survey year 03-04 is 0. Survey Geometric mean (95% conf. which may vary for some chemicals by year and by individual sample.300 (.200-. interval) Selected percentiles ( 95% confidence interval) Sample 95th .300) .300 (.300 (.200-.200-.300) . < LOD means less than the limit of detection.500) 485 538 962 Limit of detection (LOD.300 (. < LOD means less than the limit of detection.300) . population from the National Health and Nutrition Examination Survey. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th < LOD 90th * 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .300) .300) .200-.400) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th 90th . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.300-. which may vary for some chemicals by year and by individual sample.

Survey Geometric mean (95% conf.30 (1.900-1.00 (.700 (<LOD-2. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.30) .700) 90th 1. which may vary for some chemicals by year and by individual sample.600 (<LOD-1.90) .10 (.700 (<LOD-.80) 1. < LOD means less than the limit of detection.600 (<LOD-1.900 (<LOD-1. population from the National Health and Nutrition Examination Survey.6.00 (.10) .20) 1. see Data Analysis section) for Survey year 03-04 is 0.900-1. Fourth National Report on Human Exposure to Environmental Chemicals 255 .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 .3.800) .600 (<LOD-.10-1.600 (<LOD-1.10-1.30) 1.800) .20 (1. which may vary for some chemicals by year and by individual sample.50 (1.10 (.10) .700) .40) 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD .40) < LOD < LOD .900 (. Survey Geometric mean (95% conf.10 (1.10 (.900-1.600) .300 (<LOD-1.30 (1.10) 1.700) 1.S.S.900-1.50) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD 75th . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.500 (<LOD-.700 (<LOD-.10) * 03-04 03-04 * * < LOD < LOD .900) 1.900-1.900-1.10-1.20-1.70) 1.800 (<LOD-.300-2. population from the National Health and Nutrition Examination Survey.80) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD . see Data Analysis section) for Survey year 03-04 is 0.400 (<LOD-.30 (1.10-1.700) 1.400 (<LOD-1.60) 485 538 962 Limit of detection (LOD.40) 1.10-1.00) < LOD .900) .700 (<LOD-.700) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD . interval) Selected percentiles ( 95% confidence interval) Sample 95th .00-1. Serum Perfluoroundecanoic acid (PFUA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.50 (1.700 (<LOD-. < LOD means less than the limit of detection.700 (<LOD-.700 (<LOD-.00 (.300 (<LOD-.60) 640 1454 03-04 03-04 * * < LOD < LOD .900) 485 538 962 Limit of detection (LOD.00 (.80) 1.30) 1.Perfluorochemicals Serum 2-(N-Methyl-perfluorooctane sulfonamido) acetic acid (Me-PFOSA-AcOH) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.10) 1.900-1.

Rogers JM.1968--2003. Cook JC. Environ Sci Technol 2007a. Butenhoff JL. Perfluorooctanesulfonate and related fluorochemicals in human blood from several countries. Moore JA. Perfluorinated chemicals and fetal growth: A study within the Danish National Birth cohort. Grey BE.Perfluorochemicals References Alexander BH. Androgenic deficiency in male rats treated with perfluorodecanoic acid. Keller JM. Kuklenyik Z. Kuklenyik Z. Mortality of employees of a perfluorooctanesulphonyl fluoride manufacturing facility. Kuklenyik Z. Caudill SP. et al. Toxicol Appl Pharmacol 1992. Inoue K. Chemosphere 2006b. Wong LY. Polyfluoroalkyl chemicals in the U. Reidy JA. Yamashita N. Saito N.34(4):351-384. Katakura M. Yun SH.39(3):363-380. Taniyasu S. Mohotti KM. 2007b. Seneviratne HR. brominated. Fluorotelomer alcohol biodegradation yields poly. Harada K. Calafat AM. Renal clearance of perfluorooctane sulfonate and perfluorooctanoate in humans and their species-specific excretion. Corsolini S. et al. Ye Y. Serum concentrations of 11 polyfluoroalkyl compounds in the U.7(4):371-377. et al. Yoshinaga T. Yoshinaga T.115(11):1677-1682. Needham LL. Effects of ammonium perfluorooctanoate on Leydig cell function: in vitro. Perfluorinated compounds in the plasma of loggerhead and Kemp’s ridley sea turtles from the southeastern coast of the United States. Biegel LB. Kennedy GL Jr. Needham LL. sex and geographic factors on levels of perfluorooctanesulfonate and perfluorooctanoate in human serum over the last 25 years. Calafat AM. O’Connor JC. Calafat AM. Toxicol Sci 2001. et al. Kannan K. Environmental and toxicity effects of perfluoroalkylated substances.104(2):322-333. et al.S. Perfluorinated organic compounds in human blood serum and seminal plasma: a study of urban and rural tea worker populations in Sri Lanka. Kudo N. Needham LL. Perkins RG. Bookstaff RC. Crit Rev Toxicol 2004. Kumar KS. Frame SR.40:21282134. Arendt MD. Murray SM. Loganathan BG. et al.S.38(10):2857-2864. Kannan K. Calafat AM. Toxicol Appl Pharmacol 1995.46(2):141-147. Olsen J. Hekster FM.63:490496. Gaylor DW. Temporal trends of PFOS and PFOA in guillemot eggs from the Baltic Sea. Guruge KS. Rev Environ Contam Toxicol 2003. The influence of time. 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. Mandel JH. Chem Biol Interact 2000. Jarnberg U. Burris JM. O’Connor JC. Yamashita N. Olsen GW.39(1):80-84. Environ Res 2005. Grasty RC. Bignert A. Falandysz J. Environ Sci Technol 2006a. Fillmann G. J Environ Monit 2005. Watanabe T. Morikawa A. Fei C. Butenhoff JL. Chlorinated. Environ Health Perspect 2007. de Voogt P. Regul Toxicol Pharmacol 2004. Tarone RE. 256 Fourth National Report on Human Exposure to Environmental Chemicals . Environ Sci Technol 2005.179:99-121. Saito N.and perfluorinated acids. Edwards EA.134(1):18-25. Ingall GB. Inoue K.124(2):119-132. Cord serum concentrations of perfluorooctane sulfonate and perfluorooctanoate in relation to weight and size at birth.41:2237-2242. Aguilar-Villalobos M. Lau CS. Evans TJ. Koizumi A. Cook JC. Herbstman JB. Environ Health Perspect 2007. Tully JS. Reidy JA. Wijeratna S. Hurtt ME. Suzuki E.60(10):722729. population: data from the National Health and Nutrition Examination Survey (NHANES) 2003-2004 and comparisons with NHANES 1999-2000. Caudill SP. Reidy JA. Mabury SA. et al. Mechanisms of extrahepatic tumor induction by peroxisome proliferators in male CD rats. Biegel LB. Kannan K. Holmstrom KE. Kamiyama S.Koizumi A. Environ Sci Technol 2004.38(17):4489-4495. Prenatal window of susceptibility to perfluorooctane sulfonate-induced neonatal mortality in the Sprague-Dawley rat. Environ Sci Technol 2005. Peterson RE.39(23):9057-9063. The toxicology of perfluorooctanoate. Frame SR.115(11):1596-1602.113(2):209-217. Day RD.68(6):465-471. Witter FR. Olsen GW. Environ Sci Technol 2005. Kawashima Y.60(1):44-55. Rodricks J. Perfluorinated chemicals in selected residents of the American continent. and ex vivo studies. Halden RU. J Occup Health 2004. Seacat AM. McLaughlin JK. in vivo. Laane RW.115(11):1670-1676. Moore RW. Kuklenyik Z. Bandai N. Occup Environ Med 2003. population: Data from the National Health and Nutrition Examination Survey (NHANES) 1999–2000. Induction of Leydig cell adenomas by ammonium perfluorooctanoate: a possible endocrine-related mechanism. Taniyasu S. Apelberg BJ. Harada K. Characterization of risk for general population exposure to perfluorooctanoate.39(23):9101-9108. Calafat AM. Environ Health Perspect. Sasaki S. Tully JS. Needham LL. Hurtt ME. Mandel JH. Reidy JA. Liu RC. Cook JC. Dinglasan MJ. Olsen GW. Environ Sci Technol 2004.99(2):253-261. Mandel JS. Toxicol Appl Pharmacol 1990. Birth Defects Res B Dev Reprod Toxicol 2003. Hurtt ME. and perfluorinated contaminants in livers of polar bears from Alaska.

Burris JM. Serum concentrations of perfluorooctanesulfonate and other fluorochemicals in an elderly population from Seattle. and humans from Japan.S. Prevedouros K. Induction of triglyceride accumulation in the liver of rats by perfluorinated fatty acids with different carbon chain lengths: comparison with induction of peroxisomal betaoxidation. Church TR. Sterchele PF. Cousins IT. Ellefson ME. Pepper K. Olsen GW. Huang HY. Olsen GW.111(16):1892-1901. Half-life of serum elimination of perfluoroo ctanesulfonate. 2003. Dietary exposure of Canadians to perfluorinated carboxylates and perfluorooctane sulfonate via consumption of meat. Hansen KJ. Washington. Environ Health Perspect 2003a. Preliminary Risk Assessment of the Developmental Toxicity Associated with Exposure to Perfluorooctanoic Acid and its Salts. Seacat AM. Environ Health Perspect 2005. Grey BE. Gamo T. Hansen KJ. Yamashita N. birds.115(9):1298-1305. Stanton ME. Richards JH. htm.68:105–111. J Occup Environ Med 2003b.74(2):382-392.40(1):32-44. Mandel JH. Barbee BD. Hanson RG.epa. et al. Mar Pollut Bull 2005. Lundberg JK. Rogers JM. Yamashita N. Froehlich JW. A survey of perfluorooctane sulfonate and related perfluorinated organic compounds in water. Church TR. et al. Biol Pharm Bull 2003. 2007a.S. et al. Rogers JM. Olsen GW.37(12):2634-2639. Petrick G. Environmental Protection Agency (U. Subchronic toxicity studies on perfluorooctanesulfonate potassium salt in cynomolgus monkeys. Butenhoff JL. Kannan K.41(9):799-806. J Occup Environ Med 1999. Moisey J. Historical comparison of perfluorooctanesulfonate. Burris JM. Butenhoff JL.198(2):231-241. Peterson RE.51(8-12):658-668. Rogers JM.Perfluorochemicals Kudo N. Lundberg JK. fish. Burris JM.113(5):539-545.. Kannan K.1177(2):183-190. Available from URL: http://www. Butenhoff JL. Mandel JH. Miller JP.111(16):1900) Olsen GW. Thibodeaux JR. Seacat AM. Exposure to perfluorooctane sulfonate during pregnancy in rat and mouse. et al. Coordinate induction of acyl-CoA binding protein. perfluorooctanoate andother fluorochemicals in human blood.82(1):359. J Ag Food Chem 2007. Church TR. Korzeniowski SH. 2003a. Ehresman DJ. Perfluorooctanesulfonate and other fluorochemicals in the serum of American Red Cross adult blood donors. Helzlsouer KJ. Nesbit DJ. Toxicol Sci 2003. and food items prepared in their packaging. Reagen WK.perfluorohexanesulfonate. Hanson RG. EPA). Environ Health Perspect. Toxicol Appl Pharmacol 2004.26(1):47-51. Environ Sci Technol 2003. van Belle G. Kawashima Y. Mair DC. Hansen KJ. Preliminary evidence of a decline in perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) concentrations in American Red Cross blood donors. Case MT. Toxicol Sci 2002. Bronson R. Burlew MM. Exposure to perfluorooctane sulfonate during pregnancy in rat and mouse. Hanari N. A global survey of perfluorinated acids in oceans. Environ Sci Technol 2006. I: maternal and prenatal evaluations. Seymour C. (Erratum in: Toxicol Sci 2004. Butenhoff JL. Biochim Biophys Acta 1993. Taniyasu S.54(11):1599-1611. II: postnatal evaluation. Olsen GW. Butenhoff JL. Horii Y. fish. J Children’s Health 2004b.74(2):369-381. 1/15/06 Vanden Heuvel JP. Lau C. Serum perfluorooctane sulfonate and hepatic and lipid clinical chemistry tests in fluorochemical production employees. Buck RC. Thibodeaux JR. Hansen KJ.68(1):249-264. Olsen GW. Butenhoff JL. Cao XL et al. Hansen KJ. (Erratum in: Environ Health Perspect. et al. Lau C.) Tittlemier SA. Chemosphere 2007b.55:3203-3210.45(3):260-270. fatty acid binding protein and peroxisomal beta-oxidation by peroxisome proliferators. Olsen GW. Larson EB.gov/opptintr/pfoa/pfoara. fast foods. Ehresman DJ. Grey BE. et al. Zobel LR. Sources. Olsen GW. Quantitative evaluation of perfluorooctanesulfonate (PFOS) and other fluorochemicals in the serum of children. Epidemiologic assessment of worker serum perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) concentrations and medical surveillance examinations. Taniyasu S. and perfluorooctanoate in retired fluorochemical production workers.2(1):53-76. fate and transport of perfluorocarboxylates. Olsen GW. Fourth National Report on Human Exposure to Environmental Chemicals 257 . Burris JM. Toxicol Sci 2003. Mandel JH. Chemosphere 2004a. The developmental toxicity of perfluoroalkyl acids and their derivatives. Horii Y. U. Burris JM. Mandel JH. Thomford PJ.

phthalates can be released into the environment during use or disposal of the product. vinyl tiles and flooring.. Harris et al. 2005). and sediments (Clark et al. which are then absorbed (Albro et al. For the general population. 1998. 2001). Jobling et al. 1998).. 2003). There are numerous products that contain phthalates: adhesives... Infants may have relatively greater exposures from ingesting indoor dust containing some phthalates (Clark et al.. 1989). 2003. 1982. Ingested phthalate diesters are initially hydrolyzed in the intestine to the corresponding monoesters. Mortensen et al. not all phthalates Phthalates and Urinary Metabolites in this Report Phthalate name (CAS number) Benzylbutyl phthalate (85-68-7) Dibutyl phthalates (84-74-2) Dicyclohexyl phthalate (84-61-7) Diethyl phthalate (84-66-2) Di-2-ethylhexyl phthalate (117-81-7) Abbreviation BzBP DBP DCHP DEP DEHP Urinary metabolite (CAS number) Mono-benzyl phthalate (2528-16-7) (some mono-n-butyl phthalate) Mono-isobutyl phthalate Mono-n-butyl phthalate (131-70-4) Mono-cyclohexyl phthalate (7517-36-4) Mono-ethyl phthalate (2306-33-4) Mono-2-ethylhexyl phthalate (4376-20-9) Mono-(2-ethyl-5-hydroxyhexyl) phthalate Mono-(2-ethyl-5-oxohexyl) phthalate Mono-(2-ethyl-5-carboxypentyl) phthalate (40809-41-4) Mono-isononyl phthalate Mono-methyl phthalate (4376-18-5) Mono-(3-carboxypropyl) phthalate Mono-n-octyl phthalate (5393-19-1) Abbreviation MBzP MiBP MnBP MCHP MEP MEHP MEHHP MEOHP MECPP MiNP MMP MCPP MOP Di-isononyl phthalate (28553-12-0) Dimethyl phthalate (131-11-3) Di-n-octyl phthalate (117-84-0) DiNP DMP DOP 258 Fourth National Report on Human Exposure to Environmental Chemicals . dermal contact with products that contain phthalates. Various phthalate esters have been measured in specific foods. intravenous medical tubing. 1997. urinary metabolite and air phthalate concentrations are roughly correlated (Liss et al. Nielsen et al. Zacharewski et al. corresponding monoester metabolites. shampoo. some medical devices and pharmaceuticals. followed by inhaling indoor air. plastic raincoats. and teratogenicity. solvents. 1982...... Phthalates are metabolized and excreted quickly and do not accumulate in the body (Anderson et al.... lubricating oils. in humans. Phthalates are also used as solubilizing and stabilizing agents in other applications. The table shows the phthalate diesters.. indoor dust. Because they are not chemically bound to the plastics to which they are added.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. hair spray. 2003). Phthalates are often used in polyvinyl chloride type plastics. water sources. however. automotive plastics. several of the phthalates produced testicular injury. excreted in urine largely as glucuronide conjugates (Albro et al. In vitro studies showed that certain phthalates can bind to estrogen receptors and may have weak estrogenic or anti-estrogenic activity (Coldham et al. 2004. inflatable recreational toys. Absorbed monoester metabolites are usually oxidized in the body and. 1995). Okubo et al.. garden hoses. blood product storage bags. indoor and ambient air. deodorants. In chronic rodent studies. such as soap. such as plastic bags. inhalation. Parks et al. fragrances. 2000. 2006). 1997. 1985. lotions. People are exposed through ingestion. detergents. dietary sources have been considered as the major exposure route. but these effects either have not been demonstrated when tested in non-human primates or are yet to be studied. 1993). and. and nail polish. liver cancer. 2001. and personal-care products. Human milk can be a source of phthalate exposure for nursing infants (Calafat et al. but in vivo studies did not support phthalates having estrogenic effects (Milligan et al. and toys (ATSDR.. 2002). The intravenous or parenteral exposure route can be important in patients undergoing medical procedures involving devices or materials containing phthalates. to a lesser extent. Human health effects from phthalates at low environmental doses or at biomonitored levels from low environmental exposures are unknown. Dirven et al.. Phthalates have low acute animal toxicity. liver injury. and other oxidized metabolites included in this Report.. 1985. Albro and Lavenhar. Pan et al. In settings where workers may be exposed to higher air phthalate concentrations than the general population.

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

Antiandrogenic effects in male rats perinatally exposed to a mixture of di(2-ethylhexyl) phthalate and di(2-ethylhexyl) adipate. Determination of phthalate monoesters in human milk. Duty S. Angerer J. Mortensen GK. The estrogenic activity of phthalate esters in vitro.195:142-153. Hauser R. Brock JW. et al. Available at URL: http://cerhr. Scand J Work Environ Health 1985. Butala JH. Richthoff J. Skerfving S. Lovekamp-Swan T.22(3):688-695. Gans G. 6/2/09 Okubo T. Monograph on the Potential Human Reproductive and Developmental Effects of Butyl Benzyl Phthalate (BBP). Drexler H. Albro PW. gov/chemicals/dehp/dehp-eval. Calafat AM. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Davis BJ.niehs.niehs. Research Triangle Park (NC). Blood burden of di(2-ethylhexylphthalate (DEHP) and its primary metabolite mono(2-ethylhexyl) phthalate (MEHP) in pregnant and non-pregnant rats and marmosets. Jarfelt K. Hanaoka T. J Androl 2004. Am Ind Hyg Assoc J 1985. Numtip W. Occurrence and daily variation of phthalate metabolites in the urine of an adult population. 2000c [online]. Research Triangle Park (NC). Park MG. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction.103:582-587. Sumpter JP. Liss GM. Rylander L. 2000a [online].html. Jacobsen H. A variety of environmentally persistent chemicals including some phthalate plasticizers are weakly estrogenic. Meeker JD.nih. Csanády G. Silva MJ. Andersson A-M. White R. et al. et al. Hagmar L. Boehmer S.16(4):487-493. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. Environ Health Perspect 1997. Monograph on the Potential Human Reproductive and Developmental Effects of Din-Butyl Phthalate (DBP). 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 . Jobling S.html. Stringer WT. Ryan L. Hartle RW.Phthalates in human urine samples. 6/2/09 NTP-CERHR. Pan G. Akesson B. Fromme H.64(8):555-560. Baird DD. Monograph on the Potential Human Reproductive and Developmental Effects of Di(2-ethylhexyl) Phthalate (DEHP). Mechanisms of phthalate ester toxicity in the female reproductive system. Estimation of estrogenic and anti-estrogenic activities of some phthalate diesters and monoesters by MCF-7 cell proliferation assay in vitro. Zhang S. Dalgaard M. Filser J. Wang P. consumer milk. Grote K. David RM. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Hoppin JA. Available at URL: http://cerhr. Urine phthalate determinations as an index of occupational exposure to phthalic anhydride and di (2-ethylhexyl) phthalate. Harris CA.niehs. Phthalate ester exposure—air levels and health of workers processing polyvinylchloride. Draft Update Monograph on the Potential Human Reproductive and Developmental Effects of Di(2-ethylhexyl) Phthalate (DEHP).11(5):381-387. Bolte G. Jonsson BAG. Reynolds T. Balasubramanian AV. Toxicol Appl Pharmacol 2004. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Epidemiol 2005. Research Triangle Park (NC).gov/chemicals/dehp/dehp-eval. Reprod Toxicol 2005. Urinary phthalate metabolites and biomarkers of reproductive function in young men. Chahoud I. Davis BJ. Available at URL: http://cerhr. Int J Hyg Environ Health 2007.html.html. Kalita JC. Milligan SR. Reproducibility of urinary phthalate metabolites in first morning urine samples. Tsukino H. Reprod Toxicol 2004. Sumpter JP. McKee RH. Brock JW.18(1):122. Koch HM. Chen Z. Environ Health Perspect 1998. Leffers H.19(4):505-515. Park S. Environ Health Perspect 1995. 2000b [online]. Temporal variability of urinary phthalate metabolite levels in men of reproductive age [published erratum appears in Environ Health Perspect 2004. Kano K.gov/ chemicals/phthalates/bb-phthalate/bbp-eval. Kessler W. Biol Pharm Bull 2003. Yoshimura M. Ryan L. Main KM. Available at URL: http://cerhr. Meeker JD. 6/2/09 NTP-CERHR.112(17):1740].382:10841092. Skakkebaek NE.nih. Duty SM.nih.25(2):293-302. Borch J.gov/chemicals/ phthalates/dbp/dbp-eval. Hum Reprod 2007. Silva MJ. et al. Hauser R. Ladefoged O. NTP-CERHR. Relative potency of xenobiotic estrogens in an acute in vivo mammalian assay. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. 2006 [online]. Kano I. and infant formula by tandem mass spectrometry (LC-MS-MS). Environ Health Perspect 2003.26(8):1219-24. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Nielsen J. Henttu P.112(17):1734-1740.210:21-33. 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3 (13.2 (19.4) 51.6) 35.8-14.9-14.5-40.0 (14.3-21.9 (21.3 (22.3 (44.7) 23.9 (12.7-119) 99.4) 49.4 (10.7-35.4 (32.9 (28.3-74.9-49.8 (53.6) 67.9-16.5) 65.1) 68.4 (10.3) 23.3-43.1.2) 33.1) 31. and 03-04 are 0.5-36.7 (12.9) 14.1 (32.7-25.0 (15.4) 35.8-14.2) 32.9-47.5 (13.1 (14.2) 78. 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.7-17.1-61.4) 129 (98.2) 69.6-79.9 (22.8 (10.1) 32.3) 94.4) 65.1 (14.2) 66.4) 81.5 (61.0) 34.4 (53. Biomonitoring Information The median levels of MBzP in NHANES subsamples from 1999-2000.7 (11.4-120) 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 13.3-91.1 (13. 2001-2002.2 (14.1-90. NTPCERHR.7-172) 103 (74. 2000).3 (30.6-38.8-98.1-16. 01-02.9) 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 39.6 (41.2) 15.1-120) 52.3-125) Total 15.3-130) 122 (88.8 (80.6) 35.2-17.1) 67..4) 14. 2000).9-28.6-72.8 (38.0 (33.4 (32.2-38.4) 71.Phthalates Benzylbutyl Phthalate CAS No.3 (54.3 (12.8) 63.1 (58.7-16.5 (27.1-214) 166 (116-191) 145 (110-213) 88.2-40.4-16.0 (12.7-16.6) 25.7 (15.8-18. and 2003-2004 were generally similar those reported in U.7 (51. population from the National Health and Nutrition Examination Survey.0 (30. particularly male animals (McKee et al.3) 37.9) 15.8 (30.3-18.6) 29.1-18.4-25. vinyl tile. IARC considers BzBP not classifiable with respect to human carcinogenicity.5) 82.5-62.5 (26.6 (13.5) 23.0 (55.9 (13.2 (19.7-170) 169 (134-198) 152 (99.8) 24.7-15.0-106) 58.9-62.0) 70.3) 13. BzBP can be released into the environment during its production and.4) 80.2 (43.4 (53.3 (29..2-155) 91. and 0.8) 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 16.2-20.0) 24. sealants.8) 14. car care products.4) 38.1 (19.0) 16.1) 12.8-48.9 (70.8-13.1-35.8 (14.2-16.3-12.3-27.1 (10.6) 14.5-33.5-84.4-92.1 (20.8 (71.6-39.6-150) 94.2 (10.7 (80.5 (57.3.1-43.2) 14.3) 54.5-41.4) 33.0 (11.6-43.4-15.8-16.2-115) 113 (91.2 (11.7 (13.4 (59. 0.0 (43.0-130) 101 (86.9 (39.0 (15.1 (55.3-88.4 (29.5-35. including MBzP.8.6) 13.7 (70.5 (66.8-76.5 (47. People exposed to BzBP will excrete mono-benzyl phthalate (MBzP) and small amounts of mono-n-butyl phthalate in their urine.6 (66.4) 108 (96.1) 13. because it is not bound to products in which it is incorporated.2-31.6 (21.5-18.1-15.3 (29.7) 40.2) 17.2 (25.8-17.8-35. and diet is the major source for general population exposure.6) 50.6) 16.0 (20.6) 13.0) 90th 67. it can be released into the ambient air during use or disposal of the products.0 (34. and to a lesser extent. residents (Blount et al.4) 98.1 (13.2) 12.0) 23.9) 18.7-13.3 (33.0 (26.0-55.8 (28.9-190) 86.9-87.5-94.5) 214 (108-399) 235 (183-330) 255 (146-365) 125 (93.6) 95th 103 (94.2-183) 101 (78.2-116) 122 (102-143) 101 (84.5-145) 138 (106-241) 143 (127-179) 120 (99.9) 43.8-121) 79.5) 16.7-58.0 (30.5 (55.8 (71.3) 15. Food crops take up BzBP.S.1) 76.1) 14.2-16.9-30. 262 Fourth National Report on Human Exposure to Environmental Chemicals .9) 13.5-97. 85-68-7 General Information Benzylbutyl phthalate (BzBP) is a solvent and additive used in products such as adhesives.2-39.6 (13.5-14.3) 13.1-38.6-132) 103 (84.5-25.3-18.0) 33.4-24. some personal care products.5) 27.8-64.9 (11.6) 15. can produce developmental and reproductive toxicity in rodents.3) 63.8 (12.4) 12.4 (68.6-18.6 (32.2) 13.4 (31.6 (13.2) 22.4 (13.7-14.8-72.3-82.4 (48.9) 14.8 (21.1-15.8) 28.2 (47.6) 37.3-75.8) 33.4) 35.0-85.5-36.5 (67.0 (23.6) 63.6-116) 122 (102-142) 101 (85.1-39.4) 75th 35.0 (27.6) 24.7) 38.5) 15.5) 55.7 (82.1) 29.4 (27.9) 12. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.8-16.S.3-34.0) 32.6 (53.0-26.5) 30.3 (12.6-92.9) 11.4 (63. see Data Analysis section) for Survey years 99-00.7 (53.9 (16.9-27.4-127) 80.1) Selected percentiles ( 95% confidence interval) 50th 17.2) 14.6) 14.8 (86.6 (13.8-133) 89.2-19. respectively.8-17.6-92.6-17.8-41.6-29.5) 15.9 (12. 2004.1-116) 122 (93.9) 49.1-16.2-33.8 (50.3 (12.3-161) 99.5 (76.0) 20.3-122) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.4-62. interval) 15.7-82.6 (12. High dose BzBP and its monoester metabolites.7-16.

8-14.1-125) 86. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.1) 17.6 (11.8-14.9) 42.3) 14.7 (21.6-81. 2003).9) 12.4-14.7) 11. Hauser et al. 2007).4 (12.3) 13.6 (51.5-23..5-58.8) 108 (75.5) 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 .6 (24.9 (43.8 (10. interval) 14.9 (51.2 (41.3 (15.3) 36. in men attending a Boston infertility clinic (Duty et al. 2005).5-42.3) 37.8-13.1-79.3) 13. 2007).1 (21.0) 11.1-29.6) 25.4-15.0-15.6) 53.0 (49.4-17.1) 39.7) 38.4) 51.2) 26.1 (21.9 (15.6-15.5-13.8) 80.0 (12.3) 16. and females compared to males (Silva et al.8) 26.7-20.5) 16.2) 15.4 (69.5 (42.0) 49.1) 142 (99.4-116) 73.3) 67.5 (35.7-14.8-39.8 (13.7 (18.9 (12.9) 100 (80.9 (55.0-48.7-29.5) 41.4-42.6 (15.7-90.5) 46.4 (25.8-34.7 (11.5) 78.6) 12.3 (38.6-20.1-12.Phthalates York City (Adibi et al.7 (13.1-58.6-40.7 (59.3) 90.9-13.6 (11.3) 13.5-26.9-40. 2005.5 (12.9 (29.9) Total 14. 2003).8 (69.4-23.3 (24.7-15.1 (19.6) 30.7-14. adolescents compared with adults.0-109) 65.6) 38.8-85.4) 50.2-13.4) 14.4 (10.3 (12.5) 23.0-90.4-19.1 (18.2) 11.8 (57.1 (15. the adjusted geometric mean levels of urinary MBzP were significantly higher in several subgroups: children compared to adolescents and adults.0 (33.9 (10.5-38.4-79.1 (9.5) 13.5) 17.9 (54.8-80.7 (12.3-11.4-142) 134 (116-176) 136 (85.0-27.1 (53.1 (25.9-115) 57.4 (11.8) 56.8-69.2-15.6 (36.1) 35..9) 64.3 (13.1) 12.2-13.1-14.9-62.6-99.4 (34. 2004.7-69.9) 12.7 (19.3) 73.1 (43.9 (24.2-26. 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.0) 60.2-78..3-73.4) 90th 50.2) 11.6-26.4) 17.4-60.6 (57.6-12.5-99.7 (11..5-61.6) 75th 25. 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. Hoppin et al.4-27.9) 24.0) 24.0 (62.9 (22.0) 12.8-15.1 (41.3-34.1) 24.1 (21.6-47.6 (11.2) 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 12.0 (11.6-116) 74.1) 23.8 (46.9) 11.1-120) 77.2 (40.0 (41...5 (10.8 (64.7 (38.5-58.4-102) 70.7 (13.2 (56.4 (33.3) 21.7) 25.9) 12. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.0 (38.0) 15.1) 24.8) 46.6 (34.4-93.7-19.3) 14.5 (56.1) 80. 2006). DC reported median urinary MBzP levels that were about twice the levels of adults and females reported in NHANES 1999-2002 (CDC.7) 46..3-16.0-51.5) 14.3 (23.8) 68.7-397) 70.1 (23.1 (11. 2002.0 (13.6) 13.6-86.0) 13.5-31.8) 53. in young Swedish men (Jonsson et al.1-12.4 (46.8-64.0 (41.8-16.4) 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 12.3 (60.8) 33. Urinary Mono-benzyl phthalate (MBzP) (creatinine corrected) Metabolite of Benzylbutyl phthalate (BzBP) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.1 (14.5 (49.0-26.1 (13.1-27.4 (74.8-173) 195 (121-305) 229 (99.5-213) 49.4-18.7 (11.7-56.9-13.9 (15.5-79. 2004).1 (13.2) 11.2-49.5-26.4-14.7 (55.2 (27.8-13.9-23.7-20.8) 16.7) 19.8 (30..3) 29.8) 53. Finding a measurable amount of MBzP in the urine does not mean that the levels of MBzP or the parent compound cause an adverse health effect.0 (10.4-99.3-64.9-69. Weuve et al.6 (30.69-11. median urine levels of MBzP were about one-half the median levels in NHANES subsamples from 1999-2002 (Wittassek et al.7-123) 77. population from the National Health and Nutrition Examination Survey.4) 60.0-53.8) 54.7-19.2) 12.1-35.6 (19.8 (50. A small study of African-American women in Washington.5 (48.4 (13. 2002).7) 56.5-57.9 (9.4) 28.8) 24.8 (12.1 (34.73-12.9 (39.8-42.2 (69.4) 21.4) 104 (89.2) 67.7 (14.8 (11.1) 27.8-60.6) 58.9 (10.3 (35.7-31.5) 20.6-13.6 (14.0) 24.5 (10.4) 25.2-117) 95.3) 12.4 (11.2-21.9 (24.2-15.3-38.8) 71.4 (26.2-12..8) 34. and in a small sample of German residents (Koch et al.4) 13.4-90.3) 18.3) 55.2) 32.5-29.6 (30.2-57.6) 12.0) Selected percentiles ( 95% confidence interval) 50th 13.9-104) 62.1 (21.3) 89.1 (46.3 (39. In an annual sample of German university students.9-28.8-27.4) 44.8 (49..7-12.9-16.5-76.9-83.6) 73.7-61.5-16.8) 11.9) 11.7-15.7 (54.6 (22. In NHANES 1999-2000.4 (63.4 (60.0 (67.9) 52.8) 15.8) 33.8-13.4 (11.5) 10.9-14.S.8-15.4 (21.8-48.7 (23.4) 13.5 (11.7) 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 40.2-51.8) 13.4) 12.0 (12.5) 95th 77.2-17.9 (12.5 (9.4) 15.95-14.

Barr D.68:309-314. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review].S. Reproducibility of urinary phthalate metabolites in first morning urine samples. Silva MJ. Monograph on the Potential Human Reproductive and Developmental Effects of Butyl Benzyl Phthalate (BBP). Exposure to phthalates in neonatal intensive care unit infants: urinary concentrations of monoesters and oxidative metabolites. Drexler H. Int J Hyg Environ Health 2007. Dobler L. Levels of seven urinary phthalate metabolites in a human reference population. Rylander L. Hagmar L. Reprod Toxicol 2004. Giwercman A. David RM. NTP-CERHR.108(10):979-982. Hauser R.18(1):122. Environ Health Perspect 2004.114(9):1424-1431. 2000 [online]. Schettler T. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. Davis BJ. Silva MJ.nih. Singh NP. Hodge CC. Hoppin JA. Poland. et al. Urinary phthalate metabolites and biomarkers of reproductive function in young men.gov/ chemicals/phthalates/bb-phthalate/bbp-eval. Caudill SP. Ryan L. Koch HM. Helm D. Bull Environ Contam Toxicol 2002. Phthalate monoesters levels in the urine of young children. Rossbach B.111(14):1719-1722. et al.html. Duty S. Weuve J. Calafat AM. Available at URL: http://cerhr. Ryan L. Meeker JD. Calafat AM. Barr DB. Environ Health Perspect 2006. Brock JW. Caudill SP.Phthalates References Adibi JJ. Atlanta (GA). Needham LL. Environ Health Perspect 2000. Blount BC. Angerer J. Hilborn ED. Wittassek M. Urinary levels of seven phthalate metabolites in the U. Pirkle JL.112(3):331-338. Perera FP. Chen Z. McKee RH.25(2):293-302.22(3):688-695. Green RA.210(3-4):319-333. Gans G. Camann DE.93:177-185. Hu H. Butala JH. et al. Needham LL. Silva MJ. Wiesmuller GA. Hum Reprod 2007. Internal phthalate exposure over the last two decades—a retrospective human biomonitoring study. et al. et al. Silva MJ. Prenatal exposures to phthalates among women in New York City and Krakow. Jonsson BAG. 2005. Environ Health Perspect 2002. Baird DD. et al. Environ Health Perspect 2003. Brock JW. Sampson EJ. 264 Fourth National Report on Human Exposure to Environmental Chemicals . National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction.110(5):515-518. Brock JW. Environ Res 2003. Duty SM. 112(5):A270]. Research Triangle Park (NC).16(4):487-493. Jacek R. Caudill SP. Sanchez GN. J Androl 2004. 4/20/09 Silva MJ. Epidemiol 2005. Reidy JA.niehs. Richthoff J. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. et al. Eckard R. Jedrychowski W. Malek NA. Third National Report on Human Exposure to Environmental Chemicals. Koch HM. Centers for Disease Control and Prevention (CDC).

20) 4.46 (3.1-17..07 (3.5) 23. 2007).8) 677 652 703 699 1216 1088 Limit of detection (LOD.9-23.5 (11.17) 4.70 (5.80 (5.30-6.25) 01-02 03-04 01-02 03-04 01-02 03-04 4.7-18.5-24.40-3.5-16.0 (13.8 (9.00) 4.90) 12.00-11. Following oral administration of DBP to humans. Compared with the median for 6 to 11 year olds in NHANES 1999-2004 (CDC.4) 22.1-25.5) 18. 2001-2002 and 2003-2004 subsamples were similar to MBP levels reported in U.96) 3.0 (19.6 (14.50 (3.0-38.50) 7.40 (6. 2005).3-43.2-14.6 (11.97) 2.20 (7.55 (3.55) 2.1-20.72-3.00) 10.4-27.2) 5.90 (6.50) 2.0-25. in a small sample of pregnant women in New York City (Adibi et al.5 (17. 2003). Studies of children found age-related differences in urine MBP levels.7) 15.5-16.5-29.60) 3.90-2.1) 16.02) 4.30) 6. When total DBP metabolites have been measured. Fourth National Report on Human Exposure to Environmental Chemicals 265 . 2004.90 (4.9) 10..6) 17.30-13.44-2.00) 4.1) 22.9-14.10-9.10) 8. DBP can produce reproductive toxicity in male rodents (McKee et al.30) 10.7) 14.7 (7. 2001).85-6. see Data Analysis section) for Survey years 01-02 and 03-04 are 1.Phthalates Di-n-butyl Phthalate CAS No.0-18.46-5.40-3.2 (12.80 (5.5 (27. and insecticides.30) 2.56 (5.00) 7.3.70 (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 2.97-7. OSHA has established a workplace air standard for external exposure to DBP.73 (2.30 (4.0) 24. 2000.84) 4. 2000).20-9.3-20.40 (7.10-2.1) 25.10) 9.3-18.3-24.48 (2.3 (19.17 (2.7) 4.6 (10.0) 20.7 (17.94) Selected percentiles ( 95% confidence interval) Sample 95th 17.20-2.50-10.50-6.6 (29.3) 3. Biomonitoring Information Median concentrations reported in the NHANES 19992000.0 and 0.19-3. they have been referred to as monobutyl phthalate (MBP).00-4.60 (5.70) 5. 2003).20-6.56) 3. pharmaceutical coatings.6 (14.33 (2.26 (2.59) 3. mostly as MnBP (Anderson et al. Neither IARC nor NTP has evaluated dibutyl phthalates with respect to human carcinogenicity.0) 13.50) 8.2-22.2 (8.80 (3.10) 2.82-3..00 (7.9) 15. 84-69-5 General Information Dibutyl phthalates (both di-n-butyl and di-isobutyl phthalates.30) 5.6) 10. residents (Blount et al.37) 6.90 (3..10-9.30-2.. 84-74-2 Di-isobutyl Phthalate CAS No.50) 18.0) 393 342 742 729 1647 1534 01-02 03-04 01-02 03-04 2.5) 12... NTP-CERHR.50-2.4 (14.40-5.90-7.30-6.30) 10.4) 12. and in a small sample of Japanese adults (Itoh et al. 2005).6) 16.22 (3.60 (2.9 (16.3 (11.7-31.50) 90th 12.63) 3.3 (13.2 (11.20 (6.70-8.6-34.0 (13.3-30.5) 19.50-4.70) 3.80-5.90-4.40) 5.10 (4.7 (16.4) 5. Small amounts of mono-3-carboxypropyl phthalate are also produced from di-n-butyl phthalate.80-5.6 (10.20-12.6-18.73-5.6) 12.6) 26. exposure to benzylbutyl phthalate (BzBP) will also result in small amounts of mono-n-butyl phthalate appearing in the urine.5) 14.6-26.68 (2.22) 3. the median Urinary Mono-isobutyl phthalate (MiBP) Metabolite of Di-isobutyl phthalate (DBP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.00-9.70-4.3 (18.28-5. and also in some printing inks.30-7. 2004.3) 18.6-14.20) 7.3 (13.40-12.6 (13.40-4.5) 22.1 (8.97) 4.7 (17.7) 7.71 (2.3-48.9 (16.46 (2.4 (20.43) 6. about 65% to 80% of a dose is eliminated in urine within 24 hours.10) 3. 2005.5 (10.40 (2.30 (3.60-6. population from the National Health and Nutrition Examination Survey.S.6 (9.80 (2.91) 4.56 (3.50) 5.40-9. CDC.0) 12.7-31.90-4. Hauser et al. interval) 2.0-14. Survey Geometric mean (95% conf.10 (3..40-17.00-6.60 (8. NIOSH and ACGIH have established guidelines for workplace air exposure to di-n-butyl phthalate.00) 6.S.80) 75th 5. 2005).50 (6.60 (4.4-12.0) 1371 1250 1411 1355 01-02 03-04 01-02 03-04 01-02 03-04 3.7) 18.11-3.81 (3.8) 40.3-19.8) 21.46) 2.40 (2.49-2.0) 9. in men attending a Boston infertility clinic (Duty et al.6) 17. referred to as DBP) are industrial solvents or additives used in many personal care products such as nail polish and cosmetics.24-8.5 (20.3 (16.30-11.00-6.30 (1.10) 11. People exposed to dibutyl phthalates will excrete mono-n-butyl phthalate (MnBP) and mono-isobutyl phthalate (MiBP) in their urine.2-33.6 (13.67 (5.1-12.3 (16.7-20.5) 18.80 (2.40 (3. Koch et al.56-4.0 (11.6-20.20-12.00 (5.6) 16..66) 2.5) 25.1 (13.7 (9. Median MBP levels in two European studies were about two to six times higher than median levels in this Report (Jonsson et al.20 (3.3) 33.90 (4.40-4.30-3.10 (4.70-4. In addition.7 (18.

46 (2.84 (8.81) 4.65-11.51) 15..2) 24.8 (10.1) 10.93-6.3 (13..0) 15.52 (2.57-4.95) 2. the students’ median values for MiBP levels remained relatively unchanged.51) 5.33-9.47-5.2 (10.9) 12.1) 7.96 (3.0 (12.08) 75th 4.17) 90th 8.18 (1.62 (6.33) 3.7) 1371 1250 1411 1355 01-02 03-04 01-02 03-04 01-02 03-04 3.33 (2.75 (4.43) 3.28-13.1) 677 652 703 699 1216 1088 266 Fourth National Report on Human Exposure to Environmental Chemicals . 2006).5 (9.76-3.6 (15. In an analysis of NHANES 1999-2000.76 (3.0) 11.85 (2.61-3.15-4.1) 11.44 (3.39) 5.64-7.67-5.24) 3.47 (3.79-6.68) 5.4) 15.69-7.75 (6.3) 28.98 (2.21 (5..0) 3.1-24. 2004).51) 2.01-2.6 (12.8-18.2 (11.65-4.54 (4.00-3.30 (6.27-12.26-2.2) 8.74 (4.5) 15.34 (3.80-3.0) 7. ranging from more than one-tenth the NHANES median (Itoh et al.09-2.0 (8.1) 13.79-8.7 (9. to about two to fourfold higher (Fromme et al.00) 01-02 03-04 01-02 03-04 01-02 03-04 4.78) 8.76-15.7) 19.43) 3.20 (2.02 (7.38 (6.3 (17.S.6) 11.9 (9.95-3.59 (4.64-7.66) 4.84 (4. 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.35) 3.62-12.36-7.41 (2.6-19..21) 10.53-3.03 (5.99-4.1 (11. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.26 (2.29-3.5-19.38-10.76-3.47-12.8 (8.Phthalates for neonates was lower (by about half) and the median for toddlers was higher (by about sixfold) (Brock et al..18) 3.69 (2.31 (7.15) 3.80 (3.29-8.28 (4.14 (4. up to four and 13 fold.56-15. Between 1998 and 2003.19 (2.83 (2. Studies measuring urinary MnBP have reported variable median values compared to the NHANES 2001-2002 and 2003-2004 subsamples.0 (10.45) 3.3) 13.1-12.8-36.6) 13.89 (3.56) 2.3) 13.0) 393 342 742 729 1647 1534 01-02 03-04 01-02 03-04 2.73) Selected percentiles ( 95% confidence interval) Sample 95th 12.4) 7. respectively.64-10.20 (2. 2002.6 (9.56-4.39-3.30) 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.36-2.89) 6.4 (12.9 (15.57 (3.6 (8.5) 13.86) 6.69) 4.17-12.related differences in the adjusted geometric mean levels of urinary MiBP and MnBP (CDC.2-15.05) 2.31) 2.03-7.6 (8.8-13.7) 3..81 (6.7 (11.46) 3.86-4. Survey Geometric mean (95% conf.25) 5. Weuve et al.32) 7.52-3. 2004). Differences in urinary MBP population estimates by gender have also been shown (Silva et al.4-16.52) 3.6-19.18-10. 2005).33 (3.32 (3.97-2.94 (5.22 (2.7) 11.73 (5.and gender.94-12.72) 5.91-6.78-8.11-2.55-6.8 (9.72-7. interval) 2.53-4.54 (2. 2005).92 (7.4) 23. 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.9-40.11) 5. than adults in NHANES subsamples during the same time period.81 (3.57 (3.94) 6.7-28.04-5.54) 2.02-10.00 (3.1 (10.17 (2.95) 10.07 (2.66) 2.68) 3.3) 16.7) 10.1) 4.58-4. samples from German university students had consistently higher median urine levels of MnBP and MiBP.74-3.58-3.7 (21.18) 4.9 (11.31) 2.82) 4.00-3.20-2. population from the National Health and Nutrition Examination Survey.42) 2.00-7.2-13.6) 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 2.78) 9.3) 18.1-15..88 (2.7 (13.69) 6.5 (11.04) 3.20-3. while MnBP declined (Wittassek et al.81) 9.1) 15.13 (2.07-5. 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.2) 9.8) 10. 2007).10-5.43) 3.32 (7.52-20.89-5.18 (4.0-18.11 (5.53-5.20 (7.20-4.08-2. Over this time.68 (2.6 (10.9-16.37) 3.13-6.1-25.56) 5.03-11.66) 10.8-18.04) 7.82 (4.31 (2.9-26.46-11.65 (4.99) 7. 2007).80) 7.66 (8.18-4. An analysis of NHANES 2001-2002 showed similar age.79 (4.

4) 59. Survey Geometric mean (95% conf.8 (57.1 (62.5-117) 95.7-34.2) 68.2 (78.2-63.1 (28.3-67.5) 21.1) 23.2-21.5) 26.6 (55.5) 20.5-44.2) 26.1-82.9) 29.5) 36.6 (16.1) 19.7 (28.6 (44.1 (17.4) 64.4 (36.6 (65.7 (18.4) Selected percentiles ( 95% confidence interval) Sample 95th 150 (121-169) 108 (94.5 (59.5) 78.0 (31.0-19.3 (23.7 (18.1-22.9-33.4-44.4) 22.6-29.5) 17.5-27.9) 71.5-47.6 (26.0-73.1 (51.2 (21.9) 26.1 (54.3) 21.6-48. concentrations of mono-isobutyl phthalate and mono-n-butyl phthalate were measured together and expressed as a combined value.9) 36.5) 85.6 (61.9 (17.9-79.1-27.1-29.9-101) 77.9-92.5) 24.6-24.3-96.0 (25.7 (51.0) 117 (104-131) 112 (84.6) 71.4) 20.6) 21.6-20.1-75.8) 19.7 (70.8-25.2 (19.1 (18.4-31.4 (38.1-122) 122 (104-137) size 2541 2782 2605 Total years 99-00* 01-02 03-04 50th 26.0 (15.7 (38.9-22.6 (90.2 (18.8-165) 167 (143-197) 138 (110-184) 144 (115-168) 142 (111-161) 107 (89.8) 58.2-24.2) 42.7 (64.9 (17.1) 36.0) 30.3-21.5) 36.3) 23.3 (37.8-29.3) 36.5) 40.3 (17.9) 75.2-159) 92.6) 166 (127-279) 159 (110-290) 191 (150-243) 165 (121-227) 148 (106-185) 134 (110-158) 143 (117-161) 95.6-113) 108 (90.2-114) 73.4-25.5) 47.4 (84.2 (21.1) 31.5) Age group 6-11 years 99-00* 01-02 03-04 99-00* 01-02 03-04 41.3-136) 137 (107-162) 119 (90.6-31.0 (23.8) 23.6) 80.4-18.5-43.2-87.8 (19.7-92.6-40.9) 18.9.9-28.6) 35.1) 47.7 (24.6-33.7) 52.4-26.0 (18. referred to as monobutyl phthalate (MBP).1 (19.4 (25.1-80.1 (26.0) 84.0-24.7-111) 64.4.6 (19.4 (72.2) 62.9-53.4 (35.7 (33.4 (23.1-24.8-123) 101 (90.7 (16.6-37.2-49.5-47.0) 21.9-114) 116 (97.7-53.2 (75.8) 62.7) 42.7 (43.0) 38.3 (42.4-42.5) 31.9) 21.5) 37.7-121) 97.7-20.2-56.5-53.4 (71.1 (41.1 (31.6-44. respectively.7-34.3-40.6-143) 127 (99.8-42.7-42.6 (48.3) 19.1-92.3) 40.8-119) 90.8-22.3) 26.8) 43.2) 32.0-26.6-36.6) 46.1) 25.2-32.0-21.2 (59.3 (30.1 (21.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.5) 19.5 (28.8) 48.1) 46.1 (19.6-49.S.4-60.1 (34.1 (19. *In the 1999-2000 survey period. Fourth National Report on Human Exposure to Environmental Chemicals 267 .3-79.3 (60.3 (23.0) 120 (98.2-93.3 (36.3-85.5 (29.9-42.3-145) 85.2-33.5) 95.1 (36.1) 23.2 (74. population from the National Health and Nutrition Examination Survey.7-91.0) 27.1-20.4 (21.1.4 (35.0-19.2 (25.2 (58.2) 90th 98. interval) 24.8-132) 95.1 (16.6 (22.7 (22.0 (78.8) 75th 51.7 (19.0) 20.7-26.9 (20.5-42. 01-02.9 (79.5 (74.7-116) 95.6-69.0 (30.0-24.0 (36.0 (20.0 (72.5) 34.7-24.7-106) 69.4 (19.3 (30.7) 92.0 (45.6 (32.5 (59.4-20.3 (51.2-22. 1.2 (79.5-60.7) 74.1) 20.1 (19.8-111) 167 (143-223) 121 (106-136) 137 (122-156) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00* 01-02 03-04 99-00* 01-02 03-04 23.2 (17.2) 38. and 0.9) 46.1) 23.3-60.5) 65. and 03-04 are 0.3) 24.9-22.3 (56.1 (58.1) 17.2-23.2 (20.7-117) 118 (108-143) 93.7-42.5 (30.0 (17.3) 18.0-51.5-121) 106 (94.4 (35.6) 20.0-58.7) 124 (98.7-124) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites 99-00* 01-02 03-04 Limits of detection (LOD.6) 39.6) 17. see Data Analysis section) for survey years 99-00.7-127) 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 22.6-29.3-24.1-51.6) 38.9-87.1) 30.3-76.0-32.7) 28.4-159) 107 (84.9 (79.4) 52.4 (35.2) 20.0) 31.

5) 17.9) 28.8-43.5-30.4) 16.0-113) 104 (83.4) 15.3-32.6-139) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00* 01-02 03-04 99-00* 01-02 03-04 21.6-42.4-34.0 (18.6) 34.9-70.9) 52.Phthalates Urinary Mono-n-butyl phthalate (MnBP) (creatinine corrected) Metabolite of Dibutyl phthalate (DBP) and Benzylbutyl phthalate (BzBP) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.2-18.4 (23.4-65.9 (16.6 (27.2-106) 64.8) 22.2-28.2 (38.4 (19.4 (31.1 (34.1) 42.6) 14.5-15.2-85.5) 39.9-14.9) 49.2 (16.7) 42.6-23.7 (12.0 (16.4 (13.4) 53.0) 19.6-43.5 (18.4) Selected percentiles ( 95% confidence interval) Sample 95th 97.7 (19.0-38.9 (56.8) 19.3 (52.1 (46.4 (16.8 (13.7-21.3 (69.9 (37.5 (18.3) 21.6) 37.7-78.3) 18.9-34.3-20. concentrations of mono-isobutyl phthalate and mono-n-butyl phthalate were measured together and expressed as a combined value.1 (56.9-49.0) 81.0 (71.0) 70.4-135) 71.0) 108 (71.9) 62.7 (16.4) 19.7 (14.4 (17.4 (16.3-81.6-155) 91.6) 23.7 (28.0-41.6) 18.9) 24.1 (21.3 (19.8 (16.0) 53.6) 24.0 (52.3-21.1-23.3-106) 74.3-71.5) 134 (93.5-41.9 (73.1-128) 97.4-61.6 (29.6 (31.7) 20.8 (18.8) 30.1-83.6-44.1-32.4-72.0) 94.4 (20.2-48.8 (50.6-50.0-90.3 (17.4 (50.2) Age group 6-11 years 99-00* 01-02 03-04 99-00* 01-02 03-04 41.7-51.3-49.6) 39.7) 19.3) 35.8-23.9 (30.9-105) 85.6-27.5 (81.7-26.5) 21.5-16.8) 23.2-21.5) 82.2 (83.6 (25.9) 30.0) 29.S.6) 65.1 (32.5-23.6-44.0) 41. 268 Fourth National Report on Human Exposure to Environmental Chemicals .2) 31.8) 34.8-24.9 (30.9) 39.6) 64.8) 35.6) 25.9) 91.2-86.0-47.0) 55.4-164) 96.6-22.4-76.1 (61.6-23.2-22.8-32.8-24.2) 21.2) 74.5-142) 89.7-20.7 (60.4-24.7-19.9 (35.5-64.9 (64.9 (58.4-47.7 (54.8) 13.3 (28.6-128) 96.6 (57.1-99.2-27.6-74.8) 63.1) 20.3) 33.1-99.7 (27.9) 20.3) 33.9 (19.3 (42.3-26.7-42.9 (21.0-17.6-24.6 (41.1) 53.3 (76.5-37.4 (31.2) 59.7-39.5) 90th 68.3 (16.2 (35.1) 61.9-36.8) 75th 38.8) 34.2-179) 84.8 (18.3 (24.9-38.3) 19.2) 65.2 (19.1) 44.0 (34.4 (47.3-78.2-22.0) 35.4 (56.6) 31.9 (20.6-32.1) 21.9) 19.0-75.3 (17.9-56.3-17.4) 15.1-18.2-16.0-60.0 (50.3-38.5-22.4 (68.9) 14.9-68.6-26.4 (37.6-16.8) 17.0 (20.0 (26.5 (14.4) 21.6 (25.3 (52.7 (57.1) 35.7-23.8) 17.5 (64.4 (18.5-76.9-26.4 (31.5-142) 81.4-131) 81.9 (39.4) 20.3-23.1) 50.2-108) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites 99-00* 01-02 03-04 *In the 1999-2000 survey period.6-19.8) 17.9 (30.4 (17.1-115) size 2541 2782 2605 Total years 99-00* 01-02 03-04 50th 21.3 (55.0) 26.5-70.9-100) 86.2) 16.1) 37.6 (72.3) 19.8) 20.6) 83.8 (25.6 (74.0) 25.8 (33.3) 20.8 (18.6-28.7) 36.9-84.3-40.8) 28.7 (43.1-21.8-235) 137 (108-198) 88.7-28.6) 24.2) 159 (102-263) 147 (93.8 (17.2 (19.3) 17.7 (73.0 (15.7 (60.6) 38. interval) 22.6-92.3 (21.2-61.3-18.3-114) 328 393 342 752 742 729 1461 1647 1534 12-19 years 20 years and older 99-00* 01-02 03-04 Gender Males 99-00* 01-02 03-04 99-00* 01-02 03-04 17.3) 67.9-68.3) 52.0 (69.7-19.8) 40.1 (15.8 (65. population from the National Health and Nutrition Examination Survey.1) 22.6-53.4) 51.2-22.5) 91.3 (46.6-24.2-73.7-80.0 (18.0) 59.1) 20.8) 20.0) 28.3 (60.3-39.0 (27.6 (17.9 (35.1-62.6 (61.0 (61.3 (48.5 (30.3-21.5) 60.0 (43.4) 62.4 (53.4 (50.1) 17.3) 59.7 (20.8 (22.0 (70. Survey Geometric mean (95% conf.3 (17.5-21.6 (19.5-18.1 (29.3 (71.0 (19.5 (15.0) 75.4 (33.7-37.5) 84.0-19.4-103) 117 (83.4 (45.6-119) 63.7 (81.0-92.

2000 [online]. et al. Perera FP. Barr D. Fourth National Report on Human Exposure to Environmental Chemicals 269 . Chen Z. Angerer J. Yoshida K. Hagmar L. Silva MJ. Ryan L. McKee RH. et al. Needham LL. Exposure to phthalates in neonatal intensive care unit infants: urinary concentrations of monoesters and oxidative metabolites.S. Caudill SP.210(3-4):319-33.16(4):487-493. Drexler H.112(3):331-338. Bolte G. Wittassek M. Third National Report on Human Exposure to Environmental Chemicals. Barr DB. NTP-CERHR. Koch HM. et al. Hodge CC. Meeker JD.18(12):10681074.68:309-314. Silva MJ. Masunaga S. Reidy JA. Hilborn ED. Brock JW. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Caudill SP. Sampson EJ. Hauser R. Available at URL: http://cerhr. Jedrychowski W. Koch HM. et al. Blount BC. Malek NA. Pirkle JL. Calafat AM.niehs. 112(5):A270]. Levels of seven urinary phthalate metabolites in a human reference population. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Food Addit Contam 2001. Ryan L. J Androl 2004. Caudill SP. Environ Health Perspect 2000. Int J Hyg Environ Health 2007. David RM. Wiesmuller GA. Monograph on the Potential Human Reproductive and Developmental Effects of Di-n-Butyl Phthalate (DBP). Sanchez GN. Dobler L. Environ Res 2003.nih.html. et al.208:237-245.210:21-33. Green RA. Prenatal exposures to phthalates among women in New York City and Krakow. Boehmer S. Helm D. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. Silva MJ.114(9):1424-1431. Hum Reprod 2007. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. Urinary levels of seven phthalate metabolites in the U. Research Triangle Park (NC). Evaluation of the effect ofa governmental control of human exposure to two phthalates in Japan using a urinary biomarker approach. Calafat AM. Castle L. Richthoff J. Phthalate monoesters levels in the urine of young children. Reprod Toxicol 2004. Environ Health Perspect 2003. Camann DE.gov/chemicals/ phthalates/dbp/dbp-eval. Hu H. Itoh H. Urinary phthalate metabolites and biomarkers of reproductive function in young men.25(2):293-302. Occurrence and daily variation of phthalate metabolites in the urine of an adult population. Scotter MJ. Fromme H. Duty SM.Phthalates References Adibi JJ. Bull Environ Contam Toxicol 2002. Rylander L. Rossbach B. Duty S. Environ Health Perspect 2006. Drexler H. et al. Weuve J. et al. Singh NP. Butala JH. Epidemiol 2005. Springall C. Centers for Disease Control and Prevention (CDC). Massey RC. Angerer J. Needham LL.93:177-185.22(3):688-695. Brock JW.108(10)979-982. et al. Poland. Giwercman A. Silva MJ. A biomarker approach to measuring human dietary exposure to certain phthalate diesters. Atlanta (GA). Int J Hyg Environ Health 2005. Jonsson BAG. Eckard R. 2005. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Jacek R. Internal phthalate exposure over the last two decades—a retrospective human biomonitoring study.18(1):122. Anderson WA. Environ Health Perspect 2004. Int J Hyg Environ Health 2007. Schettler T. Koch HM. 4/20/09 Silva MJ.111(14):1719-1722. Gans G. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review].

400) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.500) < LOD < LOD .500 (.600) . Finding a measurable amount of MCHP in urine does not mean that the levels of MCHP or the parent compound cause an adverse health effect.400-. 0. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.50) .500) . People exposed to DCHP will excrete mono-cyclohexyl phthalate (MCHP) in their urine.400) < LOD 1.400 (. and polymers. 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. only levels at or above the 90th percentile could be characterized.400) size 2541 2782 2605 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .200-.300-.300-. 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.500 (.400 (.200-.80) .400-.70 (1.600) .500 (.00-3.500 (.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 .200-.400) 1. which may vary for some chemicals by year and by individual sample.400 (.600) .Phthalates Dicyclohexyl Phthalate CAS No.400 (<LOD-. and 0. resins. Urinary Mono-cyclohexyl phthalate (MCHP) Metabolite of Dicyclohexyl phthalate (DCHP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.00 (<LOD-1.00 (<LOD-1. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.500) .70) .200-.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. see Data Analysis section) for Survey years 99-00.600) < LOD .500 (.300-.300-.300 (. and polyvinyl chloride.90) .400-.300 (.300 (.500 (.700) .9.500 (.300) < LOD .200-.500 (.400-. Survey Geometric mean (95% conf.70) .700) .400) < LOD < LOD .10 (. Neither IARC nor NTP has evaluated DCHP with respect to human carcinogenicity.600 (.300-.400 (.50) .300 (.400 (. < LOD means less than the limit of detection.900-1.00) .500 (. population from the National Health and Nutrition Examination Survey.300-. polyvinyl acetate.S.3.10 (<LOD-1.2.500) .200 (<LOD-.10) .300 (. respectively.500) < LOD < LOD .400 (.70 (1.600) . 01-02.600) .400-.300-.00-2.400-.500) < LOD 1.300-.500-.500) .300 (.20) . and 03-04 are 0.300-.00 (<LOD-1.700) .500) 1.200-.10 (<LOD-2.400 (.300) < LOD . including nitrocellulose. 270 Fourth National Report on Human Exposure to Environmental Chemicals .500) 1.400 (<LOD-.300 (.400 (<LOD-.300) 328 393 342 752 742 729 1461 1647 1534 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .400-.500) 1.300 (<LOD-. In this Report.10 (<LOD-1.400) 1. 84-61-7 General Information Dicyclohexyl phthalate (DCHP) is used to stabilize some rubbers.300-.400 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.

170-.82 (1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 3.620) < LOD .410 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.400-.420-.53) .400-.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.43 (1.630 (<LOD-.33) .330 (.770 (.16) .34) .310) < LOD .530 (.14 (<LOD-3.910 (.660) .390 (.560) 1.53) .800-1.660) < LOD < LOD . Survey Geometric mean (95% conf.530) 1.450 (.490) .67 (1.290-.740) .770-1.830) 1.670-1.690) < LOD < LOD .910 (.05) .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 .54-6.330 (.940 (.590 (<LOD-.770) < LOD 2.17) .470) 3.670 (<LOD-.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 1.450 (.240-.36-1.690) < LOD 2.500) 3.250 (.420-.370 (<LOD-.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 .950 (. Fourth National Report on Human Exposure to Environmental Chemicals 271 .00) .S.44) .220 (<LOD-.00 (<LOD-3.06) .500-.530-.380-.33 (<LOD-3.630 (<LOD-.82) .910 (. population from the National Health and Nutrition Examination Survey.770-1.10) .910 (.510 (.360-.500 (.790-1.54) .06) .530-1.690 (.350-.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.740) < LOD < LOD .74) .710) .690-1.18) .770-1.54 (<LOD-2.480 (.11) .270) < LOD .880 (.260-.16 (<LOD-3.590 (.500) size 2541 2782 2605 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .610 (.310-.380 (.470 (.420-.22 (<LOD-1.12-1.510-.

Biomonitoring Information MEP levels in the NHANES 1999-2000. and also in men attending a Boston infertility clinic (Hauser et al.4 (62. 2002). In contrast. 2007).7 (70. and hand lotions. respectively. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. 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. 2003) and African-American women in Washington.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..Phthalates Diethyl Phthalate CAS No. and 0. 272 Fourth National Report on Human Exposure to Environmental Chemicals . deodorants.1 (71.8-111) 85. population from the National Health and Nutrition Examination Survey. Workplace air guidelines for external exposure to DEP have been established by ACGIH and NIOSH. Neither IARC nor NTP has evaluated DEP with respect to human carcinogenicity.. see Data Analysis section) for Survey years 99-00..3-110) 211 (160-278) 197 (159-243) 225 (187-270) 190 (164-219) 191 (171-214) 205 (176-238) 75. 2001-2002.3 (74.4. 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. shampoos.3 (82.1-93.9 (61.2-102) 95. soaps.2. a sample of young Swedish males entering the military had median urinary MEP levels that were somewhat higher than males in the NHANES subsamples. People exposed to DEP eliminate mono-ethyl phthalate (MEP) in their urine.S.5) 81.9-92. particularly those containing fragrances.9. Products that may contain DEP include perfumes. colognes. and 03-04 are 1. 01-02. 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. DC (Hoppin et al.7) 71. 84-66-2 General Information Diethyl phthalate (DEP) is a solvent used in many consumer products. 0.

5-114) 101 (87.2 (66. 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 . population from the National Health and Nutrition Examination Survey.0-117) 142 (119-169) 152 (126-184) 168 (141-201) 179 (161-199) 181 (164-200) 197 (174-223) 79.5-113) 122 (93. the adjusted geometric mean levels of urinary MEP were lower in the group aged 6-11 years than in either of the other age groups.. Finding a measurable amount of MEP in urine does not mean that the levels of MEP or the parent compound cause an adverse health effect. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.. 2004). This age-related trend is opposite the direction seen for other phthalates. 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.6 (77. interval) 163 (149-178) Selected percentiles ( 95% confidence interval) 50th 141 (129-157) 148 (133-162) 153 (137-177) 75th 360 (307-422) 388 (330-435) 452 (386-504) 90th 905 (753-1180) 969 (805-1180) 1110 (889-1290) Total 167 (150-185) 181 (163-202) Sample size 1950 (1670-2310) 2536 1840 (1450-2200) 2782 2040 (1640-2540) 2605 95th Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 92. 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. Analysis of NHANES 2001-2002 showed similar findings.7-110) 81. In an analysis of NHANES 1999-2000. 2003) were slightly lower than levels found in NHANES 2001-2002.S.9-110) 96.6 (65.0 (66. Other population estimates also differed by sex and race ethnicity (Silva et al. 2002). Median MEP levels found in a small sample of German residents (Koch et al.9 (82.3-105) 87. with adjusted geometric mean levels of urinary MEP that increased with age (CDC.Phthalates 2002 (Brock et al. 2005).

Meeker JD. Malek NA. Prenatal exposures to phthalates among women in New York City and Krakow. Hoppin JA. Barr DB. Reidy JA. Barr D.111(14):1719-1722.68:309-314. Environ Res 2003. Hodge CC. Koch HM. Caudill SP. Duty S. Silva MJ. Camann DE. Jacek R. Urinary levels of seven phthalate metabolites in the U. Poland. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. et al. Environ Health Perspect 2004. Angerer J. Drexler H. Silva MJ. Ryan L. Environ Health Perspect 2003. Silva MJ. Hauser R. Baird DD. Third National Report on Human Exposure to Environmental Chemicals. Singh NP. Hum Reprod 2007. Needham LL.S. Perera FP. Phthalate monoesters levels in the urine of young children. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. Centers for Disease Control and Prevention (CDC). Jedrychowski W. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004.93:177-185. Brock JW.112(3):331-338. Rossbach B. 274 Fourth National Report on Human Exposure to Environmental Chemicals .22(3):688-695. Reproducibility of urinary phthalate metabolites in first morning urine samples. 2005. Caudill SP.Phthalates References Adibi JJ. Atlanta (GA). Environ Health Perspect 2002. Brock JW. 112(5):A270]. Davis BJ. Hilborn ED. et al.110(5):515-518. et al. Bull Environ Contam Toxicol 2002.

07-4.4 (21.40-9.0 (9.10 (6.10 (2.40) 8.16-3.3 (15.00 (5.9-29.3-26.50 (3.10-5.5 (20. DEHP present in medical devices and parenteral delivery systems results in the diester rather than the monoester form being directly introduced into the blood.4) 5.30-11.7-58.3-25.30-8.6) 14.2 (10.1 (10.8 (17.23) 3.9) 15.9) 27. population from the National Health and Nutrition Examination Survey.10) 4.5 (12.1 (8.4) 13.4-20.7) 6. 1.7) 22.7 (14.8 (19.15 (1.34 (2.24-4.50 (7.90) 4.9-49.89-3.90 (1.90-5.1) 19.51) 4.40-9.6) 15.90 (4.70-8.90) 4.70 (7. After parenteral administration.50-6.50 (3. mono(2-ethyl-5-oxohexyl) phthalate (MEOHP).5 (24.68 (3.0-19.86) 2.50-20.60) 8. 2002.70 (1.70-2.60 (6.10) 2.50-2.31 (3.00) 19.0) 31. mono-(2-ethyl5-hydroxyhexyl) phthalate (MEHHP) and mono-(2-ethyl5-carboxypentyl) phthalate (MECPP).0) 328 393 342 752 742 729 1461 1647 1534 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 3.00) 2.3-64.9 (13.10 (3.0 (18.0) 11.41) 3.9-26.4-53.03-2. 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.70-6.1) 25.9-19.10-5.44) 4.77 (2.6 (41.70 (8.00 (2. packaging film.30 (3.80) 13.10-11.25-3.3 (24.7-18.5) 23.43 (3.7) 37.70 (3.00) 5.70 (1.50-3.0-84.9-48.27 (3.60) 90th 14.40) 4.9) 5.39) 3.6) 5.70-5.2) 23.9 (7.4) 23.8) 17.0-18.80-4.10-3.5) 31.7-32.7) 18.50-14.10-3.20 (4.75-4.90-8.90) 1.40) 4.5-40.10-11.5-27.4) 33.10) 3.7 (17.70) 7.8-47.0) 23.50 (2.0 (19.S.4-27.90-4.Phthalates Di-2-ethylhexyl Phthalate CAS No. and blood product storage and intravenous delivery systems.1) 29.82) 3. MEHP is primarily formed by the hydrolysis of DEHP in the gastrointestinal tract and then absorbed.10) 3.50 (8.80-8.00 (4.90 (3.2.27) 2.5) 32.00) 1.9 (15.5 (18.49 (3.90-3. Following ingestion.0. 117-81-7 General Information Di-2-ethylhexyl phthalate (DEHP) is primarily used to produce flexibility in plastics.9-28.2 (11.30-6.20 (3.90-11.6-38.79) 2.70 (1.75 (3.19-3. and in humans. and 03-04 are 1.5-17.84-4.10 (3.80 (4.9) 13.83) 2.3) 28.1-27.70) 16. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.0-18.4) 20.92-5.42-5.69) Selected percentiles ( 95% confidence interval) 50th 3.9) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.10-4.60) 3.80-3.9 (16.2) 4.00) 1.8) 15.2) 42.84) 3.10) 8.5 (30.30 (6.6-28.2) 29.40 (4.60)