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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3.2-Dichloroethene Dichloromethane (Methylene chloride) 1.5’.2'.4.5. 75 new chemicals are added for the 2003-2004 survey period and are listed in Table 1.3-Tetramethylbutyl] phenol) Triclosan (2.2-bis[4-Hydroxyphenyl] propane) 4-tert-Octyl phenol (4-[1.2-Dichloroethane (Ethylene dichloride) 1.4’-Trichloro-2’-hydroxyphenyl ether) Non-dioxin-like Polychlorinated Biphenyls 2.3’.5.2-Tetrachloroethane Tetrachloroethene Tetrachloromethane (Carbon tetrachloride) Toluene 1.5.2’.3.4.4'-Tetrabromodiphenyl ether (BDE 66) 2.1.1-Trichloroethane (Methyl chloroform) 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 2.2'.2-Dichloroethene trans-1.5'-Hexabromodiphenyl ether (BDE 153) 2.4'-Tribromodiphenyl ether (BDE 28) 2.4’.and p-Xylene o-Xylene 2 Fourth National Report on Human Exposure to Environmental Chemicals .html.4.4'.4.4'.2'.3.1.4'-Pentabromodiphenyl ether (BDE 85) 2.gov/exposurereport/chemical_selection.2'.1.4'.1.2'.4. Paradichlorobenzene) 1.5'-Tetrachlorobiphenyl (PCB 49) 2.2'.1-Dichloroethene (Vinylidene chloride) cis-1.4'-Tetrabromodiphenyl ether (BDE 47) 2.4.2-Dichloropropane 2.4’.4-Dichlorobenzene (p-Dichlorobenzene.2-Dichlorobenzene (o-Dichlorobenzene) 1.1-Dichloroethane 1.5'-Hexabromobiphenyl (BB 153) Volatile Organic Compounds (VOCs) Benzene Chlorobenzene (Monochlorobenzene) 1.4'.4. 2009 Acrylamide Adducts Acrylamide Glycidamide Total and Speciated Arsenic Arsenic.4.2'.2'4. 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 (2.4.4.4-Tribromodiphenyl ether (BDE 17) 2. Chemicals reported for the first time in the Fourth National Report on Human Exposure to Environmental Chemicals.3'. The process for selection is described at http://www.5'.2-Dibromo-3-chloropropane (DBCP) Dibromomethane 1.2'3.cdc.6'-Hexabromodiphenyl ether (BDE 154) 2.3-Dichlorobenzene (m-Dichlorobenzene) 1.What’s New in this Report What’s New in this Report In this Fourth Report. Table 1.4.2-Trichloroethane Trichloroethene (Trichloroethylene) m.3.6-Heptabromodiphenyl ether (BDE 183) 2.2'.5.5-Dimethylfuran Ethylbenzene Hexachloroethane Methyl-tert-butyl ether (MTBE) Nitrobenzene Styrene 1.4.6.5-Pentabromodiphenyl ether (BDE 99) 2.4'.2.5'-Tetrachlorobiphenyl (PCB 44) 2.2'.6-Pentabromodiphenyl ether (BDE 100) 2.

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

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

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

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

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

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

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

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

FDA. 2005).7) 75th 79.3 (53. such as potatoes and some grains.6-108) 61.8-57.4 (59.1-64. Polyacrylamides are useful water-compatible polymers used in water treatment.6-65. widely distributed in tissues.6-61. Elimination occurs mainly in the urine as mercapturic acid conjugates.2-59.7 (58. but can covalently bind to form adducts with proteins.9 (69. People may be exposed to acrylamide from foods.9-61.9 (54.2 (58.7 (55.1) 62.5-85.1-57. 217 million pounds of acrylamide were produced commercially in the U. In the general population.2 (75. 2006).0-115) 156 (120-203) 146 (129-163) 149 (125-179) 218 (172-271) 197 (172-223) 1792 1874 2994 Limit of detection (LOD.8 (91.9) 75. and an average daily intake is estimated as 0. These estimated intakes are hundreds of times lower than occupational exposures. Natural substances in the food are converted to acrylamide. and in the synthesis or compounding of dye materials. environmental releases of acrylamide can enter aquatic systems and soils where it degrades within days and does not bioaccumulate (U.3) 70.2-114) 163 (147-191) 96..0-58.8 (52.5) 58. it was discovered that acrylamide is formed when starch-rich foods.1 (52.6 (56.0 μg/kg for adults (FAO/ WHO.1 (47.4) 57.1 (88.6-104) 82.2 μg/kg/day (U. Since acrylamide has limited volatility and high water solubility.6) 73. and cosmetics (NTP-CERHR. 1990.0-104) 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 61.6) 71.2) 57. and is either metabolized to the reactive epoxide.4-60.7-64. Fourth National Report on Human Exposure to Environmental Chemicals 11 . EPA.0) 85. acrylamide is synthesized and used in the production of polyacrylamide polymer. and in some cosmetics.7-64. In humans.1) 55. 2006.0. see Data Analysis section) for Survey year 03-04 is 3.2-77.S.5) 66. 2005).7) 73.1 (73.1-61.0-66.8-55.5-80. acrylamide has produced upper airway irritation following inhalation of high levels.3-2.. soil conditioners.2-91. 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.6) 90.7) 58. and peripheral neuropathy following chronic Acrylamide Geometric mean and selected percentiles of hemoglobin adduct concentrations (in pmol/g hemoglobin) for the U.1) 101 (95.3) 63. and binding agents. drinking water.S. Animal studies indicate that acrylamide is well absorbed. as an absorbent in disposable diapers.2-118) 98. 2004.9) 58.7) 54. and well below doses known to cause nerve damage or carcinogenicity in animals.2-93.6-75. smoking.0-49. Survey Geometric mean (95% conf. EPA.6 (51.S. Tareke et al.1) 53. in permanent press fabrics. pulp and paper production.5 (52.4 (54.2) 57.6) 50.4-60.6 (81.1) 46. Acrylamide is not thought to accumulate in the body at environmental doses.5 (74.9-105) 86.3 (55.9) 63.S.5 (79. ocular and dermal irritation from direct contact with acrylamide containing materials.9-52.1 (83. (NTP-CERHR.3) 86.2-67. In 1997. gels. 2005). Fennell et al. FAO/WHO.7) 96.4-83.4-89.4) 100 (89.9) 57. in some sealing grouts.Acrylamide Acrylamide CAS No. 2005.4) 57. population from the National Health and Nutrition Examination Survey. 79-06-1 General Information Acrylamide is a small organic molecule existing as a white crystalline powder in its pure state. Recently.1-64. are heated at temperatures used for frying and baking.8 (57.0) 57. although additional exposures from cosmetic products could add a similar amount (NTP-CERHR. or to glutathione conjugates (Calleman et al.4 (51.6) 90th 141 (124-155) 03-04 03-04 03-04 03-04 03-04 03-04 03-04 59.. the main source of exposure is from the diet.4 (54.9 (60. EPA reference dose of 0.0 (57. interval) 61. 2005). 1994).6-66.4 (53.4) 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 54.0-108) 152 (139-175) 126 (111-142) 108 (86. Smaller scale applications of polyacrylamides include additives to paperboard used for food packaging. 2004).0 (69. and from dermal contact with products that contain residual acrylamide. mineral processing.7-60.S. Commercially.7 (65.8 (81.3-71.4-76.5 (44.0 (67. Estimated intakes in children are about twice that of adults (DiNovi and Howard. 2002).2-70.2 (62.7 (63. 2005).0 (53. glycidamide. but are generally above the U.

.pdf. Biomonitoring Information Acrylamide and glycidamide hemoglobin adducts (AHA and GHA.7) 61.7-62.6 (90. IARC classifies acrylamide as probably carcinogenic to humans. 1997.1-70.3) 85.who.6-64.4-59. 1997. adrenal. glycidamide (NTP-CERHR. male germinal cell injury. Vesper et al. 2005. interval) 59.2) 55.. 2004.1-62.9 (58.4) 46..4-65. thyroid. Acrylamide is clastogenic and can produce dominant lethal mutations. 2005. and other sites) (FAO/WHO. 2005.7 (57. U.3) 59.9 (57.5-66. altered gene expression in testicular tissues (Yang et al. 2001). Additional information is available from U. EPA.1) 56.2-91.7 (84.5 (42. fetal death..9 (81.0 (75. 2003.3 (56. to increase the unscheduled synthesis of DNA in tumor susceptible tissues (Klaunig et al. population from the National Health and Nutrition Examination Survey.4 (61.1 (70.1-60.4 (51.8) 60.9) 59.3) 59. see Data Analysis section) for Survey year 03-04 is 4.2-68.9-62. Klaunig et al.1 (82. 2005.7 (61.7-64.5) 75th 85. Maniere et al.. and neuronal DNA reactivity (Doerge et al. scrotal. Glycidamide Geometric mean and selected percentiles of hemoglobin adduct concentrations (in pmol/g hemoglobin) for the U. 2008). Several of these studies have shown that smokers have adduct levels that are three to fourfold higher than non-smokers. Axonal degeneration.7-86.9) 75.3-78.4-103) 79. dominant lethality).5-92..8) 45. After exposure ceases. 2005. Vesper 2005) and smoking (Bergmark.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. Hagmar et al.4 (81.0.7) 60.2 (72.5-94.0-103) 136 (123-148) 125 (116-135) 126 (119-135) 141 (126-157) 146 (123-169) 187 (169-204) 129 (111-141) 174 (157-197) 159 (143-175) 411 784 1931 2623 1529 3604 3674 03-04 03-04 03-04 64. 2008). Schettgen et al.. U. 2005.4 (90. 2005) have been demonstrated in animals.4) 83. 2006) have been demonstrated after acrylamide dosing. 2009).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 59.1 (57. Rice.. and cancer (mammary. 2005. Puppel et al..8 (51.4 (57.epa. 12 Fourth National Report on Human Exposure to Environmental Chemicals .5-64.5 (83.5 (56. 2002. In addition.7) 90. respectively) are markers of integrated acrylamide exposure over the preceding few months.Acrylamide occupational exposures.S. NTP-CERHR. Younger children may have slightly higher levels possibly due to increased intake of acrylamide-containing foods relative to body size (Dybing et al.1 (66.3) 59.7 (87.6-90.5) 71.7) 74.2) 87.2 (56.. 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.1) 60.. gov/iris/ and from the Food and Agriculture Organization of the United Nations and WHO at: http://www. 2005) and sperm DNA adducts (Xie et al.3-101) 95. most non-smokers had levels less than about 100 pmol/gram hemoglobin.9-138) 143 (130-159) 96.0-93.4) 53.0 (70. 2005. and to increase DNA reactivity when glutathione availability is reduced (Klaunig et al.4-98. Schettgen et al. EPA.5 (59. Puppel et al. EPA at: http://www. presynaptic nerve terminal binding (LoPachin.. although different analytic methods can affect results..8-48. 2002..S. Glycidamide has been shown to react with DNA (Doerge et al. Adducts are formed when either acrylamide or glycidamide react to form a permanent covalent bond with hemoglobin in the blood.9-64.9-77. 2005.9) 65.0) 118 (103-126) 121 (112-134) 113 (94.S. 2005. 2006). reproductive effects (reduced litter size. 2005.2 (63.0 (80.5) 90th 130 (120-141) 03-04 03-04 03-04 03-04 03-04 03-04 03-04 71. levels of AHA adducts decline but may remain detectable for several months (Hagmar et al. 2005).9-76...8-61.8-49.2) 65.4 (56. 2006)..1) 62. 2005). uterine. 2006.6 (66. 2005)..6-62.1-56. AHA levels have been shown to increase with dietary intake (Hagmar et al.. Survey Geometric mean (95% conf. 2004).int/ ipcs/food/jecfa/summaries/summary_report_64_final. Animal studies have shown that acrylamide can cause nerve damage (neuropathy).8 (44.2-90.5) 87. probably through its epoxide metabolite..1 (56.S. Mucci et al.9-78.0) 94.0 (52.0-62. 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.9) 87.

43:365–410. 2/3/09 Hagmar L. February. DNA adducts derived from administration of acrylamide and glycidamide to mice and rats. Haugen M.580(1-2):157-165. Osterman-Golkar S. Wu Y. Wirfalt E. 2004. Mutat Res 2005.85:447-459.580(1-2):119-129. Toxicol 2005. Alexander J. Zhang S. et al. Burgess J.cfsan. 1994).fda.. Italy. and 39% of workers with levels above 1000 pmol/gram hemoglobin had these symptoms (Hagmar et al. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 2006. Adv Exp Med Biol 2005.126(2):361-371. Acrylamide intake through diet and human cancer risk.Toxicol Appl Pharmacol 1994. References Bergmark E. Hagmar L. J Agric Food Chem 2008. Human exposure and internal dose assessments of acrylamide in food. 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.gov/chemicals/ acrylamide/Acrylamide_Monograph. Becher G. Andersen M. AHA levels were several fold to several hundredfold higher than levels in non-exposed non-smokers (Bergmark et al. 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. Duale N. Malmberg B. Mutat Res 2005. LoPachin RM. Calleman CJ. DNA damage and DNA adduct formation in rat tissues following oral administration of acrylamide. Doerge DR.nih. et al. Chem Res Toxicol 1997 Jan. Food Chem. Adv Exp Med Biol 2005. gov/~dms/acrydata. Available at URL: http://cerhr.pdf. Costa LG. 8-17 February 2005. and Research Strategies. Survey data on acrylamide in food: individual food products. Mutat Res 2005. McDaniel LP. The Updated Exposure Assessment for Acrylamide. morphological and molecular endpoints in animal models. symptoms of numbness or tingling in the extremities did not occur in exposed workers whose AHA levels were below 510 pmol/gram hemoglobin. Bruze M.int/ipcs/ food/jecfa/summaries/summary_report_64_final. Joint FAO/WHO Expert Committee on Food Additives. He F. Granath F. Mucci LA. Chem Res Toxicol 1990. Monograph on the Potential Human Reproductive and Developmental Effects of Acrylamide. Toxicol Sci. et al. Kautiainen A. Wilson KM. Cheong HK. NIH Publication No. Differences in hemoglobin adduct levels of acrylamide in the general population with respect to dietary intake.. DiNovi M and Howard D. Maniere I. Bjellaas T. Beland FA. Aprea P. Perez et al. Bridson WE. Bergmark E. Illinois. 6013-6019. Acrylamide is metabolized to glycidamide in the rat: evidence from hemoglobin adduct formation. Hemoglobin adducts of acrylamide and acrylonitrile in laboratory workers. He F. In another study. 64th Meeting: Summary and Conclusions (FAO/WHO). Tornqvist M. Rome. CFSAN/Office of Plant and Dairy Foods. Metabolism and hemoglobin adduct formation of acrylamide in humans. Spicer R. Paulsson B.html#u1004. 2001). 2/3/09 Klaunig JE. Paulsen JE. Fennell TR. Calleman CJ.Acrylamide In occupational settings. Available at URL: http://www. smoking habits and gender. Guffroy M. Snyder RW. Acrylamide neurotoxicity: neurological. Twaddle NC. Axmon A.. Simultaneous analysis of hemoglobin adducts of acrylamide and Fourth National Report on Human Exposure to Environmental Chemicals 13 . 2009 Jan 8. 2004 Acrylamide in Food Workshop: Update Scientific Issues. 2005.561:49-62. July. Determination of hemoglobin adducts in humans occupationally exposed to acrylamide. Tornqvist M.27(4):219-226. 2/3/09 Perez HL.56.pdf. Uncertainties. 1999). [Epub ahead of print] Dybing E. Doerge DR. Summer SCJ. Food and Drug Administration (FDA). Health effects of occupational exposure to acrylamide using hemoglobin adducts as biomarkers of internal dose. 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.3:406-412. Churchwell MI. Available at URL: http://www. Farmer PB. Biomarkers of human exposure to acrylamide and relation to polymorphisms in metabolizing genes. Godard T. Calleman CJ.10(1):78-84.who. Bergmark E. Toxicol Appl Pharmacol 1993. Tian G. Scand J Work Environ Health 2001. Magnusson AL. Laurentie M. 2001.. Rosen I. April 13-15.niehs.580(1-2):131-141.120(1):45-54. Fennell TR. Kamendulis LM.561:21-37. Hagmar et al. Yang JS. smokers and nonsmokers. Nordander C. 1993. et al. et al. 054472. da Costa GG. Bergmark E. Mechanisms of acrylamide induced rodent carcinogenesis. Costa LG. Toxicol Sci 2005. National Toxicology Program. Chicago.. Center for the Evaluation of Risks to Human Reproduction (NTP-CERHR). Churchwell MI. Relationships between biomarkers of exposure and neurological effects in a group of workers exposed to acrylamide.

Chae C.S. Ospina M. Broding HC. Rossbach B. Smith A.epa. et al.163(2):101-8. Lee MH. Ingham L. Drexler H. Hemoglobin adducts of ethylene oxide. Washington (DC). 14 Fourth National Report on Human Exposure to Environmental Chemicals . revised 1/3/06. Han DU. Mutat Res 2005.580(1-2):3-20. A first approach to estimate the internal exposure to acrylamide in smoking and non-smoking adults from Germany. Mutat Res 2005 Feb 7. 2/3/09 Vesper HW. Choi JH. Environmental Protection Agency (U. Vesper HW.S.50(17):4998-5006. Vesper HW. Tornqvist M.561:89-96. acrylonitrile and acrylamide-biomarkers in occupational and environmental medicine. Acrylamide. Adduction of biomacromolecules with acrylamide (AA) in mice at environmental dose levels studied by accelerator mass spectrometry. Angerer J. Available at URL: http://www. Schettgen T. Drexler H. J Agric Food Chem 2008. Int J Hyg Environ Health 2003.S. Pilot study on the impact of potato chips consumption on biomarkers of acrylamide exposure. Myers GL. Rapid Commun Mass Spectrom 2006. EPA). Marko D. Han CH. Available at URL: http://www.gov/chemfact/s_acryla. Xie Q. Fu D. Yang HJ.Acrylamide glycidamide by gas chromatography-mass spectrometry. Adv Exp Med Biol 2005. Reprod Toxicol 2005. Determination of haemoglobin adducts of acrylamide and glycidamide in smoking and non-smoking persons of the general population.207(6):531-9. propylene oxide. 1994. Anal Biochem 1999. Rice JM.htm.134(1-3):65-70. Fueller F. Environmental Protection Agency (U.gov/iris/subst/0286. 2/3/09. Benetou V. Schettgen T. Ding X. Drexler H. Puppel N. Kutting B.20(6):959-64. Tjaden Z.274(1):59-68. a carcinogen formed in heated foodstuffs. J Agric Food Chem 2002. et al. Gray JG. The carcinogenicity of acrylamide. Integrated Risk Information System (IRIS). Eriksson S. Meyers T. Ospina M. Jin Y. Liu K. Angerer J. Int J Hyg Environ Health 2004. Licea-Perez H.206(1):9-14. Toxicol Lett 2006. Schettgen T. Angerer J. Weiss T. Letzel S.56(15):6046-53. Sun H. Analysis of acrylamide.19(4):527-34. Agudo A. Toxicological effects of acrylamide on rat testicular gene expression profile. Lee SH.S. EPA).580(1-2):71-80. Automated method for measuring globin adducts of acrylamide and glycidamide at optimized Edman reaction conditions. Tareke E. Hallmans G. U.epa. Slimani N. DNA strand breaking capacity of acrylamide and glycidamide in mammalian cells. Tjønneland A. Toxicol Lett 2002. Office of Pollution Prevention and Toxics. Meyers T.txt. Cross-sectional study on acrylamide hemoglobin adducts in subpopulations from the European Prospective Investigation into Cancer and Nutrition (EPIC) Study. Liu Y. Rydberg P. U. Chemical Summary for Acrylamide. Karlsson P. September.

96 (1.50-1.087) < LOD < LOD . and various other disorders (U.140-.080-.66) 1.180) .410) .068) .910-1.094) .310-1.630 (.110 (.030-.040 (.540-.050-.310-1.187) .505 (.35 (2.96) 2.160 (.81-2.058 (.570-1.12-4.S.040-.730 (.533-. ear problems.080) < LOD < LOD .20) 1.01 (1.11) .050 (.164 (.44 (1.44) 2.65 (1. acute respiratory illness.44) 2.17) .240 (.163 (.180) .950 (.15 (2.070-.570 (.78) 2.110 (.070) .124 (.087 (.060) .126) .180) .430-1.23 (.99) 2.110-.280 (.726) .57) 2.163) .120) .190-.49) 1.63 (2.43 (1.450-.28-1.230) .480-1. Fourth National Report on Human Exposure to Environmental Chemicals 15 . Children exposed to ETS are at increased risk for sudden infant death syndrome.39 (1.110 (.75) 1.54) size 5999 6819 6320 Total years 99-00 01-02** 03-04 50th .130) . ** In the 2001-2002 survey period.063) . respectively.34 (1.630 (.92 (1.108) * .05.89) 1.310) 90th 1.20 (.084) .180 (.040 (.137-.077) .14-1.660) .030-.350 (.160) .32-2. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.04 (1.020-.990) .630 (.088-.120 (.076-. Survey Geometric mean (95% conf.23 (2.312) .53 (1.052 (<LOD-. Persons exposed to secondhand tobacco smoke (environmental tobacco smoke [ETS]) may have adverse health effects that include lung cancer and coronary heart disease.05) 1.080 (.21-1.260) 1.087-.216 (.30) 2.071) .080-.060 (<LOD-.96-4.050 (<LOD-.050-.175 (. 2004). acute respiratory infections.900-1.920 (.77 (2.350-.086 (.621-1.84-3.120 (.090-.060 (<LOD-.111-. and 03-04 are 0.800 (.154-.770) .070) 75th .066) .470-.50) 3.310) .060 (.93) .213) .88 (1. 83% of measurements had an LOD of 0.106-.Cotinine Cotinine CAS No.142-.110) .22) 2.14) .220) .860 (.400-.047-.02) 1.19) .20) . < LOD means less than the limit of detection.62 (2.234) .580) .625) .145) .62) 2.47-3. 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.260-1.40) .60-2.050) .210 (. see Data Analysis section) for Survey years 99-00.200) 1.950-1.140-.188) .02 (.120 (.120 (.20-2.790) .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 .140 (.63-2.047-.120-.070) .620-1.770-1.95) 1.060-.148-.050 (<LOD-.23-2.500 (.50 (1. DHHS.150) . 2006).12 (1.130 (.38-2.180 (. Cigarettes contain about 1.26-1. 1998).190-.53-4.053 (<LOD-. which may vary for some chemicals by year and by individual sample.14) .54 (1.99) 2. The smoke produced by burning tobacco contains at least 250 chemicals that are toxic or carcinogenic.850 (.30) 2.080 (..075 (.160-.110-.428-.059-.68) .062 (.060-.77 (1.690 (.193) .820) .28) .160 (.710 (.052 (<LOD-.930 (.180) .090-. and more than 50 compounds present in ETS are known or reasonably anticipated to be human carcinogens (NTP.220-.015. 2004). The consequences of smoking and of using smokeless tobacco products are well known and include an increased risk for several types of cancer.137 (.480-.370-.70) 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.139) * .030-.153-.5% nicotine by weight (Kozlowski et al.350-.09-2.360) . and 0.S.066 (.080-.19) 1.19-2.32) 1.48-2.201) .S.060-.77 (1.960-1.050) .12) 1.115-.110 (.620 (.110-.300) .45) 1.66 (1.94) 1.18-3.42-4.120 (.167 (. emphysema.040 (.79) 3.54 (1.30) * .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.220) . DHHS.059-. and 17% had an LOD of 0.144 (.190-.080-.50-4. cardiovascular disease.85 (1.040-.043-.87-3. and exacerbated asthma (U.068) .131 (.070 (<LOD-.180) .23 (1.55 (1.54) 1.073) < LOD .506 (.077) .670) .110 (.520 (.015 ng/mL.09-3.00) .140 (.198) * .740-1.580-1.15) 2.104-.308 (.70-2.770) .840) 3.21 (.12 (2.100-.20 (1.061) < LOD .110) .197) .17 (1.00) 1. maternal exposure during pregnancy can result in lower birth weight.76 (1.050 (<LOD-. stroke.09-3. producing roughly 1–2 mg of bioavailable nicotine per cigarette (Benowitz and Jacob. population from the National Health and Nutrition Examination Survey.090-.030 (.997-3.302) .42 (1.150) .080) < LOD .230 (.16) .066-.02) 1.600-1.510 (.44 (2.990 (.66-3.21-1.054 (.39) 3.83-2.164 (.17 (.580 (.33-2.68) 2.050 (<LOD-. Serum Cotinine Metabolite of nicotine (component of tobacco smoke) Geometric mean and selected percentiles of serum concentrations (in ng/mL) for the non-smoking U.060 (.88 (.089) Age group 3-11 years 99-00 01-02** 03-04 .057-.071 (.120-.540 (.160) .55-2.740-1.320) .22) 2789 3152 2937 3210 3667 3383 Females Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 * .49) 1.160 (.32-2.05 ng/mL.01) 3.48-3.68 (1.

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

population to environmental tobacco smoke: the Third National Health and Nutrition Examination Survey. Giovino GA. Department of Heath and Human Services. Giovino G. et al. Strauss WJ. U.iarc. International Agency for Research on Cancer. U. Kozlowski LT. 4/13/09 International Agency for Research on Cancer. Vol 83. Clin Pharmacol Ther 1994.57(1):79115. Caudill SP. Pirkle JL. Caraballo R. References Armitage AK. Cotinine as a biomarker of environmental tobacco smoke exposure. population to secondhand smoke: 1988-2002.275:1233-1240. JAMA 1996.4:313-316. Atlanta (GA): 2005.63:139-43. 4/13/09 National Cancer Institute (NCI).gov/tcrb/monographs/10/. 1988-1991. Hukkanen J. Herrera B.94(2):314-320. Absorption and metabolism of nicotine from cigarettes. George CF. Fong I.S. Brody DJ.280:152-156. Jacob III P.S. IARC Monogr Eval Carcinog Risks Hum.fr/ENG/Monographs/allmonos90. Lewis PJ.pdf.cdc. Decrease in the prevalence of environmental tobacco smoke exposure in the home during the 1990s in families with children. Racial/ethnic differences in serum cotinine levels among adult U. JAMA 1998. IARC Monogr Eval Carcinog Risks Hum. Pollack HA. 1991. Am J Public Health 2004. Available at URL: http:// cancercontrol. Pharmacol Rev 2005. Aiba M. Maurer KR. U. Flegal KM. 1988-1991. Soliman S. Benowitz NL. The Health Consequences of Smoking: The Surgeon General’s Report—Executive Summary. Tob Control 1998. and the United States. Mehta NY.280:135-140.nih.291(3):1196-1203.php. Jacob P.S. Bernert JT. 4/13/09 U. Tob Control 2006.S.S Department of Health and Human Services (U. Richter PA. [online]. Ethnic differences in N-glucuronidation of nicotine and cotinine. Tobacco Smoke and Involuntary Smoking. Metabolism of nicotine to cotinine studied by a dual stable isotope method.S. J Pharmacol Exp Ther 1999. Respiratory nicotine absorption in non-smoking females during passive smoking. Kira S. 4/13/09 Centers for Disease Control and Prevention (CDC). Pirkle JL. Third National Report on Human Exposure to Environmental Chemicals. Epidemiol Rev 1996. Benowitz NL.niosh. cigarette smokers: the Third National Health and Nutrition Examination Survey. Available at URL: http://www. Int Arch Occup Environ Health 1991. Available at URL: http://ntp. Vol 38. 4/13/09 Iwase A. Tobacco related exposures. Office on Smoking and Health [online] 2006. Metabolism and disposition kinetics of nicotine.S. Sweeney CT.18:188-204. Exposure of the U. Centers for Disease Control and Prevention. Brody DJ. Mowery PD. Pickett MA.56:483-493. Department of Heath and Human Services.114(6):853-858.gov/library/ secondhandsmoke/. Pechacek TF. Jacob P III. 2004. Herrera B. Current Intelligence Bulletin 54: Environmental tobacco smoke in the workplace. Nicotine metabolism and intake in black and white smokers. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Smoking and Tobacco Control Monograph 10 [online]. Available at URL: http://monographs.cancer. Pechacek TF. 4/13/09 Perez-Stable EJ. Coordinating Center for Health Promotion. Jacob P III. DHHS). Jarvis MJ. Summary of Data Reported and Evaluation [online] 2004.gov/eid/rmca/critdocs/ criteriadoc/33. Benowitz NL. National Institute for Occupational Safety and Hygiene (NIOSH). Centers for Disease Control and Prevention. 1999-2002. National Toxicology Program (NTP). Summary of Data Reported and Evaluation [online] 1986. 11th ed. Modin G. Centers for Disease Control.php. Bernert JT. 1999.pdf. the United Kingdom. Environ Health Perspect 2006. Trends in the exposure of nonsmokers in the U. In Report on Carcinogens. DHHS). JAMA 1998. Etzel RA. Perez-Stable EJ. Schober SE.gov/ntp/roc/eleventh/profiles/ s176toba.S Department of Health and Human Services (U. Filter ventilation and nicotine content of tobacco in cigarettes from Canada. Schwartz SS.S. Vogler GP.surgeongeneral. The Health Consequences of Involuntary Exposure to Tobacco Smoke: A Report of the Surgeon General — Executive Summary. Turner DM. Benowitz NL. Health Effects of Exposure to Environmental Tobacco Smoke: The Report of the California Environmental Protection Agency.Cotinine and public health officials determine whether people have been exposed to higher levels of ETS than are found in the general population. Smoke-free laws and secondhand smoke exposure in US nonsmoking adults. BMJ 1975. Coordinating Center for Health Promotion. et al. Sosnoff CS.niehs. Benowitz NL. Warner K. Tobacco Smoke. Houseman TH.7:369-375. June.fr/ENG/Monographs/ allmonos90. available at URL: http://mtn. Dollery CT. iarc. National Center for Chronic Disease Prevention and Health Promotion.15:302-307. Curtin LR. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Biomonitoring data can also help scientists plan and conduct research about exposure to ETS and about its health effects. National Center for Fourth National Report on Human Exposure to Environmental Chemicals 17 . Available at URL: http://monographs.

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

130-.N-diethyl-meta-toluamide (DEET) is an insect repellent that was first marketed in 1957. DEET is not registered for use on agricultural commodities. but higher DEET concentrations and different formulations may result in greater absorption (Sudakin and Trevathan. Its use is recommended for prevention of several vector-borne diseases. DEET is metabolized via hydroxylation and dealkylation pathways and eliminated in the urine within approximately 24 hours (Selim et al. People in outdoor occupations may apply DEET more frequently or use higher concentration formulations resulting in higher levels of exposure.210) 480 580 672 829 825 1126 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . see Data Analysis section) for Survey years 99-00 and 01-02 are 0.S. 2003).160) < LOD .520) < LOD . Most reports of adverse effects from overexposure to DEET involve skin reactions (Bell et al.epa.100-. have been reported as result of self-poisoning by ingestion or excessive dermal application. There are over 225 insect repellents brands containing DEET. DEET can be applied to clothing and the skin to repel biting insects. 1995.. (Kolpin et al. 134-62-3 General Information N. Fourth National Report on Human Exposure to Environmental Chemicals 19 . DEET is not genotoxic. < LOD means less than the limit of detection. DEET is not a developmental or reproductive toxicant in animals (U.110-.110 (. 2002).130) < LOD .EPA.S.180 (.150) < LOD . Human health effects from DEET at low environmental doses or at biomonitored levels from low environmental exposures are unknown.140 (.100-.N-Diethyl-meta-toluamide (DEET) N.1. EPA.EPA. which may vary for some chemicals by year and by individual sample. After absorption..140) < LOD .220) size 1977 2535 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD 90th .S.120-.170 (. 2003).180) < LOD .100-. General population exposure to DEET occurs from skin application and from inhalation of aerosol formulations.N-Diethyl-meta-toluamide (DEET) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. and it has not been rated by IARC or NTP with respect to human carcinogenicity.S.130-.S. One survey detected DEET in 74% of sampled streams in the U.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 .EPA at: http://www.110 (<LOD-.130 (. population from the National Health and Nutrition Examination Survey. 2002).130) < LOD .N.250) < LOD . 2005).130 (. Urinary N.110 (.100-. Sudakin and Trevathan.130 (.100-. Survey Geometric mean (95% conf.. About 3-8% of dermally applied DEET is absorbed.S.140) < LOD .130-. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD .140) < LOD . DEET has low acute toxicity.210 (. Additional information is available from U.180 (. DEET is also used in combination with dermal sun screens (U.130-. (U. Exposure can also occur from consuming food contaminated by DEET on hands or that was sprayed nearby. including seizures and encephalopathy.270) 688 678 518 700 598 956 Limit of detection (LOD.180 (.449 and 0.140-. Neurological effects in humans.110 (<LOD-.240) < 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 .220 (. and they range in concentration from 4% to 100%.gov/pesticides/.190) < LOD .100 (<LOD-.N-Diethyl-meta-toluamide (DEET) CAS No. 1998). 1998).560) < LOD .110 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.170 (.100-.110-.110 (.120-.

270) < LOD .190 (<LOD-.320) < LOD .350-.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 .550) 688 678 518 699 598 956 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.270-.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 .500) 480 580 672 828 825 1126 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . 1992).390-. Urinary N.250) < LOD .230) < LOD .S.N-Diethyl-meta-toluamide (DEET) Biomonitoring Information Urinary levels of DEET reflect recent exposure.410-.500 (.630) < LOD . DEET was detected in 10% of 60 Latino children in eastern North Carolina farm worker households (Arcury et al.240-.270 (<LOD-.640 (.150) < LOD .690 µg/L were measured in eight park employees who applied 71% DEET once a day (Smallwood et al.140-. representative subsamples from NHANES 2001-2002. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.300 (.440) < LOD .250-. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD . 20 Fourth National Report on Human Exposure to Environmental Chemicals . Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.93) < LOD .330 (.200 (.480 (.150-.280 (. Finding a measurable amount of DEET in urine does not mean that the level of DEET causes an adverse health effect.250 (.230-.350) < LOD .N-Diethyl-meta-toluamide (DEET) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.370) < LOD .290-.490) < LOD .370-. 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.320 (.190 (.130 (<LOD-. Urinary DEET levels as high as 5.190-. population from the National Health and Nutrition Examination Survey.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 .N.330 (.170-.350) < LOD .270 (.230-.280-1. In this survey period. Urinary levels of DEET were characterized only at the 90th and 95th percentiles of the U.240) < LOD . 2007).410 (.410 (. 2005).190 (. the limit of detection was lower than for the NHANES 1999-2000 survey period (CDC..S. Survey Geometric mean (95% conf..

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

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

K. Wong LY. Chem Res Toxicol 2001. Calafat AM. Biochem Biophys Res Commun 2003. Reprod Toxicol 2001. 1999-2000: a national reconnaissance. Hanaoka T. Koulova AI. Measurement of bisphenol A in human urine using liquid chromatography with multi-channel coulometric electrochemical detection. 2003. Ecotoxicity and the Environment (CSTEE). 2/4/09 National Toxicology Program’s Report of the Endocrine Disruptors Low-Dose Peer Review (NTP). and Hajszan.780(2):365-370. Haighton LA. National Toxicology Program Center for the Evaluation of Risks to Human Production (NTP-CERHR). Pharmaceuticals. Ema M. Kuklenyik Z. Evaluation of developmental toxicity in rats exposed to the environmental estrogen bisphenol A during pregnancy. Regul Toxicol Pharmacol 2002. Bisphenol A. Munro IC. Park S. et al. Hara K. Richter CA. Ye X. streams. Toxicol Sci 2002. Koh WS.69(22):2611-2625. Klinefelter GR. Doull J.59(4):403-408. Bradley S. Gender differences in the levels of bisphenol A metabolites in urine. Pyo MY.Scientific Committee on Toxicity. Barber LB.nih. Research Triangle Park. August 2001.europa.116(1):39-44. Caudill SP. Gray GM. Leranth. Tyl RW. et al.. Lynch BS. 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. Myers CB.it/DOCUMENTS/ Existing-Chemicals/RISK_ASSESSMENT/SUMMARY/ bisphenolasum325. hormones.68(1):121-146. Reidy JA.113(4):391-395. 4.pdf. Cunha G.Environmental Phenols References Akingbemi BT. Ekong J.102(19):7014-7019.14(2):149-157. DirectorateGeneral Health and Consumer Protection. Tsugane S. Three-generation reproductive toxicity study of dietary bisphenol A in CD Sprague-Dawley rats.35(2 Pt 1):238-254. Weight of the evidence evaluation of low-dose reproductive and developmental effects of bisphenol A. Available at URL: http://cerhr. Needham LL. Yoshinaga J. Barton L. 2007. Available at URL: http://ec. Hlywka JJ. Barr DB. Ispra. 2/4/09 European Commission. Environ Sci Technol 2002. Available at URL: http://cerhr. In vitro and in vivo interactions of bisphenol A and its metabolite.10:875-921. 2008.149:988-994.gov/chemicals/bisphenol/bisphenol. Furlong ET. Reidy JA.J. Hum Ecol Risk Assess 2004. Matthews JB. et al. Arakawa C. Proc Natl Acad Sci USA 2005. 2/4/09 Ouchi K. Occup Environ Med 2002. Kiguchi M. May 22. Imai H.pdf . Available at URL: http://ecb. niehs.137(3):353-362. Keimowitz AR. Hughes C. 2/4/09 National Toxicology Program Center for the Evaluation of Risks to Human Production (NTP-CERHR). Kim YH. and other organic wastewater contaminants in U. Nippon Eiseigaku Zasshi 2004. Watanabe S.4’-Isopropylidenediphenol (Bisphenol-A) Summary Assessment Report. Chung MK. Joint Research Centre Institute of Health and Consumer Protection. U. T. Urinary concentrations of bisphenol A and 4-nonylphenol in a human reference population.312(2):441-448. Twomey K. Brussels. Timms BG. Rat two-generation reproductive toxicity study of bisphenol A. An evaluation of the possible carcinogenicity of bisphenol A to humans. Environ Health Perspect 2008. Needham LL. Belgium. bisphenol A glucuronide. Han SS.S. November 26. McConnell EE. Endocrinology 2008. Italy. Needham LL. Urinary bisphenol A and plasma hormone concentrations in male workers exposed to bisphenol A diglycidyl ether and mixed organic solvents.pdf. Endocrinology 2004.gov/ntp/htdocs/liason/ LowDosePeerFinalRpt. with estrogen receptors alpha and beta.S. Watanabe C. Kroes R. J Chromatogr B Analyt Technol Biomed Life Sci 2002. September. Harazono A..niehs..nih. Szigeti-Buck. Cohen JT. Thurman EM. 32 Fourth National Report on Human Exposure to Environmental Chemicals .145:592-603. Exposure to bisphenol A from bis-glycidyl dimethacrylatebased dental sealants.jrc. Zacharewski TR. Kim CS. Calafat AM.nih. Kim JC. Human Health. Brine DR.S. National Toxicology Program. National Institutes of Health. Cha SW.36(6):1202-1211. population to bisphenol A and 4-tertiary-octylphenol: 2003-2004. Life Sci 2001. NC. 2/4/09 Fujimaki K. Kolpin DW. Han SY. Rhomberg et al. 2002. MacLusky. Estimation of intake level of bisphenol A in Japanese pregnant women based on measurement of urinary excretion level of the metabolite. Estrogenic chemicals in plastic and oral contraceptives disrupt development of the fetal mouse prostate and urethra.pdf . Zaugg SD. Marr MC. J Am Dent Assoc 2006. Kawamura N. NTP-CERHR Panel Report on Reproductive and Developmental Toxicity of Bisphenol A. vom Saal FS. Ikka T. 5: 505-523. Meyer MT.gov/chemicals/bisphenol/BPAFinalEPVF112607. Rubin C. European Commission. Yang M. Sottas CM. Calafat AM. Howdeshell KL. Available at URL: http://ntp. Barr JR. Environ Health Perspect 2005. NTP-CERHR Panel Report on Reproductive and Developmental Toxicity of Bisphenol A. Fujii S. Bisphenol A prevents the synaptogenic response to testosterone in the brain of adult male rats. Serizawa S.eu/ health/ph_risk/committees/sct/documents/out156_en.59(9):625-628. Joskow R. Exposure of the U. Thomas BF. and Hardy MP. C. Department of Health and Human Services. niehs. Furukawa M. N.pdf. Shin HC. National Institute of Environmental Health Sciences.

Filser JG. Vom Saal FS. Morgan MK. Kawamoto T. Wilson NK. Welshons WV. et al. An extensive new literature concerning low-dose effects of bisphenol A shows the need for a new risk assessment. Food Chem Toxicol 2002. Chang SS. Environ Res 2007. Hughes C. Colnot T. Metabolism and kinetics of bisphenol A in humans at low doses following oral administration. Witorsch RJ. Yang M. Environ Health Perspect 2005.15:12811287. Lordo RA. Chem Res Toxicol 2002. Lee SM.Environmental Phenols Volkel W. Dekant W.147(6 Suppl):S56-69. Endocrinology 2006. Arch Environ Contam Toxicol 2003. Endocrine mechanisms mediating effects of bisphenol A at levels of human exposure. Kim SY. vom Saal FS. Fourth National Report on Human Exposure to Environmental Chemicals 33 . Sheldon LS. An observational study of the potential exposures of preschool children to pentachlorophenol.103(1):9-20.113(8):926-33.44(4):546-51. bisphenol-A. Nagel SC. Biological monitoring of bisphenol a in a Korean population. Chuang JC. Low-dose in utero effects of xenoestrogens in mice and their relevance to humans: an analytical review of the literature. III. Jang JY. Csanady GA. and nonylphenol at home and daycare. Large effects from small exposures.40(7):905-12.

140-66-9 General Information 4-tert-Octyphenol.20-2. and the polyethoxy chain may consist of up to 50 ethoxy units.900 (. They are biodegraded to the corresponding alkylphenol (octylphenol or nonylphenol). is used to manufacture alkylphenol ethoxylates.40) 1..477) .60) 1.20-2. and through manufacturing waste streams (Warhurst. impaired steroidogenesis. 1996).20) 2. fish) and drinking water. 1997.50) 1. several European nations banned the use of alkylphenol ethoxylates in domestic detergents and other uses..10) 2.400 (.600-1. 2002). and some personal care products.800-1.600-1.40) 2. In rats. Alkylphenols also have been used as plasticizers and antioxidants in plastics and resins. Human exposure to alkylphenols and alkylphenol ethoxylates may occur through ingestion of contaminated foods (e.500) .60-3. Saito et al. textiles.70 (1..600) .700-1. 2002). 2004).300 (<LOD-.90) 2.600-1.20 (1. 2000.30 (1.00 (. over 500.900 (. The alkylphenols can bioaccumulate in some fish. the various alkylphenols have also been used as emulsifiers and modifiers in paints. outdoor air may have detectable levels of 4-tert-octylphenol and 4-tert-octylphenol monoethoxylates.20) size 2517 Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th .500) 75th .274-.389 (. Survey Geometric mean (95% conf.500) .507) * < LOD . Nonylphenol ethoxylates are more commonly used than octylphenol ethoxylates.300-.60-3. pesticides. to shorter chain alkylphenol ethoxylates..20-2.500) .497) * .g.70 (1. Urinary 4-tert-Octylphenol (4-[1.30) 2.80 (1. orally administered 4-tert-octylphenol was well absorbed.900 (.20) 1. and impaired spermatogenesis (e.50) 1.300-.80) 2.60) 613 652 1092 Limit of detection (LOD.00) 1229 1288 03-04 03-04 03-04 * . and was quickly eliminated from the blood (Certa et al. Disposition in humans has not been studied sufficiently. Blake and Boockfor. 2003.30) 90th 1. which are anionic surfactants used in detergents. Less frequently. Indoor and to a lesser extent. and emulsifiers.299-. industrial cleaners. streams in 30 states (Kolpin et al. altered estrus cycles and reproductive outcomes.Environmental Phenols 4-tert-Octylphenol CAS No.10 (1.30 (1.500-1. 34 Fourth National Report on Human Exposure to Environmental Chemicals .357 (.30 (1.70 (1.30) 1. < LOD means less than the limit of detection.40 (1.50 (1.400 (.500-1.g.600) 1.300 (<LOD-. In the 1990s.400) 1.40) * 03-04 03-04 03-04 .200-. leading to inhalation as another potential exposure route (Rudel et al.20-2.30 (1.000 tons of alkylphenol ethoxylates were produced annually worldwide.3.60) . and to alkylphenoxycarboxylates.50) .600) .10-2. 4-octylphenol monoethoxylate was detected in 43. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.300 (<LOD-.90) 2. an alkylphenol.300 (<LOD-.600) .500 (. Octylphenols and nonylphenols can also enter the environment directly from manufacturing waste streams.900 (..50) 1.1.50) . During the 1980s and 1990s.10 (.2.20-2. 2006.50-3. 2000. 1995. and from contact with some personal care products and detergents. altered neonatal sexual development. 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. did not bioaccumulate. Commercial formulations of alkylphenol ethoxylates usually contain a mixture of oligomers and isomers. testicular atrophy..40) 1.600-1.50-2. through sewage.80 (1. Ying et al.60-3.40) 2.S.20) 314 715 1488 03-04 03-04 * * .268-. population from the National Health and Nutrition Examination Survey. The alkylphenol ethoxylates enter the environment through human use of products containing them. Katsuda et al.10) 1.5% of 139 U. see Data Analysis section) for Survey year 03-04 is 0. These high dose parenteral effects of 4-tert-octylphenol have included altered sex hormone levels and hypothalamicpituitary suppression. Laws et al.600-1.300 (<LOD-.60-3. Several alkylphenols.80 (1.00 (.369 (..60-3.200-.400 (.. In 1999-2000. and some of their degradation products are toxic to aquatic life. which may vary for some chemicals by year and by individual sample..60-3.70 (1.20-2.3-Tetramethylbutyl] phenol) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. Bian et al.10 (.900 (. including 4-tert-octylphenol.30-2. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.00 (1.600-1.S.30 (. have demonstrated estrogenic effects particularly when injected at high doses in animals..

00) 1.00) size 2514 Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th .. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.17 (.300 (<LOD-.00 (.420) .43-3.410 (.260 (<LOD-.740 (. Fourth National Report on Human Exposure to Environmental Chemicals 35 .00 (.550-1.11) 1.62 (1. Tyl et al.53-3.10-2. (2008) showed that urinary levels of 4-tertoctyphenol were detectable in slightly greater than half of the participants of the U.1.370 (<LOD-. or their corresponding ethoxylates with respect to human carcinogenicity.435 (.06 (2.73) 2.540-1.470-1. IARC and NTP have not rated octylphenol.470) 75th . 2004.76 (2. Yoshida et al.890-2.570) .269 (.620) .730-1.910 (.276 (.320 (<LOD-.54) * 03-04 03-04 03-04 . 2001).24) 612 651 1091 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.S.280-.40-4. at lower or environmentally relevant doses (Blake et al.470-1.170-. Biomonitoring Information Urinary levels of 4-tert-octyphenol reflect recent exposure. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2. 2003.349) * < LOD . 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.270-.43) 1.630-1. 2004).450) .67-2. 4-tert-Octylphenol is not considered directly genotoxic.64 (.Environmental Phenols Myllymaki et al.. 2000.337-.15) 1.740 (.11-2.25-2.02-4.850 (..450) 1.. Finding measurable amounts of 4-tert-octylphenol in the urine does not mean that the levels of 4-tert-octylphenol cause an adverse health effect.81 (1.00) 2.560) . population from the National Health and Nutrition Examination Survey.78) 1228 1286 03-04 03-04 03-04 * . the urinary concentrations of 4-tert-octyphenol were near or below the detection limit (Inoue et al.460 (. Nagao et al.31 (1.207-.78) 3.60 (1.22) .03-6.620-1.530) .62 (1.380 (<LOD-.71) 2. Sweeney et al. 2005.33 (2.85 (1. 1999).59) 1.96-4.65-3.05-2.160-.384) * .3.50 (2.770 (.610) .20 (1.S.860 (.36-3. Kawaguchi et al.11) 2.33) 3.68-2.270 (.00) 2.68) 2.25) 2.18-4.270 (.14) 314 713 1487 03-04 03-04 * * .31-2.400) .78 (1.59 (1.41) . Urinary 4-tert-Octylphenol (4-[1.08) 1.199-.. It is unclear if estrogenic or other effects occur in animals through oral dosing.3-Tetramethylbutyl] phenol) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.640-1.03 (1.62) . Survey Geometric mean (95% conf. representative subsample of NHANES 2003-2004. In a small number of adult Japanese volunteers. nonylphenol.40 (1.43) 1.25) 90th 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.03 (1..500-1. 2001.29) 2. Calafat et al.

Marr MC. Maekawa A.36(6):1202-1211. Horie M.54(1):154-167.37(20):4543-53. Makino T. Korn LR. Watanabe G. Takai N.folliclestimulating hormone. Fail PA.44(8):1355-1361. The toxic effects of 4-tert-octylphenol on the reproductive system of male rats. 36 Fourth National Report on Human Exposure to Environmental Chemicals . Izumi S.165(3):217-226.207(1):59-68. Available at URL: http:// www. Kawaguchi M. Environmental fate of alkylphenols and alkylphenol ethoxylates--a review. Saito I. Effects of 4-tert-octylphenol given in drinking water for 4 months on the male reproductive system of Fischer 344 rats. Roche JF. Ye X. Toxicol Sci 2000. Yoshida M. 2/4/09 Ying GG. Wong LY. 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. Nair-Menon JU. Tyl RW. Chen J. Measurement of 4-nonylphenol and 4-tert-octylphenol in human urine by column-switching liquid chromatography-mass spectrometry.15(6):683-692. Phthalates. Okada F. An environmental assessment of alkylphenol ethoxylates and alkylphenols. Raychoudhury SS.116(1):39-44. Wang X. population to bisphenol A and 4-tertiary-octylphenol: 2003-2004.S. alkylphenols. Toxicol Appl Pharmacol 2000. Usumi K.57(2):255-266. Paranko J. J Chromatogr B Analyt Technol Biomed Life Sci 2004. pesticides. et al. Sakui N.71(1-2):112-122. et al. Saito Y. 1995. Toppari J. Reidy JA. testis size. Inoue K. Certa H. Sweeney T. Brody JG. Qian J. Reprod Toxicol 2001. Seto H.14(5):325-332. bisphenol A and methoxychlor in rats. Yoshida M. Reproductive effects in male and female rats from neonatal exposure to p-octylphenol. Boockfor FR. Yoshimura Y.799(1):119-125. Anal Chim Acta 486:41-50. Kawaguchi M. Ito R. Boockfor FR. Xu L. Ono H. Myers CB. Spengler JD. Karjalainen M.28(3):215-226. Irreversible effects of neonatal exposure to p-tert-octylphenol on the reproductive tract in female rats.foe. Bolt HM. Effects of neonatal exposure to a high-dose p-tertoctylphenol on the male reproductive tract in rats. Watanabe G. Inoue K. Nagao T. Wiegand HJ. Pharmaceuticals. Laws SC. Takenaka A. Environ Sci Technol 2003. Needham LL. Calafat AM. prolactin. Carey SA. Yoshimura S.S. Environ Health Perspect 2008. Warhurst AM. Exposure of the U. Millette CF.30(2 Pt 1):81-95. Meyer MT. Food Chem Toxicol 2006. Regul Toxicol Pharmacol 1999. Taya K. hormones. Indoor Air 2004. Toxicokinetics of p-tert-octylphenol in male Wistar rats. polybrominated diphenyl ethers. Seely JC. Brine DR. Arch Toxicol 1996.Environmental Phenols References Bian Q. Katsuda S. Toxicol Appl Pharmacol 2005. Infantile 4-tert-octylphenol exposure transiently inhibits rat ovarian steroidogenesis and steroidogenic acute regulatory protein (StAR) expression. Endocrinology 2000. nonylphenol. Indoor air pollution by alkylphenols in Tokyo. Nakagomi M. Toxicol Lett 2001. Chronic administration of the environmental pollutant 4-tert-octylphenol to adult male rats interferes with the secretion of luteinizing hormone. and testosterone. and other endocrine-disrupting compounds in indoor air and dust. and other organic wastewater contaminants in U.co.pdf.121(1):21-33. et al. McCoy GL. and sertoli cell number. streams. Barber LB. Environ Sci Technol 2002. Kookana R. Maternal exposure to octylphenol suppresses ovine fetal follicle-stimulating hormone secretion. 1999-2000: a national reconnaissance. Kolpin DW.18(1):43-51. Katsuda S. Song L. Muller AM. Camann DE. Williams B. Estrogenic activity of octylphenol. Furlong ET. Onuki A. Two-generation reproduction study with para-tert-octylphenol in rats.uk/resource/reports/ethoxylates_alkylphenols. Biol Reprod 1997. Blake CA. 2003. Brooks AN. Myllymaki SA. et al. Blake CA. Environ Int 2002. Thurman EM. Rudel RA. Cooper RL. Ferrell JM.141(7):2667-2673. Taya K. Zaugg SD. Fedtke N. Reprod Toxicol 2004. Bodman GJ. Maekawa A. Haavisto TE. Nicol L.

and medical devices. toys. Matsumura et al. 2004). General population exposure results from dermal and oral use of products containing triclosan. Some reports show endocrine effects are observed in amphibians and fish (Foran et al. and wound disinfection solutions. Biomonitoring Information Urinary triclosan levels reflect recent exposure. 2007).. triclosan was found in 57. Lyman and Furia. 2007. and has also been impregnated into some kitchen utensils. In the body it is conjugated to glucuronides and sulfates (Bodey et al. 2008 has shown higher levels during the third decade of life and among people with the highest household income.8-dichlorodibenzo-p-dioxin (Aranami et al. In animal and human studies. There is some concern that widespread use of triclosan and other biocides can alter antibiotic resistance in bacteria (Aiello et al. Mezcua et al. Veldhoen et al.2 µg/L) of children 6-11 years of age who participated in NHANES 2003-2004 (Wolff et al. In 1999-2000. toothpastes. 2008). representative subsample of NHANES 2003-2004. It acts by inhibiting bacterial fatty acid synthesis. 2002). Fourth National Report on Human Exposure to Environmental Chemicals 37 . Moss et al. 2006). 1976. but not by race/ethnicity and sex. Calafat et al. 1988. mouthwashes.6% of 139 U. 2007. young girls. and has not been considered mutagenic or carcinogenic (Bhargava and Leonard. Triclosan can remain present in the oral saliva for several hours after the use of toothpaste containing triclosan (Gilbert et al.. 3380-34-5 General Information Triclosan is a phenolic diphenyl ether used for over 30 years as a preservative and antiseptic agent....S. deodorants.. 2000). 2000. It can be photochemically and biologically degraded. 1987).. In a study of 90 U. a process that can result in the formation of small amounts of 2. streams sampled in 30 states (Kolpin et al. In animal studies.. Triclosan has been added to soaps. Triclosan is not considered teratogenic at maternally toxic doses. 2007). 2005.2 µg/L was comparable to the median level (8.S.S.. acne medications. IARC and NTP do not have ratings with respect to human carcinogenicity... Calafat et al. Triclosan has a low bioaccumulation potential in fish. Triclosan formulations may rarely cause skin irritation. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.. 1996.. Triclosan can be absorbed across skin into the blood stream. it is excreted over several days in the feces and urine as primarily as unchanged triclosan (Kanetoshi et al. In a U.Environmental Phenols Triclosan CAS No. 1969).. (Sandborgh-Englund et al. 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. the median urinary triclosan level of 7. Human health effects from triclosan at low environmental doses or at biomonitored levels from low environmental exposures are unknown. Finding measurable amounts of triclosan in the urine does not mean that the levels of triclosan cause an adverse health effect.. it has low acute toxicity. Triclosan enters the aquatic environment mainly through residential wastewaters.

94 (7.60 (8.4 (38.4) 25.4.4-19.4 (12.45-13.11-11.48-10.0 (11.2 (27.6) 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 9.0 (34.2 (11.43-13.45 (5.55 (4.4) 317 (231-433) 144 (96.1) 7.00-8.29-12.2 (10.Environmental Phenols Urinary Triclosan (2.50) 10.3-67.5) 11.5) 20. population from the National Health and Nutrition Examination Survey.20-13.89-11.2 (37.0-15.6) 237 (175-294) 182 (138-217) 384 (294-506) 336 (225-480) 1228 1286 03-04 03-04 03-04 13.3.6-37.4) 357 (225-456) 203 (87.6) 31.86-12.4-18.2 (13.6-14.0) 65.9-236) 193 (90.4) 51.7) 10.7 (14.1) 9.1) 50.45-10.3 (11.82 (8.40-11.8 (21.5 (11.5-341) 245 (163-334) 597 (372-992) 450 (254-750) 461 (383-527) 613 652 1092 Limit of detection (LOD. Survey Geometric mean (95% conf.50-10.4-163) 304 (134-566) 261 (198-317) 157 (113-380) 655 (310-890) 472 (406-522) 314 715 1488 03-04 03-04 16.9-61.5) 13.10) 84.90-10.9 (8.7 (28.7 (9.6-65.5-250) 574 (461-716) 380 (258-430) 1229 1288 03-04 03-04 03-04 14.6 (30.20 (7.32-14.38-18.S.4) 7.1 (15.S.1) 9.6-15.9) 7.3 (26.80 (5.0 (8.3-35.9) 8.3 (8.3) 10.1) Selected percentiles ( 95% confidence interval) Sample 95th 368 (294-463) size 2514 Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 9. interval) 12.6) 10.8-60.6 (9.6 (10.2-46.54 (8.5) 66.0-15.1) 9.16 (6.9 (11.3-15.0 (36.4) 73.70-16.60 (6.72-13.1) 11.5-14.20-11.3 (9.3) 6.7) 123 (36.0-213) 213 (160-272) 453 (263-1150) 260 (127-513) 358 (276-480) 612 651 1091 38 Fourth National Report on Human Exposure to Environmental Chemicals .8-63.18 (5.1 (8.4) 75th 43.1) 13.8) 7.6 (12.2-58.0-19.40-17.1) 9.20-10.9 (50.48 (8.93 (7.8-112) 30.1 (45.00 (4.9 (33.92-12.8) 9.6-14.3-31.8) 116 (39.6-111) 33.6) 39. Survey Geometric mean (95% conf. see Data Analysis section) for Survey year 03-04 is 2.2) 13.2-58.6) 90th 212 (172-241) 03-04 03-04 03-04 9.4.74 (5.1) 14.9) 32.21 (6.7 (39.3) 47. interval) 13.7) 292 (151-432) 132 (78.22-10.10-9.7-318) 224 (186-272) 236 (115-336) 356 (169-580) 385 (308-506) 314 713 1487 03-04 03-04 13.2) 12.2 (25.4) 90th 249 (188-304) 03-04 03-04 03-04 8.9) 75th 47.5-86.1-39.0 (26.20 (7.2-14.8-85.0) 49.6-20.0-73.4 (11.8-127) 37.6) 12.30-14.4’-Trichloro-2’-hydroxyphenyl ether) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. population from the National Health and Nutrition Examination Survey.0) 9. Urinary Triclosan (2.4 (32.2) 9.4’-Trichloro-2’-hydroxyphenyl ether) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.7 (11.8) 14.

Arch Environ Contam Toxicol 1988. phthalates. Effects of nonylphenol and triclosan on production of plasma vitellogenin and testosterone in male South African clawed frogs (Xenopus laevis). streams. Calafat AM. Ishibashi H. Kaneshima H.. Readman JW. Anal Chim Acta 1004. Ogawa H. Ebersole R. Moss T. population: 2003-2004.80(3):217-227. Shiratsuchi H. Britton JA. Kanetoshi A. Lyman FL. Odham G. Toxicology of 2.69(20):1861-1873.38(2):64-71. Katsura E. Chelimo C. Sandborgh-Englund G. et al. Adolfsson-Erici M. Biol Pharm Bull 2005. et al. Bhargava HN. Urinary concentrations of triclosan in the U. Gunderson MP.23(5):579-583. J Invest Dermatol 1976. Thurman EM. Mezcua M.4’-trichloro-2’hydroxydiphenyl ether). Br J Clin Pharmacol 1987. Hirano M. Nagao Y. Foran CM. Benson WH. Gomez MJ. Wong LY. Environ Sci Technol 2002. Erratum in: Aquat Toxicol 2007. Food Chem Toxicol 2000. J Toxicol Environ Health A 2006.67(4):532-537. Fernandez-Alba AR. Ye X. 1999-2000: a national reconnaissance. Aquat Toxicol 2006.8-dibenzodichloro-pdioxin as a photodegradation product of triclosan in water and wastewater samples. hormones. et al. Aguera A.S. Chemosphere 2007. Pharmaceuticals. Environ Health Perspect 2008. and other organic wastewater contaminants in U. The bactericidal agent triclosan modulates thyroid hormone-associated gene expression and disrupts postembryonic anuran development. Teitelbaum SL. Barber LB.66:1052-1056. Furlong ET.50(1-5):153-156. Consumer antibacterial soaps: effective or just risky? Clin Infect Dis 2007. IMS Ind Med Surg 1969.17(5):637-644. Levy SB.116(3):303-307.4. Hong HC. Furia T. Triclosan: applications and safety. Hernando MD. Howes D. Developmental evaluation of a potential non-steroidal estrogen: triclosan. 4’-trichloro-2’-hydroxydiphenyl ether.36(6):1202-1211. Kolpin DW. Skirrow RC. Am J Infect Control 1996. Pilot study of urinary biomarkers of phytoestrogens. Zaugg SD. Watanabe N. 4. Photolytic degradation of triclosan in freshwater and seawater. Wolff MS. Windham G. Larson EL. Needham LL. Pharmacokinetics of triclosan following oral ingestion in humans. Bennett ER. Pinney SM. Veldhoen N. Williams PE.45 Suppl 2:S137-S147. Clapson DJ. Reidy JA. Evidence of 2.115:116-121. Randomized trial of a hexachlorophene preparation and P-300 bacteriostatic soaps. Matsumura N. Osachoff H. Ferrer I.S. Meyer MT. Okui T.Environmental Phenols References Aiello AE.83(1):84. Gilbert RJ. Ekstrand J. Percutaneous penetration and dermal metabolism of triclosan (2. Bodey GP. Wigmore H. Environ Health Perspect 2007.38(4):361370. and phenols in girls. Aranami K. Williams FM.28(9):1748-1751. Disposition and excretion of Irgasan DP300 and its chlorinated derivatives in mice. Fourth National Report on Human Exposure to Environmental Chemicals 39 . The oral retention and antiplaque efficacy of triclosan in human volunteers. et al.524:241-247. Mar Environ Res 2000.7/2. Leonard PA.24(3):209-218.

2002.70) .33-2.350) < LOD < LOD 75th .350-2. PCP cannot be used on wood in residential or agricultural buildings. Human exposure to PCP has become less common.350 (.S. other polychlorinated benzenes. and possibly of lindane (IPCS. water and sediments because of the large amounts that were produced and used historically.530) 1.650 (.350 (. air.390 (.650) 1.65 (.47-5.350-. PCP use in the U.23 (.350 (.350 (. General population exposure to PCP may occur by inhalation of contaminated air.37 (. PCP is degraded by sunlight and metabolized rapidly by microorganisms.75) 2.76) 1.350-. hypertension.350) < LOD .350-. has been restricted.65 (.350 (.590-1.990-2.01 (<LOD-1.350 (.390 (.350) < LOD . In the environment.350 (.350 (. After a single dose.350-. 1986).350 (.510-3. population from the National Health and Nutrition Examination Survey. high dose exposure to PCP can induce a hypermetabolic state and excessive heat production as a result of uncoupling mitochondrial oxidative phosphorylation. algaecide and insecticide. so it is relatively non-persistent.30 (.350 (.350) < LOD .350-. and it is used primarily as a preservative for wood to be used outdoors (e.350) < LOD .48 (.350-..350-2.53) 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 .510-5.Fungicides Pentachlorophenol inhale it or absorb it through exposed skin. are eliminated in the urine.770 (. 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.5.350-.54-2.30) 1. and dermal contact with PCP-treated products.350 (.78) 1.350-1.350-.350) < LOD .51) 1.350) < LOD .680-1.350-. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. which may vary for some chemicals by year and by individual sample.00) 1. 1979).350) 90th . and animals.67) 1.980 (.350 (.350 (.04) 1. Human health effects from PCP at low environmental doses or at biomonitored levels from low environmental exposures are unknown.350-.32 (.76) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .350) < LOD .990 (<LOD-2.62 (.350-.47-3.80) .850-2.76) . PCP has been detected in soils. 1997).30) 1.350) < LOD .890 (. PCP is absorbed rapidly and well by all exposure routes.350) . < LOD means less than the limit of detection.30 (1. 40 Fourth National Report on Human Exposure to Environmental Chemicals . PCP also may be eliminated in urine as a metabolite of hexachlorobenzene.350-.42) 973 1190 1021 1338 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .94 (1.350) < LOD .10) 1.350-.25 and 0.53) 482 577 681 826 831 1125 99-00 01-02 99-00 01-02 * * * * .350 (.350-.350) < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result. with repeated or chronic exposure.350 (.90) 1.10) 1.350 (. and metabolic acidosis were observed in CAS No. To-Figueras et al.350-. Survey Geometric mean (95% conf.350) < LOD .350 (.350-1.350) < LOD .37) .48-2. Kohli et al.350-.350) < LOD .480-2.94 (1. ingestion of contaminated food or water.83 (2.30) .660 (. along with small amounts of tetrachlorohydroquinone and conjugates. The parent compound and conjugates. bactericide.350 (. mollusicide. the elimination half-life may be a week or more (Uhl et al.350-2. PCP is eliminated over a few days (Braun et al.350-.350 (. Effects including hyperthermia.08-3.630 (.860-2.42) 696 680 521 696 603 951 Limit of detection (LOD.350) < LOD .350-.30 (.350 (.60) 1.00) 2.350-1. 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.40 (.45-2.00 (.350-.70) 2.91 (1.350-.90) 2.50) 1.960) 1.350-1.350-.98 (1.00) 1.. PCP is distributed to most tissues and is not extensively metabolized.09) ..10 (. Acute. Since 1984.58-2.58-2.10 (<LOD-1.10 (1.500-2.350-2.890-1.350-2. utility poles and fence posts). interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.350) < LOD .73 (1. After absorption.350 (.33) . 1976..64) 1.90 (1.60) 1.S. plants.350-. herbicide.350) < LOD .18 (<LOD-1.g..

79) 1. The U.00-1.34 (.300 (.55) 1. EPA has developed standards for PCP in drinking water and the environment.29-3.760 (.35-2. 1995).69 (1.920 (. IARC has determined that pentachlorophenol is possibly carcinogenic to humans.82) 1.S.16-1.30-2.67-3. 2004.40) 1. In NHANES 2001-2002 subsamples.40) 1.25-1.48-2. Fourth National Report on Human Exposure to Environmental Chemicals 41 .. and the FDA has established a standard for bottled water.220-.57 (1.40) 1.84) 1.95) 3.400 (.830) < LOD .00-1.780-1.990 (.40-2.99) 482 577 681 825 831 1125 99-00 01-02 99-00 01-02 * * * * .67 (1.21-2.560-.25 (1.35) 1.310) < LOD .26 (1.360 (. OSHA has established an occupational standard.380-.78) 1.36) .570 (.730) < LOD .35) 1.94-3.82 (1.30) 1.06-3.320) < LOD ..13 (. chronically administered high doses of PCP were hepatotoxic. Survey Geometric mean (95% conf..06 (.67 (1. respectively) (Becker et al.52 (1.40) 1.Fungicides adults and children severely exposed to PCP through ingestion.atsdr.420) < LOD .35-2.300 (.510-.560) < LOD .25-2. population from the National Health and Nutrition Examination Survey.. Among adults in the NHANES 1999-2000 subsample.S.52) 1. In animals.73 (1.710-1. or skin absorption.cdc. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.280) < LOD .67 (1.250 (.6 and 14.290-.56) 1.500 (.950-1.430-.500-1.19) 2.9 mg/L.590-1.630 (.67-2.310-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.09-1. inhalation. 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.220-. 2003).84 (1.90) 1.270-.67 (1. 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.78) 1.900-1.300 (.260 (. EPA at: http://www. and adversely affected thyroid function (U.51) 1.09 (<LOD-2. 2000).gov/ toxpro2.11) 2.650 (.510-. environmental levels) and health effects is available from the U. 1991).84-4.26 (1.25-2.25) 1.30) 1.700-2.e. 1989).08 and 5.470 (.19 (1.gov/ pesticides/ and from ATSDR at: http://www.440 (.270-.580-.16 (. Pentachlorophenol is not mutagenic or teratogenic.780) < LOD .57 (.10 (1.610 (.08) 696 680 521 695 603 951 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.490) < LOD . respectively) (Seifert et al.320) < LOD < LOD 75th .650 (.67 (1.590) < LOD .370 (.800) < LOD 1.92) 1. carcinogenic.30 (.25 (1.67-3.290) < LOD .18) .19) 2.950-1.18 (1. children in the 1980’s. 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.94 (1.55) 973 1190 1021 1337 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * . 2003).360-..EPA. Death can result from seizures and cardiovascular collapse.500-.75) 1.S..240-.330-.75) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .850 (.250 (.950-1. In a small sample of U. the median and 95th percentile urinary PCP levels were approximately three times lower than comparable values in German adults (2. More information about external exposure (i.94 (1.10-2..910-1.06) 1.52 (<LOD-1. van Raaij et al.800-1.350) < LOD .52 (<LOD-1.S.560) < LOD .650) 90th 1.19) 2.340-.83 (1. Biomonitoring Information In NHANES 1999-2000 the median urinary PCP levels among children aged 6-11 and 12-19 years were as much as thirteen times lower compared to a sample of German children aged 6-14 years in 1990-1992 (4.0 mg/L.epa..320 (.21 (.430) < LOD .75 (<LOD-2.40) 1.320) < LOD . 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. urinary PCP levels at the 95th percentile were approximately fivefold lower than 95th percentile values measured in a nonrandom subsample from NHANES III (1988-1994) participants (Hill et al.09) 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 . 1989).S.290-.00) 1.html.

The metabolism of higher chlorinated benzene isomers. Schmid P. PCP: Human Risk Characterization [online]. Arch Environ Contam Toxicol 1989.S. available at URL: http://www. Engel R.S. Available at URL: h t t p : / / w w w. Needham LL. urine. EPA). German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Arch Toxicol 1986. Notten WR. Baker S.10:552-65. hair. Rodamilans M.Fungicides Finding a measurable amount of PCP in urine does not mean that the level of PCP causes an adverse health effect. 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. Seifert B. Seiwert M. r e g u l a t i o n s . Fast DM. Head SL.inchem. Metabolism of hexachlorobenzene in humans: association between serum levels and urinary metabolites in a highly exposed population. Smith SJ. Schulz C.18(4):469-474. Holler JS. Santiago-Silva M. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children. Environ Res 1995. Kaus S. Jones D. The metabolism/ pharmacokinetics of pentachlorophenol in man and a comparison with the rat and monkey. htm. Helm D. Biomonitoring data can also help scientists plan and conduct research about PCP exposure and health effects. Gregg M. Otero R. Blau GE. Hill RH. Pesticide residues in food-2002-Joint FAO/WHO meeting on pesticide residues. J Expo Anal Environ Epidemiol 2000. 11/30/2004.105(1):78-83. van den Berg KJ. Becker K. Shealy DB. Hill RH Jr. Pharmacokinetics of pentachlorophenol in man. Cline RE. Int J Hyg Environ Health 2003. et al. 206:15-24. Arch Environ Contam Toxicol 1989. The German Environmental Survey 1990/1992 (GerES II): reference concentrations of selected environmental pollutants in blood. Dev Toxicol Environ Sci 1979. Phillips DL. International Programme on Chemical Safety (IPCS).18:475-481. Bragt PC. Safe A. Chenoweth MB. 4/21/09 Kohli J. Effects of hexachlorobenzene and its metabolites pentachlorophenol and tetrachlorohydroquinone on serum thyroid hormone levels in rats. 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. Sala M.org/documents/jmpr/jmpmono/2002pr08. Pentachlorophenol measurements in body fluids of people in log homes and workplaces. Schlatter C. Toxicology 1991: 67(1):107-16. Environ Health Perspect 1997. 2002. et al. To-Figueras J. References Becker K. To T. Pesticide residues in urine of adults living in the United States: reference range concentrations. Uhl S. Hill RH Jr.54(3):203-208. Barrot C. Krause C. Seiwert M. Bailey SL. Needham LL. Schulz C.71:99108. Seifert B.58:182-186. Can J Biochem 1976. Environmental Protection Agency (U. 4/21/09 van Raaij JA. Braun WH. drinking water and indoor air. 42 Fourth National Report on Human Exposure to Environmental Chemicals . U. et al. Lindane. house dust.4:289296.

350-1.860) * 99-00 01-02 99-00 01-02 99-00 01-02 . 1998.600) < LOD .S.22 (.570 (.91) 973 1190 1018 1339 99-00 01-02 99-00 01-02 99-00 01-02 . which may vary for some chemicals by year and by individual sample. 90-43-7 General Information Ortho-phenylphenol (OPP. are antimicrobial agents used as bacteriostats.50) < LOD .570-2.389-.40-5. formulate.496 (.950) < LOD .580-1. Timchalk et al. 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.28-3. population from the National Health and Nutrition Examination Survey.20 (1.740 (.30) < LOD 1.90) 1. 2006).508 (. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.50-4. < LOD means less than the limit of detection.636) * .386-.50 (1.00 (1.50) .23) 695 680 520 695 603 953 Limit of detection (LOD.640) < LOD .Fungicides ortho-Phenylphenol CAS No. EPA.10) . Both have been used in agriculture to control fungal and bacterial growth on stored crops.509 (.85) 2.76) 1. interval) ..00) .890 (.50-2.490 (<LOD-.433-.20 (.780) < LOD .470 (<LOD-.670) 2. fungicides.00 (1.420 (<LOD-. General population exposure can occur via dermal.402-.23) 480 577 681 827 830 1125 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. OPP was detected in 40 of 60 different canned beers at concentrations in the low parts per billion (Coelhan et al.540-2.610-1.60 (1.30) < LOD .850 (.EPA. Survey Geometric mean (95% conf.10) 1.410-.840-1. in paints.90) .80 (2.40-7. or oral routes from residential use and by ingesting treated food or food that was in contact with treated surfaces or equipment.60 (1.480-1. whereas SOPP is not volatile and is more water soluble.3.10 (1.50-3.820 (.800-3.50 (1.600) < LOD 75th .490 (<LOD-.60-2.970 (.20) < LOD 2.930 (.10 (1.690) < LOD .624) * . Fourth National Report on Human Exposure to Environmental Chemicals 43 . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.490 (<LOD-.60-3. Estimated human intakes have been below recommended intake limits (U.645) * .S.590-2.30-2.S.621) * .00) .550-1. and as a wood preservative.10) 1.600-1.890) 1.836) * . Both chemicals degrade within hours to weeks in the environment (U.10-2.600-1.10) .90) .600) < LOD .90) 2. however.50) < LOD .00) < LOD . 1998).27 (.14 (<LOD-3.552 (.20) < LOD 1.450 (<LOD-. OPP is still used as a disinfectant fungicide for industrial applications.10) ..370-.570-.28 (.03) 1.19 (. 2006).370-.450 (<LOD-.690-1.34) 1.40 (.50) 1.632) Selected percentiles ( 95% confidence interval) Sample 95th 2.80-3.20) 2.880-2. In the past.22) 2.830 (.61) 2. SOPP is applied topically to the crop and then rinsed off.3 and 0.770 (.09) 2.560-8.17 (.30) < LOD 90th 1. small amounts of OPP have been measured in human adipose tissue (Onstot and Stanley.00-2. 2002.760-2.490 (<LOD-. or 2-phenylphenol) and its water-soluble salt. OPP is efficiently absorbed from the gastrointestinal tract and through the skin.890 (. leaving the chemical residue OPP.450 (<LOD-.466 (.570-1. Human health effects from OPP at low environmental doses or at biomonitored levels from low environmental exposures are unknown. or apply these chemicals may be more highly exposed than the general population.600-1.85) size 1991 2529 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th .20-3.40-2. Most agricultural food applications have been revoked.02) 1.40-5.00 (1.90 (1.20-2.696) * .570 (. OPP is volatile..92 (.742) * .50 (1.497 (.520 (. 2006). and sanitizers.493 (. and it has limited water solubility.364-.770 (.30-7. such as fruits and vegetables.490 (<LOD-.790) 2.750-2.600) < LOD 1.33 (. on ornamental plants and turfs. it was used in home sanitizers for surfaces. sodium ortho-phenylphenate (SOPP). Cnubben et al.370-.30) 1.00 (1.10) 2. but OPP and SOPP are still used on pears and citrus (U.390-.567 (.60 (1.30 (1.07 (. 2006).EPA.710-2.710) 3.630) < LOD .S.500-2.638) * .349-.20 (1.80) 1.498 (. 1989). Available evidence suggests that OPP does not accumulate in the body. Workers who manufacture.80) 1.610 (.10-1.90 (1.389-.860 (.88) 1. OPP is considered to be moderately toxic after acute oral doses in animal studies. inhalational.50) < LOD .

93) .epa..470 (<LOD-.53) 1. but no neurologic.900) < LOD .480-.270-.06-4. Zhao et al. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.880-1.970) 1.610) < LOD 1.620-1. Detectable levels were seen in over half the U.21) 1.08-2.47) .11) 4. Survey Geometric mean (95% conf.580-1.470) < LOD .05-2.20) < LOD 3.33) . Urinary ortho-Phenylphenol (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.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 . These metabolites may induce carcinogenicity via nongenotoxic regenerative hyperplasia of the bladder (Appel.88-4. and it has classified OPP as not classifiable with respect to human carcinogenicity. 1992.620-1. less likely.74 (1. by possible genotoxic mechanisms (Hagiwara et al.29) 1.360 (<LOD-.11 (.26) 1. Brusick.301-.410 (<LOD-.455-.S. 1984.38-3.59) 1.382 (.444 (. IARC has classified SOPP as a possible human carcinogen.248-. Biomonitoring Information Urinary OPP levels reflect recent exposure.25-6. 2005).S..52 (.06-5.940-2.04-4.28 (<LOD-4.31) < LOD .93) . Bomhard et al. 1998.990) < LOD .380 (.640-1. 1984.01) 1.24-2.00 (1. 2005).75 (1.4 mg dermally had urinary levels of OPP that were several hundred times higher than median levels found in NHANES 1999-2000 and 2001-2002 (Bartels et al.S. 2000. Finding a measurable amount of OPP in urine does not mean that the level of OPP causes an adverse health effect.91 (1.58) 2..311-.EPA 2006).29) 1..860 (. 1999. or. 1986)..43) 3.980 (<LOD-1.11-1.496 (.09 (1.86 (1.750 (. 2002.670 (.4) 3.44 (1.S.690 (.08-1. population in the subsamples from NHANES 1999-2000 and 2001-2002 (CDC.403-.910 (<LOD-1.343 (.17 (.28 (2.810) < LOD .11) < LOD 90th 1. Nakagawa et al.S.24-2.514 (.43 (1. 2002.670 (. U. 2002).27) < LOD ..38) 1.600-1.64 (2.550) < LOD .560-2.840 (. CDC.860 (. Ito et al.770-2..78 (2.09-3.900-1. 2005.484) * .40-13.12) < LOD 1.910 (.84 (1. ortho-phenylhydroquinone and ortho-phenylbenzoquinone.0) 1.93) 1.560) < LOD 75th .02 (. 44 Fourth National Report on Human Exposure to Environmental Chemicals .550 (. 1997.453 (.21-2.09-6.61 (.510 (<LOD-.950) < LOD .91) 695 680 520 694 603 953 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.07) 2.410 (<LOD-..08) 1. U.666) * .580) < LOD .800-1.00 (.329-. In high dose animal studies. Additional information is available from U.508) * .780-14.440 (..17 (.43-2.291-.320 (<LOD-.59) .62) .93 (1.568) * .650-1.97 (2. reproductive. or developmental toxicity was observed (Bomhard et al.75 (1. Biomonitoring studies on levels of OPP provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of OPP than are found in the general population.13) 1.43-2.780 (.38) 973 1190 1018 1338 99-00 01-02 99-00 01-02 99-00 01-02 .38) 2.791) * .. 1999.96) 1.550-.11 (.51-3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.385 (. OPP or SOPP produced carcinomas of the bladder only after phase II detoxification pathways were saturated.EPA 2006). OPP was not found to be mutagenic. Murata et al.EPA at: http:// www.81) 1. Pathak and Roy.18) 2.810-1. population from the National Health and Nutrition Examination Survey.558) Selected percentiles ( 95% confidence interval) Sample 95th 2.61 (2.30) 480 577 681 826 830 1125 99-00 01-02 99-00 01-02 .17) 2.500) < LOD . Dermally applied OPP was not carcinogenic in a 2-year experimental study in animals (NTP.33-2.46) < LOD 1.32) 1.590) * .510-.420 (<LOD-.89 (1. Smith et al.96 (1.17) * 99-00 01-02 99-00 01-02 99-00 01-02 .420 (<LOD-.750-2. Volunteers exposed to 0.69 (1.32) 3.656) * .61 (1. 1993.06 (1.473) * .750 (.980 (. leading to production of two metabolites.670) < LOD . Kwok et al.96-4.910-1.12-2.96 (1.361-.21 (.460-.353-.gov/pesticides/. interval) .570) < LOD 1.Fungicides anemia.

Mutat Res 1993.S. EPA 739 R-06004. Moore GA.epa.EPA). Bromig KH. 1989. Timchalk C.50(11):3351-3358. Timchalk C. Shirai T. Christenson WR.S. van de Sandt JJ.45(5):460-481. Hagiwara A. St John MK. Hakkert BC. Imaida K. Environmental Protection Agency (U. food additives and natural products as promoters in rat urinary bladder carcinogenesis. Moriya K. Bartels MJ. Pathak DN. Tayama S. Urinary physiologic and chemical metabolic effects on the urothelial cytotoxicity and potential DNA adducts of o-phenylphenol in male rats. Turteltaub KW. Office of Toxic Substances. Atlanta (GA). Hagiwara A.32(6):551-625.17(8):411-417.pdf. Glas K. Cano M. Smith RA.S. Coelhan M. Toxicol Appl Pharmacol 1998. Reregistration Eligibility Decision (RED) for 2-phenylphenol and salts (Orthophenylphenol or OPP).703(12):97-104. Determination and levels of the biocide ortho-phenylphenol in canned beers from different countries.nih. U.niehs. J Agric Food Chem 2006. Toxicol Appl Pharmacol 1999. Fourth National Report on Human Exposure to Environmental Chemicals 45 . Herbold BA. Environmental Protection Agency (U. In vivo genotoxicity of sodium orthophenylphenol: phenylbenzoquinone is one of the DNA-binding metabolite(s) of sodium ortho-phenylphenol. Selim S.gov/oppsrrd1/REDs/ phenylphenol_red. U.159(1):18-24. 4/9/09. Brendler-Schwaab SY.28(6):579594. Arnold LL. Vogel JS. Environ Mol Mutagen 2005. Carcinogenesis 1999. Kawanishi S. Eastmond DA. 90-43-7) in Swiss CD-1 mice (dermal studies). Meuling WJ. Relationship between metabolism and cytotoxicity of ortho-phenylphenol in isolated rat hepatocytes. The carcinogenicity of the biocide ortho-phenylphenol. Buchholz BA. Brzak KA. Bartels MJ. Comparative in vitro-in vivo percutaneous penetration of the fungicide ortho-phenylphenol. Inoue S. Ito N. Elliott GR. Arch Toxicol 2000. Richter M.43(7):14311437. Bomhard EM. Detection and characterization of DNA adducts formed from metabolites of the fungicide ortho-phenylphenol. 2006. Nakagawa Y. 2005. Leser KH. Eadon G. 4/13/09 Onstot JD. McNett DA.20(5):851-857. J Agric Food Chem 2002. IARC Sci Publ 1984. Kwok ES. Oxidative damage to cellular and isolated DNA by metabolites of a fungicide orthophenylphenol. Identification of SARA compounds in adipose tissue. Xenobiotica 1998. Bartels MJ. Freyberger A. Fukushima S. EPA). Shibata M. Dose-dependent binding of ortho-phenylphenol to protein but not DNA in the urinary bladder of male F344 rats. Centers for Disease Control and Prevention (CDC). Sangha GK. Ito N. March 1986. Determination of orthophenylphenol in human urine by gas chromatography-mass spectrometry. Gierthy J. Third National Report on Human Exposure to Environmental Chemicals.Fungicides References Appel KE. Drugs.150(2):402-413. Mendrala AL. Analysis of genotoxicity and the carcinogenic mode of action for ortho-phenylphenol. National Toxicology Program (NTP). The pharmacokinetics and metabolism of 14C/13C-labeled ortho-phenylphenol formation following dermal application to human volunteers. rat and man. July 28. et al. NTP Technical report on the toxicology and carcinogenesis studies of ortho-phenylphenol (CAS No. Roy D. Biochem Pharmacol 1992. Available at URL: http://www. Bormett GA.54(16):5731-5735.pdf. Narang A. EPA-560/5-89-003. Brusick D. O-phenylphenol and its sodium and potassium salts: a toxicological assessment. Zhao S.(56):399-407. Hirose M. Available at URL: http://ntp. J Chromatogr B Biomed Sci Appl 1997. Sangha G. Hum Exp Toxicol 1998.S. Bartels MJ. et al. Long-term toxicity and carcinogenicity study of sodium o-phenylphenate in B6C3F1 mice. Christenson WR.286(2):309-319..74(2):61-71. Fukushima S. Crit Rev Toxicol 2002.35(2 Pt 1):198-208. Food Chem Toxicol 1984. Regul Toxicol Pharmacol 2002. Murata M.22(10):809-814. Comparative metabolism of orthophenylphenol in mouse. Moldeus P.gov/ntp/htdocs/LT_ rpts/tr301. Roberts AL. Stanley JS. Cnubben NH.

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

Finding measurable amounts of acetochlor mercapturate in the urine does not mean that the levels of acetochlor mercapturate cause an adverse health effect. Acetochlor has low acute toxicity. 2006). In animals. However. and hydroxymethyl ethyl aniline (U. this metabolite is not a marker of exposure to most plant metabolites or environmental degradates. 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. and has been detected in watersheds of agricultural lands (Battaglin et al. NTP and IARC do not have ratings regarding human carcinogenicity. 2000. U.EPA 2000. Acetochlor is moderately toxic to fish and honey bees.. 2-hydroxyethyl-6-methylaniline. 2006). renal injury. Davison et al. CAS No. 2000). 1994.S.. animals have demonstrated tumors of the lung... Jefferies et al. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.S. Acetochlor is not mutagenic. and thyroid (U. People exposed to acetochlor will excrete acetochlor mercapturate in their urine.e. 2000. but other pathways occur. 2000.EPA.S.EPA.. Human health effects from acetochlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown. Estimated human intakes of acetochlor have been below recommended limits (U.epa. Fourth National Report on Human Exposure to Environmental Chemicals 47 . General population exposure to acetochlor may occur through diet or drinking water. including one that produces 2-methyl-6ethylaniline and its reactive metabolite.0 μg/L (Curwin et al. and it is unlikely to be genotoxic at relevant doses (Ashby et al. however. 2006). but it has produced testicular atrophy. a major pathway for acetochlor metabolism involves mercapturate conjugation. Hladik et al. Additional information about external exposure (i.S. Acetochlor degrades in water to acetochlor sulfonic acid and acetochlor oxanilic acid.. 2006). Feng and Wratten. Urinary levels of acetochlor mercapturate were generally not detectable in the NHANES 2001-2002 subsample (CDC. nasal epithelia. mainly corn. 1998).EPA considers acetochlor likely to be carcinogenic in humans. remains in soils for up to 3 months.gov/ pesticides/. 1996). which are often more prevalent in the environment.Herbicides Acetochlor Biomonitoring Information Urinary levels of acetochlor mercapturate reflect recent exposure.S. in some species and at doses above maximum tolerated doses.. the latter which may account for some observed effects (Coleman et al. Acetochlor is microbiologically degraded. Acetochlor mercapturate was measured in the urine of farmers actively spraying the pesticide and the geometric mean was 8. Urinary acetochlor mercapturate levels of 0.. Plants can degrade acetochlor to 2-ethyl-6-methylaniline. Kolpin et al. 2005). EPA at: http://www.S. 2005). It is absorbed by plants and inhibits plant protein synthesis. environmental levels) is available from U. 1989.5 to 449 μg/L were measured in commercial applicators within 24 hours following its application (Barr et al. 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 not shown developmental or fetal toxicity in chronic animal studies. 2007). and neurologic movement abnormalities (U.EPA. 2005...

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. 48 Fourth National Report on Human Exposure to Environmental Chemicals . 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.1. 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. Survey Geometric mean (95% conf. Urinary Acetochlor mercapturate (creatinine corrected) Metabolite of Acetochlor Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.S. 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.S. < LOD means less than the limit of detection. Survey Geometric mean (95% conf.Herbicides Urinary Acetochlor mercapturate Metabolite of Acetochlor Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. see Data Analysis section) for Survey year 01-02 is 0.

Volume 65.S. Environmental Protection Agency (U. Davison KL. Barr DB.cornell.cce. Number 15. Hines CJ. Tinwell H.15(6):500-508. Hladik ML.S. sulfonamide. Centers for Disease Control and Prevention (CDC). 1998.S.24(10):1003-1012. Dialkylquinonimines validated as in vivo metabolites of alachlor. imidazolinone. Hodgson E.111(5):749-756. Feng PCC. Jefferies PR. Sanderson WT.S. Coleman S. Peter CJ. Comparative metabolism of chloroacetamide herbicides and selected metabolites in human and rat liver microsomes. Hsiao JJ. Green T. 2000. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. Wilson AG.37(4):10881093.html. Barr DB. Striley CA. Andrews HF. Deddens JA. Thurman EM. Atlanta (GA). EPA). Evaluation of the potential carcinogenicity and genetic toxicity to humans of the herbicide acetochlor. Reynolds SJ. et al. Bravo R. reservoirs and ground water in the Midwestern United States. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. Feil VJ.gov/oppsrrd1/reregistration/REDs/acetochlor_tred. Environ Sci Technol 2005. Available at URL: http://www. pages 3682-3690. Chem Res Toxicol 1998. Kolpin DW. J Expo Sci Environ Epidemiol 2007. Hein MJ. Burkhardt MR.11(4):353359. Finding minimal herbicide concentrations in ground water? Try looking for their degradates. Larsen GL.EPA): http://pmep. acetochlor.Herbicides References Ashby J. Heederik D.edu/profiles/herbgrowthreg/24-d-butylate/acetochlor/acetochlor_pet_100. Casida JE.pdf. Fourth National Report on Human Exposure to Environmental Chemicals 49 . Sci Total Environ 2000. Available at URL(non U. Kier L. Camann DE. and metolachlor herbicides in rats. Wratten SJ. Olsson AO. Environmental Protection Agency (U. Federal Register: January 24. 2005. Lefevre PA. March 2006.108(12):1151-1157. Environ Health Perspect 2003. Xenobiotica 1994. U. J Agri Food Chem 1989. Battaglin WA. Hum Exp Toxicol 1996. Furlong ET.248(2-3):115-122. Occurrence of sulfonylurea. Barr DB. EPA 738-R-00-009. Sci Total Environ 2000. Rose RL. and other herbicides in rivers. Identification of human urinary metabolites of acetochlor in exposed herbicide applicators by high performance liquid chromatography-tandem mass spectrometry. Roberts AL. Whyatt RM.248(2-3):123-133. Kinney PL.S. et al. EPA).15(9):702-735. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. Comparative metabolism and elimination of acetanilide compounds by rat. Ward EM.17(6):559-566. Barr JR. Acetochlor (Harness) Pesticide Petition Filing 1/00. epa. 5/30/06 U. Report of the Food Quality Protection Act (FQPA) Tolerance Reassessment Progress and Risk Management Decision (TRED) for Acetochlor. Third National Report on Human Exposure to Environmental Chemicals. et al. Alavanja MC. Linhart SM. Quistad GB. Curwin BD. 5/30/06. Environ Health Perspect 2000.39(17):6561-6574. J Expo Anal Environ Epidemiol 2005. Linderman R.

EPA.S. 1998). Animal carcinogenicity studies have demonstrated tumors of the nasal turbinates. Tessier and Clark. corn cropland was treated with alachlor. 1989. Jefferies et al.. but shows little bioaccumulation. 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. Alachlor itself is not considered mutagenic. General population exposure to alachlor may occur through consumption of contaminated food or drinking water. peanuts and other crops. mean values of urinary concentrations of alachlor metabolites. alachlor is quickly absorbed after oral doses and mostly excreted as metabolites within a week (IPCS. (2003) showed that 2.. about 20-25% of the U. 2003). as measured through conversion to deethylamine. Biomonitoring Information Urinary levels of alachlor mercapturate reflect recent exposure. 1994. soybeans. WHO. Finding measurable amounts of alachlor mercapturate in the urine does not mean that the levels of alachlor mercapturate cause an adverse health effect. U.. and uveal degeneration. the latter may account for some observed effects (Davison et al. 1997. 1988. 1996). U. Alachlor and its degradates are leachable from agricultural soils and have been detected in watersheds of agricultural land including ground and surface waters (Battaglin et al. 1998. the dermal exposure route is potentially significant for applicators. 1999 and 2007.EPA considers alachlor to be a probable human carcinogen at high doses. though positive genotoxic results are reported for several metabolites of alachlor (Brown et al. 1998). Alachlor is highly toxic to freshwater fish and slightly toxic to birds and some invertebrates..S. In chronic animal testing. 1998. U. In animal studies. 1995. Additional information about is available from U. but has not shown developmental or reproductive toxicity in mammalian systems (U.EPA. 2003)..gov/pesticides/. 1996. 1998. In animals. Hill et al. 1996. 2005).2% of a reference population had detectable alachlor equivalents by immunoassay in their urine. 2005. IPCS. USGS. but another metabolic pathway can produce 2.S. In a study of applicators and workers exposed to alachlor. 2003). WHO. Estimated human intakes have been below recommended limits (U. mercapturate conjugates were predominant metabolites. alachlor has demonstrated hepatotoxicity.S.Herbicides Alachlor CAS No.S. 1999. WHO. Human health effects from alachlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown. Hladik et al. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Since the late 1980s alachlor use has been declining. ranged from 0.. formulators. and thyroid only at either maximum tolerated doses or related to species-specific pathways (Heydens et al. 1995).1 to 1.1 mg/L at various collection times (Sanderson et al. 2000.S. 2000. People exposed to alachlor will excrete alachlor mercapturate in their urine (Driskell et al. 50 Fourth National Report on Human Exposure to Environmental Chemicals . whereas 60% of applicators had detectable amounts. EPA at: http://www. Alachlor has a soil half-life of a few weeks. Feng and Wratten. It is both metabolized in plants and degraded microbiologically in agricultural soils into as many as 19 metabolites and degradates.EPA. It is absorbed by plants and inhibits plant protein synthesis.. Kolpin et al. 2003).S. 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. but this metabolite is not a marker of exposure to most plant metabolites or environmental degradates which are often more prevalent in the environment. and field workers.. but not likely at low doses.6-diethylaniline and its reactive metabolite. including corn. U. NTP and IARC do not have ratings regarding human carcinogenicity. Alachlor has low potential for acute toxicity. and on non-crop land for general weed control..EPA. stomach.EPA. 1998).. In 1993-1995. Urinary levels of alachlor mercapturate were generally not detectable in the NHANES 2001-2002 subsample (CDC. Because it can be absorbed through skin.S. hemosiderosis.epa. WHO. Hines et al.

Urinary Alachlor mercapturate (creatinine corrected) Metabolite of Alachlor Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. which may vary for some chemicals by year and by individual sample. see Data Analysis section) for Survey year 99-00 is 1.S.S. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 1942 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 50th < LOD < LOD 75th < LOD 90th * 99-00 99-00 99-00 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 463 662 817 99-00 99-00 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 950 992 99-00 99-00 99-00 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 679 507 586 Limit of detection (LOD. 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. < LOD means less than the limit of detection.18. Survey Geometric mean (95% conf. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 1942 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 50th < LOD < LOD 75th < LOD 90th * 99-00 99-00 99-00 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 463 662 817 99-00 99-00 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 950 992 99-00 99-00 99-00 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 679 507 586 < 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.Herbicides Urinary Alachlor mercapturate Metabolite of Alachlor Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. Survey Geometric mean (95% conf. population from the National Health and Nutrition Examination Survey. Fourth National Report on Human Exposure to Environmental Chemicals 51 .

Biological monitoring of commercial pesticide applicators for urine metabolites of the herbicide alachlor. Quantitative assessment of the mutagenic potential of environmental degradative products of alachlor. Feil VJ. EPA).S. and metolachlor herbicides in rats. J Ag Food Chem 1995. Barr DB. Kimmel EC.int/water_sanitation_health/dwq/chemicals/en/alachlor. Deddens JA. Background document for development of WHO Guidelines for Drinking-water Quality. The Quality of Our Nation’s Waters Pesticides in the Nation’s Streams and Ground Water. Kolpin DW. Roberts AL. Kolpin DW.pdf.56(9):883-889. Sanderson WT. Available at URL: http://www. 1997.39(17):6561-6574. 1998. Life Sci 1988. Environ Health Perspect 2003.gov/oppsrrd1/ REDs/0063.S. Geological Survey (USGS). Circular 1291. Kier LD. and other herbicides in rivers. Thelin GP. Larsen GL. reservoirs and ground water in the Midwestern United States. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. World Health Organization.47(6):503-517. 4/2/09 U. Finding minimal herbicide concentrations in ground water? Try looking for their degradates. No. Centers for Disease Control and Prevention (CDC). Kinney PL. 1999. Xenobiotica 1994. J Agri Food Chem 1989. Peter CJ. ALACHLOR. Lau H. Gilliom RJ).S. Hull RD.44(18):1325. acetochlor. Hsiao JJ.43(25):2087-94. Clark JM. Am Ind Hyg Assoc J 1995. Bull Environ Contam Toxicol 1996. Supplemental Technical Information (available on-line only). Biagini RE. Erratum in: Life Sci 1989. Linhart SM. Camann DE.111(5):749-756. Wratten SJ. 2/27/09 U. Jefferies PR. Andrews HF. WHO/ FAO Data Sheets on Pesticides.395(2-3):159-171. Mutat Res. MacKenzie B. Reregistration Eligibility Decision (RED) Alachlor. World Health Organization (WHO).S.24(10):1003-1012. DNA adduct formation by alachlor metabolites.epa. 2007. Occurrence of sulfonylurea. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. who. March 2006. Hines CJ.248(2-3):123-133. Brown MA. December 1998. Hill AB. An evaluation of the carcinogenic potential of the herbicide alachlor to man. Striley CA. Comparative metabolism and elimination of acetanilide compounds by rat. Henningsen G. imidazolinone. U. Environmental Protection Agency (U. Wilson AG. Casida JE. 2/27/00 52 Fourth National Report on Human Exposure to Environmental Chemicals . Hum Exp Toxicol. 2003. Sacramento.18(6):363-391.43(9):2504-2512.gov/nawqa/pnsp/pubs/circ1291/ supporting_info. Shealy DB. Brown KK. Tessier DM.php. Dialkylquinonimines validated as in vivo metabolites of alachlor. Sci Total Environ 2000. International Programme on Chemical Safety (IPCS). Dialkylquinoneimine metabolites of chloroacetanilide herbicides induce sister chromatid exchanges in cultured human lymphocytes. Available at URL: http://www.usgs. Available at URL: http:// www. et al.org/documents/pds/pds/pest86_e. Martens MA. 98-4245 (by Barbash JE. 1996.56(6):853-859.pdf. 1999. Hines CJ. Heydens WF. revised February 15. Quistad GB. Environ Sci Technol 2005. Feng PCC. Shoemaker DA. Water-Resources Investigations Report: Distribution of Major Herbicides in Ground Water of the United States Water Resource Investigations Report No. Ann Occup Hyg 2003. EPA 738R-98-020. Atlanta (GA). Alachlor in Drinking-water. California. 1992-2001. 2005.htm. Identification of a major human urinary metabolite of alachlor by LC-MS/MS. Available at URL: http://water. Whyatt RM. Quistad GB. 2/27/09 Jefferies PR. Sci Total Environ 2000. Biagini R. Casida JE. Burkhardt MR. Geological Survey (USGS).Herbicides References Battaglin WA.248(2-3):115-122.37(4):10881093. 86.11(4):353359. Thake DC. Chem Res Toxicol 1998.inchem. Geneva. Third National Report on Human Exposure to Environmental Chemicals. Casida JE. Davison KL. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. Furlong ET. Barr JR. et al. Thurman EM. Driskell WJ. Tolos W. Hladik ML. Hill RH Jr. sulfonamide.

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

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

Heederik D. Clayton CA. Toxicol Sci 2000. Jones AD. the urinary geometric mean levels for herbicide applicators in Ohio and Wisconsin were about 6 μg/L (Hines et al. et al. atrazine was detected in only four children (Arcury et al. 2003. Bersani M. Fleenor-Heyser DG. Chen H. et al. Geneva. 2005). 3/11/09 Laws SC. Tyrey L.64(9):672-678.58(2):366-376. 82. Stoker TE.org/documents/pds/pds/pest82_e.115(8):1254-1260. Quandt SA. Toxicol Sci 2000. Goldman JM. A risk assessment of atrazine use in California: human health and ecological aspects. Sanborn JR. Blewett C. Cooper RL. Reynolds SJ. Eldridge JC. Breckenridge CB.99(8):5476-5480.109(6):583-590.76(1):190-200. Third National Report on Human Exposure to Environmental Chemicals. World Health Organization. Stuart AA. Tapia J. et al. Catenacci G. Grzywacz JG. Noriega N. Barr DB. Stoker TE. Lee M. Short-term effects of chlorotriazines on estrus in female Sprague-Dawley and Fischer 344 rats. demasculinized frogs after exposure to the herbicide atrazine at low ecologically relevant doses. Ferrell JM. Hermaphroditic. Simpkins JW. Deddens JA. Hines CJ. 2005. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa.43(2):155-167. 2000). Atrazine disrupts the hypothalamic control of pituitary-ovarian function. References Adgate JL. Ferioli A. Aldous CN. Extrom PC.Herbicides Biomonitoring Information Urinary levels of atrazine mercapturate reflect recent exposure. Brown KK. McElroy WK. Biomonitoring studies on levels of atrazine mercapturate provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of atrazine than are found in the general population. Eldridge JC. Gillis JH. Steroids 1999. Ann Occup Hyg 2003.53(2):297-307. J Toxicol Environ Health 1994. Wetzel LT. In a study of 60 farm worker children. 3/11/09 Arcury TA. J Expo Anal Environ Epidemiol 2005. levels of atrazine mercapturate were generally not detectable (CDC. Determination of urinary residue levels of the N-dealkyl metabolites of triazine herbicides. Curwin BD.. WHO/ FAO Data Sheets on Pesticides. Carr WC Jr. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.69(2):217-222. Eberly LE.. Barbieri F.. Vonk A. 2005). Available at URL: http://www. Perry et al. Maroni M. Schmid J. 2007).2 μg/L in 15 farmers studied several days after spraying the pesticide (Curwin et al.cdc.gov/toxprofiles/tp153. Environ Health Perspect 2007. Finding measurable amounts of atrazine mercapturate in urine does not mean that the levels of atrazine mercapturate cause an adverse health effect. Saiz SG. Agency for Toxic Substances and Disease Registry (ATSDR). Sanderson WT. Atlanta (GA). Striley CA. International Programme on Chemical Safety (IPCS). Gammon DW.. Pest Manag Sci 2005.atsdr. In a small number of field workers. The geometric mean of urinary atrazine mercapturate was 1. urinary concentrations ranged from 5-1756 μg/L (Lucas et al. et al.61(4):331-355. Mendoza M. 1999) and 83 Minnesota children with multiple urine collections during 1997 (Adgate et al. Cottica D. Ferrell JM. Biological monitoring of human exposure to atrazine. Toxicological profile for atrazine. atrazine mercapturate was infrequently detected at the detection limit of < 1 μg/L. J Toxicol Environ Health 1994. 1996. The effects of atrazine on female wistar rats: an evaluation of the protocol for assessing pubertal development and thyroid function. Seiber JN. diamino-S-chlorotriazine and hydroxyatrazine. Toxicol Lett 1993. Determination of atrazine metabolites in human urine: Fourth National Report on Human Exposure to Environmental Chemicals 55 .47(6):503-517. Hayes TB. No. Bradway DE. Hein MJ.inchem. Short-term effects of chlorotriazines on estrus in female Sprague-Dawley and Fischer 344 rats. Environ Health Perspect 2001.. 1993).html. Biagini RE.43(2):155-167.. Moseman RF. Freeman NC. Laws SC. et al. Shoemaker DA. The mammary tumor response in triazine-treated female rats: a thresholdmediated interaction with strain and species-specific reproductive senescence. et al. Toxicol Sci 2003. In small studies of Maryland residents in 19951996 (MacIntosh et al.. Proc Natl Acad Sci USA 2002. Wetzel LT. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. Centers for Disease Control and Prevention (CDC). Collins A. Lucas AD. Available at URL: http:// www. Cooper RL. In the NHANES 2001-2002 subsample. Pfeifer KF. Stevens JT. Gillis JH. Through immunoassay atrazine equivalents (detected mostly as atrazine mercapturate).30(2):244-247. Lioy PJ. Barr DB. Cooper RL. Pubertal development in female Wistar rats following exposure to propazine and atrazine biotransformation by-products. 2001). Goodrow MH.15(6):500-508. Stoker TE. ATRAZINE. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample.htm. Barr DB. J Agric Food Chem 1982. 2001 [online]. Pesticide urinary metabolite levels of children in eastern North Carolina farmworker households.

May 2003a. A risk characterization for atrazine: oncogenicity profile. Determination of the effect of tridiphane on the pharmacokinetics of [14C]-atrazine following oral administration to male Fischer 344 rats. 3/11/09 U. 2003b. 4/2/09 56 Fourth National Report on Human Exposure to Environmental Chemicals . A longitudinal investigation of selected pesticide metabolites in urine.67(2):198-206. Toxicology 1990. Exposure parameters necessary for delayed puberty and mammary gland development in LongEvans rats exposed in utero to atrazine. Ann Epidemiol 2000.S. Toxicol Sci 2000. 0062. Toxicol Appl Pharmacol 2004. U. Osborne DW. Chem Res Toxicol 1993. Stoker TE. Toxicol Appl Pharmacol 2002.27(6):599612. Sanderson JT. March 2006. Guidici DL. The Quality of Our Nation’s Waters. Stoker TE. Supplemental Technical Information (available on-line only). The effects of atrazine metabolites on puberty and thyroid function in the male Wistar rat. 1992-2001. Urinary biomarkers of atrazine exposure among farm pesticide applicators.gov/scipoly/sap/meetings/2003/june/ finaljune2002telconfreport. Crit Rev Toxicol 1997. Environmental Protection Agency (U. Wetzel L. EPA Office of Pesticide Programs.pdf. Dagenhart D.epa. Office of Prevention.9(5):494-501. Timchalk C. Dryzga MD.gov/nawqa/pnsp/pubs/ circ1291/supporting_info. Rayner JL. Ryan PB. Singzoni B. Washington (DC).61(1):27-40. White paper on potential developmental effects of atrazine on amphibians. Induction and inhibition of aromatase (CYP19) activity by various classes of pesticides in H295R human adrenocortical carcinoma cells.S. MacIntosh DL. EPA). Hammerstrom KA. Perry M.6(1):107-116. Sathiakumar N.pdf.S.56(2):69-109.10(7):479. Interim Reregistration Eligibility Decision For Atrazine. Cooper RL. Kastl PE. Breckenridge CB. J Toxicol Environ Health A 1999. Tortorelli J.gov/oppsrrd1/REDs/ atrazine_ired. Lansbergen GW. van den Berg M.usgs. Boerma J. Delzell E. revised February 15. J Expo Anal Environ Epidemiol 1999. Available at URL: http://www.S. The effect of atrazine on puberty in male Wistar rats: an evaluation in the protocol for the assessment of pubertal development and thyroid function. Case No. Environmental Fate and Effects Division. Fenton SE. Available at URL: http://water. Guidici DL. Wood C. Langvardt PW.Herbicides development of a biomarker of exposure. A review of epidemiologic studies of triazine herbicides and cancer. Available at URL: http://www. EPA). Laws SC.S. Needham LL. Laws SC.epa. Toxicol Sci 2002. Pesticides and Toxic Substances. Cooper RL. Stevens JT. Environmental Protection Agency (U. Pesticides in the Nation’s Streams and Ground Water. Christiani D.195(1):23-34.php.182(1):44-54. 6/1/09 U.58(1):50-59. Circular 1291. Geological Survey (USGS). 2007.

< LOD means less than the limit of detection.00-2.4-D have been below recommended intake limits (U.. 2.560-1.420) < LOD . It is poorly bound in soils.250 (<LOD-. which may vary for some chemicals by year and by individual sample. 2. Recent estimates of chronic intakes of 2.952 and 0. Once absorbed.230-.Herbicides 2.4-D may occur during residential applications. Kohli et al.610 (.80) 1. headache.27 (.4-D is eliminated mostly unchanged in the urine with an elimination half-life ranging from 10 to 33 hours (Arnold et al. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 1..60) 1. 2007). dizziness. hypotension. It was first registered with U.4-D or exposed for prolonged periods.740 (.4-D at low environmental doses or at biomonitored levels from low environmental exposures are unknown.930-1. by direct contact with agricultural and residential areas after applications.560-.910) 1. but at higher levels they are herbicidal.55 (1.320) 90th .4-D can be applied either as an aqueous salt or as oil-soluble esters.07 (.10 (<LOD-1.310) < LOD .810-1.370-.910) < LOD .260 (<LOD-.250 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. it acts as a plant growth hormone.51 (1. although dermal exposure may be significant for herbicide manufacturing plant workers exposed to high concentrations of 2.22) < LOD .350) < LOD < LOD < LOD . Intentional overdoses and unintentional high dose exposures to chlorophenoxy acid herbicides have resulted in weakness. 2004). Acid and salt forms are much less toxic to fish and aquatic invertebrates than the ester forms..EPA in 1948.10 (<LOD-1.890) < LOD . 1974.420-. As much as 62 million pounds of 2. 2. with a half-life of several days to several weeks.730 (.22) 962 1135 1015 1278 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .550-1.4-D is rapidly absorbed via oral and inhalation routes.03) 695 659 520 668 589 892 Limit of detection (LOD.32 (1.400) < LOD .48) < LOD 1.210-.S.20 (. 2. abdominal pain.410) < LOD .660) 1. Fourth National Report on Human Exposure to Environmental Chemicals 57 .27-2.4-D) controls broadleaf weeds in residential. renal and hepatic injury.13) < LOD . and mecoprop).20 (<LOD-1. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.680-1. 4-D.690 (.21) 1. 2005). these herbicides can enhance plant growth.30 (<LOD-2.S. the chlorophenoxy herbicide 2. and delayed Urinary 2.4-D has low acute toxicity.210 (<LOD-. and it is often mixed with other chlorophenoxy acid herbicides (such as dicamba. and aquatic environments.2.310 (.330 (. myotonia. 1989. Survey Geometric mean (95% conf.24 (.S. It is rarely detected in ground waters (USGS.16) < LOD .37) size 1977 2413 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD 75th < LOD .49) 477 546 677 797 823 1070 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD .4-Dichlorophenoxyacetic Acid CAS No.690-1.70) 1.540-. MCPA.610-. agricultural.670-1.4-dichlorophenoxyacetic acid (2.230 (<LOD-.490) < LOD < LOD < LOD .4-Dichlorophenoxyacetic acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.690 (. nausea.690 (.08) < LOD . Human health effects from 2.890 (.05-2. population from the National Health and Nutrition Examination Survey.490 (.910) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .02-1.27 (1.EPA. Sauerhoff et al. It is not well absorbed through the skin.40) 1.440-1.EPA. 1977).S.760 (. Similar to other chlorophenoxy herbicides.960-1.930 (.10) < LOD 1. General population exposure to 2. in 2001 (U.4-D were used in the U. 94-75-7 General Information Widely used throughout the United States.S. At low levels. and by consuming food or drinking water contaminated with 2.43) 1.66) < LOD 1.

670 (<LOD-1.640 (. 2005. Frank et al. 2005. 1994). In previous samples of the U.4-D had urinary levels several hundred to several thousand times higher than the 95th percentiles of the NHANES subsamples (CDC.. 2002.26) 962 1135 1015 1277 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .41 (1.08 (.560-.14 (.13 (.890) < LOD 1.270-. Average post-application urinary levels of 2..790) 1. eyes.S.73) .620-.Herbicides neuropathy (Bradberry et al.890-1.gov/pesticides/. Post-application levels in farmers and home gardeners were dependent on Urinary 2.340 (.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.550-.40) 695 659 520 667 589 892 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.S.29) 477 546 677 796 823 1070 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD .720 (.3.EPA 2005). 2002. IPCS.480 (. 2.24) 1.27-1. 2005. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 1995.440 (.610-.590 (<LOD-1.S.08 (.4-Dichlorophenoxyacetic acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U..660 (..S. Acute high doses administered to laboratory animals produced ataxia.340-. 1992).7.350 (<LOD-.380 (<LOD-. 58 Fourth National Report on Human Exposure to Environmental Chemicals . 2000). U. Hill et al.670 (.4-D was not found to be genotoxic or carcinogenic in animal studies (Garabrant and Philbert.810-1. 2005. other exposures.4-D production plant workers and a few forestry workers spraying 2.780) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD . 2005).980) < LOD 1. Biomonitoring Information Urinary levels of 2.270 (<LOD-.410) < LOD < LOD < LOD . 2006.680) < LOD .780-1. 2005). IPCS.EPA. 2. Knopp et al.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 .380) < LOD .330-.740 (..380-. Kutz et al. 2004). such as soft tissue sarcoma and non-Hodgkin’s lymphoma..410) 90th . or teratogenic effects in chronic rodent studies (Charles et al. 1996.670 (.700 (.780 (. 1989).16) 1. 1995).4-D are eye irritants.780) .. 1996. 2005). interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 1. U.08 (.820-1. 1996. IARC considers the chlorophenoxyacetic acids group of chemicals as possibly carcinogenic to humans. Additional information is available from U.. It is unclear whether these associations are related to the chlorophenoxy herbicides.32 (<LOD-2.13 (. Epidemiological studies have reported associations of several types of cancer. IOM. 2001. Survey Geometric mean (95% conf.4-D reflect recent exposure. or to contaminants in the herbicide formulations (specifically 2. Pearce and McLean. 1980.580-. in small samples of children (Hill et al. population from the National Health and Nutrition Examination Survey. U.380 (<LOD-.490 (.930-1. developmental.520-. 2.920) < LOD 1.4-D levels were detectable in less than a quarter of the individuals studied. thyroid.850) < LOD .05) . adrenals and gonads (NTP. population (Hill et al.56) .660) < LOD .EPA.17 (. myotonia. liver. with the exposure to chlorophenoxy herbicides as defoliants or contaminated herbicides.epa.990-1.390) < LOD < LOD < LOD . CDC.EPA at: http://www. IPCS.810-1.790) < LOD .35) < LOD . and evidence of histological injury to the kidneys.560-.410 (<LOD-..S. 1985. 2003. 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.470) < LOD . U.610-.19) .EPA.. The acid and salt forms of 2. 2005).590 (<LOD-1.S.39) < LOD 1. Kolmodin-Hedman and Erne.S. and of adults and children (Baker et al. urinary 2.570) < LOD .4-D does not have significant reproductive.8-tetrachlorodibenzo-pdioxin) (Garabrant and Philbert.410) < LOD 1.

4-dichlorophenoxyacetic acid (2. Xenobiotica 1974.4-D).4-D and 2. Shealy DB. Tandon JS.4 dichlorophenoxyacetic acid (2.71(2):99-108. Arch Toxicol Suppl 1980. Mandel JS.inchem.51(3):152-159. Dichlorophenoxyacetic acid. et al.10(6 Pt 2):789-798. Barr DB. Barr DB. geometric mean urinary levels of 2. 3/17/09 Knopp D.4-D than levels found in the general population.niehs. National Toxicology Program (NTP).5-T). cfm?objectid=06FF8DA6-E5A1-90CD-3F26562CEC5CDDE5. Finding a measurable amount of 2. Gupta BN. Chapman P. van Ravenzwaay B. Khanna RN. Sanderson WT. Needham LL.4-D.4-dichlorophenoxyacetic acid and its forms.4:97-100.4-D will result in an adverse health effect. 914. Gregg M. Quantification of selected pesticide metabolites in human urine using isotope dilution high-performance liquid chromatography/ tandem mass spectrometry. Honeycutt R. Needham LL.4-.4-dichlorophenoxyacetic acid in man.php?record_id=10603. Forestry workers involved in aerial application of 2. J Toxicol Environ Health 1992.4-dichlorophenoxyacetic acid in the chemical industry: results of a five year biological monitoring study. Dhar MM.. Board on Health Promotion and Disease Prevention. The pharmacokinetics of chlorinated phenoxy acid herbicides: a literature.31 Suppl 1:90-97. Survival and Growth Curves from NTP Toxicity Studies. Ripley BD. Available at URL: http://ntp. et al. Mandel et al. Garabrant DH.nap. International Programme on Chemical Safety-INCHEM (IPCS). Developmental toxicity studies in rats and rabbits on 2. the amount of pesticide applied.4-D in urine provide physicians and public health officials with reference values so that they can determine whether other people have been exposed to higher levels of 2.. Wilson RD. Cole DC.nih. 2005. Kutz FW. Arch Environ Contam Toxicol 1989. In farm families. Updated March 7. Fast DM. Scand J Work Environ Health 2005. Campbell RA. Pesticide residues in urine of adults living in the United States: reference range concentrations. Beasley VR. Vet Hum Toxicol 1989. Biomonitoring for farm families in the farm family exposure study.4-D were highest in the farmers who applied the 2. the number of acres to which it was applied (Curwin et al. Hein MJ. J Environ Sci Health B 1992. 2005 Charles JM. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.60(1):121-131. Harris SA. Available at URL: http:// www.. Alexander BH. Baker SE. TOX-63: TOXICITY REPORT CURVES. To T. Environ Res 1995. Stephenson GR. and the use of protective clothing or equipment (Arbuckle et al. Curwin BD. 1992). Scand J Work Environ Health 2005. 2006. TOX-63 Peroxisone Project (2. Assessment of exposure to 2. Ritter L. Beeson MD.4-D): exposure and urinary excretion. Review of 2.27(1):23-38.gov/index. Bus JS.32(4):233-257. Holler JS. Solomon KR. Harris et al. Murphy RS. 2005). References Arbuckle TE.15(6):500-508. Driskell WJ.edu/catalog. Veterans and Agent Orange: update 2002. Biomonitoring of herbicides in Ontario farm applicators. Estimation of occupational exposure to phenoxy acids (2. Available at URL: http:// www.37(2):277-291.Herbicides the time since application. Atlanta (GA). Tables.htm. Kolmodin-Hedman B. Toxicol Sci 2001. Baker BA. Arnold EK. Selected pesticide residues and metabolites in urine from a survey of the U. other family members had levels ranging only slightly higher than the 95th percentile levels in NHANES 1999-2000 and 2001-2002 subsamples (CDC. Absorption and excretion of 2. Bailey SL. Baker S. Erne K. Arch Environ Contam Toxicol 1985.S. et al. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children. Heederik D. Exposure of homeowners and bystanders to 2. Brody D. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa.4-dichlorophenoxyacetic acid (2. J Expo Anal Environ Epidemiol 2000. Occup Environ Med 1994. Sircar KP. Third National Report on Human Exposure to Environmental Chemicals. 3/17/09 Institute of Medicine (IOM).4:318-321. Hill RH Jr. Sirons G J. Carter-Pokras OD. Crit Rev Toxicol 2002. Acquavella JF. Centers for Disease Control and Prevention (CDC).4.31(2):121-125. 2005. Head SL. Hill RH Jr. Smith SJ. Committee to Review the Health Effects in Vietnam Veterans of Exposure to Herbicides (Fourth Biennial Update. Frank R. 2.. Philbert MA. 2005).4-D in urine does not mean that the level of the 2. Cook BT.4-Dichlorophenoxyacetic Acid).org/documents/jmpr/jmpmono/v96pr04. J Expo Anal Environ Epidemiol 2005 Nov. Reynolds SJ.31 Suppl 1:98-104. general population. Kohli JD. Hanley TR Jr. Biomonitoring studies of 2. Washington (DC): National Academies Press. Pesticides residues in food: 1996 evaluations Part II Toxicology. 3/17/09 Fourth National Report on Human Exposure to Environmental Chemicals 59 .4-D) epidemiology and toxicology.18(4):469-474.4:427-435. 2003.

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

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

740) 679 700 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.200 (<LOD-. Survey Geometric mean (95% conf. population from the National Health and Nutrition Examination Survey.240) 679 701 957 Limit of detection (LOD. see Data Analysis section) for Survey year 01-02 is 0.S. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Urinary Metolachlor mercapturate (creatinine corrected) Metabolite of Metolachlor Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.670 (<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 . 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.S. < 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 . population from the National Health and Nutrition Examination Survey. Survey Geometric mean (95% conf.220) < LOD 1192 1346 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .Herbicides Urinary Metolachlor mercapturate Metabolite of Metolachlor Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.200 (<LOD-.500) < LOD 1192 1345 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .440 (<LOD-. 62 Fourth National Report on Human Exposure to Environmental Chemicals .

acetochlor. J Expo Anal Environ Epidemiol 2005. Heederik D. Feng PCC. Environ Sci Technol 2005. Peter CJ. Sci Total Environ 2000. 6/1/09 Whyatt RM. Sanderson WT. Kinney PL. Thelin GP. 2007. Wratten SJ.php. Available at URL: http://water. Circular 1291. Metolachlor in Drinkingwater. U. 1999. California. Kolpin DW. Environ Sci Technol 2007. 1998. Deddens JA.15(6):500-508.ESTfeature_gilliom. Furlong ET. Rose RL. Feil VJ.S. J Agri Food Chem 1989. Environmental Protection Agency (U.108(12):1151-1157. Dialkylquinonimines validated as in vivo metabolites of alachlor. Environ Health Perspect 2000.gov/nawqa/pnsp/pubs/files/051507. and metolachlor herbicides in rats.int/water_sanitation_health/dwq/chemicals/ metolachlor.111(5):749-756. Kolpin DW. Environ Health Perspect 2003. Quistad GB. Hein MJ. Geological Survey (USGS). et al. Xenobiotica 1994. Supplemental Technical Information (available on-line only). reservoirs and ground water in the Midwestern United States. April 1995.248(2-3):115-122.usgs. Background document for development of WHO Guidelines for Drinking-water Quality. Pesticides in U. R. Hodgson E. sulfonamide. Brown KK. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. Thurman EM. Linderman R. streams and groundwater. et al. Davison KL.24(10):1003-1012. Gilliom RJ). Casida JE.S.11(4):353359. Shoemaker DA. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. and other herbicides in rivers. EPA 738R-95-006. Sacramento.pdf. Barr DB. Occurrence of sulfonylurea. Barr DB. 3/27/09 Fourth National Report on Human Exposure to Environmental Chemicals 63 . Linhart SM. Available at URL: http://www. Alavanja MC.41:3409-3414. Curwin BD. Coleman S.epa. Available at URL: http://water.gov/nawqa/pnsp/pubs/circ1291/ supporting_info. usgs.who. Atlanta (GA). The Quality of Our Nation’s Waters Pesticides in the Nation’s Streams and Ground Water. Chem Res Toxicol 1998. Centers for Disease Control and Prevention (CDC). 4/2/09 U. Comparative metabolism and elimination of acetanilide compounds by rat. 3/26/09 U.usgs. Reregistration Eligibility Decision (RED) Metolachlor. Jefferies PR. Hladik ML. Available at URL: http://water.gov/nawqa/ pnsp/pubs/wrir984245/text. Reynolds SJ. 1992-2001. Andrews HF. Geological Survey (USGS). 2005.Herbicides References Battaglin WA.S.S.pdf. Available at URL: http://www. Finding minimal herbicide concentrations in ground water? Try looking for their degradates. EPA). Ann Occup Hyg 2003. World Health Organization (WHO). Camann DE. revised February 15. 98-4245 (by Barbash JE.39(17):6561-6574. Gillion. Water-Resources Investigations Report: Distribution of Major Herbicides in Ground Water of the United States Water Resource Investigations Report No.pdf 3/30/09 Hines CJ. March 2006. Comparative metabolism of chloroacetamide herbicides and selected metabolites in human and rat liver microsomes.S. Hsiao JJ. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. Sci Total Environ 2000. imidazolinone. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns.37(4):10881093.248(2-3):123-133. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. Striley CA.gov/oppsrrd1/ REDs/0001.47(6):503-517. Roberts AL. Ward EM. Larsen GL. Biagini RE. Burkhardt MR.html. Barr JR. 2003. Third National Report on Human Exposure to Environmental Chemicals.

.5-T use as a herbicide in 1985.5-Trichlorophenoxyacetic Acid CAS No. Survey Geometric mean (95% conf. Nelson et al. Once absorbed into the body. 2.5-trichlorophenol and other degradates. 1992. nausea. 2.. Kohli et al. 1989.4.4.4.4.4.4.5-T was once applied as either an aqueous salt or as an oil-soluble ester.4.8-tetrachlorodibenzo-p-dioxin (TCDD) led to the discontinuation of 2.4. abdominal pain. but higher levels are herbicidal. 2. see Data Analysis section) for Survey years 99-00 and 01-02 are 1.5-T) is a chlorophenoxy acid herbicide that is no longer registered for use in the United States.4. Agent Orange). * Not calculated: proportion of results below limit of detection was too high to provide a valid result.4. 1986. Epidemiological studies have reported associations of several types of cancer. Given the commercial unavailability of 2.2 and 0. 1992). with an elimination half-life of approximately 19 hours (Arnold et al. Human health effects from 2.Herbicides 2. Chlorophenoxy herbicides act as plant growth hormones. it is not well absorbed through the skin. 64 Fourth National Report on Human Exposure to Environmental Chemicals ..5T is rapidly absorbed via oral and inhalation routes.4-D were used as defoliants in the Vietnam War (e.5-T is eliminated mostly unchanged in the urine. and concern about contamination with 2. 93-76-5 General Information 2.7. 2007).4. 2004). Intentional overdoses and unintentional high dose occupational exposures to chlorophenoxy acid herbicides have resulted in weakness.. renal and hepatic injury.5-Trichlorophenoxyacetic acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.5-T has been rarely detected in ground waters (USGS. such as soft tissue sarcoma and non-Hodgkin’s lymphoma. these herbicides can enhance plant growth..5-T degrades to 2.4. population from the National Health and Nutrition Examination Survey.5-T (Holson et al. Teratogenic and developmental effects have been reported in studies of multiple rodent strains treated with high doses of technical grade 2..5-T in soil varies with conditions. and delayed neuropathy (Bradberry et al.4. with the exposure to chlorophenoxy herbicides as defoliants Urinary 2. The half-life of 2. the general population is unlikely to be exposed to it.5-T.g. Omer. hypotension. ranging from several weeks to many months. myotonia.1.5-Trichlorophenoxyacetic acid (2. Although 2.5-T and 2. At low levels. headache.4.S. 1974).5-T at low environmental doses or at biomonitored levels from low environmental exposures are unknown. Mohammad and St. dizziness.4. 2.3. < LOD means less than the limit of detection. 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. which may vary for some chemicals by year and by individual sample.4. Ester forms of 2.

* Not calculated: proportion of results below limit of detection was too high to provide a valid result.4. or to contaminants in the herbicide formulations (specifically 2. IPCS.4.EPA at: http://www.gov/pesticides/. IARC considers the chlorophenoxyacetic acids group of chemicals as possibly carcinogenic to humans. 1980)..7. 2.5-Trichlorophenoxyacetic acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. Mean urinary levels of 2.3. 2005. Urinary 2.4. other exposures.S. population from the National Health and Nutrition Examination Survey. Biomonitoring Information Urinary levels of 2. Survey Geometric mean (95% conf.EPA. Biomonitoring studies on 2.8-tetrachlorodibenzop-dioxin) (Garabrant and Philbert.4. Pearce and McLean.5-T also were below the limit of detection (Kutz et al.5-T reflect recent exposure. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1814 2537 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 430 580 618 830 766 1127 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 891 1192 923 1345 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 652 679 483 700 531 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. urinary levels of 2.epa.000 times higher than the detection limit for the NHANES 2001-2002 data (Kolmodin-Hedman and Erne. similar to results of NHANES II (19761980). It is unclear whether these associations are related to the chlorophenoxy herbicides. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.4. IOM.5-T itself is not mutagenic. Finding a measurable amount of 2. Additional information is available from U.5-T measured after a day of exposure in a few asymptomatic herbicide applicators were 35. 2005).4.S.4.S. U.5-T does not mean that the level will result in an adverse health effect. Fourth National Report on Human Exposure to Environmental Chemicals 65 .5-T than levels found in the general population. In the NHANES 1999-2000 and 2001-2002 subsamples (CDC. 2004). 2003. 1996.5-T in urine also provide physicians and public health officials with reference values so that they can determine whether other people have been exposed to higher levels of 2.4.5-T were generally below the limit of detection.Herbicides or contaminated herbicides.4. 1992). in which urinary levels of 2. 2002.

210:250-255. Committee to Review the Health Effects in Vietnam Veterans of Exposure to Herbicides (Fourth Biennial Update. Gaines TB. Review of 2. Agricultural exposures and non-Hodgkin’s lymphoma.pdf. Wolff GL. 3/17/09 66 Fourth National Report on Human Exposure to Environmental Chemicals .4-.8(5):551-60.epa.htm. Washington (DC): National Academies Press. Kutz FW. Centers for Disease Control and Prevention (CDC). Tandon JS. 3/17/09 Institute of Medicine (IOM). S. 914. Pearce N. LaBorde JB. general population. Washington (DC): U.Herbicides References Arnold EK.EPA). Toxicol Rev 2004. LaBorde JB. Dichlorophenoxyacetic acid. Erne K. Murphy RS. discussion 5-7.4:318-21. Bradberry SM.4-D/2.inchem. May.4-D) epidemiology and toxicology. Beasley VR.5-T). Absorption and excretion of 2. Scand J Work Environ Health 2005. Mohammad FK.4. U. Fundam Appl Toxicol 1992.4.4. The pharmacokinetics of chlorinated phenoxy acid herbicides: a literature. St Omer VE.5-trichlorophenoxy acetic acid in man. Arch Toxicol Suppl 1980. Poisoning due to chlorophenoxy herbicides. Khanna RN.37(2):277-91. McLean D. Crit Rev Toxicol 2002. Behavioral and developmental effects in rats following in utero exposure to 2.4-dichlorophenoxyacetic acid (2.5-trichlorophenoxyacetic acid (2. 2.32(4):233-257.4. Gaines TB. Available at URL: http://www. Nelson CJ. McCallum WF. Environmental Protection Agency (U. Gaylor DW. II.31 Suppl 1:1825. Vale JA. J Toxicol Environ Health 1992. 3/17/09 Kohli JD.4. Garabrant DH. 2004. Selected pesticide residues and metabolites in urine from a survey of the U.23(2):65-73.org/documents/jmpr/jmpmono/v96pr04. gov/oppbead1/pestsales/01pestsales/market_estimates2001.5-t mixture.31(2):121-125. Atlanta (GA). Available at URL: http:// www. Veterans and Agent Orange: update 2002. 2003.5-T in four-way outcross mice. Vet Hum Toxicol 1989.5-T).19(2):298-306. Gupta BN. 2005.S.4. Pesticides residues in food: 1996 evaluations Part II Toxicology.edu/catalog. Dhar MM.2000 and 2001 market estimates. Cook BT. Philbert MA.S. Multireplicated dose-response studies with technical and analytical grades of 2. International Programme on Chemical Safety-INCHEM (IPCS). Nelson CJ. Proudfoot AT.4. Developmental toxicity of 2. et al. Brody D. Board on Health Promotion and Disease Prevention. Holson JF. Pesticide industry sales and usage . Third National Report on Human Exposure to Environmental Chemicals.4. Available at URL: http:// www. Kolmodin-Hedman B.4-D and 2. et al.5-T). Estimation of occupational exposure to phenoxy acids (2. Neurobehav Toxicol Teratol 1986. Fundam Appl Toxicol 1992.php?record_id=10603. Holson JF. Arch Int Pharmacodyn Ther 1974.EPA. Developmental toxicity of 2. Multireplicated dose-response studies in four inbred strains and one outbred stock of mice.nap. I.5-trichlorophenoxyacetic acid (2. Office of Prevention Pesticides and Toxic Substances.19(2):286-297.S. Sheehan DM. Carter-Pokras OD. Sircar KP.

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

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

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

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 .080 (.056-.4) 14.2) 12.1) 14.5 (16.090 (.3 (18.6 (14.1 (13.100) . interval) Selected percentiles ( 95% confidence interval) Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * * 50th < LOD < LOD 75th < LOD .1) 10.130-.110 (.098 (.086-.048 (<LOD-.7 (14.5) 15.083-.8-17.096-.093) .102 (.103 (.062-.055 (.070) .3-21.160 (.4) 19.120 (.9 (13.9 (12.158) . 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 9.30 (8.2) 15. < LOD means less than the limit of detection.4) 21.101) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.130) .2-15.138 (.062 (.7-19.073-.90) 90th 15.3 (14.0) 19.059 (.080) .140) . see Data Analysis section) for survey years 01-02 and 03-04 are 10.084-.177) Sample size 2159 1952 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD .054-.049-.120) .1-18.9-22.120 (.112) 95th .70 (7. which may vary for some chemicals by year and by individual sample.2) 11. Survey years 01-02 03-04 Geometric mean (95% conf.10 (<LOD-16.5 (<LOD-11. which may vary for some chemicals by year and by individual sample.1 (18.103 (.120-.090-.80-10.110) .8 (18.40-9.058) < LOD .8-19.160 (. Survey years 01-02 03-04 Geometric mean (95% conf.069) < LOD < LOD .1) 20.090-.109 (.110-.054-.4 (12.147 (.8-17.110) .9 (12.202) 539 456 484 487 980 885 < LOD means less than the limit of detection for the lipid adjusted serum level.090 (<LOD-.116) .130) .7) 15.060) .6-33.8-25.6) 9.00-14. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.4) 95th 20.0-21. 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.3 (19.6 (15.5-15.130 (.4-18.100) .180) .5 and 7.150 (.2) Sample size 2159 1952 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD 10.062 (.160) .0 (15.190) .130) .8-24.053 (<LOD-.109-.0 (11.S.149) .0-25.2) 14.50) 15.3 (18.60-10.4) < LOD < LOD 16.054-.7) 716 587 1443 1365 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD 9.140-.077-.150 (.100-.5) 19.110 (.8.00 (8.30 (8.80 (<LOD-10.0 (10.108-.130-.088-.4) 20.8) 14.090-.1-24.3 (13.075) < LOD .6 (15.6-24.1-19.9 (13.1) 15.4) 539 456 484 487 980 885 Limits of detection (LOD.9 (14.138) .117) < LOD .4-17.063-.064) 90th .170) .5-17.S.5) 21.070 (<LOD-. population from the National Health and Nutrition Examination Survey.1) 13.139 (.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. population from the National Health and Nutrition Examination Survey.089 (.130-.0) 21.50 (8.100 (.1) 15.6) 19.9-38.7-22.242) .124) .139 (.070-.0) < LOD 9.6-24.8) < LOD 8.077 (.8 (9.180) .064 (.0 (10.120 (.113 (.140 (.100-.1-16.6) 16.7 (15.7 (<LOD-15.109-.112-.40-10.9-23.080-.1) < LOD 9.100-.8 (11.8) 15. Fourth National Report on Human Exposure to Environmental Chemicals 79 .80-9.190) .110 (.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.5-17.4 (12.182) 716 587 1443 1365 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD .

atsdr.47:1059-1087. toxicology.66(4):229-234. 1991. et al. and epidemiology in the United States. Available at URL: http://www. 2007 [online].cfsan. Exposure to low doses of the environmental chemical dieldrin causes behavioral deficits in animals prevented from coping with stress. Cancer Epidemiol Biomarkers Prev 2000. David VL.27:405-421. Cox.59:229-234. Six high-priority organochlorine pesticides. Chapin RE. Ellis H. Soto AM. Hartvig HB. Ginsburg KS. Facca A. Toxicol Lett 1992. Wienburg CL. Mink PJ.352:1816-1820. Psychopharmacology (Berl) 1987. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. plasma dieldrin. Environ Health Perspect 2001. Organochlorine insecticides in substantia nigra in Parkinson’s disease. United States Geological Survey (USGS). Schulte P. 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. Basit A. Needham LL. Smith AG. Handbook of Pesticide Toxicology. Demographic and seasonal influences on human serum pesticide residue levels.Organochlorine Pesticides in the NHANES 2001-2002 and 2003-2004 subsamples (Edwards and Priestly 1994). The E-SCREEN assay as a tool to identify estrogens: an update on estrogenic environmental pollutants. J Toxicol Environ Health 1989. Garrett N. Frey JM. Serrano FO. PA. 15. Stehr-Green. Kitzazwa M. bioaccumulation. 2 Classes of Pesticides. No:429-436.gov/~dms/ pesrpts. Organochlorine exposure and risk of breast cancer. Priestly BG. 1989.91(1):122-126. pp. International Programme on Chemical Safety (IPCS). 4/21/09 Jorgenson JL. Brock JW. Patterson DG Jr. 4/21/09 Hoyer AP. Edwards JW. Anantharam V.14:95-102. 1992-2001. and lymphocyte sister chromatid exchange. September 2002. Environmental Health Criteria 91. 731-915. Aldrin and Dieldrin [online]. Chemosphere 2004. Kanthasamy AG. Available at URL: http://www.html.html. Reprod Toxicol 2000. Teta MJ.fda.cdc. Patterson DG Jr. New York. Kanthasamy A. Song S. Available at URL: http://pubs. Grandjean P. Evaluation of epidemiologic and animal data associating pesticides with Parkinson’s disease. Carlson JN. Chung KL. Andersen A. Toxicological profile for aldrin/dieldrin [online].109(Supp1):113-139. J Occup Environ Med 2005. Part A 2000.64-65 Spec. Chlorinated Hydrocarbon Insecticides. Daniel SE. Neurotoxicol 2005. Narahashi T. are nonestrogenic in transfected HeLa cells. Inc. References Agency for Toxic Substances and Disease Registry (ATSDR).inchem. 80 Fourth National Report on Human Exposure to Environmental Chemicals . Jorgensen T. et al. Toxicity of dieldrin for dopaminergic neurons in mesencephalic cultures. Environ Health Perspect 1995. Olea N. 4/21/09 Bates MN. Sanchez-Ramos J. McIntosh LJ. Rosellini RA. Finley B.9:1357-1367.org/documents/ehc/ ehc/ehc91. VT.54:1431-1443. Academic Press. Dieldrin-induced neurotoxicity: relevance to Parkinson’s disease pathogenesis.26:701-719. Serum organochlorine levels and breast cancer: a nested case-control study of Norwegian women.usgs.htm. Grajewski B. Aldrin and dieldrin: A review of research on their production environmental deposition and fate. Food and Drug Administration (FDA). Tully DB. In Hayes WJ. Turner W. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.gov/toxprofiles/ tp1. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. either singly or in combination. Revised Feb.150:263-271. Vol. Li AA. Mann D. J Toxicol Environ Health. Mumtaz MM. Lancet 1998. August 2008. Exp Neurol 1998. 6/1/09 Ward EM. Effect of occupational exposure to aldrin on urinary D-glucaric acid.gov/ circ/2005/1291/. Jr and Laws ER. Int Arch Occup Environ Health 1994. Corrigan FM. Roy ML. Pesticides in the Nation’s Stream and Ground Water. Shore RF. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Sodium and GABA-activated channels as the targets of pyrethroids and cyclodienes. 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. Available at URL: http://www. Fernandez MG. Jr. Eds. Buckland SJ.103(Suppl 7):113-122. Sonnenschein C.

5-65.8-43.8) 52.9 (36.4) 18.8 (10.6 (16.5.5-13.9 (29.0-13.7 (<LOD-32.5) 37.8 (10.82-11.3 (11.1 (40.6-24.9 (11.7 (34. Since 1992.20 (<LOD-11.0-33.6) 48.1 (11.0-12.2-21.8-61.7-56.9 (18.2-49. fish. Technical grade chlordane had contained 7% trans-nonachlor.9-42.1) * 11.6) 9.4) 22.7) 19.7 (10.0) 37. Both pesticides are persistent in soils and sediments and have been detected in water from agricultural run-off and near production and disposal facilities (ATSDR.7 (32.0) 75th 20.9) 11.3 (26. 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.0-25. and 7.7) 28.5-47.9-21.0) 21.7 (19.5) 38.6-24. heptachlor use has been limited to treatment of fire ants near power transformers. Heptachlor was used as a soil and seed treatment and for termite control in and around buildings until 1988.5 (33.. Chlordane is not currently produced or used in the U.3 (27.2) 22.7 (17.Organochlorine Pesticides Chlordane CAS No.6-12.3 (25.4) 29.S.6-53.5) 44.2-26.10-11.8-33.8) 53.0 (<LOD-12.9 (31.30-11.9) 13.6) 23.7 (43.70 (<LOD-10. population from the National Health and Nutrition Examination Survey. and dairy products are the usual sources of exposure to these chemicals in the general population.8-23.1 (<LOD-12.6) 20.8.4) 12.1 (17.1) 16.7 (<LOD-13.3-45. < LOD means less than the limit of detection.4-51. which results in exposure to the fetus and nursing infant Serum Oxychlordane (lipid adjusted) Metabolite of Chlordane Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U.1-65.63 (8.3-45. Survey Geometric mean (95% conf.0-67.1-51.2) 34.8-73.3) 18.9) 23.6) 49.3) 10.5 (34.5 (31.8-42.2-49. Consequently.1 (15.7-70.8-31.6) 9.2 (37. 1994.0 (16.8) size 1661 2249 1978 Total years 99-00 01-02 03-04 50th < LOD 11.0 (32.8 (40.1-25. 76-44-8 General Information Chlordane and heptachlor are structurally related organochlorine pesticides and were used in the U.5-42.3 (<LOD-19.6) 8.3 (9.3-43.10 (8. in addition to trace amounts of numerous other related compounds (ATSDR.2) 36.9 (15. 2007). 10. Fourth National Report on Human Exposure to Environmental Chemicals 81 . 01-02.6) 36.0) 20.1 (20. Both of these chemicals and their metabolites can cross the placenta and are excreted into breast milk. Until 1988.9 (26.5) 628 557 462 350 501 493 559 1031 898 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.2-56.8-20.6) < LOD 11.1 (<LOD-12.9-40.S. 2007).1) 30.8) 27.2 (10. see Data Analysis section) for Survey years 99-00.6 (9.8-32. interval) Selected percentiles ( 95% confidence interval) Sample 95th 44.1 (25.8 (42.0 (20. and in soil.8 (17.1) * 11.9 (15.5.4) 37.9) 11.6 (25.2 (21.4 (30.7) 42.9 (11.0) 31.3) 41. Heptachlor and chlordane and their metabolites bioaccumulate in fatty animal tissues.4) < LOD < LOD < LOD 23. buildings.5) 21.6) 39.5-32.4) 39.2 (28.4 (31.4 (30.4) < LOD 11.5) < LOD < LOD 9.4-40.7) 31.1 (16.0-61.7-14.1) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * 12.36-11.4 (35.2) 46. the technical grade product of each chemical contains 10%-20% of the other chemical.8) 663 752 595 998 1497 1383 20 years and older Gender Males 99-00 01-02 03-04 * 11.3-32.0 (26. and 03-04 are 14.1-19.4 (10.4 (22.2) 33.9) 23.69-10.7-25.90 (8.4 (<LOD-12.74 (<LOD-10.8) 18.4-45. 57-74-9 Heptachlor CAS No.6-18.9) 31.7-39.9) 37.89-10.5 (8.1-50.0) 27. 1994).7) 19.1 (<LOD-12.2) < LOD 11.9) 17.5) < LOD < LOD < LOD < LOD 13.5-40.3 (28.5-43.7) 9.2) 37.37 (8. respectively.5-44.9) 10.9) 36. which may vary for some chemicals by year and by individual sample.6 (43. As a result of the manufacturing process.10-18.2) * 12.3 (21.9-21.1-15.7 (42.2-28.5) 9.2) < LOD 11.3-49.5-38.5) 10.3) 18.5 (<LOD-12. lawns.7-12.1 (44.9 (17.0 (37.6) 48. from the early 1950’s until the mid-1980’s.9 (21.2 (41.20-11.8 (18.9) 39.3) 37.1) 22. foods high in fat such as meat.9 (26.7) 35.9-38.5) 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 * * * * 11.3-24.2 (39.0-18.1 (27.6) 11.1) < LOD < LOD < LOD < LOD < LOD 8.2 (9.8) 52.0) 41.8) 44.5 (41.2 (36.8 (17.3) 10.9) 47.8-33. chlordane was used to kill termites and other insects on agricultural crops.6 (9.S.7 (34.3 (20.4-14.5-41.4-21.1-25.5) 56. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.1) 30.1) 90th 34.20-10.6-45.

070-. 1977b.091) .160 (.270 (.269 (.287) .080) .170) .057 (.133) 90th .140-. The major metabolite of heptachlor is heptachlor epoxide.S.200-.130) .290-.115-.130 (.320) .286 (.058 (.053-.070 (<LOD-.430) .250 (. Le Marchand et al.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 * * * * .208 (.302) .250-. Smith. 1981). 2007.286 (.074-.077) .240-.049 (<LOD-..348) .130-. interval) Selected percentiles ( 95% confidence interval) Sample 95th .310 (. Survey Geometric mean (95% conf.170) .510) . 2001.120-. Chlordane and heptachlor are absorbed after oral.199-.148-.070) . Human health effects from either chlordane or heptachlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown.560) .231) .070 (<LOD-.250 (.055-.400) . Shindell and Ulrich.070 (<LOD-.190-. Elimination of all these chemicals from the body occurs over months to years.083 (. No clear evidence of excessive cancer rates was demonstrated in human epidemiologic studies (ATSDR.280-.080 (.300 (.360) .130-.087-.300) .100-.126) . characterized by seizures and paralysis.310) .065-.203-.290) .068) .291) size 1661 2249 1978 Total years 99-00 01-02 03-04 50th < LOD .210-.271 (.070 (<LOD-.061-.076) < LOD .128 (. EPA has established environmental criteria for chlordane and heptachlor. and the U.430) .340) .110 (<LOD-. 1991). IARC.140-.180-.253-.320 (.140 (.350) . heptachlor.210 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Rogan. 2007).092) .053-.146) < LOD < LOD . 1977a.330 (.066-.410) .Organochlorine Pesticides (Dallaire et al.260 (. 1986).230-.400) . Chronic feeding studies with either chlordane or heptachlor have demonstrated reduced fertility.060 (<LOD-.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. which is also persistent in the body (ATSDR.168-.240 (.160) .230 (.050-.280 (.350 (.130-.280-.104-.340) .148) .069 (<LOD-.225 (.370 (.170) .070-.190-.200-. The U. 82 Fourth National Report on Human Exposure to Environmental Chemicals . and inhalation exposure.310) .170) .070) < LOD < LOD < LOD < LOD < LOD .240-. high doses of either chlordane or heptachlor block inhibitory neurotransmitters and result in central nervous system toxicity.450) .057-.050 (<LOD-. FDA established allowable residues of chlordane.056 (.165-.130) .200 (.245-. to heptachlor.062) < LOD ..310) .170-.280-.300) .320) .440) .063 (.063) .130-.180-.180) .290) .207 (.120-.189-.090) . chronic doses of heptachlor have produced liver enlargement and injury.204 (.227) < LOD . 1996.207) .220-.073) < LOD < LOD < LOD < LOD . 2002.063 (.270 (.115 (.079) < LOD < LOD < LOD . which may vary for some chemicals by year and by individual sample.063) * .066 (.140) .189 (. In laboratory animal studies.150) .150-.210 (.120-..090-.300) .320 (.220-.315 (.300) .130 (.126 (.370 (.083) .063 (.290-. IARC considers chlordane and heptachlor as possibly carcinogenic to humans. and alterations in immune function of offspring.110-. and heptachlor epoxide in foods and bottled water.070-.320) 663 752 595 998 1497 1383 20 years and older Gender Males 99-00 01-02 03-04 * .136) .077) .280) . 1991.108-.100 (<LOD-.320 (.106-.112 (.104) .180) .S. 2006).140 (.077) .260-.242-.190-.213) * .370 (.100-.130-.373) .160) .075 (.140 (.S.090) .230) .058-.120 (.070 (.300-.140 (. Subtle neurodevelopmental effects have been observed rodents after prenatal exposure to heptachlor (IPCS. Acute. neonatal mortality.270 (.068-..062) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * .280 (.258-.066 (<LOD-.064) < LOD .320 (.220 (.230 (.066-. Epidemiologic studies have not demonstrated teratogenic or developmental effects (Baker et al.240) .150 (.380) .071 (.246-.230-.079) .082 (.223) .047 (<LOD-.149 (. both chlordane and heptachlor induced hepatic cytochrome P450 enzymes and increased the incidence of liver tumors (NTP.073 (.077) .058-. population from the National Health and Nutrition Examination Survey.080 (.150 (.119 (.170) . Chlordane is metabolized primarily to oxychlordane and to a lesser extent.260 (. OSHA has established occupational exposure criteria. 1986).068) 75th . dermal.216-.080) .130 (.290 (.100 (.067 (.080) . Takahashi et al.258 (.310-.063 (.057) * .150 (.450) .048-.160) .200-. and NIOSH and ACGIH have recommended workplace exposure levels for each pesticide.260 (.146) .230-.350 (. 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. and breast milk is a major excretion route in lactating women.063-.290-.

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

S. and 7.0-16.9) * * * Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 8.5) 19.3 (13.6 (11.7 (13.9-29.6 (16.3) 18.6) 13.2 (<LOD-25.6) 22.2-16.8) 13.3) 16.5) < LOD 14.8 (13.3) 27.0 (15.8-24.3-18.90 (<LOD-9. 01-02.6) 14.8 (18.7-19.8 (13.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.8 (18.8) 21.8-24.9-23.6-21.3) 18.0 (11.8-24.7 (16.7-18.5 (11.3) 22.0-17.0-54.5.5) 598 553 460 336 503 490 539 1041 888 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. 10. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.9) 15.0) size 1589 2259 1963 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th 90th 15.4 (<LOD-54.3 (<LOD-25.5 (<LOD-32.20 (<LOD-9.7 (10.4) 18.2) 20.6) < LOD < LOD < LOD 27.8-23.8.9-29.5 (11.10-13.5 (<LOD-21.2) 13.5 (18.8) 19.6-17.9 (15.0) 13. and 03-04 are 14.6 (13. interval) Selected percentiles ( 95% confidence interval) Sample 95th 24.2 (18.4 (11. 84 Fourth National Report on Human Exposure to Environmental Chemicals . respectively.5 (10.1 (16.2) 26. see Data Analysis section) for Survey years 99-00.50) < LOD < LOD < LOD 17.6 (<LOD-27.0-17.4 (15.8) 19.2 (<LOD-62.7-25. < LOD means less than the limit of detection.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 7.1) 13.4 (<LOD-19.8) 15.6 (12. Survey Geometric mean (95% conf.1-16.6.6 (16.8) 13.8 (<LOD-23.8) 14.3) 18.0-19.9 (12.2 (<LOD-16.1 (19.2-17.2) 15.9-25.0) 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 13.6 (14.1-15.1) 20.2-27. population from the National Health and Nutrition Examination Survey.3) 10.2-27.8) 16.8) 20.4 (11.8) 14.1-38. which may vary for some chemicals by year and by individual sample.4) 21.40) 15.1) 23.8 (15.9-16.1-29.3) 23.6 (8.8-46.

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

8 (28.2-23.5) 19.0 (62.1) 17.2) 17.6-88.0 (13.3) 19.5) 9. and 03-04 are 14.1 (10. 86 Fourth National Report on Human Exposure to Environmental Chemicals .8) 80.6 (32.9 (28.6) 13.S.1 (47.6 (50.5) 20.8-16.9 (36.2-37.6-54.0 (48.4-22.5-17.9-22.7 (35.1-51.3-32. population from the National Health and Nutrition Examination Survey.1) 17.5) 90th 55.2) 39.8) 47.0 (60.6) 54.1) 31.9-89.8-67.0-143) 112 (68. interval) 18.8 (12.0-123) 74.3 (14.3) 18.7 (16.0) 40.7-77.5.5 (15.7) 28.0 (16.4) 55.1-126) 67.8 (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.5) 14.70 (<LOD-12.3) size 1933 2286 1955 Total years 99-00 01-02 03-04 50th 17.3-86.3-39.2-18.7-38.0 (15.4 (30.2-18.1) 16.1) 18.9-65.6-66.8-19.3) 30.0) 75th 31.6 (57.0-93.7-22.7) 15.7-20.3-21.7-23.9-65.2 (60.3) 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.8 (15.3) 36.8 (28.4-52.4) 16.2) 19.86-13.1-16.5) 14.9 (16. and 7.4 (45.9-58.9) < LOD < LOD < LOD 20.2 (25.3 (16.0-24.1) 78.8 (17.2 (64.7 (11.0) 664 758 589 1269 1528 1366 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 17.8-129) 74.3-58.0) 19.2-17.7-21.8.5 (45.0-93.5-95.0 (16.7) 56.9 (47.6) 10.2-21.8) 51.3 (17.4) 20.2 (7.1 (41.1-55.3 (58.0) Selected percentiles ( 95% confidence interval) Sample 95th 79.0-37.0) 33.9 (<LOD-14.4 (11.7) 35. 01-02.0-68.5-111) 68.6) 56.0) 49.0 (19.6) 84.5) 77.2 (15.6 (<LOD-14.2) 34.5-19.8 (71.9) 922 1062 955 1011 1224 1000 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 * 11.0-113) 68.5 (15.5 (13.6 (56.2-16.1-20.1-28. Survey Geometric mean (95% conf.9 (15.0 (42.2-88.7) 78.6 (56.1) 14.2) 20.7-35.9-64.3 (14.3) 32.1-18.2 (59.5) 78.1 (48.3 (49.6-82.4) 107 (84.8 (26.0-23.1) 18.5) 22.0) 18. 10.1-34.1 (17.7 (13.7) 17.9-40.0-22.3) 16.9-35.9-36.7-17.1) 17.5) 26.9) 14.9 (51.4 (12.5) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * 20.6-19.7 (28.3 (45.7-113) 68.5 (44.9-69.5-69.8-79.0-38.4-67.9) 14.9 (29.2 (14.4-35.6 (12.6) 60.9-45.8 (19.0-59.6) 82.8 (26.3) 30.6) 25.0) 13.6 (15.7 (30.0 (13.6-22.7) 78.8-21.0) < LOD < LOD 8.8 (11.8-110) 59.4) 59.9 (51.8 (28.4 (28.5 (25.7) 73.0 (42. see Data Analysis section) for Survey years 99-00.8) 19.8 (<LOD-20.1-22.8-16.1 (22.8-90.8-41.7 (59.6 (16.5) 36.0-20.2) 59. < LOD means less than the limit of detection.7-160) 86.8 (30.5) 35.4 (16.8 (16.7) 52.1) 17. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.9) 51.1) 17.7 (59. respectively.4-18.6-20.4-23.4) 48.5-36.5.3 (56. which may vary for some chemicals by year and by individual sample.3-30.5) 30.2 (26.1) 17.4 (67.9 (19.6 (52.3-57.7 (18.8 (42.3-50.9 (66.5-87.7-34.7-32.9-20.8 (49.9) 51.7) 59.1-34.0 (15.1) 17.1 (65.7 (74.2 (19.8 (45.8-90.7) 14.2 (27.3) 32.6) 56.2) 30.2 (14.8-19.3-74.1) 32.7-29.1) 62.9 (15.8-77.3) 25.6) 34.5) 48.5-20.7-18.2) < LOD 10.4) 19.1-16.0-23.3) 15.0 (14.2 (36.4-62.10 (<LOD-11.1) 30.3) 18.4-36.1) 78.8 (26.8 (13.0 (29.

119) Selected percentiles ( 95% confidence interval) Sample 95th .410-1.108) 75th .177-.098) . Fourth National Report on Human Exposure to Environmental Chemicals 87 .090 (.490 (.098-.417 (.520 (.497-.090-.220) .160 (.440-.430-.220 (.330-.237) .232) .093-.095-.390) .210 (.128 (.460) .210 (.079-.211) 90th .250) .367) .240 (.355 (.171-.340-.237) .130 (.317 (.930) .080 (.091) .126) .110 (.540) .310 (.078 (.220 (.461 (.260) .279-.310) .580 (.109 (.120) .110) .580 (.140) .122) .093-.240) .400-.190-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.240-.840) .127) < LOD < LOD .141) .310-.120 (.440) .590 (.055 (<LOD-.094 (.343 (.205 (.103 (.091-.090 (<LOD-.116) .060-.114) .150) .161) .242) .460-.080-.120 (.085-.234) .20) .093) .161-.400) .111-.520 (.220 (.069) .173-.390-.090-.145-.085-.288-.047-.558) size 1933 2286 1955 Total years 99-00 01-02 03-04 50th .510 (.260) .470 (.135 (.490) .116-.130) .690) .190-.430-.125) .100-.320-.078-.371) .186-.110 (.108) .093-.110 (.559) .410-.550 (.106 (.630) .130) .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 .390 (.190-.070 (.120) .061-.370 (.460) .420 (.097) .129) .120) .082) .210) .105 (.590) .400-.170 (.420) .390 (.183 (.470 (.310-.390 (.590 (.760 (.327 (.600) .089 (.490-.120 (.120) .210) .390) .210-.286-.310-.096-.400 (.099-.120-.250) .290-. Survey Geometric mean (95% conf.108 (.350 (. population from the National Health and Nutrition Examination Survey.395) .124) .112 (.220 (.600 (.104-.180-.080-.160-.684) .414 (.340-.470 (.190-.300) .110 (.301-.220 (.100 (.109 (.285-.079-.150) .565) 922 1062 955 1011 1224 1000 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 * .480) .071 (<LOD-.100-.272-.158-.068-.830) .113) .395-.690) .220 (.062 (.490 (.106 (.100 (.120-.112 (.520) .330-.090-.390 (.651) .081-.134) .092 (.069-.830) .310-.360-.087 (.080-.330 (.041 (<LOD-.090-.100-.098 (.130) .113) < LOD .084-.250) .130) .202 (.180-.080-.500) .110 (.103 (.240) .106 (.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.280) .117) .210 (.580 (.096-.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.573 (.210) .640 (.360-.130) .350-.054-.340) .120-.565) .230 (.100) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * .190-.122) .098 (.288 (.080) .060) .380 (.099-.130) .324 (.131) .470-.111 (.220 (.090-.220 (.125 (.110 (.470-.081 (. interval) .510-.450) .240) .S.190-.130 (.594) .100-.409-.370 (.300-.085-.180-.458 (.060 (<LOD-.119) < LOD < LOD < LOD .320-.186 (.116 (.090-.104 (.680) .400 (.210-.960) .397-.110-.680 (.800) .430-.630) .096) .191 (.270-.130) .630) .141) .092 (. which may vary for some chemicals by year and by individual sample.405) .090) .

41:145–148. 1979-1980. Covaci A.inchem. Organochloride pesticide residues in human milk in Hawaii. J Occup Med 1986. Temporal trends of organochlorine concentrations in umbilical cord blood of newborns from the lower north shore of the St. Royce W.atsdr. Sci Tot Environ 2006.84:151-161.atsdr. Lulek J.niehs. Hertz-Picciotto I. Available at URL: http://ntp. Chashchin V. International Agency for Research on Cancer (IARC).330:55-70. Dewailly E. Available at URL: http://www. Smith AG.111:349355. maternal serum and milk from Wielkopolska region. Baker DB. Determinants of serum polychlorinated biphenyls and organochlorine pesticides measured in women from the child health and development study cohort. Trends in birth defects for a Hawaiian population exposed to heptachlor and for the United States. Organochlorine exposures and breast cancer risk in New York City women. International Agency for Research on Cancer (IARC) . Distribution of polychlorinated biphenyls. 2001. et al. 79. In Hayes WJ. et al. LeMarchand L. Willman E. et al. New York. Bull Environ Contam Toxicol 1981:27:506-511. Darnerud PO. Gilman A. Available at URL: http://www. gov/toxprofiles/tp12. Organochlorines in Swedish women: determinants of serum concentrations.gov/ntp/ htdocs/LT_rpts/tr008.9:1-109.html. Arch Pediatr Adolesc Med 1996. Vol.org/site/foundation/ research/projects2. Bjerselius R. Berkowitz GS. Handbook of Pesticide Toxicology.inchem. Wong L. Canada). May 1994.150:981-990. Ayotte P. Environ Health Perspect 2002. August 2007. 1986. Atuma S. Bioassay of chlordane for possible carcinogenicity. Concise International Chemical Assessment Document 70 Heptachlor [online].nih.50(3):108-118.nih. Available at URL: http://www.htm. Wolff MS. Chlordane and heptachlor [online].heptachlor. Takei G. Van Oostdam JC. Loo S. Laliberte C. KalubaSkotarczak A.gov/toxprofiles/tp31. Chlorinated Hydrocarbon Insecticides.pdf. Environ Res 2000. Keller JA.Summaries & Evaluations. Available at URL: http://www.cdc. National Toxicology Program (NTP). Bleiweiss IJ. Estimation of Human Exposure to Heptachlor Epoxide and Related Pesticides in Hawaii. Shindell S and Ulrich S. Saidein D.cdc.gov/ntp/ htdocs/LT_rpts/tr009. 1963-1967. Evaluation of human exposure to the heptachlor epoxide contamination of milk in Hawaii. Eds. et al. 6/1/09 Rogan WJ.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). 2006.110:617-624. Glynn AW. Toxicological profile for heptachlor and heptachlor epoxide [online].niehs. An evaluation of serum pesticide residue levels and liver function in persons exposed to dairy products contaminated with heptachlor. 6/1/09 National Toxicology Program (NTP).110(8):835-838. Charles MJ. Wohlleb JC. 731-915. 2 Classes of Pesticides. Barker J.org/documents/iarc/ vol79/79-12. Bioassay of heptachlor for possible carcinogenicity.28:497501. 1993. Inc. Brower S. Natl Cancer Inst Carcinog Tech Rep Ser 1977a. Environ Health Perspect 2003. 1994-1997 organochlorine compounds.html. Takahashi W. 1991 pp. Siegel BZ.pdf. Kolonel LN. Hawaii Med J 1991. Mortality of workers employed in the manufacture of chlordane: an update. Academic Press. Odland JO.htm. Circumpolar maternal blood contaminant survey. Environ Health Perspect 2002. Jr and Laws ER. Head SL. Voorspoels S. Arch Environ Health. Aune M. Natl Cancer Inst Carcinog Tech Rep Ser 1977b. Muckle G. 4/21/09 Baker DB. 4/21/09 Dallaire F. Pollutants in breast milk. Senie R.259(3):374-377. Jr. Poland. Tartter P. Vol. organochlorine pesticides and polybrominated diphenyl ethers in human umbilical cord serum. Stehr-Green P. Dendle WH. A Report to the Hawaii Heptachlor Research and Education Foundation. 4/21/09 James RA. JAMA 1988. Hansen JC.html. 4/21/09 Agency for Toxic Substances and Disease Registry (ATSDR).372:20-31. Available at URL: http://ntp.org/ documents/cicads/cicads/cicad70. Sci Total Environ 2004. 9/25/07 International Programme in Chemical Safety (IPCS). Lawrence River (Quebec. Jaraczewska K. Toxicological profile for chlordane [online]. Drews K.8:1-123. Available at URL: http://www. Granath F. Dewailly E. 88 Fourth National Report on Human Exposure to Environmental Chemicals .

In the body.6-33.8-39. see Data Analysis section) for Survey years 99-00. p. 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.7 (19. fish.6 (22. 2002. It is still used in some countries.7 (15.0 (18.2 (<LOD-40. < LOD means less than the limit of detection. Fourth National Report on Human Exposure to Environmental Chemicals 89 . as well as in plant and animal tissues.9) 29.1 (33.S. and dairy products. Only a small proportion of DDT is metabolized and excreted (Smith.9 (10. These chemicals are highly persistent in soil. and water. o.p’-DDT (65%-80%).70 (8.6 (31.0) 19.0 (18.p’-DDT (15%-21%). In the general U. population from the National Health and Nutrition Examination Survey. continues to be the primary source of DDT exposure. which may vary for some chemicals by year and by individual sample. DDT can be absorbed after ingestion.S.2-95.50-11. DDT was used at one time as a treatment for head and body lice.2) 155 (59. 1991).8-17. 1988).8) 36. 2008.5 (23.0-37.2-dichloroethenylidene)-bis[4-chlorobenzene] (DDE) and 1.9 (<LOD-20.9 (21.7.3-16.00 (<LOD-10.5-54.9) 14.3) 21.0-155) 83. including 1.2-65.3-236) 24.5 (23.5 (14. population.4) < LOD 17.8. Smith. 01-02. food. interval) Selected percentiles ( 95% confidence interval) Sample 95th 28.8) 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. and trace amounts of several related compounds. 1991).1’-dichloro-(2.0-35. sediments. and 03-04 are 20.10-13.9-34. Gunderson.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. Survey Geometric mean (95% conf.1 (23. DDT and DDE are distributed to all body tissues with the highest concentrations found in adipose tissues (ATSDR.3) 22. inhalation.0-53.9 (10. DDT is converted to DDE and several other metabolites. air. Both Serum p.5-36.1 (<LOD-39.1’-(2. The biodegradation half-life of DDT in soil varies from 2 to 15 years. Food imported from countries that still use DDT may contain the chemical or its residues.S.1-27.6) 635 566 461 356 514 490 564 1061 890 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.9 (10.1-71.p'-Dichlorodiphenyltrichloroethane (DDT) (lipid adjusted) Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U.0-27.9) < LOD < LOD 9.5) < LOD < LOD 9.1) 31.5 (15.90 (<LOD-12.10 (<LOD-12.6 (9.8) 15.0 (10.7) < LOD 18. resulting in fetal exposure.2) < LOD < LOD 9. particularly for endemic vector and malaria control.3 (<LOD-21. depending on conditions.2) 30.0 (21.8-23. DDT and DDE can cross the placenta.2-bis(p-chlorophenyl) ethane (DDD). DDT is converted in the environment to other more stable chemical forms.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 12.9) 17.0) 20. which is a mixture containing p.4 (23.9-28.0) 40.4) < LOD < LOD < LOD 61.7-16.8-26.3-590) 293 (104-541) 48.2 (11.8) 30. or dermal exposure. when virtually all use of it was banned.3 (<LOD-31.3 (27.5) 25. and 7. after World War II until 1972.0-15. although DDT and DDE intakes have decreased over time (FDA. 17.7) 12.6 (<LOD-25.6 (25.Organochlorine Pesticides Dichlorodiphenyltrichloroethane (DDT) CAS No. respectively.3) 28.5) size 1679 2305 1965 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * * 11.p’-DDD (4% or less).3) 21. DDT usually refers to the technical product. It was produced and used in the U.4. particularly meat.5) 23.0) 26.

1996).054-.150-.140) .120 (<LOD-..084 (.200 (.g.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 .p’-DDE can produce anti-androgenic effects (Gray et al. Several reviews of cancer epidemiologic studies have concluded that a link between DDT and breast cancer is inconclusive (Beard.330-4. Human health effects from DDT at low environmental doses or at biomonitored levels from low environmental exposures are unknown.150-.00 (.150 (<LOD-.130 (<LOD-.068-. have not been consistently demonstrated (Beard.180-.203) .079) < LOD < LOD .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 . resulting in exposure to nursing infants (Rogan. 2006).190-1. and o. 2006).075) 1.180 (.143) < LOD < LOD . Studies of DDT exposure and pancreatic cancer.420) .260) .167) size 1679 2305 1965 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * * . 90 Fourth National Report on Human Exposure to Environmental Chemicals .230) . 2006). Animal studies reported reduced fertility.. overt signs of acute human toxicity include vomiting. which may vary for some chemicals by year and by individual sample. polychlorinated biphenyls.128 (.105-.180) .087 (. and duration of lactation. A workplace standard for DDT has been established by Serum p.064 (.230) .240) . both DDT and DDE may induce specific cytochrome P450 isozymes (Nims et al. accidental exposures.078 (. 2006. 2002. 1956). tremor.086 (.570-4.130 (<LOD-.095) < LOD .313 (. DDT may bind to estrogen receptors (Chen et al. reproductive organ abnormalities.132-.130-.290) .190 (. Reproductive effects in humans affecting birth weight. Survey Geometric mean (95% conf.170-.180 (. 2002. 2001).p'-Dichlorodiphenyltrichloroethane (DDT) (whole weight) Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U. 2006. although the risk for preterm delivery may be related to maternal DDE levels (Longnecker et al. 2002. interval) Selected percentiles ( 95% confidence interval) Sample 95th .142 (.627) ..130 (<LOD-. premature delivery. lung cancer. 1998).071 (.p’-DDD and p.074-.170) .S.106-.108 (.080-. 2001).180) . 2002.059-. In high dose.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.146 (.530 (.530) .. Longnecker et al. other organochlorines.114-.Organochlorine Pesticides chemicals are excreted in breast milk. 2006. and altered behavior after neonatal exposure (Eriksson and Talts.170 (. Jusko et al.051 (<LOD-.069) .146 (.048 (<LOD-. Mariussen and Fonnum.. It is difficult to attribute outcomes in human studies solely to DDT because of potential co-exposure to other persistent organohalogen chemicals (e.34) .063 (<LOD-.140-. 2000.098-.250 (.250-1.01) .. Hayes et al..400 (. 2001). Beard.189-..106) .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 .220) . 2001). and leukemia have also been inconclusive (ADSDR.201 (.. dioxins and furans). Jusko et al.112 (. Epidemiologic studies of children with environmental exposure to DDT and DDE have not demonstrated neurologic or developmental abnormalities (Gladen et al. fertility.106) < LOD < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.071-.190 (.220) .26) 1. In laboratory animals.00) .150) .061) < LOD < LOD < LOD . population from the National Health and Nutrition Examination Survey. Calle et al...343) < LOD .120-.400) . 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.065-.240 (.. 1995. Gladen and Rogan. 1997).150 (<LOD-.078-. 2004. Snedeker.160-. and seizures. Gray et al.62 (.

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.epa. 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. and the most recent median levels for German adults and children are similar to levels in this Report (Becker et al.S. Declining DDE levels over time have also been observed in the German population. EPA at: http://www. and 7.Organochlorine Pesticides OSHA and a guidance established by ACGIH. Biomonitoring Information DDE persists in the body longer than DDT. Compared to females in the NHANES 1999-2000 subsample. 2005). respectively. Heudorf et al. In general. and 03-04 are 18. Survey Geometric mean (95% conf.e. A study of New Zealand adults sampled in 1996-1997 reported median DDE levels that were about threefold higher than the median for adults in the NHANES 1999-2000 subsample (Bates et al. 8. 01-02. 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. 2004). 2002. Stehr-Green.3.S.8.. Smith.6 (81. compared to levels observed in this Report (Anderson et al.. the lipid-adjusted geometric mean levels of DDT and DDE were each fivefold to tenfold higher than the 95th percentile and geometric mean levels.6. respectively. see Data Analysis section) for Survey years 99-00.html. population declined by about fivefold to tenfold. levels of DDT and DDE increase as a person ages as a result of cumulative exposure (ATSDR. 1998. 1991). NTP considers DDT as being reasonably anticipated to be a human carcinogen. In a population-based sample of men and women from eastern Slovakia. population from the National Health and Nutrition Examination Survey.. Link et al.gov/ pestcides/ and from ATSDR at: http://www. 2002.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. mean DDE levels were about fivefold higher among women of southern Spain exposed by virtue of Serum p. 2004). Since the 1970’s.. Fourth National Report on Human Exposure to Environmental Chemicals 91 .7-119) 113 (100-140) 93... for males and females in the NHANES 19992000 subsample (Pavuk et al.S..gov/ toxpro2. IARC classifies DDT (p. mean serum levels of DDT and DDE in the U.cdc. More information about external exposure (i. 2003. so serum DDE levels may be an indicator of historic exposure and may be higher than DDT levels in the same person. environmental levels) and health effects is available from the U.. 2003).p’-DDT) as a possible human carcinogen.atsdr. 1989).7-129) 297 (256-344) 338 (303-376) 268 (217-332) 108 (97.

07 (5.1) 7.6) 13.00-1.68) 2. 1991).66-2.17-3.2 (19.01-5.66-4.43-8.6) 9.99) 1.30 (1. Consumers of Great Lakes sport fish had mean serum DDE levels that were only slightly higher than nonconsumers.3) 16.64-2.4) 14.82) 1.45 (1.71 (5.14) 2.4 (12.69) 4. serum levels of o.8-90.66) 4.31-12.57-2.6) 11.1 (8.43 (5.7) 9.600) .51 (1.557) 1.01-1.75 (8.87-16.01) 1.0 (9.63 (1.3-43.76) 1.4 (8.3) 13.18 (6.6) 8.33-1.61 (1.870 (.34-11.75) 1.5) 7.46 (1.6 (8.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.25) 1.55-9.1) 40.97-4.0) size 1964 2298 1956 Total years 99-00 01-02 03-04 50th 1.860 ng/L) and DDE (about 14.91) 3.7) 13.65) 1. 1989).48-4.56) 2.40 (3.21) 3.59 (1.6) 12.5) 10.37-16.09-1.04 (6..30-1.81 (7.8 (14.890-1.17 (3.456 (.10-1.66) 1. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.S.15-4.88-35.85-10.07) 1. A small study of Indian men with background exposure reported mean serum DDT and DDE levels that were around fiftyfold higher than the 95th percentile for DDT and tenfold to twentyfold higher than the geometric mean DDE levels among males in this Report (Bhatnagar et al.82 (1.5) 5. 2005).79) 4.13 (1..6) 9.680-1.84 (3.32-1.9 (26.53-15.69 (1.11 (2.40-4.8 (9.49 (1.51-8.64) 3.3 (9.57-3.4) 13.5) 22.81-18.45 (1. Serum p.75 (4.90-8.p’-DDT.66-17.1) 12.10) .00 (6.9) 5.p’-DDT were below the limits of detection.32 (1.54-7.36 (3.49 (1.65 (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 .26-10.10-5.534-.3) 937 1069 955 1027 1229 1001 Females 99-00 01-02 03-04 Race/ethnicity Mexican Americans 99-00 01-02 03-04 3.43-4. considerably higher than levels in this Report (Smith.81) 11.13-2.76 (2. less than one percent had detectable serum levels of o.29 (1.68-4.965-1.80) 1.0) 2.93 (7.57) 2.26-2.22) .25 (1.77 (1.58) 1.12-1.623 (.22-1.11-1.21) 90th 7.7) 16.796 (. 2004).35) 1.1 (9.37 (1.34) 6.32-1.80 (2.646) .58) 1.63-15. In the NHANES 1999-2000.58) 75th 3.04-1.79) Selected percentiles ( 95% confidence interval) Sample 95th 11.520 (.06) 1.24) 1.52 (3.6) 9.91 (6.47 (1.91-3.97 (3. 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.69) 8.39 (3.p’-DDE in serum does not mean that the level of the chemical causes an adverse health effect.79) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 .02) 1.01-11.85 (1.963-1.5) 16.9-17.70-3.2) 19.80) 3.6 (9.32 (1.40-8.18-1. 1971).84-3.57 (1.02-8.03-1.06) 3.39) 1.2 (9.25) 8. 2001-2002 and 2003-2004 subsamples.27-1.00 (. interval) 1.59 (4.76-3.8) 686 758 588 1278 1540 1368 20 years and older Gender Males 99-00 01-02 03-04 1.32) 1.6 (7.20 (.71) 32.23 (7.55 (2.88 (2.730) .61-2.3) 10.6) 9.2 (6. High mean levels of whole blood DDT (about 3..02 (2.50-17.05 (3.37-10.994-2.91-2.26) 3.9-38.2 (9.46-2.26 (1.59) 3.51) 1.75) 6.0 (12.7 (8.71 (6.27) 3.59) 6.12 (.01-15.24 (1.51) 3.10) 2.4) 9.49 (6.16-1. Finding a measurable amount of p.30-1. population from the National Health and Nutrition Examination Survey.38 (1.53) 7.18) 1.51-15.18-4.9 (15.18-1.488-.7-20.14-9.36) 3. In a subsample of NHANES II (19761980) participants.47) 3.56-6.3 (8.726) .66) 1.p’-DDT (Stehr-Green.57 (3.38 (1.6 (17.80) 1.62-6.49) 8.36-11.500-.48 (6.76) 1.01-1..22 (7.90) 22.7-19.25-14.56-2.05) 1.07) 1. 2004).37-1.51-49.41 (1.31-2.41-12.50 (2.9) 7.71) 12.34) 2.40-4.19) 4. 309 versus 268 ng/g lipid.83 (1.69 (2.72) 1.25-16.7-48.820-1.419-.53 (2.01) 1.92 (3.46 (1.14) 2.56-3.28) 1.78 (4.Organochlorine Pesticides nearby agriculture (Botella et al.43-4.37-4.53) 1.p’-DDT.39-2.36-2.516 (.92) 1.92 (3. or p.69 (.68 (2.385-.00) 7.430-.57-13.66) 3.8 (13.52-6.635) 1.8 (13.36-1. which is similar to the overall geometric mean of 260 ng/g lipid in the NHANES 1999-2000 subsample (Bloom et al.18-3.561 (.611-1.57 (1.590 (.85-4. Workers involved in production or application of DDT developed neurologic abnormalities associated with blood levels around 100-300 mg/L.4-19.63 (1.19-14.25 (.31 (1.77 (1.32-9.81 (1.30 (1.52 (1.81-5.54 (1.87 (5.70) 1.34-3.16 (2. Survey Geometric mean (95% conf.59 (1.14-1.34 (7.490 ng/L) were found many years ago in a study of pesticide workers in Argentina (Radomski et al.03-4.13) 4.96) .72) 1.14 (1.54) 8.2) 26.75) 2.96) 1.01-11.24-17.60-13.44) 1.8) 15. o.39-1.12 (6.63 (6.2-32.

17. and 03-04 are 20. population from the National Health and Nutrition Examination Survey. which may vary for some chemicals by year and by individual sample.S. < LOD means less than the limit of detection.8. see Data Analysis section) for Survey years 99-00. respectively.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. and 7.Organochlorine Pesticides Serum o. 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.4. 01-02. * 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 .7.

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

Vena JE. Garrett N. Sci Tot Environ 2006. Toxicological profile for DDT. Klebanoff MA. Gray LE Jr. Katz SH. 4/21/09 Anderson HA. Herrman T. Rivas A. Zaidi SS. Kashyap R. Hum Reprod Updat 2001.html. hexachlorobenzene. Profiles of ortho-polychlorinated biphenyl congeners. et al. CA Cancer J Clin 2002. Patterson DG Jr. Heudorf U. Ellis H. and other chemicals. Atuma S. Baker RJ.html.53(8):1161-1172. selected elements. et al. Organochlorines in Swedish women: determinants of serum concentrations. a biostable metabolite of dichloro(diphenyl)trichloroethane (DDT). Cueto C. Link B. 4/21/09 Gladen BC.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR).162:890-897. et al. Piechotowski I. Lancet 2001. Thun MJ. Effects of environmental antiandrogens on reproductive development in experimental animals.7(3):248-264. Available at URL: http://www.17(6):692-700. Wolf CJ. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. Furr J. Hurd C. Falk C. Environ Health Perspect 1998. Klebanoff MA.72:261265. JAMA 1956. Hanrahan L. Environ Res 2005. Angerer J. Gabrio T. Neurotoxicol 2000. et al. Bloom MS.97(2):178192. Environ Health Perspect 2004. Henley SJ. Bjerselius R. DDE and shortened duration of lactation in a northern Mexican town. Hediger ML. Transcriptional activation of the human estrogen receptor by DDT isomers and metabolites in yeast and MCF-7 cells. Hayes WJ. lindane (g-HCH). FDA total diet study. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. and dichloro(diphenyl)ethylene (DDE). Epidemiology 2006. Frumkin H. Biochem Pharmacol 1997. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. Current internal exposure to pesticides in children and adolescents in Germany: blood plasma levels of pentachlorophenol (PCP).1-dichloro2. Neonatal exposure to neurotoxic pesticides increases adult susceptibility: a review of current findings. Talts U. Available at URL: http://www. Savitz DA.96:34-40. Buckland SJ. Olea-Serrano MF.54:1431-1443. et al. India.. Maternal serum level of 1. Ostby J. Levels of DDT. Krause C. Environ Health Perspect 2003. Longnecker MP.206:485-491. Beard J. Zoellner I. J Assoc Off Anal Chem 1988. Food and Drug Administration (FDA). Cerrillo I. Saiyed HN. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods.205:297-308. Vorojeikina DP. Association between maternal serum concentration of the DDT metabolite DDE and preterm and small-for-gestational-age babies at birth. Organochlorines and breast cancer risk.fda. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Burse VW. Biomonitoring of persistent organochlorine pesticides. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. April 1982 to 1984. Kulkarni PK. Granath F. Crespo J.atsdr.gov/~dms/ pesrpts. Prenatal DDT exposure in relation to anthropometric and pubertal measures in adolescent males. Bhatnagar VK. Paepke O. Jr. and HCB residues in human blood in Ahmedabad. Needham LL. Calle EE. Becker K. Gunderson EL. Rogan WJ.85:504508. Fourth National Report on Human Exposure to Environmental Chemicals 95 . Durham WF. et al. Kaus S. Am J Public Health 1995. Bates MN.112(17):1761-1767. Aune M. Olson J.21(1-2)37-48. Zhou H. Zhou H. DDT and human health. Parks L. Chemosphere 2005. Botella B. Lambright C. Exposure of women to organochlorine pesticides in Southern Spain. Maternal DDT exposures in relation to fetal and 5-year growth. Brock JW. Jusko TA. Olson JR. dietary intakes of pesticides.gov/ toxprofiles/tp35. Koepsell TD. Notides AC. and polythelia among male offspring. Schulz C. HCH.2-bi(p-chlorophenyl)ethylene and risk of cryptorchidism. Klebanoff MA. Gladen BC. Needham LL. Gray KA. Greenfield TA. Willman EJ.355:7889. Charles MJ. Am J Epidemiol 2002.52:301-309. Int J Hyg Environ Health 2003. Int J Hyg Environ Health 2002. August 2008. Arnold SF.106(5):279-289.358:110-114. dichlorodiphenyldichloroethylene. Environ Res 2004. and Mirex among male Lake Ontario sportfish consumers: the New York State Angler cohort study. Olea N. et al. September 2002. Davis MD. Swanson MK. hypospadias.58:1185-1201.cdc. Chemosphere 2004. Jr. DDE.111:349355. et al. Bull Environ Contam Toxicol 2004.155(4):313-322. Seiwert M.cfsan. Glynn AW. Lepom P. Chen CW. Barr DB. and DDD [online]. Darnerud PO. et al. Longnecker MP. The effect of known repeated oral doses of chlorophenothane (DDT) in man. Moysich KB. Eriksson P. Needham LL. Brock JW. Drexler H.71(6):1200-1209. The Great Lakes Consortium.

Pollutants in breast milk. Pavuk M. Rey AA.109:35-47. Smith AG. J Toxicol Environ Health Part A 1998. and dieldrin. Arch Pediatr Adolesc Med 1996. Chlorinated Hydrocarbon Insecticides. Handbook of Pesticide Toxicology. J Toxicol Environ Health 1989. Inc. Jr. Environmental exposure to PCBs and cancer incidence in eastern Slovakia. and DDD in male rat liver and cultured rat hepatocytes. DDE. children and newborn infants.20(2):186-193.150:981-990. DDE. New York. Lynch CF. Jones CR. In Hayes WJ. Pesticides and breast cancer risk: a review of DDT. Blood levels of organochlorine pesticides in Argentina: occupationally and nonoccupationally exposed adults. Rogan WJ. Deichmann WB. Vol. Thomas PE.53:455-477. Reddy AB. Stehr-Green.36:253-589. Comparative pharmacodynamics of CYP2B induction by DDT. Demographic and seasonal influences on human serum pesticide residue levels. Petrik J. Snedeker SM. Lubet R. et al. 2 Classes of Pesticides. Cerhan JR.27:405-421. Fox S. Environ Health Perspect 2001. PA. Chovancova J. Schecter A. Crit Rev Toxicol 2006. 1991 pp. Nims R. et al. Neurochemical targets and behavioral effects of organohalogen compounds: an update. 96 Fourth National Report on Human Exposure to Environmental Chemicals .Organochlorine Pesticides Mariussen E. Fonnum F. Eds. 731-915.54:1509-520. Radomski JL. Academic Press. Chemosphere 2004. Astolfi E. Jr and Laws ER. Toxicol Appl Pharmacol 1971.

Endrin is absorbed rapidly after ingestion. 1987). Survey Geometric mean (95% conf.8.50) < LOD 5. endrin is converted rapidly to its major metabolite. interval) Selected percentiles ( 95% confidence interval) Sample 95th 5. 1992). and inflammation (Smith. Fourth National Report on Human Exposure to Environmental Chemicals 97 . endrin has been detected with declining frequency in U.10 (<LOD-5.S. 2008).S. endrin blocks inhibitory neurotransmitters in the central nervous system resulting in excitation and seizures (Narahashi et al. largely the result of historical agricultural application or run off from contaminated soils (ATSDR.40) < LOD 547 433 487 446 1000 831 Limit of detection (LOD.20 (<LOD-5.30 (<LOD-6. endrin usually is not detected in serum of exposed individuals.20 (<LOD-5. or from contact with contaminated soils and sediments in areas where endrin was applied. EPA. 1991). Hepatic effects of endrin exposure have included necrosis. 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. Further conversion occurs to 12-ketoendrin and various conjugated metabolites which are excreted in urine and feces. Kavlock et al. Endrin was not widely used as a termiticide. 72-20-8 General Information Endrin.30) < LOD 5.S. total diet surveys (FDA.50) < LOD < LOD < LOD 5. 1979.S. manufactured.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... characterized by generalized seizures in previously healthy persons occurred in Pakistan when sugar contaminated with endrin was ingested (Rowley et al.. fatty infiltration. All uses of the pesticide in the U. 1996. which may vary for some chemicals by year and by individual sample. anti-12hydroxyendrin.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 5.40-5. 1992).60 (5. unlike aldrin and dieldrin. Endrin was used as an insecticide.10 (<LOD-5. Over time.09 and 7. Skeletal abnormalities and cleft palate in the offspring were associated with endrin when it was fed to pregnant laboratory rodents (Chernoff et al.Organochlorine Pesticides Endrin CAS No. Because it is metabolized so rapidly. or discarded. rodenticide and avicide.. endrin can persist for years. a stereoisomer of dieldrin. is no longer manufactured in the U. inhalation or dermal exposure routes. In the body. Endrin has been detected in soils. unless the dose is high and the exposure is very recent. Endrin does not accumulate in body tissues (IPCS. 1991). < LOD means less than the limit of detection. Smith. and occasionally at low levels in sediment and surface waters. have been cancelled by the U. Ketoendrin is a major photodegradation product (IPCS. 1981). 1992). 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. IPCS. see Data Analysis section) for Survey years 01-02 and 03-04 are 5. 1992.40 (<LOD-6. General population exposure can occur after ingestion of endrin residues on food items imported from countries where endrin is still used. At high doses. High doses produced renal tubular necrosis and diffuse kidney degeneration in animals. Human health effects from endrin at low environmental doses or at biomonitored levels from low environmental exposures are unknown. Depending on soil conditions.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. An epidemic of acute endrin poisoning.

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

9:1357-136. 1992. Grajewski B. Sodium and GABA-activated channels as the targets of pyrethroids and cyclodienes.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Vol.21:141-150. 4/21/09 Bates MN.atsdr.org/documents/ehc/ehc/ ehc130. Whitehouse DA. pp. Andersen A. Patterson DG Jr. 4/21/09 International Programme on Chemical Safety (IPCS). Food and Drug Administration (FDA). Chernoff H. Available at URL: http://www. 2 Classes of Pesticides. Available at URL: http://www. Olea N. Academic Press. II. Hardjotanojo W.gov/~dms/ pesrpts.cdc. New York. Frey JM. Ellis H. Toxicol Lett 1992. Rowley DL. I. Chernoff N.fda.htm. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. et al. Saleem M.gov/toxprofiles/tp89. Gray LE. Jr and Laws ER. Crespo J. Rab MA. Endrin [online]. Gray LE.html. Cerrillo I. Toxicological profile for endrin [online]. Cancer Epidemiol Biomarkers Prev 2000. Toxicology 1979. Turner W. Sokal D. Chlorinated Hydrocarbon Insecticides. Eds.inchem. Environ Res 2004. 4/21/09 Kavlock RJ. Chemosphere 2004. Environmental Health Criteria 130.html. Narahashi T. Needham LL. Botella B. Gray J.96:34-40.cfsan. Schulte P. Pediatrics 1987. Hanisch RC. No:429-436.64-65 Spec. Liddle J. 731-915. Gray JA. Fetotoxic effects of prenatal exposure in hamsters. Ginsburg KS. Jr. Perinatal toxicity of endrin in rodents. Exposure of women to organochlorine pesticides in Southern Spain. August 1996. Burse VW.13:155-165. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Kavlock RJ. Patterson DG Jr. 1991. Hanisch RC. Olea-Serrano MF. Ward EM. In Hayes WJ. Rogers E.79(6):928-934. Convulsions caused by endrin poisoning in Pakistan. Smith AG. Buckland SJ. Roy ML. Available at URL: http://www. Handbook of Pesticide Toxicology. Fetotoxic effects of prenatal exposure in rats and mice. Toxicology 1981. et al. Garrett N. Perinatal toxicity of endrin in rodents. et al. Fourth National Report on Human Exposure to Environmental Chemicals 99 . FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Rivas A. Serum organochlorine levels and breast cancer: a nested case-control study of Norwegian women. August 2008. et al. Inc.54:1431-1443.

The general population may be exposed to HCB through diet. < LOD means less than the limit of detection.3 (14.3) < LOD < LOD 29. see Data Analysis section) for Survey years 99-00.4.2) < LOD < LOD 13.6) < LOD < LOD 26.3 (22. water.1) < LOD < LOD 15.3) < LOD < LOD 20.4 (11.8 (26.8 (15.4) < LOD < LOD 22.5-15.1-20. Survey Geometric mean (95% conf.9-20. and elimination occurs by renal and fecal routes.4 (22. 2.9-24.8) 583 554 460 350 511 488 636 1052 888 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.3) 24.3 (22. air.5-TCP) and 2.7 (19.9) < LOD < LOD 28. It is a persistent chemical and bioaccumulates in both aquatic and terrestrial food chains (ATSDR.5-14.3 (20.6 (23. HCB may be created as either a byproduct or an impurity in the manufacturing process for certain chemicals and pesticides.5-trichlorophenol (2. 2008. and foods with a high fat content. and 03-04 are 118.6 (21. HCB is slowly metabolized. wildfowl.0-19.7-22. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.0-16.4.5-33.2 (24.0) < LOD < LOD 24. Although it is not manufactured as an end-product in the U.S.1-16. and sediment (Barber et al.1 (14.6) 591 747 588 1111 1530 1373 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * 14. 1988).6 (24..9) < LOD < LOD 16. 118-74-1 General Information Hexachlorobenzene (HCB) was used from the 1930’s to the 1970’s in the U.1 (13.3) * * 15.0 (18.2-15..7) 807 1058 957 895 1219 1004 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * 16.8 (22.7-21.2-15.6) < LOD < LOD 25.9 (14.1) * * 15. distributes widely throughout the body.9-32. Urinary metabolites include pentachlorophenol (PCP). population from the National Health and Nutrition Examination Survey.7-26.0-28. Hexachlorobenzene has entered the environment as a result of industrial activities and pesticide applications.9 (23. particularly by consuming fish.8-15.0 (18.5-18.S.7-30.2 (14. Workers in chemical manufacturing industries may be exposed to HCB via inhalation or dermal pathways. 1976). respectively.6-26.0) * * 15.7-15.8.6-19. HCB is well absorbed after oral administration.9) < LOD < LOD 15..9) < LOD < LOD 19. and has been detected in soil. and 7.6-33.6) < LOD < LOD 26.8) < LOD < LOD 27.3-22.3 (12. 100 Fourth National Report on Human Exposure to Environmental Chemicals .7-16.9 (25. 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.S. or game taken from areas with HCB contamination.3 (16.2 (13. EPA cancelled its use in 1984. and accumulates in fatty tissues where it persists for years. 2002).5) < LOD < LOD 18.7 (15.9) < LOD < LOD 20.4 (18.9 (25.9-17.0 (14. Gunderson. 2005). 31.3-26.9-30.7 (27.1 (17.4) < LOD < LOD 33.9) 19..2 (17. HCB has been detected in fewer foods since the 1980s (FDA.9-15. which may vary for some chemicals by year and by individual sample. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD 28.4) < LOD < LOD 18. breast milk is an additional route of elimination in nursing women.9) < LOD < LOD 20.4-16.7) * * 14.2-31.4) < LOD < LOD 14.7) < LOD < LOD 24.7-16. 1997).6-32. primarily as a fungicide and seed treatment until the U.8) size 1702 2277 1961 Total years 99-00 01-02 03-04 50th < LOD < LOD 14.6-44.7-29. The FDA dietary surveys have shown that over time.0) < LOD < LOD 15.6-TCP) (To-Figueras et al.4) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * 13.4.4.0-25.6) < LOD < LOD 14.7) < LOD < LOD 75th < LOD < LOD 90th * * 15.5-14.4) < LOD < LOD 23.0.3-20.0 (25. these metabolites can also be produced after exposure to other chlorinated compounds (Kohli et al. 01-02.5-15.2 (14. Therefore.7 (15.5 (14.5 (13.0) < LOD < LOD 15.4) < LOD < LOD 19.4 (18.Organochlorine Pesticides Hexachlorobenzene CAS No.2) < LOD < LOD 29.S.1 (14.6) < LOD < LOD 24.4-15.4.5 (13.6-trichlorophenol (2.

109) * * . The U.182 (. reproductive and developmental toxicities.097) .085-.123 (.102) < LOD < LOD .115 (. anorexia. environmental levels) and health effects is available from the U.140 (.111) < LOD < LOD .062-.epa.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.159-. Human health effects from HCB at low environmental doses or at biomonitored levels from low environmental exposures are unknown.167) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * . and many died before 2 years of age (Peters et al.186 (.html.129) < LOD < LOD . interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD .141) < LOD < LOD .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 * * .095 (.123 (.097) < LOD < LOD .gov/pesticides/ and from ATSDR at: http://www. Biomonitoring Information Serum concentrations reflect the body burden of HCB.S.118-.091-. as well as hypertrichosis.cdc. acute doses produce central nervous system depression and seizures.212) size 1702 2277 1961 Total years 99-00 01-02 03-04 50th < LOD < LOD .143-.082-.203) < LOD < LOD . population from the National Health and Nutrition Examination Survey. 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.088-. Chronic feeding studies in animals have demonstrated kidney injury.092 (. and liver and thyroid cancers (ATSDR.081 (.094 (. Fourth National Report on Human Exposure to Environmental Chemicals 101 .118) < LOD < LOD .179 (.152) < LOD < LOD .191 (. With chronic exposure.086) < LOD < LOD .107-.087 (.178-.120 (.065 (.174-.176) < LOD < LOD . IARC classifies hexachlorobenzene as possibly carcinogenic to humans.135-.095-.163-.099) < LOD < LOD .083) < LOD < LOD .090 (.104 (.099) < LOD < LOD .148-.077-.225 (.097 (.167 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.S. a consequence of these heme abnormalities is a condition known as acquired porphyria cutanea tarda.132) < LOD < LOD .gov/toxpro2.088-.147-.163) < LOD < LOD . very high.100) < LOD < LOD . immunologic abnormalities.078 (.111-.085) * * .113-. This condition. 1982. HCB interferes with normal heme synthesis.173) < LOD < LOD .175) < LOD < LOD .157-..090 (..090-. 2002). EPA at: http://www.079 (.073-.107) < LOD < LOD .Organochlorine Pesticides chemical. and the FDA has established a bottled water standard for HCB.089-.163 (.196) < LOD < LOD .102 (.125 (.121 (.155) < LOD < LOD .072-.e. Schmid.081-.092-.258) < LOD < LOD .126) .069) < LOD < LOD .145-. ACGIH has developed workplace exposure limits for HCB.118-.156 (.114-.060-.089-.160 (.176-.169-. More information about external exposure (i.095) < LOD < LOD 75th < LOD < LOD 90th * * . Infants were exposed transplacentally and through breast milk.atsdr.123 (.203) < LOD < LOD . which is manifested by increased deltaaminolevulinic acid synthase activity and decreased uroporphyrinogen decarboxylase activity.069) * * . In humans. and NTP classifies hexachlorobenzene as reasonably anticipated to be a human carcinogen. thyromegaly.095) * * .130) < LOD < LOD .092 (. EPA has established a drinking water standard.171 (. arthritis. Survey Geometric mean (95% conf.098 (.092 (.095 (.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 * * .064 (.147 (.090 (.088-.086-.145-.S.099) < LOD < LOD .094) < LOD < LOD .114-.127-. 1960).122) < LOD < LOD . and weakness.086-.190 (.157 (. which may vary for some chemicals by year and by individual sample. 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.

Kohli J. Canada).9% of participants had quantifiable levels (Stehr-Green. 4/21/09 Barber JL. 2006). 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. Lawrence River (Quebec.111:349355. 2005)..77:173182.71(6):1200-1209. distribution. Lackmann GM. declines in background HCB levels ranging from around 50%90% have been documented in studies using cord blood (Dallaire et al. Gocmen A. Hexachlorobenzene in the global environment: emissions. Peters HA. Bradman et al. Santiago-Silva M.135(4):400404. In the 1976-1980 NHANES subsample.html. 2002. et al.. only 4. Atuma S. Jones KC. Sci Tot Environ 2005. Ozalla D. Kemper FH. Herrero C. Can J Biochem 1976. References Agency for Toxic Substances and Disease Registry (ATSDR). Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. 2002. Toxicological profile for hexachlorobenzene update [online]. Gunderson EL. 2002. Schwartz JM. Available at URL: http://www. Paepke O. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Lepom P.81(2):82-85. Environ Health Perspect 2003. J Assoc Off Anal Chem 1988. 102 Fourth National Report on Human Exposure to Environmental Chemicals . Bradman A. Barr DB. Finding a measurable amount of hexachlorobenzene in serum does not mean that the level of the hexachlorobenzene causes an adverse health effect. Fenster L. Glynn et al. Epidemiology of hexachlorobenzene-induced porphyria in Turkey: clinical and laboratory follow-up after 25 years.gov/~dms/ pesrpts. Schulz C. Environ Health Perspect 2002.. Int J Hyg Environ Health 2002. Arch Neurol 1982. Bertram HP. 1989). however. Jones D. Available at URL: http://www. IARC Sci Publ 1986. Safe A. Bryan GT. Zoellner I. et al. Muckle G.44 mg/L.110(8):835-838. Aune M.. lower than the limit of detection (on a lipid adjusted basis) in NHANES 1999-2000 and 20012002. 2002).17:388–399. Polychlorinated biphenyls and hexachlorobenzene in full-term neonates. and other chemicals. Urinary porphyrin excretion in a human population highly exposed to hexachlorobenzene. Hexachlorobenzene content in human whole blood and adipose tissue: experiences in environmental specimen banking. but approximately five times higher than the overall geometric mean level in 2003-2004 (Becker et al.. HCB levels were directly related to age.54(3):203-208. April 1982 to 1984. Sala M. than the limits of detection (on a whole weight basis) in NHANES 19992000 and 2001-2002 (Herrero et al.cfsan. Link B. September 2002. Over the past two decades.349:144. Cripps DJ. Kaus S. Otero R. Piechotowski I. Biol Neonate 2002. Temporal trends of organochlorine concentrations in umbilical cord blood of newborns from the lower north shore of the St. FDA total diet study. Lackman. Organochlorines in Swedish women: determinants of serum concentrations. Dogramaci I. et al. 2005). 2005. As a result of the lower limit of detection in NHANES 2003-2004. but overall. dietary intakes of pesticides. Herrman T.atsdr. Becker K... Gabrio T. 2003). Reference values updated. Dallaire F. Krause C. and the geometric mean concentration of HCB in whole blood was 0. et al. J Exp Sci Environ Epidemiol 2007. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. 1986. Link et al. Seiwert M. van Wijk D. 1999). Sweetman AJ. 4/21/09 Glynn AW.. Biomonitoring of persistent organochlorine pesticides.. Chemosphere 2005. Food and Drug Administration (FDA). Granath F. 2002) and among children (Link et al. Lecha M. Laliberte C. Residency near industrial or agricultural areas has been associated with higher serum HCB levels (Barber et al. In a representative sample of the 1998 German adult population.gov/ toxprofiles/tp90. Bjerselius R. 2002.fda. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Darnerud PO. The metabolism of higher chlorinated benzene isomers. factory workers chronically exposed to HCB and residents near the factory had serum HCB levels that were 150 to 50 times higher.58:1185-1201.. Bertram et al. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. 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. trends and processes.Organochlorine Pesticides in the NHANES 1999-2000 and 2001-2002 subsamples. Dewailly E. levels. Agerelated increases of HCB in body fat and serum have been consistently noted in general population studies (Becker et al. respectively. Lackmann. Eskenazi B.205:297-308.cdc. HCB detection in serum also was proportional to age. Holland NT. Factors predicting organochlorine pesticide levels in pregnant Latina women living in a United States agricultural area.html. August 2008.39(12):744-749.. selected elements. more HCB levels were quantified. Arch Dermatol 1999. In Spain. Muller C. Ayotte P.

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

containing about 64% alpha and 10%-15% gamma isomers.8 (10.0-111) 70.7 (62.4) < LOD 9.5 (14.6-89.5-29.0) 35.90-8. Survey years 99-00 01-02** 03-04 Geometric mean (95% conf.3) 51.0) 71. exists in several isomeric forms.6 (16.6 (17.3 (42.0-70.6) 16. HCH isomers.0-21. Lindane (1%) lotion and shampoo are available by prescription for singleuse application to treat human scabies and head lice.6 (22.7-20.5) 29.9 (62.8 (23.8-16.6) 36.9 (9. commonly known as lindane.3-38. EPA cancelled agricultural uses of lindane (ATSDR.68 (<LOD-10.2 (18.2-20.0 (37. soil.9-24.1 (9.2-42.4 (12.4) 51.7) 18.7-69.60-13.46-11. However. Technical grade HCH is a mixture of all four isomers. < LOD means less than the limit of detection.6) 653 758 589 1240 1533 1370 20 years and older 10.36.2-98.5 (11. 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. Lindane has a half-life of about two weeks in soils and water.7 (30.4 (16.8-19.1 (9.5528.4 (52.1 (12.5-123) 49.43 (<LOD-9.2 (31.1-15.4-111) 84.7) 27. 6.5 (8.4) 27.8-68.0) 17.7-26.76.7 (<LOD-16. 01-02. 319-85-7 gamma-Hexachlorocyclohexane CAS No.3-56.8.2) 13.8 (9.7-166) 70.4) 901 1067 952 992 1224 1007 Females 11.6) 50.04-10.2-87.9 (26.1 (21.66-12.90) 7.0 (19.6-20.8) 39.50) 8.7) 10.7) 32.6) 35.1) 71.2 (34.4) 44. can be used as an insecticide and has been used to kill soil-dwelling and plant-eating insects. see Data Analysis section) for survey years 99-00. and sediment as a result of historic production and use.4 (50.9-81.0-23.4) 11.7) < LOD < LOD < LOD < LOD < LOD < LOD 37.8) < LOD 10. which may vary for some chemicals by year and by individual sample.0 (14.8) 27.7) 23.2 (29.2) 9.2-22.7) 97.9) 17.5 (24. environmental levels declined.9-178) 48.9) 81.1 (30.7 (53.90-8.5) 67. and have been used either as fungicides or to synthesize other chemicals.0) 7.5) 22. water. **In survey period 2001-2002.3 (13.6-42.7) 73.Organochlorine Pesticides Hexachlorocyclohexane CAS No.0-34. interval) 9.8-54. beta.5) 90th 42.7) 10.0 (<LOD-12. The gamma isomer. and delta.8 (17.3 (42.4) < LOD < LOD < LOD 46.9 (30.8 (33.5 (43.2 (50.8) 7.8 (21.0) 8. It is no longer produced or sold in the U.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. 2005).3) 37.5) 16.9-14. 608-73-1 beta-Hexachlorocyclohexane CAS No.4-45. The other isomers can be formed during the synthesis of lindane.20-16. 104 Fourth National Report on Human Exposure to Environmental Chemicals .70-19.0 (8.6-135) 69.7 (35.6) 47.2 (48.1) 31.6 (10.6-14. 58-89-9 General Information Hexachlorocyclohexane (HCH).09) < LOD Gender Males 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD 14. so they can accumulate in fatty tissues of animals.6-37.7 (25.2-55. See the section “What’s New” at the beginning of this Report for details.S.1-27.80 (6. population from the National Health and Nutrition Examination Survey.4 (11.8 (32.8-199) 134 (85.1-32.1-32.80 (<LOD-14.2-46.5 (16.6 (33.1 (16.3 (26.0-70. the U.7 (29.7 (13.5) 632 563 460 403 513 487 702 1051 887 Non-Hispanic blacks Non-Hispanic whites Limits of detection (LOD. HCH does not bioaccumulate to an appreciable extent in plants (ATSDR.3) 14.8) * * * * * * 15.70 (6. As pesticide applications of HCH were increasingly restricted or eliminated.5) 40.8) 95th 68. and 03-04 are 9. 2005).1-37.0) 41.5) 11.3) 34.7-96.S.8) 12.1) 12.9) Selected percentiles ( 95% confidence interval) Total * * 50th < LOD < LOD < LOD 75th 19.3-85.1) 12.9 (32. each result has been multiplied by 1.6 (40. particularly alpha and gamma have been detected widely in air.6-62.6-18.6) 18.4 (8.8-87.9-21.2-52.3) 25.1 (11.0 (33.8 (64.61-12.56-12. In 2006.6-47.87 (9.30-11. gamma.7) 56.70-12. and 7.9 (50.5 (37. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.1 (18.3 (62.2) 62.2) 142 (99.1-49.2 (9.9 (11.1 (27.7-69. formerly referred to as benzene hexachloride.1-16.4-73.1) 13.9 (40.S.2-67. including alpha.7-96.5) 14.0 (35.70 (8.4-50.4) Sample size 1893 2291 1959 Age group 12-19 years 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD 21.1-36.9) 15.89 (<LOD-9.9) 45.4) 10.2-17.0-20. respectively.9-51.2) 36.9-56. HCH isomers are lipophilic.4) 21.8) 52.

080-.125) < LOD < LOD < LOD .100-.066) Selected percentiles ( 95% confidence interval) Total * * 50th < LOD < LOD < LOD 75th . for lindane.37) 1.480 (.160-.050 (.260) . the serum half-life was about 20 hours among children (Ginsburg et al.480) .110) .220-.380 (.080-. FDA pesticide monitoring program has shown a temporal decline in the detection of lindane.340-.072 (.297-.047-.Organochlorine Pesticides exposure to HCH is through the diet.070) . 1971.350) . 1983)..065 (. paresthesias.32) .310) .124-.308-.130 (.190-.096) .140) .360-. Fourth National Report on Human Exposure to Environmental Chemicals 105 .077) < LOD .190) .150) .065 (.442 (.080) * * * * * * .560 (. When animals were chronically fed lindane at high doses.058) < LOD Gender Males 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD .250-. 1986).062 (.144 (.580 (. **In survey period 2001-2002.190-1.086) < LOD < LOD < LOD < LOD < LOD < LOD .400) .910 (.620-1.073-.410-.210) .120 (.090 (.460) .120-.089) . hepatic enzyme induction.220) .091) .5528. Acute high doses of lindane after ingestion or excessive skin application of the 1% lotion have produced seizures in humans.01 (.080 (.290 (.280-.118 (.700) .167 (.250-. population from the National Health and Nutrition Examination Survey.089-.059-. ataxia..080 (.234 (. or dermal exposure.130-.244-.. Survey years 99-00 01-02** 03-04 Geometric mean (95% conf.310 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.840) .330-.140) .100-.070-.190) .100) .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 . Gunderson 1988).290 (.360) .200 (.057-.103-.070-.056-.710) .060) .051 (<LOD-.216 (.410 (. tremors.080-. 1981). respectively.260) .067 (.412 (. Human health effects from HCH isomers at low environmental doses or at biomonitored levels from low environmental exposures are unknown.570 (.119) .139 (.390-.260-.077) < LOD .080) .050-. The beta isomer accumulates in fatty tissues and is metabolized more slowly.083) .210-.240-.310) .319) .110) .081-.050 (<LOD-.290) .360 (.390 (. 2008.057 (<LOD-. HCH crosses the placenta and is also excreted in breast milk (Radomski et al.173-.370-.305) .120 (.191-.510) .S.070 (.587) 653 758 589 1240 1533 1370 20 years and older .480 (. EPA has established a drinking water standard.382-.051-.103) 90th . and FDA has established a bottled water standard and food residue tolerances for lindane.140) .056-. 2002).281 (. from 6% of samples in 1982-1984 to 2% in 1994 (FDA. HCH isomers are absorbed after inhalation.090 (.070-.220 (.078 (. which may vary for some chemicals by year and by individual sample. 1996. OSHA and ACGIH have established workplace standards and guidelines.294-.100 (.460 (.470 (.057-.120-.S.120 (.521 (.140 (. See the section “What’s New” at the beginning of this Report for details.501) .290) .420-.200-.180-.350 (.048 (<LOD-. enlarged livers. HCH isomers are metabolized to chlorophenol metabolites that are excreted in the urine (Angerer et al.175 (.620) .057) < LOD Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 99-00 01-02** 03-04 .130) .150) . Distribution is mainly to fatty tissues.050 (<LOD-.287 (.083 (.814) .170-.S.690) . Saxena et al. and memory loss (Nigam et al.222 (.050 (.064 (. interval) .410) .250 (.110-.600) .069) .100-.064) .05) . Workers who directly handled HCH have complained of headache.450) .470) .680) .120) . Acute high dose toxicity in rodents affects the central nervous system producing decreased activity. probably by blocking inhibitory neurotransmitters in the central nervous system.240 (.290 (.100) .340) .100 (.068-.400) .221-.150 (.103 (.092 (.250 (. ingestion.040-. U. 1977).170-.070 (.254) 95th .200-.450-.410) .160) .300-.118-.330 (.120-. Pesticide applicators or agricultural workers could be exposed to HCH by inhalation and dermal pathways.160 (.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.. After dermal application of lindane 1% lotion.131-.270 (. 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. and nephropathy developed (IPCS.230-. The U.404) .090-.210 (.560) .120) .191-.146-.110) .320 (.050) .050-. each result has been multiplied by 1.050-.450 (.050-. Rogan.090 (.150-.098 (.372 (.058 (<LOD-.174) .214) .661) 901 1067 952 992 1224 1007 Females .220-.250) .062 (.580-1.331 (. resulting in a half-life of about seven years. and seizures.067) .250 (.280-..210 (.

In populationbased studies of New Zealand adults and German adults and children.e. environmental levels) and health effects is available from the U. the maximum and 95th percentile beta-HCH values. 01-02. which were considerably lower (as much as twentyfold) than mean levels reported in small studies of adults in Spain (Botella et al. 2004.. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.. were similar to the 95th percentiles in this Report. 2005. Biomonitoring Information Because of its longer half-life.. 106 Fourth National Report on Human Exposure to Environmental Chemicals . see Data Analysis section) for Survey years 99-00.gov/pesticides/ and from ATSDR at: http:// www. 1998). and 03-04 are 14. beta-HCH may be detected in a higher percentage of the general population than are the other HCH isomers. Additional factors associated with higher beta-HCH levels include rural residence. 1971.8.. 2005. male sex. which may vary for some chemicals by year and by individual sample. Link et al.5. 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. Radomski et al. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD < LOD size 1799 2280 1960 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD < LOD 90th * * * Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 660 758 593 1139 1522 1367 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 863 1060 952 936 1220 1008 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 631 563 461 380 509 490 646 1045 884 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.html... respectively. 2002). 1998. 1991. 10. respectively. and a diet that includes meat (Becker et al.Organochlorine Pesticides hexachlorocyclohexane isomers as possibly carcinogenic to humans. More information about external exposure (i.epa.. 2004). 2001-2002. Kutz et al. 2004) and India (Bhatnagar et al. Stehr-Green. Stehr-Green.atsdr. 1989.S. Studies of general populations have shown declining beta-HCH levels since the 1970s (ATSDR. aged 9-11 years.. 2002. Survey Geometric mean (95% conf.. In NHANES 1999-2000. studies in populations with environmental exposure have reported lindane levels below the limit of detection in most persons (Anderson et al.. 1989).. Sturgeon et al. and 2003-2004. Bates et al. In recent years.S. 1991. < LOD means less than the limit of detection.5. serum levels of lindane were generally below the limits of detection. and 7. EPA at: http://www. population from the National Health and Nutrition Examination Survey.. older age. In an earlier (1996-1997) sample of German children. Becker et al. Kutz et al. and NTP classifies hexachlorocyclohexane isomers as reasonably anticipated to be human carcinogens.gov/toxpro2.cdc.

. 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. A study of Swedish women aged 54 years and older reported a median beta-HCH level that was slightly higher than the geometric mean for women reported in the NHANES 1999-2000 survey period (Glynn et al. in this Report (Nigam et al. respectively. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.. 1986. Radomski 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. In a small study of adults who consumed sport fish from the Great Lakes. 2003)... Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.S. 2005). the median beta-HCH levels were similar or slightly higher than the 95th percentile in this Report (Anderson et al. Fourth National Report on Human Exposure to Environmental Chemicals 107 . population from the National Health and Nutrition Examination Survey. 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.Organochlorine Pesticides 2001-2002 survey period (Link 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). which may vary for some chemicals by year and by individual sample.. Biomonitoring studies on levels of HCH isomers provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of HCH isomers than are found in the general population. 1998). 1971). Survey Geometric mean (95% conf.

Serum hexachlorocyclohexane residues in workers engaged at a HCH manufacturing plant. available at URL: http://www. Zoellner I. Falk C. Darnerud PO. August 2005. Bjerselius R. Rothman N. Patterson DG Jr. Arch Toxicol 1981. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods.120:1-82. Heinrich R.inchem. Occupational exposure to hexachlorocyclohexane. Majumder SK. Bhatnagar VK.205:297-308. Buckland SJ. Stehr-Green. Needham LL. Environ Res 2004. Cancer Causes and Control 1998. Piechotowski I. children and newborn infants. and other chemicals. selected elements. Environ Health Perspect 1998. Visweswariah K.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Bates MN. Seiwert M. Chemosphere 2005. Absorption of lindane (g benzene hexachloride) in infants and children. Chemosphere 2004. Kutty D. Gabrio T. The Great Lakes Consortium. Gunderson EL. Herrman T. org/documents/jmpr/jmpmono/2002pr08. Garrett N.96:34-4Food and Drug Administration (FDA). Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population.57(4):315-320. Nigam SK. Demographic and seasonal influences on human serum pesticide residue levels. Environ Health Perspect 2003.html. Aune M. Link B. et al. Ellis H.cdc.111:349355.html. Lowry W. et al.htm. Cerrillo I. Botella B. Wood PH. Rogan WJ.20(2):186-193. Karnik AB. Atuma S. Rev Environ Contam Toxicol 1991. Olea-Serrano MF. Saxena MC. and HCB residues in human blood in Ahmedabad.48:127-134. Radomski JL. Toxicol Appl Pharmacol 1971.54:1431-1443. Arch Pediatr Adolesc Med 1996. Olson J.52(1):59-67.27:405-421. Bai KM.fda. International Programme on Chemical Safety (IPCS). et al. Blood levels of organochlorine pesticides in Argentina: occupationally and nonoccupationally exposed adults. Burse VW. Reisch JS. et al. Astolfi E. J Pediatr 1977. Brock JW. HCH.150:981-990. 108 Fourth National Report on Human Exposure to Environmental Chemicals . Hanrahan L. VI. Granath F. April 1982 to 1984. Olea N.atsdr. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. Glynn AW. PA. et al. Bottimore DP. Saiyed HN. Organochlorine pesticides and polychlorinated biphenyls in human adipose tissue. Exposure of women to organochlorine pesticides in Southern Spain. Deichmann WB. Pollutants in breast milk.71(6):1200-1209. 2002. Kaus S. Becker K. Krishna Murti CR. Kulkarni PK.72:261265. Lindane. Brinton LA. Pesticide residues in food-2002-Joint FAO/WHO meeting on pesticide residues.106(5):279-289. Bhargava AK. Toxicological profile for hexachlorocyclohexanes update [online]. 4/21/09 Ginsburg CM.9(4):417-424.91:998-1000. Sturgeon SR. Crespo J. Available at URL: http://www. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Int J Hyg Environ Health 2002. 4/21/09 Kutz FW. gov/toxprofiles/tp43. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. dietary intakes of pesticides. Lepom P. Levels of DDT. et al. Krause C. Placental transfer of pesticides in humans. Biomonitoring of persistent organochlorine pesticides.58:1185-1201. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. Rey AA. J Toxicol Environ Health 1989. Available at URL: http://www. Zaidi SS. August 2008. Metabolism of gammahexachlorocyclohexane in man.cfsan. Bull Environ Contam Toxicol 2004. 4/21/09 Anderson HA.gov/~dms/pesrpts. Kashyap R. Int Arch Occup Environ Health 1983. Angerer J. Serum concentrations of organochlorine compounds and endometrial cancer risk (United States). Maass R. Rivas A. Paepke O. et al. Int Arch Occup Environ Health 1986. Raju GS. Needham LL. Potischman N. FDA total diet study. Schulz C. J Assoc Off Anal Chem 1988. Siddiqui MKJ. India. Organochlorines in Swedish women: determinants of serum concentrations. Needham LL.

4) < LOD 63.6) 9. 1991). Some states and the U..4) 617 548 459 398 500 484 688 1049 884 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. soil. and 03-04 are 14.0-374) 11.5 (9.3-225) 15. since 1977.4 (8.5-425) 40.S.70-40. Human health effects from mirex at low environmental doses or at biomonitored levels from low environmental Serum Mirex (lipid adjusted) Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U.5 (<LOD-115) 153 (30. 1985.40 (<LOD-13. respectively.7) < LOD 66. Mirex can cross the placenta and be excreted in breast milk.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. where it was applied directly to soil and by aerial spraying.S.10-37. mirex was detected in human adipose samples. which may vary for some chemicals by year and by individual sample.7 (12.0 (<LOD-108) < LOD < LOD 50.8) < LOD 15.1 (13. In studies conducted in the 1970’s and 1980’s.7 (<LOD-47.Organochlorine Pesticides Mirex CAS No.90-29. aquatic organisms. and 7. after which it is widely distributed in the body and stored in fat.2 (7.4-230) 18.7) 8.2-230) 13.. see Data Analysis section) for Survey years 99-00.3 (15.5-82. water. Ingested mirex that is not absorbed is eliminated in the feces within about 48 hours. Mirex contamination of Lake Ontario and adjacent waterways has been well documented (ATSDR.S. population from the National Health and Nutrition Examination Survey. Mirex binds strongly to soil.5-291) 11.1) 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. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 57.5 (<LOD-42.6 (<LOD-108) 9. Mirex is absorbed through the skin and from the gastrointestinal tract.3) < LOD < LOD < LOD < LOD < LOD < LOD < LOD 15.6) < LOD < LOD < LOD < LOD 71.1 (8.6 (<LOD-23.10 (<LOD-15.3 (15. 2385-85-5 General Information Mirex has not been produced or used in the U.8 (<LOD-73. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. (Kutz et al. 01-02. its major uses were as a flame retardant additive and as a pesticide to kill fire ants and yellow jackets in the southeastern U.8 (12. Mirex has been detected in air. and foods. EPA have issued public health advisories or warnings that fish from contaminated lakes and rivers may contain mirex.0 (14.0 (12.6-305) 15.6) size 1853 2257 1951 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th 15. resulting in exposure to newborns and nursing infants. it is a highly persistent chemical in the environment. Occupational exposure is limited to workers at sites where mirex contamination is present. disposal. where it has a half-life of 12 years.2) 51. Fourth National Report on Human Exposure to Environmental Chemicals 109 .70-24.5.70 (<LOD-15. especially those from persons living in the southeastern U. 1995).S.6. or pesticide application.8. sediments.3) 887 1052 949 966 1205 1002 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 13. < LOD means less than the limit of detection. Formerly.4) < LOD 15. 10.S.1 (<LOD-65. Mirex is not metabolized in the body.1 (<LOD-104) < LOD < LOD < LOD < LOD 39. animals. Survey Geometric mean (95% conf. 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.6 (<LOD-31.

064 (<LOD-.430 (.090 (<LOD-.79) . and the FDA monitors foods for pesticide residue and has established an action level for mirex in fish tissue.090-1..090 (<LOD-. and 2003-2004 subsamples.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 .470 (.635) < LOD .S. The U..Organochlorine Pesticides exposures are unknown.256 (.077 (<LOD-.100 (<LOD-. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD . EPA has established environmental standards for mirex. serum mirex levels were generally below the limits of detection (Stehr-Green.atsdr.090-1. which may vary for some chemicals by year and by individual sample. 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.e.gov/toxpro2. environmental levels) and health effects is available from the ATSDR at: http://www.090-1.089-.102) < LOD < LOD < LOD < LOD .055-.062-.110 (<LOD-.106 (.090 (<LOD-.170) < LOD .html.240) < LOD < LOD < LOD < LOD < LOD < LOD < LOD .S. 110 Fourth National Report on Human Exposure to Environmental Chemicals . 1991).450 (. 2001-2002. 2004).080-1. In addition.053-. Inuit mothers from three Arctic areas had geometric mean serum mirex levels that were threefold to sevenfold higher than nonInuit mother from other Arctic regions. 7. population from the National Health and Nutrition Examination Survey.059 (<LOD-.052-.41) . 2005)..450) 1.080-1. 1989). 1995. Smith.268) < LOD .79) .7 ng/g of lipid.8.220 (<LOD-.054 (<LOD-.079 (<LOD-.37) .108 (. Laboratory animals fed high doses developed liver enlargement and liver tumors. 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.08 (. and NTP classifies mirex as reasonably anticipated to be a human carcinogen.cdc.73) .470) .220) .070-1. Survey Geometric mean (95% conf. In samples obtained between 1994 and 1997.02) .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 . IARC classifies mirex as possibly carcinogenic to humans. Biomonitoring Information In the NHANES 1999-2000.510) < LOD < LOD .174) 617 548 459 398 500 484 688 1049 884 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the lipid adjusted serum level. 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. and 4.084) * * * 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 .610) < LOD < LOD < LOD < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result. More information about external exposure (i. developmental abnormalities including cataracts and edema in the offspring have been reported (ATSDR. The geometric mean mirex levels of the Inuit mothers were 8.92) . as well as in a subsample of NHANES II (1976-1980) participants.690) .410 (.140 (<LOD-.100 (<LOD-.470) .106) < LOD .093 (.112 (. reproductive toxicity included decreased fertility and testicular damage.170-3.310 (.370 (.170) size 1853 2257 1951 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .

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

0) 14. Both chemicals have been detected in air.4.0 (3. Such workers would probably Urinary 2.40 (2.4.72) < LOD 1. Historically. soils.0) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 1. 1999)..20) < LOD 5. and polychlorinated benzenes (Kohil et al. 1999).30-11. General population exposure may occur by ingesting contaminated food or water and by inhaling contaminated air.30) < LOD < LOD < LOD < LOD < LOD 1. 88-06-2 Metabolites of Organochlorine Pesticides and Other Environmental Chemicals General Information The chlorophenols.20) < LOD 1. public drinking water systems did not detect 2. other organochlorines.4.80-41.0) < LOD 5.0) 2.8-tetrachlorodibenzo-p-dioxin occurs during the synthesis of 2.30-27.0) 2. but they may be produced as by-products during manufacturing of other chlorinated aromatic compounds.4. hexachlorobenzene.20) < LOD 90th 5.0) 2.S.42 (<LOD-12.30-44.50 (.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. population from the National Health and Nutrition Examination Survey.5-Trichlorophenol CAS No.10-3. recent sampling of U.60 (. 2. including hexachlorobenzene and hexachlorocyclohexanes.60 (2.30-40. 112 Fourth National Report on Human Exposure to Environmental Chemicals .0 (4.40) < LOD 4.6-Trichlorophenol CAS No. 2006).6-TCP were used as intermediates in the production of certain pesticides.30-27.20-71.940-3. interval) Selected percentiles ( 95% confidence interval) Sample 95th 16.60) < LOD 8.27) 482 570 681 815 831 1112 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD 1.03) 9.40 (1. Survey Geometric mean (95% conf.980-3.6-TCP was also used as a wood preservative and may still be used in production of some fungicides (ATSDR.980-3.00 (2. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.0) 5.31 (<LOD-9.60 (4.6-TCP).4.40-11.4. 2.50 (2.27) 696 661 521 696 603 939 Limit of detection (LOD.S.0 (3.3. Trichlorophenols have been detected in fish taken from waters near waste water treatment and industrial discharges (ATSDR.60-18.5-trichlorophenol.30-3.0) 2.4.71 (<LOD-8. 2. EPA.5TCP and 2.20-36.0 (4.9 and 0.00 (3.19 (<LOD-6.40 (2.5-Trichlorophenol Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.0 (4.6-trichlorophenol (2.0) < LOD 973 1178 1021 1319 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .60-8. are metabolites of several organochlorine chemicals.7. Environmental sources of these compounds include industrial discharges or run off from pesticide facilities or disposal sites.4. Occupational exposures.4.0 (8.00-8. 1976).50-63.71 (<LOD-8. usually at herbicide production or waste incineration facilities.40 (2.50) < LOD 1.0) 2.30) < LOD 4. Exposure to trichlorophenols also may result from metabolism of lindane.40) < LOD 6.00-3.0) < LOD 11. 95-95-4 2.4.900-2.57 (<LOD-15.4. which may vary for some chemicals by year and by individual sample.0) < LOD 5.7) 24.80 (1.40-18.40 (. < LOD means less than the limit of detection.63) 18.0) < LOD 5.5-trichlorophenol (2.50-25. 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.40 (.42 (<LOD-8. and sediments.9 (<LOD-121) 9.0) < LOD 11. surface water.Organochlorine Pesticides 2.0) 2.950 (<LOD-1.S.5-TCP) and 2.40 (1.50-16.30-27.80) < LOD 1.40 (2.6-TCP in any of the samples (U. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.40) < LOD 1.30 (. may occur by inhalation or dermal routes.0 (5.90-33.00-3.80 (2. however.8) 21.9.4.20 (4. Formation of 2.0) < LOD 21. Trichlorophenols are no longer manufactured commercially.920-3.50 (1.

4. Human health effects from 2.50) < LOD 2.53-3.68-4.37-11.980 (<LOD-1.6-TCP had increased rates of hepatic tumors.24) < LOD 6.49 (1.24-11.36 (1.93-11.2 (2. 2004).05-17.55 (4.Organochlorine Pesticides be exposed to mixtures of chlorophenols.57 (<LOD-7.19-4.1) 2.83-12.3) < LOD 973 1178 1021 1318 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .20-6.24) < LOD 5.4. but almost twenty times higher than 95th percentile values reported in German adults aged 18-69 years (Becker et al. Laboratory animals chronically fed high doses of 2. animals showed hepatocellular abnormalities..6-TCP at low environmental doses or at biomonitored levels from low environmental exposures are unknown.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. was similar to the corresponding percentile for 6-11 year olds in NHANES 1999-2000 (Hill et al.5-TCP nor 2.44 (1.78 (3.0 mg/L.920-2. Radon et al.5-TCP.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. which includes trichlorophenols.4) 5.3 mg/L in a nonrandom subsample from NHANES III (Hill et al.6) 4.75 (3.13-13.78-19.7 (4.e. The 95th percentiles for 2.67 (1.64 (4.. and other chlorinated compounds.28-25. the 95th percentile urinary 2. IARC classifies combined exposures to polychlorophenols. Fourth National Report on Human Exposure to Environmental Chemicals 113 .9 (5.31) < LOD 2.17) 9. and lymphomas.15) < LOD 2.4.88-16.46 (1. urinary 2. Neither 2. Urinary 2. However.4 (6.4. More information about external exposure (i.32) < LOD 4.11) 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 2.78) < LOD 1.5) 11.02) < LOD 7.1 (<LOD-58.80 (1.11) 482 570 681 814 831 1112 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD 1. 2003.86 (3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.6-TCP were developmental or reproductive toxicants in animals (ATSDR 1999).4. Biomonitoring Information In the NHANES 1999-2000 and 2001-2002 subsamples.4..html.4.S. recent small studies have not demonstrated increased exposure to trichlorophenols in workers who dredged contaminated soils or incinerated waste materials (Agramunt et al.atsdr.29 (1.gov/toxpro2.00-29.47-8. Among 6-11 year old children in NHANES 1999-2000.53-3.16) < LOD 90th 5.05-8.8 (5. furans.4.6-TCP. NTP classifies 2. population from the National Health and Nutrition Examination Survey.02-3.8) < LOD 9. interval) Selected percentiles ( 95% confidence interval) Sample 95th 11.2) < LOD 5.8) 4.2) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 2....3 mg/L reported in German adults aged 18-69 years (Becker et al..37) 16.4.6) 4.33) < LOD < LOD < LOD < LOD < LOD 2.820-2. 2003). IARC considers the experimental evidence for animal carcinogenicity inadequate for 2. 1989). 1995) and up to 19 times higher than the 95th percentile value of 1.cdc.37) 696 661 521 695 603 939 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.4) < LOD 3.. Survey Geometric mean (95% conf.90 (4.00) < LOD 4.2) 2.57 (<LOD-7. In the same 2-6 year old children.6-TCP levels at the 95th percentile were up to eight times higher than 3. environmental levels) and health effects is available from ATSDR at: http://www.67 (1.4) < LOD 3.43) < LOD 12.24) < LOD 1. 1989). in addition to dioxins. 7.43 (2.44 (.27-17.62-20.16 (.00-19.75 (<LOD-6.73 (<LOD-8.95 (3.24 (3. At lower doses.5-TCP among adults in this Report and in a nonrandom subsample from NHANES III (Hill et al.74) 11.4.9) 12.19-12.4.3 (5. leukemias.82 (<LOD-32. the 95th percentile urinary 2.4..0) 7.69 (2.5-TCP and limited for 2.6) 4.5-TCP or 2.57 (3.4.6-TCP as reasonably anticipated to be a human carcinogen.5) < LOD 12.68 (<LOD-8.60-3. 1995) were similar.69-18.79-4. 2003).81 (<LOD-9. as being possibly carcinogenic to humans.

80 (2.4.3) 23.60) 6.0 (20.40-2.4.40-2.70) 3.0 (8.40-32.6-22.0) 9.80-7.0-41. 0.4.52 (2.20 (3.30) 4.7) 33.09) 15.2) 25.3) 37.0) 19.98-11.52-3.60 (2.6-TCP (0.0-68. see Data Analysis section) for Survey years 99-00 and 01-02 are 1.5-TCP level of 0.0) 14.00-4.7-16.60) < LOD 5. which may vary for some chemicals by year and by individual sample.8 (9.4 (8.5-TCP or 2.45-9.73-9.80-25.20-3.0 (8. Sawmill workers exposed to chlorophenol wood preservatives had urinary 2. 2004).89-6.80-20.35-3.53) 4.0 (13.7 mg/L.26 (2.8-13.75 (8.95-6.6-Trichlorophenol Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.6-19.98-7.24 (2.0 (16.8-24.70-6.60 (3.20) 4.18-3..0 (11.90 (4.31 (3.60-37.S.4.58-3.6-TCP were monitored in a group of hazardous waste incinerator workers from 19992002.69 (3.0-37.4.0) 17.0-50.0) 12.1 (8.0) 10.10) 2.5-TCP or 2.95 (4.7) 21.0) 7.53) 2.23) 2.4. 114 Fourth National Report on Human Exposure to Environmental Chemicals .5-TCP or 2.7-3.00-21.4 (17.5-TCP and 2.5-TCP and to the median 2.36-5.70 (2. < LOD means less than the limit of detection.0) 13.1) 16.0) 9. Mean values of 2.78 (2.5-46.30-2.60 (3.30-11.0 (15. for males in NHANES 19992002 (Agramunt et al. 1998).9 (13.40) 4.45 (2.84) 2.5 mg/g creatinine) were similar to the limit of detection for 2.0 (4.0 (6.80 (3.57 (<LOD-2.23) 3.0 (9.6TCP values.0) 17.0) 11. Urinary 2.46-3.40) 3.0) 13.4.70 (2.59) 4.40) 2.0 (15.5-TCP and 2.4.3.0 (14.7 (9.68 (<LOD-2.00 (4.14 (2. the median urinary 2. Biomonitoring data will also help scientists plan and conduct research about 2.50-5.70) 1.0 (6.31) * 2.Organochlorine Pesticides A small study of adults who ate Great Lakes sport fish reported a mean urine 2.6 (12.51-12. Urinary 2.90) 2.74-3.85 (2.1-25.28) * 2.4 (10..0) 15.6-TCP provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of 2.30-33. Survey Geometric mean (95% conf.76) 3.4.32) * 3.8) 18.6) 21.12) 2.45) < LOD 11.65 (5.80-6.8-15.36 mg/g creatinine.3 (11.79 (5.99) 6.95) 3.06) * 2.20-23.4.90 (3.7 (13. Biomonitoring studies on levels of 2. 1991).6-TCP than are found in the general population.70-6.0) 6.67) 4.6-TCP exposure and health effects.20 (3.40 (2.80 (2.0 (12.5-TCP or 2.00 (1.10-3.9 (11.40) 2.4.1 (10.89 (3.0) 11.30-2.4 (9.6-TCP level.0 (14.3-17.2) 12.07 (<LOD-3.20-6.4.87-14.4.70-3.74 (2.0 (20.00 (2.01-6.58 (1.59-6.6TCP causes an adverse health effect.63) 90th 15.36 (1.40 (2.0-38.0) 19.50 (2.9) 13.0 (6.49 (6.4.09-7.0-18.0) 14.4.0) 7.6 (11. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.0 and 1.66 (8.02) 2.4.6) 970 1178 1019 1325 99-00 01-02 99-00 01-02 99-00 01-02 2.3 (11.0-44.6 mg/g creatinine) and 2.4.6-TCP levels that were as much as 450 times higher than the median level among adults in the NHANES 1999-2000 subsample (Pekari et al.0) 13. population from the National Health and Nutrition Examination Survey. respectively.0) 10.08 (2.65) 15.4.9) 694 677 519 696 602 931 Limit of detection (LOD.2 (14.6-17.40-14.85) * 3.6) 26.2) 481 574 678 820 830 1109 99-00 01-02 99-00 01-02 2.4.32-4.80) 1.70) 5.90-8.78 (2. 2003).0 (7.23-2..0 (14.2-0.8) 32.04) 2..7) * 99-00 01-02 99-00 01-02 99-00 01-02 4.60-21.70) 5.60-3.55-3.40-7.48-26.10-3.4-17.3-26.18) Selected percentiles ( 95% confidence interval) Sample 95th 25.28) 24.0) 13.54) 6.32) 3. interval) 2.47 (3. In harbor workers exposed to chlorophenol-contaminated river silt.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 2.44) 75th 4.45 (5. Finding a measurable amount of 2.67-12.3) 20.4.25-11.33-4.10) 6.92 (2. was about six times lower than the median urinary levels for males in this Report (Radon et al.5-TCP (0.10-2.91-4.0-43.0-38.72-10.40-4.6-TCP in urine does not mean that the level of 2. similar to the limit of detection for this Report (Anderson et al.0-54.56 (3.10 (5.

33-2.19-5.51-21.75) 75th 4.10 (6.13 (1.8) 12.52) 2.20-2.00 (2.9) 8.63 (<LOD-2.3-37.53) * 2.56 (7.38 (4. population from the National Health and Nutrition Examination Survey.72-16.88) 1.88 (2.4 (12.9) 481 574 678 819 830 1109 99-00 01-02 99-00 01-02 2.87) 2.09-3.99-2.5) 11.9-34.0 (9.15 (1.60-2.33) * 2.5 (8.65-21.50-8.83-6.4 (11.9 (9.95-2. Fourth National Report on Human Exposure to Environmental Chemicals 115 .25-17.9-64.1 (8.6 (5.29 (6.3 (9.49) 4.38 (2.44 (3.81-9.4.5) 12.26) * 99-00 01-02 99-00 01-02 99-00 01-02 4.51) 18.1) 14.11) 10.88) 5.15 (6.5 (7.65) 2.67-17.8) 21.38-5.98 (1.88) 4.87-6.71 (3.88) 4.6-31.33 (1.13-6.16-10.1 (13.92) 4.25 (3.52 (3. interval) 2.30-2.63-13.41-6.38) 22.7) 25.7 (14.32-19.5) 11.06-2.63 (2.27-9.6 (10.62-15.25 (3.55-2.41 (3.56) < LOD 11.56-5.6 (9.40 (2.40 (7.77) 2.08-2.29-4.29-4.1) 694 677 519 695 602 931 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.0) 10.87 (3.02 (1.82) 2.00) 4.21-11.04-16.26-13.4) 9.17) 2.43-7.53) 4.65) 18.9) 8.52 (5.17-4.01 (3.73-22.89) 10.63) 4.22 (<LOD-2.8) 19.76-8.9-29.51 (2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.17) 13.82-2.42) 2.6) size 1989 2502 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th 2.22-2.94-13.78 (2.5 (10.18-2.25-15.66-4.5) 8.35 (3.52) 2.9) 7.49-3.50 (2.8 (7.6) 970 1178 1019 1324 99-00 01-02 99-00 01-02 99-00 01-02 2.14-2.6) 12.06) 4.22 (3.48-2.76) 1.6 (9.00) 4.81) Selected percentiles ( 95% confidence interval) Sample 95th 21.83-6.23 (1.1-32.43 (2.43 (<LOD-2.10-9.9) 19.5) 9.26 (6.91 (3.59 (2.8 (8.6) 8.23) 4.90) 2.04-2.0) 8.25-2.00 (3.91-2.S.6 (12.18-4.05 (6.78) 2.0 (11.88-7.02) 3.3) 8.83 (3.87-7.98) 10.Organochlorine Pesticides Urinary 2.53-11.6-Trichlorophenol (creatinine corrected) Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.82 (8.9-32.5-28.6 (6.89-2.77-4.87) * 2.65-2.05 (3.76) 4.24 (1.76) 2.73) 5.88) * 2.6) 13.72) 32.68) 2.54 (2.22-9.91 (7.32 (2.68) 2.3-23.28-4.58 (4.2 (8.60 (4.6 (22.1) 11.47-5.7) 6.0 (6.82 (3.46-14.90 (1.8) 11.81) 2.2) 19.53 (3.1-21.70-9.96) < LOD 4.4) 8.14-13.33 (7.83-5.10) 4.7-36.06) 11.63-15.9 (9.42 (2. Survey Geometric mean (95% conf.4) 4.2 (12.63) * 4.2 (13.78) 90th 12.22 (1.2 (7.79-17.

45:440-445. Hanrahan L. Baker S.EPA). Radon K.pdf. Can J Biochem 1976.54(3):203-208. Szadkowski D. Environ Health Perspect 1998. Seifert B. Domingo JL. Int J Hyg Environ Health 2003. Bailey SL. et al.gov/safewater/ccl/pdfs/reg_determine2/report_ ccl2-reg2_ucmr1_occurrencereport. 5/19/09 116 Fourth National Report on Human Exposure to Environmental Chemicals . Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. Becker K. Urinary excretion of chlorinated phenols in saw-mill workers.cdc. et al. Burse VW. Needham LL. Jones D. Am J Ind Med 2004. Toxicol Lett 2003. Jarvisalo J. Kohli J. Corbella J. Smith SJ. Arch Environ Contam Toxicol 1989. Chlorophenol exposure in harbor workers exposed to river silt aerosols. Luotamo M. Falk C. Poschadel B. et al. Domingo A. December 2006 Draft. 206:15-24. Hill RH Jr. Wegner R. html. Safe A. 4/21/09 Agramunt MC. July 1999. U. 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]. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Olson J. Lindroos L. Needham LL.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR).atsdr. Head SL. The Great Lakes Consortium. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children. Environ Res 1995. To T.epa. Shealy DB. Toxicological profile for chlorophenols [online]. Pekari K.18(4):469-474. Available at URL: http://www. Holler JS. Baur X.63:57-62. Available at URL: http://www. S. Pesticide residues in urine of adults living in the United States: reference range concentrations. Gregg M. Int Arch Occup Environ Health 1991. Environmental Protection Agency (U.gov/toxprofiles/tp107. Heinrich-Ramm R. Kaus S.71:99108. Fast DM. Aitio A. Schulz C. The metabolism of higher chlorinated benzene isomers. Monitoring internal exposure to metals and organic substances in workers at a hazardous waste incinerator after 3 years of operation.S. Seiwert M. Anderson HA. Hill RH Jr.146:83-91.106(5):279-289.

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

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

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

1-23.9-18.56 (6.3) 14.30 (4.86-15.840-1.37 (3.54 (3.32 (. 120 Fourth National Report on Human Exposure to Environmental Chemicals .2) 672 678 473 509 696 578 595 948 752 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.70 (4.2) 16.0 (6.40-14.0-28. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.740-2.51) 2.80) .8) 11.620-1.60 (1.20 (.56 (1. and 03-04 are 0.26-6.0 (7.71-9.80 (4. and 0.20 (. interval) 1.10) < LOD < LOD 4.70) < LOD < LOD 75th 3.39 (3.80) 3.5 (8.5-16.28) 1.40-16.0) 10.72) 5.00-7.83 (5.1) 13.44-38.50 (2.9 (8.08 (<LOD-2.4 (9. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.10 (2.00 (5.7) 11.20-30.52-11.13-2.58 (5.16) 4.35-11. see Data Analysis section) for Survey years 99-00.8 (9.758-1.40 (.40-19.00-12.13 (2.82-12.34-3.0) 11.600 (<LOD-1.81) 1.9) 952 1187 928 997 1333 1003 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.15) 14.20 (.70) .1 (10.00-27.91) 4.44 (2.4) 17.97) 90th 7.5) 15.33-18.00) 3.0 (8.0) 6.2.4 (9.757-2.717-1.0) 11.05-7.70-19.01) * * 1.810-1.52) 6.50-36.90-5.29) * * 1.80) 2.86 (1.81) 11.0) 20.623-1.70-23.70 (2.2.9) 14.0) 7.16 (2.03 (.954 (.3-15.2 (7.60-11.27-3.1 (9.599-1.70) < LOD < LOD 1.0 (7.0) 15.970-2.1.70-14.8) 19.82) 10.90) 3.30 (2.53) 4.0) 6.26 (5.80 (2.99 (5.7 (14.81) 11.00 (1.02-5.1) 10.90) 2.43-12.61 (3.6) 18.8 (14.27-15.4) 18.52) * * 1.0) 10.2) 14.17-3.20-7.0-27.00-27.6) 7.50 (.0) 11.2 (9.780) < LOD 3.61) 4.10 (.93-24.0) 6.13 (2.80-24.4) 20.2) 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 1.750-1.670-1.38-5.15-12.40-1.0) 10.74 (8.12-19.85 (3.90 (1.35-12.4 (7.00-12.530 (<LOD-2.20 (.44-3.14) * * .48-7.10 (2.47) * * 1.94) * * .7 (12.98-12.0 (7.830 (<LOD-3.60) < LOD < LOD 4.58) Selected percentiles ( 95% confidence interval) Total * * 50th 1.60-18.94) 3.2 (11. respectively.2-20.30 (2.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.2 (14.00-19.1) 95th 13.860-2.12) 4.9) 8.00) 3.80) 11. 0.58 (2.02) 4.35-16. < LOD means less than the limit of detection.80) 2.60-25.98-5.55-6.79-7.3) 17.66) * * 1.0 (7.08-2.50-5.80) 2.46) 10.30-6.55-8. 01-02.90-4.21) 9.57-7.0) 11.07-10.45 (2.11 (.20 (2.71 (2.26-8.73) * * .21 (.68-7.93 (4.490-2.2 (7.981 (.67) 3.19) 9.290 (<LOD-.40-11.00 (4.0 (9.39 (8.32) 1.8) 7.70-11.23-5.2) 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 1.0 (5.2 (14.56-13.579-1.S.4 (7.63) 1.8) 7.8-32.0 (6.80-4.10-7.58 (3.96-3.0) 5.2) 16.60) .2 (7.0) 9.5 (11.22 (.0) 12.8 (12.89) 9.0) 5.50 (4.33 (5.20-4.40-5.76 (2.0) 10.890 (<LOD-2.290 (<LOD-1.74 (8.80) .0 (8.1-17.3) 16.04) < LOD 1.10) < LOD .42-3.08-15.36-4.0 (12.30-4.56 (4.50) 2.0 (8.0) 5. which may vary for some chemicals by year and by individual sample.0 (9.955 (.47) 5.0) 10.97) 8.8 (8.10 (.95) 5.60 (5.34-7.5) 20.80) 4.5-17.2 (9.700-1.42) .79 (5.0 (4.80-22. population from the National Health and Nutrition Examination Survey.

500-1.90-8.94 (4.06-2.1 (6.23) 4.41) Selected percentiles ( 95% confidence interval) Total * * 50th .5-20.68-4.540-1.45-5.40-12.31 (3.2 (6.03-6.04-6. interval) .37 (4.5-16. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.8) 12.98-5.2 (10.7) 18.1 (7.8) 16.1) 4.1 (10.02-14.7) 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 .88-15.40 (3.75) 2.75 (3.7) 12.82-14.0 (8.9 (5.46-5.37) 9.24-3.883 (.5) 12.53) 9.6 (9.03 (2.67) 4.40-5.89-3.30 (1.80 (7.54-4.80 (2.9 (9.2) 9.66-15.79-9.40-14.71) 10.996 (.28 (4.57) 4.61-29.83) 8.28) 10.94-23.4) 4.77 (6.20-8.98) .9) 12.79-3.57 (4.55-20.83 (7.9) 16.42 (3.82-14.69 (4.47 (1.7 (8.932 (.84) 7.3) 16.73 (1.4) 13.13) 4.61 (1.82-6. population from the National Health and Nutrition Examination Survey.5) 7.608-1.34 (6.818 (.40) < LOD < LOD 75th 2.69) 4.54-11.85 (6.900 (.7) 5.47 (3.43 (.89) * * 1.21-23.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.710 (<LOD-1.560-1.61 (1.870-2.87 (3.27) < LOD 2.44 (2.37-3.0) 7.04 (1.43) 2.87-5.09 (.3) 12.80) 9.30) 2.4 (4.67) 1.98) 9.960 (<LOD-2.34 (6.11-6.574-1.98-22.890 (<LOD-1.2) 7.56-13.05 (1.820 (.6) 8.66 (1.9-28.54-2.60) 2.00 (4.650-1.790 (.00-19. Fourth National Report on Human Exposure to Environmental Chemicals 121 .10-13.34) * * .5-13.780 (<LOD-1.1) 4.5) 8.95 (3.8) 6.57 (6.74) 4.00) 8.7 (9.S.53-11.41) .0) 6.25) < LOD .40-28.3) 15.05 (.40-3.1 (8.960 (.10 (3.31-14.98) .35 (1.02 (7.57-10.2) 8.510-1.61-13.8) 7.1 (9.60) * * .62-5.14 (3.1) Sample size 1949 2519 1928 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.56) 7.23 (4.533-1.81-5.00 (4.66 (5.8) 8.43 (3.02-2.15-10.35) < LOD < LOD 3.41-12.47 (3.6 (10.00-17.76-4.01-2.4 (9.25) 6.1-15.56) 4.2 (8.6) 11.62) .9 (9.28 (2.7 (10.81 (1.19 (4.2) 13.74) 90th 7.440 (<LOD-2.36) * * 1.94-22.47) 2.69) 2.87 (1.78 (2.88-10.47) * * .3) 5.3) 952 1187 927 997 1332 1001 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.45-11.03) 2.54-15.84 (5.633-1.46) 2.54) .924 (.830-1.570-1.75 (7.93-9.890 (<LOD-1.920 (.51-5.6) 13.60-9.4) 4.18 (.45-5.855 (.750 (<LOD-1.29 (2.8 (10.95) 2.430-1.5) 11.53 (6.71-2.03) 2.93-5.34) < LOD < LOD .37 (5.29) * * .5 (4.28-9.32-12.38 (1.67-19.28 (5.40) 4.98 (3.66-34.09-11.58) * * 1.6) 9.69-10.2) 95th 12.1 (11.09) 2.37-5.94 (2.38) .620-1.773-1.88 (5.75-7.85) 2.860 (.72) 11.93) 9.39 (2.50) 7.88) 2.5) 7.76) < LOD .00-13.03 (7.42) 12.94-10.80 (6.07 (.566-1.92-5.2) 5.94-9.56) .05) .26) * * .52) 4.7) 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.02 (2.82-26.68) < LOD < LOD 3.2) 5.75) 14.90-5.64-5.549-1.66 (2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.9) 11.5-32.92-2.

37 (3.00-18.67) 4.29) < LOD < LOD < LOD < LOD 3.62-17.12 (4.22 (6.45 (3.84-4.80-12.33-11.77-14.40) < LOD < LOD 75th 2.50-5.0 (10.60) < LOD < LOD 2.30) 3.4-17.61 (3.5 (9.70 (1.7) 10.0-24.0) 6.0 (10.580-2.00 (.74) * * * * * 1.80-14.8) 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 1.20) .31-7.3 (9.14 (6.0) 13.18 (3.80 (5. respectively.3) 10.30) 8.24 (2.50-4.35 (6.22) 8.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.30) < LOD < LOD .3 (9.15-6.90 (2.6) 11.3) 20.7) 14. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th .41-5.7-21.0-24.35) 4.20) 3. which may vary for some chemicals by year and by individual sample.46-4.7) 15. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.58.6-41.51) < LOD 1.80-21.81-6.90 (2.90 (1.0) 14.670 (<LOD-1.86-10.3) 22.18) * * * * * * * * 1.670 (<LOD-1.60 (6.70-9.7) 22.00-9.8-21.78) 5.66) 4.00-4.5 (8.10-4.3) 14.92) 9.0) 19.6) 14.63-14.7) 16.2) 14.0) 9.01 (2.0) 9.0 (14.80) .4 (10.77-3.7-19.80) 5.49-4.6 (10.5) 471 576 310 664 822 717 814 1121 938 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * .0 (9.90-31.3 (11.66-13.0 (8.0) 7.88) 3.89 (2.39 (5.30) 3.27) 4.28 (7.00-16.0 (13.34-3.90 (6. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.99 (3.41) 3.90) 4.3 (12.740 (<LOD-1.98-9.90 (5.90-9.90) 8.2 (9.42 (1.6-19.90-15.1-23.0) 13.04 (3.3 (6.8) 8.5.00) 3.75 (3.9-17.90 (6.00) < LOD .0 (9.17 (7.8 (12.6 (10.22 (6.670 (<LOD-1.4 (10.34-10.1 (10.9) 16. < LOD means less than the limit of detection.7 (11.8-20.7 (10.3) 8.20-8.910 (<LOD-2.82) 8.27 (7.89) 2.40 (2.27 (3.6) 14.95-9.34 (6.34-5.00) 8.60 (5.25 (2.96) 90th 7.90 (6.80 (2.20-4.3 (7.2 (7.31-12.00-4.30) < LOD < LOD 4.80-3.80-6.27) 9. 01-02.10 (.970 (<LOD-2.4 (14.70-5.9) 95th 14.10-15.4) 7.39-13.4) 11.70-9.11-6.73) 7.1 (10.75 (2.10 (<LOD-1.5) 21.9 (7. 122 Fourth National Report on Human Exposure to Environmental Chemicals .1) 11.0 (5.0) 12.00) 3.20-18.0) 23.5.52 (6.0-19.8-17.670 (<LOD-1.06 (2.8-20.70-8.95 (5.50) 5.9-15.80-4.20 (<LOD-2.6) 18.9 (12.90 (6.22-12.70 (8.8) 9.53 (3.60 (2.95 (2.16-1.9) 10.88) 10.80-8.0 (7.650-1.67) 3.0 (15.80 (2.61-32.680 (<LOD-1.5 (8.8 (12.0) 12.20) 3.0-29.80) .92-17.90 (2.40 (2.6) 952 1187 946 997 1332 1019 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * 1.0) 14.72) 2. 0.0-33.24-5.50) .10) 6.5-26.0) 11.50) 3. see Data Analysis section) for Survey years 99-00.64) 10.90-15.0) 11.9) 9.70) 2.31) 1.4) 672 678 498 509 695 579 595 948 757 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.96) 3.37) 2. and 03-04 are 0.58 (1.9-14.67-10.0) 18.10-10. population from the National Health and Nutrition Examination Survey.47-6.00) 7.46-28.29-4.00-18.15-2.0) 12.27) .S.35-3.97-4.790 (<LOD-1. and 0.59-3.

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.59-3.S.21) * * * * * 1.7 (8.1 (19.7-19.74-4.4-16.72-4.67 (1.12 (7.27) 5.70-2.4 (11.2) 16.30-5.51-10.27) 1.00 (5. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.09-11.67 (7.04) 9.77 (2.910 (<LOD-1. Fourth National Report on Human Exposure to Environmental Chemicals 123 .7) 14.6) 14.80) 3.71 (1.18) 2.86-3.99 (4.93 (<LOD-2.1) 20.30) 8.0 (10.5 (11.00) 8.2-15.69-11.32) 2.4) 6.01-5.38 (2.0) 14. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.760 (<LOD-1.42) 8.7) 14.2 (9.83 (6.50 (6.3-15.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.00 (7.55) .5 (9.71) < LOD < LOD 2.70-35.940) < LOD < LOD 1.88-7.3-17.21-21.77 (2.97) < LOD .28) 6.920 (<LOD-1.07) 2.54 (7.92) 3.30) 2.5 (10.25 (4.4) 7.23-3.6) 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 * * * .48 (2.61 (2.00 (<LOD-1.6) 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 1.91) 3.6 (10.4-18.86) 9.6 (12.86 (3.2) 12.3-21.11 (5.30) 7.6) 12.27) < LOD .78 (6.37) 3.15 (1.4-16.55 (2.78-10.16 (3.92 (5.9-17.00 (<LOD-1.87 (3.0 (8.42-19.28 (1.93-10.690 (.11-3.20-3.89-3.3) 12.68-10.2) 12.5-17.9 (9.07-3.2) 10.37-5.68) .890-2.3) 8.34) < LOD < LOD < LOD < LOD 3.95) 90th 8.06 (<LOD-1.54) 9.89-10.91-9.8 (10.03 (2.38) 1.83 (7.4) 9.4) 16.9 (9.590 (<LOD-.2) 8. population from the National Health and Nutrition Examination Survey.79-6.7) 15.41 (7.16-14.94 (5.95) 3.2 (9.29 (5.07 (5.96-10.4) 7.0 (11.78 (4.68-19.85-17.73 (5.530-1.29 (2.64-11.3-17.1) 10.6 (11.14 (2.32-8.5 (15.1 (8.54-5.12) < LOD < LOD 4.2) 15.93 (6.7) 9.0 (13.6) 95th 16.6) 471 576 310 664 821 715 814 1121 937 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * .27-13.36 (2.82-11.52-3.6-19.42) 7.4) 15.5) 10.89-3.75-3.2) 12.9 (9.28-12.7 (11.973 (.6) 13.93 (2.38-13.5) 8.19) 3.620 (<LOD-.7 (10.29-2.8) 16.82-8.8) 14.33-10.6 (13.45) 6.27) * * * * * * * * 1.63 (2.2-30.68-4.4) 7.94-14.43 (2.3) 6.55) 16.5) 13.7) 12.72) 4.38 (1.6) 6.97-4.8 (8.89-13.950) .75-3.0-21.78) 4.15) < LOD < LOD 75th 2.47-9.07) 2.00 (3.89) 5.53-8.00 (2.780-1.810 (<LOD-1.2) 19.05-3.3) 9.85-8.79-9.81 (7.9) 19. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th .03 (6.5) 22.39-17.99) 2.74-19.8) 11.95 (2.0-19.38 (.7-23.6) 7.9-25.44-6.63 (6.4-15.96-11.6 (13.29) 3.850 (<LOD-1.7 (10.3 (7.1 (13.06) .88 (1.58 (4.51-7.45) 3.25-9.50-17.34-18.89 (2.33) 3.5 (8.89 (3.03) 3.02-4.3-34.09-11.6 (11.1) 13.00) 2.77) 3.9) 16.

22-3.11-3.58 (1.83 (2.40 (1.54-2. 124 Fourth National Report on Human Exposure to Environmental Chemicals .780) .83) 1.70-7.95-5.15) 2.46) 1.31) 95th 2.14 (1.750-1.60) 3.42-2.30-3.840 (.49) .74-5. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.970) 1.587) * * .05-3.26) .459 (.618) * .13) .04) .00 (1.10) 1.540 (.73 (1.830 (.70-2.930) < LOD .17) 1.95) 2.80) 5.670) .60 (2.49) 2.560-.380-.30) 2.60-4.31) 2.40 (1.30) 4.10) 1.30 (.55 (3.600-1.00-2.23-3.550 (.09 (.20-2.89-6.46 (2.490 (<LOD-.57 (2.50) 1.77 (1.20) 3.910 (.05-2.90 (1.467 (.98-3.50-2.76 (1.20 (2.54 (2.18 (1.20 (1.20) 2.30 (.79) .1.690) .585) * * .79) .260 (<LOD-.860) < LOD < LOD .50 (1.80) 3.440-.160 (<LOD-.790 (.01-3.17) 1.80) 3.280-.20) 3.740 (.690-.27 (2.47) 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 * .580-1.50-2.36-4.96-3.380-.30 (.710) .240 (<LOD-.38) 1.690-1.00) 1.880) < LOD 75th .570 (.16) 2.303-.74) 3.65 (2.730) .500 (<LOD-.29-2.820 (.26 (2.20 (1.45 (1.29) 1.08 (2.22-8.89) 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 * .41-5.336-.2.960-1.700) .759) * .30-1.740-1.15) 2.960 (.70 (1.30-3.97 (2.32 (1.720-1.210 (<LOD-.20-2. population from the National Health and Nutrition Examination Survey.80) 2.90) 2.94 (3.57 (1.549 (.22-2. 0.22-3.54) .35) 1.18 (.83) 2.70 (1.780 (. see Data Analysis section) for Survey years 99-00.63 (1.690 (.34) 2.950) 90th 1.32-1.70 (1.880 (.86) 3.88) 1.20-1.570-1.570 (.13) 2.960) 1.457 (.08 (2. which may vary for some chemicals by year and by individual sample.S.80 (2.449 (.11-3.46 (1.89) .37-2.850) < LOD .455 (.61 (1.75-2.390-. and 03-04 are 0.50 (1.749 (.550 (.425 (.25-1.50 (1.657) * * .73 (2.810) .94 (2.96-5.80 (1.450 (<LOD-.720 (.30) 4. < LOD means less than the limit of detection.91) 2.930 (.17-4.21) 3.89) 672 678 478 509 695 553 595 948 745 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.22 (1.380) .50 (1.680-1.00) 2.33-2.597) * .10-1.30 (1.400) .69-4.20-3.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.700) .68-5.83) .64 (1.00-4.388-.580-.710 (.510 (.45 (1.16) 1.80) 2.77-2.750) 1.27 (3.75 (2.16-3.353-.87-3.89) 1.990-1.48 (1.48 (2.98 (2.01) .980) 1.10) 1.590-.740-.01-1.32) 3.620-1.78) 952 1187 907 997 1332 998 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * .800 (. 01-02.720-1.460-.20 (1.710 (.970) .880) < LOD .201-.46-3.10-1.960) .60) 2.80) 3.820 (.31-3.382-.14-1.740 (.780 (.78) .453 (.94) .04) 1.45-4.20) 1.960) .390-.350-.98) .86 (1.570 (<LOD-.505 (.592) * 50th .19-1.930-1.600 (<LOD-.31-3.90) 3.90) 2.398-.39) 2.584) .45 (2.680-1.41 (2. and 0. respectively.592) * .50 (1.592-.760 (.359-.95 (2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.90-4.570) * .03) 1.510 (<LOD-.34) 2.20) 1.47 (1.59-2.930) 1.570 (<LOD-.09.940) < LOD .20) 2.10) 3.73-5. interval) Selected percentiles ( 95% confidence interval) Total * .340-.949) .350-.910-1.343 (.76-6.83 (2.30) 1.59-6.650-.600-.910) 1.

230 (<LOD-.390-1.05 (1.20) 1.71) .400) .250 (<LOD-.08-2.71) 2.07) 1.98) 1.22) 1.07) 1.43) 2.00-1.305 (.70 (2.310 (<LOD-.300-.04-5.77-3.08-3.25-3.840) 1.57-4.19 (1.730) .136-.44-2.940-1.790 (.73 (2.253-.97 (1.22-2.760) < LOD 75th .400-1.47 (1.43) 2.61) 2.630) * .67) 1.70 (3.47 (1.270-.75) 6.447 (.403) .720 (. population from the National Health and Nutrition Examination Survey.61-3.99) 2.00-3.08) 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 * .58-6.310 (<LOD-.04) 95th 2.440-1.550-.90) 2.07 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.270 (<LOD-.08-2.11 (.08) 2. Fourth National Report on Human Exposure to Environmental Chemicals 125 .470) .448 (.03-1.560-.560-.47-4.380) .580-.13 (1.590) * 50th .700 (.680 (.20-2.08 (2.22) .520 (.39) 2.79 (1.79) 1.510 (.16-1.67 (1.670 (.55-3.77-4.49 (1.490 (.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 * .64 (2.50) 1.870) .550) .97) 2.77 (3.07) 1.690) < LOD < LOD .88 (1.66 (2.740) .32) 2.720-1.11) 1.61 (3.53) .42-6.453 (.760) .320-.645) .640 (.52 (1.05-4.39 (1.590-1.62 (1.92 (1.285-.S.45 (1.280 (<LOD-.850) 1.830) 90th 1.49-4.250 (<LOD-.02-3.32) 1.20-7.515) * * .700 (.510-.377-.840) 1.03-2.17) 2.08-2.990-1.710 (.72) 1.97 (1.16) 1.07) 5.41 (.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.29-4.88) .23) 2.370-.57 (3.33) .94) .09) .38 (1.740) < LOD 1.460-1.22-3.67 (1.22 (2.80) 2.348-.17) 2.32-1.65) 2.22-3.660-.790) .24) 4.52) 3.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.62 (2.36) 3.97) 1.310-.71 (1.980-1.535 (.710 (.82 (2.318-.57 (1.63 (1.38 (2.485) * * .550-1.75 (1.18-2.320-.30-2.380-1.60) 1.43) 1.05) < LOD .460) .57-2.64 (2.84 (2.87 (2.60 (2.67-3.04-1.270-.23) 2.07-2.234 (.870 (.23) 3.58) 3.05) 1.480) .500-.393 (.76) 1.42-8.330-.32) 5.820) 1.31-1.58 (1.597) * .509 (.81) 2.700 (.350) .66) .380-.82) 2.78) 3.580 (.50 (1.75 (2.34 (1.580) .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 * .920) .08-3.520-.552 (.800-1.950-2.750 (.368) * .06) 4.480-1. interval) Selected percentiles ( 95% confidence interval) Total * .180 (<LOD-.880) 1.99) 1.84-6.42) .38-3.08-3.820) .23 (.471-.444-.510 (.591 (.590 (.742) * * .830 (.72 (1.470 (<LOD-.540-.330 (<LOD-.00 (3.45 (2.69 (3.60) .55 (1.16-2.640 (.02-3.67) .42 (.335-.92) 3.02-6.75-3.840) .750 (.390) .560 (.550-.412-.61-3.44) 2.688) * .89-3.10) 2.739) * .08-3.72-4.91 (1.11-2.92-8.460 (.710 (.910) < LOD .73-3.900) 1.30) 3.08 (.69 (1.22) 4.300 (<LOD-.14 (2.95) 1.07-3.23) 1.17-2.05-2.800) < LOD .32 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.43 (1.89 (1.06-2.530 (.930-1.60 (1.28 (1.72 (2.372 (.33 (1.640 (.

0) 3.0) 45.50-5.0 (24.98 (1.25-3.3 (24.21 (1.0 (17.44) Selected percentiles ( 95% confidence interval) Total * 2.61-2.61 (1.58-2.8) 41.8 (12.71) 5.83-2.70 (1.0 (38.0) 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 2.0 (40.6-22.64-8.20 (2.30) 11.0) 33.80-2.10 (1.690-3.0 (26.50-2.2) 31.2 (12.8-24.87-7.40) < LOD 1.0-29.00 (.0 (19.1) 38.46-6.8) 671 678 498 509 695 579 595 947 757 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.0 (38.26 (.60) < LOD 1.41) 1.3 (12.23-2.0-39.30) 4.0-260) 34.0-53.0 (20.8) 39.21 (4.4-22.3 (14.80-18. 01-02.8 (26.5) 69. which may vary for some chemicals by year and by individual sample.69) 2.0-110) 42.0 (8.19-2.53) 1.4-76.11) 2.0-39.44) 2.09 (4.1 (10.13 (1.0 (20.40) < LOD 2.07-5.75-14.4) 38.3) 31.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.11 (4.43-7.50-17.54 (1.83 (1.1-20.0-62.0) 6.57-2.0) 18.7 (12.0-41.49-2.4 (15.53) 40.3) 28.2-26.0 (38.1-25.8-21.16) * 1.83-2.45) 2.00 (.81-3.0-47.12) 1.18) 20.78) 9.0-92.10 (1. 126 Fourth National Report on Human Exposure to Environmental Chemicals .4 (19.80) 90th 38.46-2.0 (32.45) 2.3) 33.26) 75th 11.0-49.10-13.7) 20.10 (1.9 (27.7 (28.58) 16.2-27.0) 16.05) 1.6-54.90-8.0-69.70 (.05-3.3 (10.0 (38.48-2.05) * 2.0 (13.S.23-2.79 (1.53 (1.470 (<LOD-1.3 (12. interval) 1.0) 20.48-2.44) 3. and 03-04 are 0.59 (1.0-230) 35.1 (25.0 (38.1 (11.0) 8.9) 48.80) 1.74-2.82 (1.2-27. population from the National Health and Nutrition Examination Survey.9) 18.06) * 2.30-14.610 (<LOD-1.0) 3.9 (19.66-5.7 (12.92) * 2.9 (23. and 0.0 (33.2-80.5-74.78 (1.9-51.93-3.9) 17.0) 19.77 (1.92-5.5) 30.0-58.10-4.1-40.1-19.52 (4.2-39.7) 47.41-4.0-41.2) 16.33 (5.0) 30.71-2.6) 52.70) 1.70-17.41) 5.8 (12.1) 140 (46.67 (1.44-7.4.32 (2.600-2.0 (6.42) 1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.88) 1.29-4.20) 1.96) 5.660-2.29-9.81-2.830-4.0) 20.17-2. 0.0) 15.6 (15.77) 38.99 (2.0) 4.36-2.9 (19.0-110) 34.0) 28.0 (11.0 (21.1-46.0 (8.2-33.1 (25.72 (1.1-47.23) 9.0) 3.29) 2.5-20.0 (38.2-47.80) < LOD 1.0 (37.70-6.54 (3.70) 1.60 (2.21 (3.0) 4.1) 38.8) 32.88) 3.19) 2.79-2.4) 19.0) 28.20-4.530-4.95 (5.13) 12.94 (1.3 (23.10) 39.9 (10.76 (2.27-6.5 (24.0) 5.70 (7.40-4.59 (1.90) 11. see Data Analysis section) for Survey years 99-00.2-62.04 (<LOD-2.83 (3.8) 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 1.0) 15.0-52.8) 62.1 (22.14) 5.0) 16.1 (26.5-45.0) 42.0) 471 575 310 664 822 717 813 1121 938 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 2.0-58.0) 4.5-40.35-6.6 (9.13 (1.31-6.12 (3.0) 17.40) 50th 2.71 (4.48) 5.41) 1.18.0 (25.50-7.0) 3.3) 26.70) 5.86 (1.06 (1.9-21.70 (1.40-16.30 (.0) 31.97) 6.0-53.76 (2.63-6.0 (38.16) 2.53) * 2.6 (11.0) 13.7-22.04-8.10 (1.98) * 2.91 (4.0-41.85) * 2.1) 95th 48.90 (1.50 (2.80) .02 (2.0) 17.2 (19.90 (1.64-3.10 (7.4 (10.86-3.0-50.18) 14.65 (4.0-31.0-43.04) 3.0) 32.0 (8.1) 18. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.5-27.7-41.3) 38.50-20.6 (26.79 (2. < LOD means less than the limit of detection.9) 38.41 (1.6-27.18) 6.85 (1.00-24.0-62.46 (.8 (22.5.10) .830-3.0 (7. respectively.6-45.57-2.

96-16.00) 6.58-2.71) 8.9-18.5-97.07) 9.4 (9.3) 13.5-43.59-2.79-17.06) 1.0) 3.4-21.23) < LOD 2.1) 27.23-1.8 (7.870-3.1) 52.22-2.51) .1-22.9) 12.2 (16.8-45.7 (18.0-40.21 (4.95-16.4 (25.43-2.26-4.7-20.9-41.9-95.1) 25.52 (1.2) 41.14 (.59-2.7-38.1 (33.7 (18.46-6.5 (15.9 (19.55 (2.2) 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.2) 13.28 (1.1) 13.7) 23.19) 5.22 (2.6) 112 (40.09 (5.40-4.67-3.7-37.8) 3.70-4.9) 54.8) 31.19 (1.82) 1.66 (1.48) 1.3 (20.68 (1.7) 26.0) 30.2 (22.9 (10.3 (8.80-8.33) 2.16 (1.66) 8.7) 34.58-17.83) .46) 1.84-13.56) 1.67 (1.31) 2.2-34.71 (1.6) 19.6) 23.1) 27.6) 3.18) * 2.7 (11.4-67. Fourth National Report on Human Exposure to Environmental Chemicals 127 .5) 70.0-71.7-43.3-27.38-1.2 (15.5 (34.2) 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 2.1-60. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.51) < LOD 1.62) 4.67-16.6) 11.2) 13.19) 5.6 (11.26-2.32-3.17-3.9-36.5 (6.0 (25.28) 1.11-2.3 (10.20) Selected percentiles ( 95% confidence interval) Total * 1.1) 15.S.4) 12.69-5.9 (39.2 (8.14-8.29-5.0 (6.680-4.46-22.22 (.27 (6.3 (9.96) 2.0 (14.5 (15.86) * 3.61 (1.16 (1.4-34.8) 15.02 (.11) < LOD 1.80 (1.40 (2.50 (2.37-2.1 (25.870-3.06) 75th 9.3-22.4-71.9 (26.90 (.3 (10.5 (17.4 (25.9 (13.0) 48.1) 17.95-16.6-49.6-38.6 (24.52-4.9) 3.16 (1.00-16.33) < LOD 1.18-1.3-42.9-52.38-5.64 (1.94-20.43) * 2.2) 36.02) * 1.72) 2.9) 3.7) 30.30) 28.35) .88 (4.5-36.4 (19.38 (3.95 (2.5-190) 30.7) 66.88 (4.54-15.0 (32.2) 4.40-7.79 (2.27) 50th 2.01 (.7 (24.8) 23.08 (1.7-19.0 (23.75 (1.25-3.0-118) 29.4 (21.1) 25.20-5.750 (<LOD-1.7) 15.4) 12.16-2.7-109) 22.1 (12.99-4.60 (.5 (8.86) * 2.70 (1.9 (7.0 (39.2 (21.03) 1.0) 47.8-37.4 (11.67 (1.00) 1.1) 13.91 (6.12 (1.888-1.61-22.83 (.670-1.8-26.7) 61. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.68) 47.06-1.47 (1.1-63.8) 11.46-5. interval) 1.860 (<LOD-1.9-37.57) 4.62 (2.3) 28.19-6.5 (13.8-34.61-2.45 (1.4 (12.94) 19.2-70.6 (27.35 (2.2-38.53) 1.07-2.75 (1.0 (23.930 (<LOD-1.0) 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 1.2-47.37 (1.4) 14.88 (1.8-43.02) 1.7 (10.93) 5.2-28.48 (4.5) 27.6 (7.0) 13.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.75) * 1.44) 9.41 (2.36 (4.00 (4.24 (1.63-5.3-19.4-39.899-2.2) 471 575 310 664 821 715 813 1121 937 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 1.1 (39.91-2.19-14.6) 7.2 (9.35) 1.9) 24.43-12.66 (1.12) 3.34) * 1.9) 24.69-18.7) 95th 51.88 (1.890-4.0) 25.45-1.08) 1.27) 10.0 (19.32 (3.97 (1.38) 5.36) 10.40 (5.47-17.54-2.8) 32.5 (41.6-32.15 (.18) 3.1 (34.1 (50.7-47.6-51.59-15.4) 3. population from the National Health and Nutrition Examination Survey.57 (6.33-5.6) 3.03-2.0-70.39 (1.870-3.0) 10.27-3.1) 36.07-2.82 (2.17) 2.2) 33.56 (2.47 (3.50-5.60) 4.4 (5.22-3.0 (17.75-6.06) 1.95) 90th 32.33) 1.36-13.94) 1.23) 37.71-2.76-2.

940 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.640) .570) .120 (<LOD-.117 (. 128 Fourth National Report on Human Exposure to Environmental Chemicals .220 (<LOD-.410) < LOD < LOD < LOD < LOD .140) .700-1.10) .650 (.680-1.830) < LOD .610 (.990) .370-.230-.380-.160) .12 (.720-1.720) .42) .140-.230) .990 (.210 (.130-.430 (.730) .470-1.10 (.380-.620 (.099-.870 (.390) < LOD < LOD .680) .090 (<LOD-.490 (.10) .130-.050-.090 (<LOD-.310) < LOD < LOD < LOD < LOD .090 (<LOD-.640 (.640-1.280) < LOD < LOD < LOD < LOD .130) .120-.00) .930 (.S.850) < LOD .700-1.13) .450 (.090 (<LOD-.310 (.360-.03) .780) < LOD 1.171) * * .150) .260 (.190 (.1.310 (.560 (.460 (.310) < LOD < LOD < LOD < LOD .700-1.190 (.370-.42) .320 (.540) .550) .650-1.640) .290) < LOD < LOD < LOD < LOD Non-Hispanic whites Limit of detection (LOD.690-1.390 (.170-.450 (.850 (.870) < LOD .650) .380-.820 (.720 (.680-1.420-.650) .330-.740) < LOD .540 (<LOD-.860-1.100 (. 0.860) .05.300-1.30) . and 03-04 are 0.290 (<LOD-.650-1.430-.820 (.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 .20) .410-. see Data Analysis section) for Survey years 99-00.840) .220 (.540) 672 678 498 509 694 579 595 947 757 Non-Hispanic blacks .990) .080 (<LOD-.10) .870 (.900 (.160-.40) .130 (.530-.400-.410-1.084-.110-.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 * * * * * * . which may vary for some chemicals by year and by individual sample.830 (.350) .140-.190 (.700-1. < LOD means less than the limit of detection.870 (.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 * * * * * * * * * .30) .180) .210 (.610-.450 (.300-.680 (.770) < LOD 95th .240 (<LOD-.080 (<LOD-.130) .730-.830) .140-.870 (.630 (.610 (.770 (.600 (.160) .410-.290) < LOD < LOD < LOD < LOD 90th . 01-02.30) .470 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.460-.610-1.15) .290) < LOD < LOD < LOD < LOD .350) < LOD < LOD < LOD < LOD .660 (.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.540) .310-.36) .090 (<LOD-.32) .200) < LOD < LOD .120-.150 (<LOD-.320-.090 (<LOD-.130-.162) * * * * * .360-.630 (.830 (. respectively.850 (.58) .270 (.840) . population from the National Health and Nutrition Examination Survey.760) < LOD .1.560 (. and 0.870 (. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th 75th .510-1.440-1.60) 1.

190 (.110) .230 (<LOD-.084-.410 (. population from the National Health and Nutrition Examination Survey.450) .270 (.730) .360 (.810 (.140-.860 (.290) < LOD < LOD < LOD < LOD 90th .140-.110) .230) < LOD < LOD < LOD < LOD .050 (<LOD-.610-1.800-1.740) < LOD 1.880 (.330-.140-.300 (.570 (.00) < LOD .110) .940) .310) < LOD < LOD < LOD < LOD Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.09) .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 * * * * * * .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 .110) .260) .700 (.36 (1.380-.510) Sample size 1949 2515 1962 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * .057-.03 (.080 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.161) * * .140-.116 (.990) .500-1.510-.38) 1.670-1.570-.03 (.140) .640-1.080 (.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.67) .360) < LOD < LOD < LOD < LOD .330-.650) < LOD .380-.410) < LOD < LOD .260-.070 (<LOD-.190 (.750) < LOD 95th .550 (.700-1.500 (<LOD-.100 (<LOD-.600-1.110-.860 (.740 (.300-.62) 1.060-.170 (.410) .520-.400 (<LOD-.150-.280) < LOD < LOD < LOD < LOD .990) .080) .360-.570-1.670 (.450 (.120) .780 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.330 (.070 (<LOD-.200 (.500) .580) .100-.230-.070 (<LOD-.320 (<LOD-.170 (.410 (.240-.520) 672 678 497 509 693 578 595 947 756 Non-Hispanic blacks .410-.440-1.390-.03) .310) < LOD < LOD < LOD < LOD .01 (.86) .870) .360-.400) .200 (.940) .180-.670 (.111) * * * * * .210 (.580 (.700) . Fourth National Report on Human Exposure to Environmental Chemicals 129 .970) .02) .S.070 (<LOD-.410-.270) < LOD < LOD < LOD < LOD .43) .700 (.720 (.12) < LOD .380-.860-2.19 (.710-1.78) .14) 1.460 (.890 (.540) .120) .380-1.760) .730) .330 (.650-1. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th 75th .560 (.140-.29 (.600) .730) .580-1.220) < LOD < LOD < LOD < LOD .370 (<LOD-.340-.170) < LOD < LOD .960) .720 (.380 (.190-.090 (<LOD-.540 (.850 (.86) .880-1.540 (.490-1.470 (<LOD-.300-.03 (.550 (.580 (.660-1.390-.330-.580) < LOD .780) < LOD 1.60) .440 (.250-.66) 1.58) 1.20) 1.220 (.730 (.090 (.02-1.24) .24 (.

0 (4. population from the National Health and Nutrition Examination Survey.590 (.425-1.600 (.07) 1.30-6.0) 5.03 (.0-40.20) < LOD < LOD < LOD < LOD < LOD 1.07 (3.21-3.30 (.30-3.0 (7.07 (3.05-3.62) 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 * * * * * * .00 (1.47 (3.66) 4.960 (.40-7.6) 672 678 498 509 695 552 595 947 752 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.800-4.35-10.40-20.07-3.53 (2.350-.32 (1.20 (1.43-4.640 (.90 (2.01) 5.23-6.691 (.10-3.68) 2.63) 32.0-40.39) .1.110 (<LOD-.60) 1.59-5.0 (5.0 (13.80 (4.6) 5.00-17.40) 1.61 (1.52 (1.260-.400-1.07 (1.960 (<LOD-1.0) 4. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.620-1.15) 19.94-8.0) 2.40) 2.52) 5.770) 2.74 (3.70) 2.0 (6.830 (.74) 5.360-1.00) .0 (4.0-38.0) 2.83) 2.0) 4.08.70-30.05 (3.28-9.580 (.88-3.0) 4.90-9.35) 5.30 (2.48) 13.0) 2.0) 5.880) 5.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.0-38.0) 2. and 03-04 are 0. which may vary for some chemicals by year and by individual sample.87) 12.70-3.26 (2.0 (17.30 (1.3) 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 * * * * * * * * * .90 (1.250 (<LOD-.00) .840 (.840-3.87) 5.67 (1.0) 7.0 (16.12) * * * * * * * * .60) .0) 4.0 (17.99) 19.910) 2.65) 1.0 (5.11 (1.0) 2.90-28.890 (.05 (2.85-3. and 0.50) .20 (1. respectively.0 (3.30 (1.840 (<LOD-1.35) 11.80) < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 4.62-8.33 (4.40-4.51 (2.15) 14.18) 1.610) < LOD < LOD < LOD < LOD < LOD 2.0) 5.210-1.90) .13 (3.76 (1.0) 3.30-7.640 (. 0.720) 2.11) .39 (2.0 (17.49 (1.96 (1.10 (.20-17.14) 2.90) .36-3.30 (1.380-.70-50.10 (3.510-.50) 2.99 (1.730 (.14) .82-4.870) < LOD < LOD .67) .31-10.49) 17.20-4.20-4.45 (2.67 (2.0) 5.480-.99) 11.800) 17.07-3.38-3.00 (.29-10.30) .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 .10 (3.690 (.63 (3.51-8. 01-02.52 (1.55-4.12-1.1.800) 90th 13.40 (1.14-5.350-.24-7.0-39.31) . 130 Fourth National Report on Human Exposure to Environmental Chemicals .00-17.48 (2.49 (1.0) 2.080-1.0 (17.83-3.770 (<LOD-1. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th 2.70-17.32-9.190-1. < LOD means less than the limit of detection.30) 95th 19.40-8.11) 13.0) 2.0 (5.900 (.0-38.94 (1.37) .10-9.40 (1.S.97) 20.0-44.370-.170-1.70-7.330 (<LOD-1.94-3.90) .53-7.86) 4.42) .850) 16.0 (17.42) 2.21) 3.0 (5.10-3.28) .740 (.28) 1.750-2.0 (5.97) 20. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.90-20. see Data Analysis section) for Survey years 99-00.00) 1.55-8.750-1.610 (.53) 20.46 (1.90-37.83-3.36-3.

50) 11.8) 7. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.64-4.9) 5.790) 11.790 (.51-4.8) 1.340-.47-10.04-16.07-21.340-.57 (.08) .85 (1.10) 2.73 (4.31) .85-3.7) 6.39) 20.17 (1.55) 21.02 (1.33-5.660) < LOD < LOD .14-6.29-4. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.48 (4.38 (2.11) .88) 17.40-2.56) .18) 1.53) 27.370) < LOD < LOD < LOD < LOD < LOD 1.748 (.740-1.6) 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 * * * * * * * * * .96-8.31) .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.92 (2.22-27.25 (1.79 (.600 (<LOD-1.57-40.21-3.33 (1.5) 2.40-12.23-7.14 (1.75) 5.2-38.52 (. population from the National Health and Nutrition Examination Survey.97) .890 (.13 (2.40 (.940-4.5 (11.74 (2.80) 3.800-2.0 (4.12-4.1) 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 * * * * * * .7) 5.11-5.06 (.770) .55 (3.71 (.830 (.00-19.05) .57) 8.620-3.18) * * * * * * * * .470 (.240-.83-11.260-.88 (2.8) 2.35 (.7 (12.67 (2.02) .49-2.31-7.91) 2.65 (2.66-47.5) 2.710 (<LOD-1.17) 5.10 (2.840-3.370-1.580) 1.9 (11.02 (.32-6.59 (1.8-33.5 (8.67) 2.10-3.310-.84) 9.86 (3.260-.50) .55) 21.340-.450 (.370 (.03) 2.41 (4.98 (4.69) 2.56) 2.190-1.67-6.33 (3.690-5. Fourth National Report on Human Exposure to Environmental Chemicals 131 .330-1.560 (.09-3.37) 4.430) 1.60) < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 4.83 (4.71 (2.24) 3.8) 7.36 (.7 (6.50 (4.5-40.5 (9.2 (8.270 (<LOD-.47-10.390-.8) 4.29 (4.5) 7.25-9.1 (7.S.89 (2.650) 90th 10.22) 2.970-3.02-4.580 (.150 (<LOD-.33-4.250 (<LOD-.12 (4.540-1.62 (1.1 (5.44-11.69-7.03) 16.830-3.51-44.50 (2.04 (1.30 (4.86) .590) 2.47) 5.500 (.48-42.860-2.47) .33-3.96) 2.57) 1.540 (.3) 2.07 (2.4) 2.15) 9.32) 9.90-6.64) 30.580) 16.28-6.340 (.9) 6.01 (1.41) 18.40) 1.4 (4.80 (.670 (.8 (20.270-.96-25.8) 2.44) .7) 4.630-1.960 (.4-34.31-18.1) 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.7) 3.580-1.67) 1.88 (.45 (1.700) < LOD < LOD < LOD < LOD < LOD 1.43) .0 (9.00) .650 (.320-1.81-17.360 (. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th 1.61) Sample size 1949 2517 1927 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .62-17.18) 95th 21.25-38.430 (<LOD-.56 (1.0) 4.780-4.700) 6.1) 2.850-3.91-4.88-3.60 (1.820) .27 (2.82-11.53) .730-3.474-1.3) 3.930) .48-7.77 (.820 (.

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Keefe TJ. metabolite clearance. Lewis JA. Neurotoxicol Teratol 1998. Vitayavirasak B. O’Malley M.nap. Wickremasinghe AR. Masala G. and spatial learning in monkeys and rats. Ruberu DK. Occup Environ Med 1995. Narang A. Muniz J. Scherer J.php?record_id=2126&page=1. Hore P. 1993 [online].12(2):134-141. Weerasekera G. Buccafusco JJ.12(2):153-172. Arch Environ Contam Toxicol 2000.68(3):209-227 Maizlish N. Office of Prevention Pesticides and Toxic Substances. Hansen S.345(8958):11351139.113(4):504-508. Lancet 1995. London L. U. Salvini S.332(1-3):71-80.26(2):199-209. Irish RM. discrimination. Organophosphate pesticide exposure and neurobehavioral performance in agricultural and non-agricultural Hispanic workers.pdf. Weisskopf C. Jenkins B. Marshall E. McConnell R. Tumino R. Dinoff TM. low-level organophosphate exposure on delayed recall. Washington (DC): U.44(4):352-357. Aprea C.S. Effects of occupational exposure to organophosphate pesticides on nerve and neuromuscular function. Heaton RK. gov/oppbead1/pestsales/01pestsales/market_estimates2001. National Research Council (NRC). Berry H. Buchanan D. Petchuay C. National Academy of Sciences.58(11):702710. Rohlman D. vibration sense and tremor among South African farm workers. Samuels S. Environ Health Perspect 2006. Muniz J. Caltabiano LM. 2004. Am J Ind Med 1987. Daniell WE. McCauley L.epa. Lasarev M. EPA. Smit LA. Available at URL: http://www. Chronic neurological sequelae to organophosphate pesticide poisoning. Steenland K. Russo J. Lambert WE. Phillips J. Santana J. Nell V. Environmental Protection Agency (U.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Krieger RI. Scand J Work Environ Health 1998. Fourth National Report on Human Exposure to Environmental Chemicals 133 . 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. Neurotoxicity among pesticide applicators exposed to organophosphates. Terry AV Jr. Variation in organophosphate pesticide metabolites in urine of children living in agricultural communities. Am J Public Health 1994. The presence of dialkylphosphates in fresh fruit juices: implication for organophosphorus pesticide exposure and risk assessments. J Occup Environ Med 2002. Occup Environ Med 2001. Burcar PJ. et al. Thompson ML. Washington (DC). Chrislip D. Lu C.338(8761):223-227. Bull Environ Contam Toxicol 1994. Stokes L. Rosenstock L. Prendergast MA.20(2):115-22. Beach J. The Pesticide Health Effects Study Group. Lancet. Pesticide industry sales and usage . Gillham R. Available at URL: http://books. Robson MG. Malathion deposition. Frasca G.52(2):190-195.84(5):731-736. Pesticides in the Diets of Infants and Children. Int J Occup Environ Health 2006. Effects of chronic. Kidd M. J Toxicol Environ Health A 2005. Pilkington A. et al. Mounce LM. Saieva C. Effects of long-term organophosphate exposures on neurological symptoms. low-level exposure to the organophosphate diazinon. Twenty-four-hour urinary excretion of ten pesticide metabolites in healthy adults in two different areas of Italy (Florence and Ragusa). et al. Johnson C. Stephens R. Jamal GA.S. 1/12/09 Peiris-John RJ. and cholinesterase status of date dusters and harvesters in California. 1991. Bradman A. Visuthismajarn P. May. Pedersen L. van der Hoek W. 4/7/09 Young JG. Takamiya K. Seiber J. EPA). et al. Sci Total Environ 2004. Arch Environ Health 1975. Neuropsychological effects of long-term exposure to organophosphates in sheep dip. A behavioral evaluation of pest control workers with short-term.2000 and 2001 market estimates. Chronic central nervous system effects of acute organophosphate pesticide intoxication. Association between in utero organophosphate pesticide exposure and abnormal reflexes in neonates. S.114(5):691-696. Myers JE. Arch Environ Health 1988. Stark A. Eskenazi B. Environ Health Perspect 2005.38(4):546-563.52(10):648-653. Barr DB.edu/ openbook.30(2):98-103. Lasarev M. Rodnitzky RL. Occupational exposure to organophosphate pesticides: a neurobehavioral study. Keifer M. Chronic neurological sequelae of acute organophosphate pesticide poisoning. Calvert IA. et al. Biological monitoring of organophosphate pesticides in preschool children in an agricultural community in Thailand. Ames RG. Levy LS.43(1):38-45. Rothlein J. Bravo R. Neurotoxicology 2005. Schenker M. Savage EP.24(1):18-29. Claypoole K. Gladstone EA. Spurgeon A. Monitoring of urinary alkyl phosphates in pestcontrol operators exposed to various organophosphorus insecticides. Rothlein J.

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 . In addition to reflecting exposure to the parent insecticide. The table below shows the parent organophosphorus insecticides and their metabolites measured in this Report. see the section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites.5. 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. the level may reflect exposure to the environmental degradation products of these pesticides. These metabolites differ from the dialkyl phosphate metabolites because each specific metabolite derives from one or only a few parent insecticides.Organophosphorus Insecticides: Specific Metabolites Organophosphorus Insecticides: Specific Metabolites General Information The specific metabolites of the organophosphorus insecticides discussed in this section are those that are often measured in biomonitoring studies. parathion and methyl parathion are metabolized to para-nitrophenol. malathion is metabolized to malathion dicarboxylic acid. For example.

and sprayed to kill mosquitoes.22 (1.20-16.04-10.10 (1.3) 8.21) 3.89-2.00) 1. but can be detected in streams receiving runoff from application sites. 2002).63 (8.16) 2. Approximately 80.62-2.20-4.50 (2.28) 2.53 (1.67 (2.5.77 (1.47-13.89 (2.39-2.32-1.83) 1.15 (1. interval) 1.40) 2. Chlorpyrifos is not well absorbed through the skin but dermal exposure can be significant when other routes of exposure are low.0) 14.20 (4.8-15.24-1. and dust.05) 1.66-15.30-11.40 (5.19 (1.70 (1.59-2.60-2.34) 1.0) 7.80) 2.30 (4.40) 9.02) 1.30-9. Chlorpyrifos is Urinary 3.97) 7.17 (1.70-16. Approximately 21-24 million pounds per year were used domestically from 1987-1998.39) 4.68 (7.9) 11.9 (9..10 (4.10 (5.50 (2.4 (10.1) 5.51-2.44-5.64) 3.5-24.35) 2.40 (5.29-1.96) 3. air.6) 7.0) 8.31-2.61 (1.0) 12.27 (7. 2921-88-2 Chlorpyrifos-methyl CAS No.14) Selected percentiles ( 95% confidence interval) Sample 95th 10.0) 9. It has low leachability.0) 10.99-4.0) 12.EPA.63 (2.30 (2.09 (2. For instance.72) 2.60-3.40 (6.78 (7.6-Trichloro-2-pyridinol Metabolite of Chlorpyrifos and Chlorpyrifos-methyl Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.57 (2.43-2. USGS.10-17.25) 1.44 (3.4 (8.3 (10.50-4.2) 972 1183 1022 1326 99-00 01-02 99-00 01-02 99-00 01-02 1.51 (1.38 (3.19-3.90 (2. chlorpyrifos was no longer registered for indoor residential uses in the United States. Chlorpyrifos is very toxic to fish and aquatic invertebrates and shows modest degrees of bioconcentration.30-12. Chlorpyrifos is a broad spectrum organophosphorus insecticide that has been widely used to control insects on food crops such as corn. dermal.and post-construction structural applications for termite control were to be phased out by 2005 (U.91) 16.86) 4.3 (11.77-15.90) 3.50 (1.63 (1.30-2. and inhalation routes.0 (13.50 (1.24-3.95) 7. 2002). Inhalational and dermal routes of exposure are important in pesticide formulators and applicators.61-7.9 (7.03) 99-00 01-02 99-00 01-02 99-00 01-02 2. 2007).0) 12.26) 7.52-2.43-2.0 (9.70-17.20-2.22) 2.20) 2.000 pounds are used per year.30-1.13-3.30 (2.7) 8.61) 75th 3.10) 6. It also has been applied directly on animals to kill mites.4 and 0.7-23.70-11. Survey Geometric mean (95% conf. 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.97-7.2 (10.4-15.EPA. Chlorpyrifos is degraded in agricultural soils with a half-life of several months.51) 1.98-15.70 (1. in 142 urban homes and preschools in North Carolina.30) 4.71 (6. Estimated intakes from diet and water have not exceeded recommended intake limits.30-5.60-3.67 (1.02 (7.80-10.9) 697 660 521 701 602 947 Limit of detection (LOD.05-5.8) 10.47 (4. Chlorpyrifos-methyl is an organophosphorus insecticide also used in agriculture and not registered for residential use. 5598-13-0 General Information The chemical 3.44-2.4) 481 573 681 823 832 1113 99-00 01-02 99-00 01-02 1.60 (4.77-6.0) 15.5. 2005).00-8.20) 4.30) 4.31-2.0 (7.30) 5.20-14.50-2. The general population may be exposed to chlorpyrifos via oral.0) 11.0) 12.09 (3.90-8. Fourth National Report on Human Exposure to Environmental Chemicals 135 .5) 7. 1999.59) 2.70) 1.94 (4.76 (1.4.25) 3.32) 2.60-4.60) 5.45 (1. chlorpyrifos and TCPy were detected in all indoor air and dust samples (Morgan et al.0 (10.46-2.70-5.76 (1.04-10.9 (10.8) 9.50-14.77) 1.0 (7.1-16.92 (1.71 (2.9-18.95 (4.00) 3.20 (2.29) 90th 7.47-11.97) 2.90 (3.66-4.90-4.6-trichloro-2-pyridinol (TCPy) is a metabolite of chlorpyrifos and chlorpyrifos-methyl.80 (1.37) 5.10) 2.00) 2.90-2.80) 4.90 (1.0) 6. Exposure can also result from contact with contaminated surfaces.70-15.0-28.0 (7.90 (6.40-13.02 (1.20-3.40-10.67 (2.3) size 1994 2509 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th 1.35) 1.72-4.87-6.0 (7.55-5.81-2.S.20-11.68-2.0) 18.50-4.97) 2.80-8.50 (2.28-3. After 2001.36 (4.01) 1.60 (2.88 (1.5 (8.7) 9.7) 13.40-2.79-2.S. pre.47) 1.37 (4.3 (8.84) 1. and is infrequently detected in ground water (IPCS.4 (9.0) 10. applied to structures to kill termites.90-7.0 (7.80) 1.37 (1.10 (3.60 (5. population from the National Health and Nutrition Examination Survey.50-5.0) 8.90 (1.71 (1.90) 7.74-9. and on plants for days to several weeks.00-24.03) 1.50-2.20) 2.20) 10.50-8.74 (1.S.80) 12.40-26.0) 12.80 (7.Organophosphorus Insecticides: Specific Metabolites Chlorpyrifos CAS No.52-12.91 (1.97) 4.0) 10. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.47-9.13 (1. staying bound to soil particles.

95 (3.81 (3. Recent in vitro and in vivo animal studies suggest that effects on neuronal morphogenesis.58-5.24 (1.940-1.71 (1.86 (1.24-1.3) 9.. Once absorbed.35) 1. resulting in excess acetylcholine at nerve terminals.66-11..89) 4.76 (2..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 1.93 (1.37 (1.63 (4.7) 697 660 521 700 602 947 136 Fourth National Report on Human Exposure to Environmental Chemicals .0) 481 573 681 822 832 1113 99-00 01-02 99-00 01-02 1.11-9.05) 3.14) 1.23) 14.94-14.83) 1.44 (1.50 (4. The metabolite TCPy does not inhibit acetylcholinesterase enzymes.09-3.8) 9. cholinergic effects..16) 6.25-1.91) 1.97) 3.94-12.58 (4.85-4.76 (3.44 (1. and producing acute symptoms such as nausea.56 (4.39) 6.01) 1.29 (3.77) 1.86 (3.23-1.20 (2.0) 12.47 (1.4) 4.80-4.30-4.91) 10.88 (1. Betancourt et al.33 (.47 (5.27-1.42 (5..73 (1.97 (2.25-11.S. 2006.97 (3.14-8.59) 3.57) 2.33-7.75) 6. 1984).49-2.35-1.59-2.79-13.88-9.58) 1.70-4.55 (4.72) 2.07) 1. Overt cholinergic toxicity from chlorpyrifos has been described following suicidal ingestion and unintentional high level occupational exposure.55 (1.16 (4. paralysis.30-1.7) 7. and other metabolites.82-4.91-4.21-6. TCPy is more persistent in the environment than chlorpyrifos itself (U.03) 1.97) 3.56-2.55) 1.05-3. Two observational studies of pregnant women and their offspring exposed to chlorpyrifos at environmental levels have found inconsistent relationships with birth outcomes of weight and length (Eskenazi et al.3 (7.2 (7.26-14.48 (1.71) 3.02) 7.86 (1.87-3.06-4. Urinary 3.27-7. Ricceri et al.53 (2.39 (2.09 (1.54) 5.93) 5.41 (1.38) 3.6) 10.91) 1.35) 2.33 (5.82 (3.98 (7.58 (1.34-1.64-7.72) 1.92 (1.58 (1.48 (2.28) 2. ubiquitous lowlevel environmental exposures in humans would not be expected to result in inhibition of cholinesterase activity.20-1. 2002).49-2.47-2.92) 3. 2006a.24-4.88-8.1 (10.49-2.01) 3.93 (4. interval) 1.31-1.46 (1.05-1.42 (6.24) 75th 2.44 (5.51 (1.8) 972 1183 1022 1325 99-00 01-02 99-00 01-02 99-00 01-02 1.EPA. Survey Geometric mean (95% conf.56 (1. 2006. 2000).44 (5. Howard et al..60-3.17-4. Thus.21-1.82 (2.95 (1.88-8.96) 3.80) 3.12-3.22-6.39-1.05-4.11) 7.47 (1.9 (12.57-2.85 (2.45-1.40) 1.42-2.85) 4.58) 5.56) 5.00) 1.5.32) 1.62) 1.99) 1..66) 1.07) 5.09-2. 2005.81) 2.00-8.43 (4.24-24.93) 2.11 (2. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”).88 (1.31) 1.00 (7.52 (5.6) 9.28) 2.43-10.01) 3.69 (1.80-6.60 (1. Chlorpyrifos is eliminated from the body primarily in the urine with a half-life of approximately 27 hours (Nolan et al. weakness.00-13. In addition to being a metabolite of chlorpyrifos and chlorpyrifos-methyl in the body.88-10. and seizures.1-38.02 (5.39 (4.91 (3.2) 6.25-12.91-13.97-3.92-2.19-1.85 (3.98 (6.85) Selected percentiles ( 95% confidence interval) Sample 95th 8.33) 2.99-8.93 (2.0) 6.24) 5. 2005. and behavior may occur at systemically nontoxic doses or at doses of chlorpyrifos that do not result in cholinergic signs (Aldridge et al.3) 8.62) 90th 5. Slotkin et al. vomiting.05-8.06 (1.11 (2.6-Trichloro-2-pyridinol (creatinine corrected) Metabolite of Chlorpyrifos and Chlorpyrifos-methyl Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.3) 8.. phosphorothioates such as chlorpyrifos are metabolically activated to the “oxon” form which has greater toxicity than the parent insecticide.08) 6. Based on animal data and human cholinesterase monitoring during occupational exposure.19) 3.64 (1.15 (4. These organophosphorus insecticides share a mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system.1-21.1 (7.33 (1.78 (1.66 (1.45 (1.22 (4.75 (1.12) 1.19) 6. Metabolic hydrolysis leads to the formation of TCPy.44-6.84-6.S. population from the National Health and Nutrition Examination Survey.09-1.5) 5.01) 99-00 01-02 99-00 01-02 99-00 01-02 3.83-2.12-1. Roy et al.63-2. 2005.5 (6. the detection of TCPy in a person’s urine may reflect exposure to the environmental degradates.88) 6.72-2. Chlorpyrifos and chlorpyrifos-methyl both demonstrate moderate acute toxicity in animal studies.91 (4.57) 9. chronic exposure to chlorpyrifos may be associated with slight alterations in some components of neurophysiologic testing (Steenland et al.56) 2.31-4.19-2.53-5.Organophosphorus Insecticides: Specific Metabolites rapidly absorbed following ingestion. TCPy can also occur in the environment from the breakdown of the parent compounds.57-2. neurotransmission.90-9.82) 8.46 (2.49 (1.65-15.0) 10. 2006b).74) 1.24-5.91) 2.68) 1.68) 6.17-4. In pesticide applicators. Human health effects from chlorpyrifos or chlorpyrifosmethyl at low environmental doses or at biomonitored levels from low environmental exposures are unknown.22 (6.64-2.36) 1.63 (5.83-11.54 (2.85) 1.06 (5.0) 16..22) 1.65-11.44 (6.80-11.62-7.

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

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Biological monitoring of exposure of the general population to the organophosphorus pesticides chlorpyrifos and chlorpyrifos-methyl by determination of their specific metabolite 3. Exposures of preschool children to chlorpyrifos and its degradation product 3. Herrick RF.51(1):53-65. U. Available at URL: http://www. Brain Res Dev Brain Res 2005. Barr D. Levin ED. Ryan PB. Pellizzari E. Morgan MK. Baker BA. mothers and fathers living in farm and non-farm households in Iowa. Toxicol Appl Pharmacol 2005.niehs. Steenland K. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. Toxicol Sci 2006. Howard AS. Sanderson WT. Robertson GL. et al.nih. Environ Health Perspect 2006.Organophosphorus Insecticides: Specific Metabolites Centers for Disease Control and Prevention (CDC). Hein MJ. Scand J Work Environ Health 2005. Gurunathan S.S. Chuang JC. Reid TM.6-trichloro-2-pyridinol. Temporal variability of urinary levels of nonpersistent insecticides in adult men.114(10):1542-1546. Rauh V.15(3):271-281. 2921-882. Jones PA. Mandel JS. Environ Health Perspect 2006a. Environ Res 1995. Lein PJ.6-trichloro 2-pyridinol in their everyday environments. Environmental Health Criteria 198. Wartenberg D. J Expo Anal Environ Epidemiol 1999. Seidler FJ. Chlorpyrifos: pharmacokinetics in human volunteers. 4/7/09 Perera FP.org/documents/jmpr/jmpmono/ v99pr03.71:99108.31 Suppl 1:98-104. Yang D. Toepel K. Barr DB. Freshour NL.

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

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

380 (<LOD-.670 (<LOD-1.27) < 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 . population from the National Health and Nutrition Examination Survey. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2481 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .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 .S.200 (<LOD-. Survey Geometric mean (95% conf. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.200 (<LOD-. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2480 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .560) < LOD 659 700 920 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. Fourth National Report on Human Exposure to Environmental Chemicals 141 . 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. 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.2. < LOD means less than the limit of detection.S.270) < LOD 659 701 920 Limit of detection (LOD.Organophosphorus Insecticides: Specific Metabolites Urinary 3-Chloro-7-hydroxy-4-methyl-2H-chromen-2-one/ol Metabolite of Coumaphos Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.

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

population from the National Health and Nutrition Examination Survey.Organophosphorus Insecticides: Specific Metabolites Diazinon CAS No. Prior to 2000. and other metabolites. It has been infrequently detected in general groundwater sampling but has been detected in streams receiving runoff from application sites (IPCS. 333-41-5 General Information The chemical 2-isopropyl-4-methyl-6-hydroxypyrimidine is a metabolite of diazinon. Estimated intakes from diet and water do not exceed recommended intake limits (U. 2004).S. diazinon produced wild bird kills before use restrictions were in place. USGS. and particularly when it was ingested in granular form. It is toxic to birds.05) < LOD < LOD 644 678 484 700 554 956 Limit of detection (LOD. Fish and aquatic invertebrates show modest degrees of bioconcentration and are very sensitive to toxic effects.45 (<LOD-3.49 (<LOD-2. < LOD means less than the limit of detection. vegetable. which may vary for some chemicals by year and by individual sample.7. aerial.11) < LOD < LOD < LOD < LOD 454 580 632 829 756 1126 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 894 1191 948 1344 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1. an organophosphorus insecticide that is used to control insects on nuts. phosphorothioates such as diazinon are metabolically activated to the “oxon” form which has greater toxicity. Diazinon is not well-absorbed through the skin.EPA. Before these restrictions. Survey Geometric mean (95% conf. but is rapidly absorbed orally (IPCS. 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. 1998). in some pest strips. Inhalational and dermal routes of exposure can be significant for pesticide applicators. Fourth National Report on Human Exposure to Environmental Chemicals 143 . diazinon was widely used in residential and garden application. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.EPA. fruits. diazinon cannot be sold for residential use. It is also used for cattle ear tag applications to control flies and ticks and. seed and foliar applications are planned to be phased out (U.S. 1998. in the past. but these uses have been phased out. Once absorbed.2 and 0. Diazinon is biologically and chemically degraded in soils with a half-life of about a few weeks. and forage crops. 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. 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. 2007). Metabolic hydrolysis leads to the formation of 2-isopropyl4-methyl-6-hydroxypyrimidine. see Data Analysis section) for Survey years 99-00 and 01-02 are 7. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”). 2004). since 2004. about 13 million pounds of diazinon were used annually on agricultural sites in the United States. Experimental diazinon exposure in people has demonstrated its rapid elimination into urine.S. Most granular formulations.

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. 1992).. Intoxications in humans from intentional overdose. diazinon and other organophosphorus insecticides share a mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system.. Biomonitoring Information Urinary levels of 2-isopropyl-4-methyl-6hydroxypyrimidine reflect recent exposure. and producing acute symptoms such as nausea.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. or reproductive toxicant (IPCS.S.76 (<LOD-3. Diazinon is not considered to be a mutagen.S. vomiting. respectively. paralysis. cholinergic effects. Additional information about external exposure (i.. population from the National Health and Nutrition Examination Survey.e. In the U. subsamples of NHANES 1999-2000 and 20012002. Thus. 1986 Rajendra et al.cdc. 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. At high doses. 2002). * Not calculated: proportion of results below limit of detection was too high to provide a valid result.epa. most of the measurements of 2-isopropyl-4-methyl6-hydroxypyrimidine in urine were below the limit of detection. teratogen. EPA at: http://www. environmental levels) and health effects is available from ATSDR at: http://www. In two nonrandom samples of United States adults and children. and indoor applications have been documented. The U.EPA considers diazinon unlikely to be carcinogenic in humans. 1998). Survey Geometric mean (95% conf.Organophosphorus Insecticides: Specific Metabolites from dialkyl phosphate metabolite excretion (Garfitt et al. animal carcinogen. In addition to being a human metabolite of diazinon. Seifert and Pewnim.S. 2000. In animals.gov/toxpro2.45 and 1.48) < LOD < LOD 644 678 484 699 554 956 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.. 2-isopropyl-4-methyl-6-hydroxypyrimidine was detectable in 57% and 43% of the 130 and 140 participants.atsdr. respectively (Baker et al.html and from U.72 (<LOD-4. 2-isopropyl-4-methyl-6-hydroxypyrimidine can also occur in the environment from the breakdown of the parent compound. 1998). Human health effects from diazinon at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 2003). and seizures. in the 2001-2002 subsample (CDC. 144 Fourth National Report on Human Exposure to Environmental Chemicals ..49 μg/L. weakness.gov/pesticides/. diazinon does not accumulate in tissues (IPCS. Diazinon has moderate acute toxicity in animal studies.S. the detection of 2-isopropyl4-methyl-6-hydroxypyrimidine in a person’s urine may reflect exposure to the environmental degradate. 1986. Olsson et al.. There has been only limited study of diazinon at systemically non-toxic doses that do not result in cholinergic signs (Anthony et al. agricultural. although the 95th percentiles for children 6-11 years old and for non-Hispanic blacks were 1. resulting in excess acetylcholine at nerve terminals.

2005. Carrier G. Environmental Protection Agency (U. Beeson MD. Available at URL: http://www. 6/1/09 Fourth National Report on Human Exposure to Environmental Chemicals 145 . revised February 15. Anal Bioanal Chem 2003. Mason HJ.usgs.. Fenske RA. Alteration of mice L-tryptophan metabolism by the organophosphorous acid triester diazinon. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. 1998. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine. Interim reregistration eligibility decision (IRED.S. Nguyen JV. Atlanta (GA).376(6):808-815. Ann Occup Hyg 2006. Barr DB. Swan et al.epa. Effect of sublethal levels of diazinon: histopathology of liver. Driskell WJ.pdf. Exposure to the organophosphate diazinon: data from a human volunteer study with oral and dermal doses. Brunet RC. J Expo Anal Environ Epidemiol 2000. Banister EW. Redmon JB. 1/14/09 U. Barr DB. Baker SE. 1992-2001. Swan SH. Toepel K.10(6 Pt 2):789-798.114(2):260-263. Sadowski MA.Organophosphorus Insecticides: Specific Metabolites 2005). Barr DB.50(5):505-515. The Quality of Our Nation’s Waters. Third National Report on Human Exposure to Environmental Chemicals. 4/7/09 Lu C. Environmental Health Criteria 198. (2003) found that 2-isopropyl4-methyl-6-hydroxypyrimidine was detectable in 96% and 58% of the subjects. Needham LL. 2006).S. Seifert J. urinary 2-isopropyl-4-methyl-6-hydroxypyrimidine levels were below the limit of detection (Bouchard et al. Dumas P. Biochem Pharmacol 1992. Quantification of selected pesticide metabolites in human urine using isotope dilution high-performance liquid chromatography/ tandem mass spectrometry. EPA). Barr DB. Pesticides in the Nation’s Streams and Ground Water. Banister E. Irish R.org/documents/ehc/ehc/ehc198. Cocker J. References Anthony J. Effects of chronic intake of diazinon on blood and brain monoamines and amino acids. Drug Chem Toxicol 1986.9(2):117-131. In 23 children. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. International Programme on Chemical Safety-INCHEM (IPCS). 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. Oloffs PC. Bull Environ Contam Toxicol 1986. Liu F. March 2006. 2007 [online]. Noisel N.S.37(4):501-507.inchem. Biological monitoring of exposure to organophosphorus insecticides in a group of horticultural greenhouse workers. U. Oloffs PC.gov/ oppsrrd1/REDs/diazinon_ired. et al. Diazinon.htm.44(11):2243-2250. Rajendra W. May 2004.134(1-3):105-113. Kruse RL.gov/circ/2005/1291/. Drobnis EZ. Garfitt SJ. 2006). Bouchard M. Study for Future Families Research Group. EPA 738-R-04-006. Pewnim T. Available at URL: http://pubs. Geological Survey (USGS). Toxicol Lett 2002. In a small number of men visiting fertility clinics in Missouri and Minnesota. Olsson AO. Semen quality in relation to biomarkers of pesticide exposure. Available at URL: http://www.. Environ Health Perspect 2003. Jones K. In 54 Canadian greenhouse workers.111(12):1478-1484. Bravo R. Environ Health Perspect 2006. Diazinon. 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. Centers for Disease Control and Prevention (CDC). urinary 2-isopropyl-4-methyl-6hydroxypyrimidine was detected in less than 14% of multiple samples collected during varied diets (Lu et al.

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

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

6/1/09 148 Fourth National Report on Human Exposure to Environmental Chemicals .109(6):583-590. 1992-2001. Environ Health Perspect 2006. Blasiak J. Environ Health Perspect 2001. Centers for Disease Control and Prevention (CDC). J Expo Anal Environ Epidemiol 1999. Trzeciak A. Freeman NC. Atlanta (GA).epa. Lu C. Available at URL: http://www. Brunet RC. Eskenazi B. Gosselin NH. Reregistration eligibility decision (RED) Malathion.22(1):7-17. July 2006.73(1):182-94. Eberly LE. htm. Lu C. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population. Jewell NP. Bradman A. Fenske RA. Swan SH.56(10):2393-2399. Grether JK. Malathion deposition. Malathion (addendum). 6/1/09 U. Albertini RJ. MacIntosh DL.9(5):494-501. 2005. J Expo Anal Environ Epidemiol 2005. Toepel K.S.77:1009-1010. Lioy PJ. Toxicol Sci 2003 May. Nicklas JA. Prasad SB. Pluth JM. Weltzien E. The Quality of Our Nation’s Waters. A longitudinal investigation of selected pesticide metabolites in urine. Carrier G. Increased frequency of specific genomic deletions resulting from in vitro malathion exposure.15(2):164-171.inchem. Geological Survey (USGS). Am J Epidemiol 1990. 4/7/09 Kissel JC. Curl CL.Organophosphorus Insecticides: Specific Metabolites References Adgate JL. Barr DB. Giri S. Environ Mol Mutagen 1993. Neutra R. Kedan G.74(2):following table of contents.132(4):794-795. Needham LL. Hammerstrom KA.112(10):1116-1124. Samuel O. metabolite clearance. Arch Environ Contam Toxicol 2000. Szyfter K. Barr DB. Harley K. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample.pdf. Barr DB. A toxicokinetic model of malathion and its metabolites as a tool to assess human exposure and risk through measurements of urinary biomarkers. Erratum in: Toxicol Sci 2003 Aug. Jaloszynski P. Griffith W. and cholinesterase status of date dusters and harvesters in California. Harris JA.gov/circ/2005/1291/. Petitti D. et al. Hertz-Picciotto I. International Programme on Chemical Safety-INCHEM (IPCS). O’Neill JP. EPA 738-R06-030. U. Available at URL: http://www. Cancer Res 1996. Clayton CA. Ryan PB.org/documents/jmpr/jmpmono/v2003pr06. Krieger RI. March 2006. EPA). Comparison of organophosphorus pesticide metabolite levels in single and multiple daily urine samples collected from preschool children in Washington State.usgs. Dinoff TM. Third National Report on Human Exposure to Environmental Chemicals.514(1-2):223231.S.445(2):275-283. Reproductive outcome in women exposed to malathion. Dumoulin MJ. Environmental Protection Agency (U. In vitro studies on the genotoxicity of the organophosphorus insecticide malathion and its two analogues. Bouchard M. Am J Public Health 1987. Goldhaber M. Genotoxic effects of malathion: an organophosphorus insecticide using three mammalian bioassays in vivo. 2007 [online].gov/oppsrrd1/REDs/ malathion_red.S. Pesticides in the Nation’s Streams and Ground Water. Bravo R. Sharma GD. Mutat Res 1999. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. revised February 15. Available at URL: http://pubs. Pesticides residues in food: 2003 FAO/WHO Meeting on Pesticide Residues. Rappaport E. Giri A. Flessel P. Mutat Res 2002. et al.114(2):260-263. Irish R. Quintana PJ.38(4):546-553. Environ Health Perspect 2004. Thomas D. Genetic toxicity of malathion: a review. Hooper K. Kizer KW: Exposure to aerial malathion application and the occurrence of congenital anomalies and low birthweight. et al. Barr DB.

00 (2.90 (1. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Urinary para-Nitrophenol Metabolite of Ethyl Parathion.32 (1.30-16. 1977).50-14. and oral routes can occur in pesticide and agricultural workers (Muttray et al.61) < LOD 1.80 (1.730 (<LOD-.33) 2.50 (1. and Nitrobenzene Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.12) < LOD < LOD 1.66 (2.10) 22.47) 2.16) < LOD 1.70 (2.27) 2.37-4.30-3. O-ethyl-O-(4-nitrophenyl) phenylphosphonothioate. Ethyl and methyl parathion are infrequently detected in groundwater sampling (USGS.70-3.02) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .70-6. Morgan et al.90-11.700 (<LOD-.40) 1.71) 971 1164 1018 1313 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .44) 2.49 (1. more slowly absorbed through the skin.0) 3.01-4.70 (2.30 (2.770 (.10-1. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. with limited applications in agriculture.40-4.34 (3. Survey Geometric mean (95% conf. 56-38-2 General Information Para-nitrophenol is a metabolite of the insecticides methyl parathion.15-3.80 (2.50) 3.90-9.92) 5. 2000).EPA.11) 2.940 (<LOD-2.10 (3. Increased risk of exposure via dermal.01) 695 660 518 679 603 941 Limit of detection (LOD.60-19.85 (2.50) 1.. Both are toxic to birds.10 (3. Many previous registered agricultural uses of methyl parathion have been cancelled (U. 2006).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 1.37-2. Estimated intakes from diet and drinking water have been below recommended limits.70 (3. Methyl Parathion.60-24. peak domestic use was as high as 5-6 million pounds per year.50 (1.80) 2.40-3.67) < LOD 1.0) 3. which may vary for some chemicals by year and by individual sample. 2007).50-9.71 (3.37) 2.0) 3.Organophosphorus Insecticides: Specific Metabolites Methyl Parathion CAS No.19 (.910) < LOD < LOD . Methyl parathion is not registered for residential use in the United States. and has a short half-life in soils and on plants.00 (2.79) 4.40) 2.48) 90th 2.70) 2.70-3.20) 5.58) 3. the potential for human exposure to either ethyl or methyl parathion through the diet or drinking water is low.860 (<LOD-1.20-5.70 (2.10 (<LOD-6.11-4.45) 5.10-11.50 (1.69 (2.60-36.50 (1.21 (2.70-6.22-3. all registered uses were voluntarily cancelled (U.1.28-4.67 (1.72 (3.74) 5. Fourth National Report on Human Exposure to Environmental Chemicals 149 . interval) Selected percentiles ( 95% confidence interval) Sample 95th 5.57-4.990-1.0 (3.70 (<LOD-3. In animal studies. first registered in 1948.30 (1.71 (2. and eliminated rapidly from the body after absorption (Kramer et al.850) < LOD . binds tightly to soils resulting in low leachability.60 (4.61) < LOD 1. ethyl parathion. Once absorbed. on cereal grains. phosphorothioates such as methyl and ethyl parathion are metabolically activated to the “oxon” forms which have greater toxicity than the parent insecticides.. and aquatic invertebrates. Methyl parathion use is highly restricted.60) 1.69) 4.70) 2.0) 3.300-. 2003).24) 479 565 680 813 830 1099 99-00 01-02 99-00 01-02 * * * * < LOD .S.02-6.S.32-1.18-3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.37-4.910) < LOD < LOD < LOD 1. In the 1990s.41-4.50 (2. population from the National Health and Nutrition Examination Survey. methyl parathion was rapidly absorbed after ingestion.32-1.20 (2. It had been applied to cotton. 2002.70) 2.21-1. < LOD means less than the limit of detection. and to a lesser extent.8 and 0.26 (1.20 (<LOD-2.50 (2.40 (1.45 (1.0) 2.30-5.50) 3.298-00-0 Ethyl Parathion CAS No.33 (1.01) 4.10) 4. Ethyl parathion.0) 3.60-5. but by 2003.. fish.910) < LOD .05) 4.13-1.62 (1.S. Metabolism of ethyl or methyl parathion leads to the formation of paranitrophenol.28 (1.40-4.09-1. Methyl parathion has low water solubility. pulmonary.00) 3.EPA.50) 2.70-6. and of the chemical nitrobenzene.46 (3.0) 4. was once a restricted-use insecticide with limited applications on certain agricultural crops.89 (2. Given its limited use.28 (1.92-2.80 (2.40) 4.57) 1.32-3.91-3.790 (<LOD-.36-1.

06) 971 1164 1018 1312 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD . 150 Fourth National Report on Human Exposure to Environmental Chemicals .59 (1. ethyl parathion. paralysis.790-1.45) 695 660 518 678 603 941 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.440 (<LOD-.16-4.57) 6. Jaga and Dharmani.26) 17.41-2.80 (1. The metabolite.800-1..96 (1.04 (2.07) 2. but lists ethyl parathion as a possible human carcinogen. In addition to being a metabolite of methyl and ethyl parathion.78) 2.15-10.26 (1.60) 2. accidental exposure.05) 4.950) < LOD .20) 3.640) < LOD < LOD 1.21-21. retinal atrophy and sciatic nerve degeneration have also been observed (IPCS.720 (<LOD-.35-3.67-2.20 (3.97 (2.400 (<LOD-.39) 1.. 2004). and unintentional acute or chronic high-level occupational exposure (Hill et al.79 (1.33-3.73 (1.790-.870) < LOD .43) 4.500) < LOD < LOD . In large doses.23) 1. 1995.87 (1.S. and other metabolites.01 (. EPA at: http://www. and seizures.930 (.21) 1.35-3.33) 479 565 680 812 830 1099 99-00 01-02 99-00 01-02 * * * * < LOD ..48-4.00) 2. U. 2005.55) 2.67 (3.29 (2.96 (1. 1995).30-1.80 (1.78-2.91 (1.93 (2.92 (2. Parathion and methyl parathion have high acute toxicity in animal testing. teratogenic. At high animal doses of methyl parathion.880 (.31-3.57-7.. Karanth and Pope et al.56-2. para-nitrophenol can also occur in the environment from the breakdown of the parent these organophosphorus pesticides and from nitrobenzene.01 (2. 1991).00 (1.14-3.79) 1.71) 1. WHO. interval) Selected percentiles ( 95% confidence interval) Sample 95th 4.77-7.epa.38-3. 2006. and producing acute symptoms such as nausea.atsdr.08-3.730-1.37-1.88) 1.EPA considers methyl parathion unlikely to be carcinogenic to humans.07 (1.10) 90th 2. environmental levels) and health effects is available from ATSDR at: http://www.44-3.370 (<LOD-.970 (.e.29) 1.13-12.39 (1. 2004). Survey Geometric mean (95% conf.840 (.680 (<LOD-1.. cholinergic effects.. paranitrophenol.60-2.04) 1.98-7.97-10.95) 1. methyl parathion. Methyl Parathion.Organophosphorus Insecticides: Specific Metabolites Metabolites”).01-3.940 (<LOD-1.3) 2.31) < LOD .11-4.cdc.33-6.9) 1..60 (1. 1978..78-2.13) 4.94-47.720-1.17) .2) 2. Additional information about external exposure (i.00 (1. 1990. IARC does not consider ethyl parathion and methyl parathion classifiable as human carcinogens.20) .33-3. or generally to have reproductive toxicity at doses below those causing acetylcholinesterase inhibition in most animal studies (IPCS.850-1.09) 2.72-2.84) 3. Slotkin et al.76-14.2) 2.980 (. Methyl parathion is not considered genotoxic.94-4.530) < LOD < LOD < LOD . and other organophosphorus insecticides share a common mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system. population from the National Health and Nutrition Examination Survey.57-2.29) 2.03) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD . Thus.08 (1.70) 3.82) < LOD . Urinary para-Nitrophenol (creatinine corrected) Metabolite of Ethyl Parathion.15) 3.89 (2.4 (3.930 (.08) < LOD . 2003.html and from U.61) 4. the detection of para-nitrophenol in a person’s urine may also reflect exposure to the environmental degradate.44-3.S. gov/toxpro2.540) < LOD .71 (1.1) 2.25 (2. Human health effects from parathion or ethyl parathion at low environmental doses or at biomonitored levels from low environmental exposures are unknown.430 (.11) 1.90 (1. gov/pesticides/.88 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.83 (1.7) 3. 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.830-1.25) 1.89 (2.S. does not inhibit acetylcholinesterase enzymes. Lores et al.86 (2. Zurich et al. and Nitrobenzene Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. vomiting. 2006.97 (<LOD-4.82 (2.55 (<LOD-3. weakness.17-4.23) 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 .78 (2. resulting in excess acetylcholine at nerve terminals.970 (.30) 3.91) 1.310-.690-1. Orsorio et al.10 (1. Overt cholinergic toxicity and death from methyl and ethyl parathion have been described following suicidal ingestion.

S. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. J Anal Toxicol 1990.21(1):5767. oral or dermal administration. Organophosphorus pesticide poisonings in humans: determination of residues and metabolites in tissues and urine.71:99108. CDC. 2005). Rockhold RW. 2003) and in 482 pregnant females from an agricultural region of California (Eskenazi et al. Arch Environ Contam Toxicol 1977. Hill RH Jr. 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. Kedan G. Hill et al. Barr JR. References Barr DB. Fourth National Report on Human Exposure to Environmental Chemicals 151 .110 Suppl 6:1085-1091. Baker SE. 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.33(5):270-276. Dharmani C. Guizzetti M. Pharmacokinetics of methyl parathion: a comparison following single intravenous. 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. 2004). J Expo Anal Environ Epidemiol 2005. end-of-shift urinary para-nitrophenol levels ranged from 190 to 410 µg/ gram of creatinine (Leng and Lewalter..5 mg (500 µg)/g creatinine for workers at the end of shift. Pesticide residues in urine of adults living in the United States: reference range concentrations. 1995. 2002. Chicago area methyl parathion response. Wellman SE. Third National Report on Human Exposure to Environmental Chemicals.9:311-320. Available at URL: http:// www. 2002). 1999). Hetzler HL. McClure PC. Hryhorczuk DO. Hill RH Jr. Pathak S. Barr DB.inchem. et al. Costa LG. Pesticide workers may have much higher levels following pesticide applications. Lin LI.15(2):164-171. Environ Res 1995.S.56(7):449553. Lu C.. population (Olsson et al. Bailey SL. Finding a measurable amount of para-nitrophenol in urine does not mean that the level will result in an adverse health effect. Moomey CM. and many residents were symptomatic (Barr et al. McCann et al. Ashley DL. Arch Environ Health 1978. Harley K. Atlanta (GA). Kissel JC. Slach EF. Moseman RF. Occup Environ Med 1999. Head SL. and levels were similar or slightly lower that those in a small convenience sample of the U. Toxicology 2005. DiPietro E. Runkle KD. Effect of organophosphorus insecticides and their metabolites on astroglial cell proliferation. 2005. Karanth S. Pope C.110 Suppl 6:1075-1078. Head SL. Cline RE.Organophosphorus Insecticides: Specific Metabolites Biomonitoring Information Urinary levels of para-nitrophenol reflect recent exposure. Morgan DP. 1995).25(5):599-606.org/documents/jmpr/jmpmono/v95pr14. Giordano G... 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. Eskenazi B. Griffith W.. Comparison of organophosphorus pesticide metabolite levels in single and multiple daily urine samples collected from preschool children in Washington State. et al. McCann KG. Neurotoxicol Teratol 2003. Environ Health Perspect 2004. Jewell NP. a range of values several hundred times higher than levels found in the U. Turner WE. Parathion-Methyl (addendum). Needham LL. Curl CL. 2005. Gregg M. Baker RC. et al. Barr DB. 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. 4/7/09 Jaga K. Measurement of p-nitrophenol in the urine of residents whose homes were contaminated with methyl parathion. Leng G. Laboratory investigation of a poisoning epidemic in Sierra Leone. Environ Health Perspect 2002. Clark JM. Centers for Disease Control and Prevention (CDC). Role of individual susceptibility in risk assessment of pesticides.215(3):182-190. Weltzien E. general population (CDC. Bradman A. Lores EM. 2002. Bradway DE. ACGIH recommends a BEI of 0. International Programme on Chemical Safety-INCHEM (IPCS).14(4):213-216. et al.112(10):1116-1124. Shealy DB. 2005. Age-related effects of chlorpyrifos and parathion on acetylcholine synthesis in rat striatum.. Environ Health Perspect 2002. et al.htm. J Biomed Sci 2002. Kramer RE.. Barr DB.6(2-3):159-173. Rubin et al. Urinary excretion of paranitrophenol and alkyl phosphates following ingestion of methyl or ethyl parathion by human subjects. Rev Environ Health 2006. Methyl parathion: an organophosphate insecticide not quite forgotten. 2005). Alley CC. Baker S. Lewalter J.

Esteban E.S. Yacovac R. Available at URL: http://www. Pesticides in the Nation’s Streams and Ground Water. Environ Health Perspect 2002. Toxicol Appl Pharmacol 2004. 2004. 0153. revised February 15. The Quality of Our Nation’s Waters. Costa LG. Available at URL: http://www. Interim reregistration eligibility decision (IRED) for Methyl Parathion. Facts.Organophosphorus Insecticides: Specific Metabolites Muttray A. Ethyl parathion. Environ Health Perspect 2006. Available at URL: http://www. May 2003.04/106. Barr DB.pdf. Kieszak S.gov/oppsrrd1/REDs/factsheets/0155fct. September 2000. Seidler FJ. Anal Bioanal Chem 2003.int/water_sanitation_health/dwq/chemicals/ methylparathion. Hill RH Jr. Osorio AM.114(10):1542-1546. 2007 [online]. Rubin C. pdf. Olsson AO.who.376(6):808-815. et al. Am J Ind Med 1991. EPA). Environmental Protection Agency (U. Schilter B. Environmental Protection Agency (U. Jung D. Assessment of human exposure and human health effects after indoor application of methyl parathion in Lorain County. WHO/SDE/WSH/03.S. Ohio.epa. Letzel S.E.S.20(4):533-546. EPA). Methyl parathion in drinking water. 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. 1/14/09 U. Sadowski MA.201(2):97-104.usgs.gov/circ/2005/1291/.S. Geological Survey (USGS). Rosenberg J.110 Suppl 6:1047-1051. March 2006.pdf. Tate CA. 1/12/07 U. Backer G. Hill G. EPA-738-FOO-009. Involvement of glial cells in the neurotoxicity of parathion and chlorpyrifos. U. External and internal exposure of wine growers spraying methyl parathion. R. Ames RG.D. Monnet-Tschudi F. Slotkin TA. Dunlop B. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine. gov/oppsrrd1/REDs/methylparathion_ired. Toxicol Lett 2006. Honegger P. 6/1/09 World Health Organization (WHO). Investigation of a fatality among parathion applicators in California. Nguyen JV.epa.162(2-3):219-224. Levin ED. 1995-1996.S. Ryde IT. 5/19/09 Zurich MG. 152 Fourth National Report on Human Exposure to Environmental Chemicals . Case No. Available at URL: http://pubs. Mengle DC. 1992-2001.

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

see Data Analysis section) for Survey year 01-02 is 0.470 (.S.460) 1165 1316 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . Urinary 2-(Diethylamino)-6-methylpyrimidin-4-ol/one (creatinine corrected) Metabolite of Pirimiphos-methyl Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. < LOD means less than the limit of detection.250 (<LOD-.880) 567 810 1104 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD .700-.680 (<LOD-.700-1.Organophosphorus Insecticides: Specific Metabolites Urinary 2-(Diethylamino)-6-methylpyrimidin-4-ol/one Metabolite of Pirimiphos-methyl Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.17 (.55) .00) 669 687 929 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.94) .210 (<LOD-. interval) Selected percentiles ( 95% confidence interval) Sample 95th .610 (<LOD-1.200-.740-1.300-1.850 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.07) .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 .670) 567 810 1104 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD .780 (<LOD-1.780 (.15) < LOD .840) 669 687 929 Limit of detection (LOD.31) .2. 154 Fourth National Report on Human Exposure to Environmental Chemicals .820) < LOD < LOD .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 .21) < LOD .210-.S.210-1.27) . which may vary for some chemicals by year and by individual sample.740 (.08) 1165 1316 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .410 (<LOD-1. population from the National Health and Nutrition Examination Survey.840 (.430 (<LOD-. 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.780 (.500 (. Survey Geometric mean (95% conf.580-1. Survey Geometric mean (95% conf.780 (<LOD-1.950) < LOD < LOD 1. interval) Selected percentiles ( 95% confidence interval) Sample 95th .670 (<LOD-1.760 (<LOD-.64) .

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

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

EPA at: http://www.50(2):245-255. Estrogenicity of pyrethroid insecticide metabolites. Ose K.. Hu et al. Garey and Wolff. 2006. et al. choreoathetosis. Xenobiotica 1997.23(6):665-673. Indoor pyrethroid exposure in homes with woollen textile floor coverings. salivation. Fredriksson A. Idel H. fenvalerate. Environ Health Perspect 1999. Pogo BG. Leng G. 2005). Moniz AC.. Bernardi MM.205(6):459-472. cyfluthrin was the most frequent pyrethroid associated with symptomatic effects (irritant respiratory and dermal effects. Neurodevelopmental consequences of gestational exposure (GD14-GD20) to low dose deltamethrin in rats.. 2006. Okuno Y. Generally. Kim HS. Behavioral and endocrine changes induced by perinatal fenvalerate exposure in female rats. Moniz et al. Lazarini CA. September 2003. J Reprod Dev 2004.. J Environ Monit 2006. Kamita Y..108(1):78-85. 2003. Spinosa HS. Human doseexcretion studies with the pyrethroid insecticide cyfluthrin: urinary metabolite profile following inhalation. Adhami VM. Idel H. epa. on immature and adult mice: changes in behavioral and muscarinic receptor variables. Shukla Y. 2002). et al. The pyrethroids in general use are not considered teratogenic or to have significant reproductive toxicity (ATSDR. 2000. Yang J.gov/pesticides/ and from ATSDR at: http://www. Berger-Preiss E. neurochemical changes in cholinergic.. 2006).atsdr. McCarthy et al. 1999. Toxicol Appl Pharmacol 1991. Neurotoxic effects of two different pyrethroids.107(3):173-177. Estrogenic and antiprogestagenic activities of pyrethroid insecticides. Kim TS. Assessing estrogenic activity of pyrethroid insecticides using in vitro combination assays.Pyrethroid Pesticides and other ion channels may also explain some pyrethroid effects. Toxicol Appl Pharmacol 2006. Human cases of systemic poisoning are rare and usually result from accidental exposure or intentional ingestion of pyrethroid insecticides. Kuhn KH. 2005). Kim IY. Toxicokinetics of pyrethroids in humans: consequences for biological monitoring. 2003. Leng G. Chen JH. Wolff MS. Estrogenic potential of certain pyrethroid compounds in the MCF-7 human breast carcinoma cell line. Abell AD. Go V. Soderlund et al. 2001. the pyrethroids are not considered genotoxic in in vitro testing or carcinogenic in animal testing (WHO.. Lewalter J.8(1):18-21. 2002. paresthesias) reported in agricultural workers from 1996 to 2002 (Spencer and O’Malley.251(3):855-859. References Agency for Toxic Substances and Disease Registry (ATSDR). [Effects of fenvalerate on reproductive and endocrine systems of male rats] Zhonghua Nan Ke Xue 2002. In California. Song L. Elwan MA. tremor. Lazarini et al. Yamada T. Guillot TS. Ranft U. Lee SJ. Regul Toxicol Pharmacol 2002. motor activity. Shafer. Kuhn K. et al. Elwan et al. 2005). 2003. IARC considers deltamethrin and permethrin as not classifiable as to their human carcinogenicity. Kunimatsu T. Lack of (anti-) androgenic or estrogenic effects of three pyrethroids (esfenvalerate. Neurosci Lett 2001.. 2004. Biochem Biophys Res Commun 1998. Concomitant exposure to organophosphorus insecticides may increase pyrethroid toxicity by slowing metabolic clearance of the pyrethroid. Wolff MS. and striatal dopamine levels in male and female rats..35(2 Pt 1):227-237. and catecholaminergic pathways and behavioral changes have been demonstrated at subacute and subchronic doses for some pyrethroid pesticides (Aziz et al. Bernardi MM. Seth PK. Wang SL. cdc. Bull Environ Contam Toxicol 1999. Sugiri D. Ray et al. Wieseler B. Levsen K. and permethrin) in the Hershberger and uterotrophic assays.62:101-108. Florio JC.27(12):1273-1283.S. Miller GW.gov/toxprofiles/ tp155.html.html. Additional information about pesticides is available from U. 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.211(3):188-197.gov/toxpro2.8(1):197-202.. 2005).. WHO. 1998. though a few pyrethroid pesticides and some metabolites have shown weak or inconsistent estrogenic effects on standardized assays (ATSDR.27(4):609-614.. Effects of prenatal exposure to deltamethrin on forced swimming behavior. Shaw IC. 2002). Toxicological profile for pyrethrins and pyrethroids. Kunimatsu et al. hypersensitivity. et al. Kang IH. Kim et al. Cruz-Casallas PE. Signs and symptoms of acute pyrethroid poisoning after massive ingestions include agitation. Zhao RC. Caudle WM. McCarthy AR. Available from URL: http://www. Fourth National Report on Human Exposure to Environmental Chemicals 157 . Shin JH.atsdr. Int J Hyg Environ Health 2002.300(3):161-165. Lemonica IP. 2003. 1991. Garey J. Pauluhn J. Agrawal AK.cdc. In developing rodents. Pyrethroid pesticide-induced alterations in dopamine transporter function. Sunami O. Varoli FM. Garey J. Thomson BM. Eriksson and Fredriksson. Transient dermal paresthesias have been reported among pesticide applicators after direct contact with certain types of pyrethroid pesticides. bioallethrin and deltamethrin. Leng A. Go et al.. Neurotoxicol Teratol 2005. 2001. Hu JY. Leng G. dopaminergic.1/15/09 Aziz MH. Neurotoxicol Teratol 2001. Richardson JR. Eriksson P. Salzgeber SA. and seizures (ATSDR.

Available at URL: http://www. Mechanisms of pyrethroid neurotoxicity: implications for cumulative risk assessment. Permethrin Facts (Reregistration Eligibility Decision Fact Sheet).Pyrethroid Pesticides Ray DE.S. Crofton KM. 5/26/09 U. Environ Health Perspect 2005.epa. pdf. J Toxicol Clin Toxicol 2000.38:95-101.171:3-59. Permethrin.gov/oppsrrd1/REDs/ factsheets/permethrin_fs.pdf.epa. Shafer TJ. Pesticide and Evaluation Scheme. 5/26/09 U. Forshaw PJ.S. and therapy. June 2006b.10. 19962002. Reregistration Eligibility Decision for Cypermethrin. Soderlund DM. Revised February 25. 2007. Pyrethroid illnesses in California. Available at URL: http://pubs. 2005. Clark JM. et al. Geological Survey (USGS). World Health Organization (WHO). U.S. sumithrin synthetic pyrethroids for mosquito control.int/hq/2005/WHO_ CDS_WHOPES_GCDPP_2005. Available at URL: http://www. synergies. 5/26/09 158 Fourth National Report on Human Exposure to Environmental Chemicals . EPA).htm. Lesser JE.S.186:57-72. The metabolism of cypermethrin in man: differences in urinary metabolite profiles following oral and dermal administration.S. EPA). 5/26/09 U. Environmental Protection Agency (U.gov/ circ/2005/1291/. Sheets LP. Xenobiotica 1992. Spencer J.epa.22(8):983-991. Piccirillo VJ. Rev Environ Contam Toxicol 2006. EPA). 5/26/09 Woollen BH. June 2006a. Safety of pyrethroids for public health use. Mullin LS.S. Available at URL: http://www.113(2):123-136. Environmental Protection Agency (U.gov/oppsrrd1/REDs/cypermethrin_red. April 2002. Developmental neurotoxicity of pyrethroid insecticides: critical review and future research needs. Available at URL: http://whqlibdoc. 1992–2001. Environmental Protection Agency (U. Sargent D. Pesticides in the Nation’s Streams and Ground Water. O’Malley M. Marsh JR.S. Pyrethroid insecticides: poisoning syndromes. Meyer DA. Toxicology 2002. resmethrin.htm.gov/pesticides/ health/mosquitoes/pyrethroids4mosquitoes.usgs.who. March 2006. Laird WJ.

Cyfluthrin accounted for one-third of pyrethroid-related worker illnesses reported in California from 1996-2002.S. 2001) showed that urinary levels of 4-fluoro-3-phenoxybenzoic acid at the 95th percentile ranged from either slightly higher or lower than the detection limit in the U.. Biomonitoring Information Urinary levels of 4-fluoro-3-phenoxybenzoic acid reflect recent exposure to cyfluthrin or its environmental degradate. 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. 2005.95 µg/L. Fourth National Report on Human Exposure to Environmental Chemicals 159 .. 2006). Degradation of cyfluthrin to 4-fluoro-3-phenoxybenzoic acid occurs in the environment. Following an indoor application exposure. In 57 volunteers entering areas previously spot-sprayed with various pyrethroid pesticides (including cyfluthrin)..68359-37-5 General Information The chemical 4-fluoro-3-phenoxybenzoic acid is a specific metabolite of the pyrethroid insecticide cyfluthrin. representative subsample in NHANES 2001-2002 (CDC.. 2003). but it can also reflect direct exposure to 4-fluoro-3-phenoxybenzoic acid formed in the environment. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. most of which were dermal and respiratory irritations (Spencer and O’Malley. 2006) and estimated daily intakes based on urinary levels in children were considered to be below acceptable daily intakes (Heudorf et al.. 2004). In an analysis of 217 urine specimens from a nonrandom sample of United States residents.Pyrethroid Pesticides Cyfluthrin CAS No. 2006) and 1177 urban adults and children (Heudorf et al. Biomonitoring studies of 4-fluoro3-phenoxybenzoic acid in urine provide physicians and public health officials with reference values so that they can determine whether other people have been exposed to higher levels of cyfluthrin than levels found in the general population.. median urinary levels of 4-fluoro-3-phenoxybenzoic acid were slightly less than the limit of detection in the NHANES 2001-2002 subsample (CDC.. the mean elimination half-life of cyfluthrin from the plasma was 16 hours (Williams et al. Urinary levels of 4-fluoro-3-phenoxybenzoic acid were generally below the limit of detection (0. Leng et al.S. (2004) reported a geometric mean concentration of 4-fluoro3-phenoxybenzoic acid of 0. the presence of 4-fluoro-3-phenoxybenzoic acid in urine not only reflects the metabolic transformation of cyfluthrin. Baker et al. Finding a measurable amount of 4-fluoro-3-phenoxybenzoic acid in urine does not mean that the level will result in an adverse health effect. 2003).2 μg/L) in the U. representative 2001-2002 NHANES subsample (CDC. Urinary levels for adults and children in these studies were similar (Heudorf et al. 2005). Studies in Germany of 396 children and adolescents (Becker et al. 2003). 2005). 2001. Cyfluthrin is rapidly metabolized and eliminated from the body. Thus.

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

population from the National Health and Nutrition Examination Survey.S.Pyrethroid Pesticides Urinary 4-Fluoro-3-phenoxybenzoic acid (creatinine corrected) Metabolite of Cyfluthrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Fourth National Report on Human Exposure to Environmental Chemicals 161 . Survey Geometric mean (95% conf. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1949 2538 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 473 580 662 830 814 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 950 1193 999 1345 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 666 680 517 700 594 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.

Heudorf U.77(1):67-72. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. Angerer J. Int J Hyg Environ Health 2003. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides.186:57-72. Sugiri D. 19962002. Atlanta (GA). Int J Hyg Environ Health 2006.Pyrethroid Pesticides References Baker SE. Centers for Disease Control and Prevention (CDC). 162 Fourth National Report on Human Exposure to Environmental Chemicals . et al. Berger-Preiss E. Barr DB. Hadnagy W. Seiwert M. Int Arch Occup Environ Health 2004. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides. Angerer J. Angerer J.46(3):281-288. Third National Report on Human Exposure to Environmental Chemicals. Isotope dilution highperformance liquid chromatography-tandem mass spectrometry method for quantifying urinary metabolites of synthetic pyrethroid insecticides. Butte W. Leng G.209(3):221-233. Ball M. Angerer J.13(2):112-119. Int J Hyg Environ Health 2006.209(3):293-299. Williams RL. Kolossa-Gehring M.206(2):85-92. Heudorf U. Human exposure to indoor residential cyfluthrin residues during a structured activity program. Schulz C. Hoppe HW. Becker K. Ranft U. Pyrethroid illnesses in California. Olsson AO. Heudorf U. Arch Environ Contam Toxicol 2004. Rev Environ Contam Toxicol 2006. Environ Health Perspect 2001. J Expo Anal Environ Epidemiol 2003. Idel H. O’Malley M. Bernard CE. Spencer J. 2005. Drexler H.109(3):213-217. Krieger RI. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine.

21) .170 (.110-.380-.210) 90th . interval) Selected percentiles ( 95% confidence interval) Sample 95th 1. Kuhn et al.740-1.520) . 1999).2dimethylcyclopropane carboxylic acid in urine not only reflects the metabolic transformation of any of the three pesticides.270 (.960 (.770-1. and cis-Cypermethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.68) . the presence of trans-3-(2.400-.200-.350) .08) .240) .470 (.380 (. ciscypermethrin and cis-cyfluthrin.380) .220-.180) .2-dimethylcyclopropane carboxylic acid is a metabolite formed from cis-permethrin.670-2. Survey Geometric mean (95% conf. The presence of cis-3-(2.180 (. trans-cypermethrin.280-.340-.550) .160 (<LOD-.160 (.53) . but it can also reflect exposure to cis-3-(2.300 (.680) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .370-.and trans-isomers.330) .210) .12 (.28) 468 580 667 831 816 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .470-1.430-.740-2. The chemical trans-3(2.580) 1.490-1.630) .270 (. The cis-isomer of permethrin has more potent insecticidal activity than transpermethrin.43) . 1985.680 (.160 (.262) * * * < LOD < LOD .610) .220-.120-.155-.2-dimethylcyclopropane carboxylic acid that is formed in the environment from the degradation of these pesticides (George.220) . 1985.500 (.200) .47 (.140 (<LOD-.630 (.790) .68 (.or trans-3-(2.880 (. transcypermethrin and trans-cyfluthrin.S.120-.77 (.510 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.07 (.140 (.1.920) 1.44 (.200 (.2-dichlorovinyl)-2. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.10) 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 .202 (.530 (.630-.670 (.710-1.950-2.1 and 0.340) .740 (.490-.200) .260 (.15) .. 52315-07-8 CAS No. which may vary for some chemicals by year and by individual sample.490-.440 (.Pyrethroid Pesticides Cyfluthrin the cis-metabolite is found in the urine. Biomonitoring Information Urinary levels of cis.2-dichlorovinyl)2.310) .570-.500 (. cis-cypermethrin.2-dimethylcyclopropane carboxylic acid Metabolite of cis-Permethrin.570 (.900 (.460-.68) .2-dimethylcyclopropane carboxylic acid is a metabolite formed from trans-permethrin.68359-37-5 Cypermethrin Permethrin CAS No.80) .600) .460 (.690) .670-1.13 (.300-.670-1. Generally.270 (.870) 1.110 (<LOD-.08) 947 1193 1004 1346 99-00 01-02 99-00 01-02 99-00 01-02 * * .200-.2-Dichlorovinyl)-2.700) .330 (.2-dichlorovinyl)-2.120-.2dichlorovinyl)-2.370 (. population from the National Health and Nutrition Examination Survey.730 (.610) .780) .460-1.850 (.250 (.410) .2-dimethylcyclopropane carboxylic acid in urine not only reflects the metabolic transformation of any of the three pesticides.220-.580-1.790 (..2dichlorovinyl)-2. and ciscyfluthrin.110-.110-.410) . cis-permethrin.770) .640 (. < LOD means less than the limit of detection. Similarly. cis-3-(2.820 (.35) .2-dichlorovinyl)- CAS No.120-. more of the trans-metabolite than Urinary cis-3-(2.630) .24) 1.52645-53-1 General Information Several pyrethroid pesticides are formulated as a mixture of cis. Fourth National Report on Human Exposure to Environmental Chemicals 163 .680-3.300 (.790-1.28) 671 680 518 701 591 957 Limit of detection (LOD.890 (.300-.200-.380-.54) .790-1.32) .200) < LOD < LOD < LOD .490-1. and trans-cyfluthrin.230) .11) .2-dimethylcyclopropane carboxylic acid formed in the environment from the degradation of these pesticides (George.280 (.890 (.340) .710) .740) 1. In the body.240) .510 (.420-. Kuhn et al.220-.600 (.380-.35) 1.510 (.210-.730 (.150 (. trans-permethrin. Cyfluthrin.50) .910-5.600-1.250-.650-1.2-dichlorovinyl)-2.730 (. but can also reflect exposure to trans-3(2. 1999).270-.

Survey Geometric mean (95% conf.250) 90th . Cyfluthrin.260 (.2-dimethylcyclopropane carboxylic acid reflect recent exposure to either their parent pyrethroid pesticides or their environmental degradates.11 (.840 (. 2006..390-.360-1.2-dichlorovinyl)-2. post- Urinary cis-3-(2.420 (.130-..14) 671 680 518 700 591 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.380) .2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of cis-Permethrin.250) . 2002).230-. population from the National Health and Nutrition Examination Survey.550) .59) .2-dichlorovinyl)-2.750 (.260 (.640) 1. urinary levels of cis-3-(2.340) .67) .320) .33 (.21) .250) .600 (.920 (.200 (. though the 95th percentile levels increased several fold after exposure to nearby pest control operations (Leng et al. Urinary levels of the two chemicals in adults were similar to those in children in these studies (Heudorf et al.290 (.49) . 2001) showed urinary levels of cis.540 (.11) .260 (.180 (.80) . 2004).200) .560) . Studies in Germany of 396 children and adolescents (Becker et al. the levels at 24-72 hours were slightly less than the 95th percentile in the NHANES 2001-2002 subsample (CDC.Pyrethroid Pesticides 2.2-dimethylcyclopropane carboxylic acid levels at the 95th percentile were about one-third of the 95th percentile in the NHANES 20012002 subsample (CDC.390-.430-1..710-3.270) .59 (1.24) .250-.and trans-3-(2.11) ..2dichlorovinyl)-2. median urinary levels of trans-3-(2.2dimethylcyclopropane carboxylic acids at the 95th percentile that were similar or slightly less than the 95th percentiles in the U. In a study of volunteers.230-.2-dichlorovinyl)-2.440 (.300) ..140-.590) .710 (. 2006).680-1.470-1.150-.2-dimethylcyclopropane carboxylic acid did not increase.340) .59) .680 (.290-.300) .400 (.230 (.370-.550 (.450-.580-1.260-.12 (. Other studies have provided evidence that urinary levels of cis.700) .220 (.530 (.280 (. and cis-Cypermethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.700) .560) 1.104-.300-.290) . 2005). 2006).250 (<LOD-.430 (.2dichlorovinyl)-2. 164 Fourth National Report on Human Exposure to Environmental Chemicals . 2003). representative NHANES 2001-2002 subsample (CDC. 2005).450-1.810 (.280-.390 (..550) .190) .150-. In a study of urban residents in Germany (Berger-Preiss et al..570) .and trans-3(2.440-.300 (.640-1.08) 468 580 667 830 816 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .400-1.430-.2-dichlorovinyl)-2.540 (.2-dimethylcyclopropane carboxylic acid did not increase at 24-72 hours after exposure to nearby pest control operations (Leng et al.880) . These studies indicated that intake is mainly from the diet and that dermal absorption contributes little to intake (Heudorf et al.300 (.680-1.170) < LOD < LOD < LOD . 2004. the median and 95th percentile of urinary levels of cis-3-(2.080-.230-.690-1..410) .190 (.640 (.500 (.580) .2dimethylcyclopropane carboxylic acid at the 95th percentile were about half the 95th percentile in the NHANES 20012002 subsample (CDC.S.840 (.250-.890 (.31) .S.11) 1. 2005).29 (.220) . 2005).270) .170 (.830) .590 (.270-.200-.190) .160 (<LOD-. 2006.370-.260) . 2005) In a small group of indoor pest-control operators. Schettgen et al.290) .220 (.67 (.900 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1. In the same residents.450 (.640-.37) . 2002).320-.540) .440 (. Lu et al.380-.150-.340-. In these volunteers.700-2.12-2. 2006) and 1177 urban adults and children (Heudorf et al..2-Dichlorovinyl)-2...03) 1. the levels at 24-72 hours were slightly less than the 95th percentile in the NHANES 2001-2002 subsample (CDC.03) size 1951 2538 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD 75th .350 (. urinary trans-3-(2.250-.180-.800 (.890) .370-.510-1.240 (<LOD-.270 (.440-.33) .380 (.2-dimethylcyclopropane carboxylic acids in children were related to residential pesticide use and house dust levels (Becker et al.210-.138 (.780) 1. Estimated daily pyrethroid intakes based on urinary levels in the German children were below the acceptable daily tolerances (Heudorf et al. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 2001.530 (.200-.520) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .750-1.350) .550-1.182) * * * < LOD < LOD .11) 947 1193 1004 1345 99-00 01-02 99-00 01-02 99-00 01-02 * * .550-1.780 (. 2003).640-1.170 (.120 (.

91 (1.26 (.27 (1.490-1.54 (1.39-5. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.400-.500) .89 (2.49-3.850-1.17 (.560 (.7) 2.660) 1.55-4.58) 961 1184 1015 1341 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .55-3.520) .40 (1.76-3.750) .77) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .25 (1.70) 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 . however.17-1.49-3.410-.2-dimethylcyclopropane carboxylic acid Metabolite of Cyfluthrin.66) 691 680 518 690 595 954 Limit of detection (LOD.56 (1.95) 3.66) . 2005).41 (1.560 (.410-. which may vary for some chemicals by year and by individual sample.17 (.56) 2.68) 2.2-dichlorovinyl)-2.620) < LOD 2.09 (.20 (.22 (1.39 (1.37 (1.530) .63) 1.28 (2.570) 90th 1.56) 2. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.580 (.2-dimethylcyclopropane carboxylic acid (Hardt and Angerer.87 (1.14-6.63) 1.700-1.08-6.970 (.03-1.20 (.440 (<LOD-. trans-Cypermethrin. 2005).23) 2.68-2.2-dichlorovinyl)-2.710 (.03-1.S. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.90) 1. Fourth National Report on Human Exposure to Environmental Chemicals 165 .69) 1.670) . and trans-Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.77 (1. population from the National Health and Nutrition Examination Survey.410 (<LOD-.42 (2.01 (1.95) 2.and trans-3-(2.680-1.43) 2.20 (. Biomonitoring studies on urinary levels of cisor trans-3-(2.410 (<LOD-. 2003) were similar to the 95th percentiles for adults in the NHANES 2001-2002 subsample (CDC.830-1. Urinary trans-3-(2.23 (.68) 1.760) .470 (.420 (<LOD-.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. Survey Geometric mean (95% conf.2-dimethylcyclopropane carboxylic acid in urine does not mean that the level causes an adverse health effect.19 (2.49-5.07-3.60) .84 (1.910-1.76-4.460-.08-4.800-1.2-Dichlorovinyl)-2.610) 1.81) 2.840-1.64-4. Finding a measurable amount of cis.42) 1.560 (.10) 2.56 (1.55-5.08) 1.54) 4.14-2.730) .460-.77) 1.860) .910-1.480-.28 (1.25-3.16) 1.Pyrethroid Pesticides application median urinary levels of summed cis.77) 2.670) .97-11.820) .13) .60-4.62 (1.470 (<LOD-.19 (3.11-1.490 (<LOD-.550 (.07 (1.19) 1.01) 4.12-6.810-1.50 (1.60) 1.59 (1.700) . < LOD means less than the limit of detection.35) 1. were up to 27 times higher than the 95th percentile for adults in the NHANES 2001-2002 subsample (CDC.920-1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 3.66) 478 576 675 826 823 1123 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .41-14.2dichlorovinyl)-2.940 (.4 and 0.520-.11-2.68-3.69 (1.780 (.94 (1.68) 1. The maximum post-application urinary levels.48) 4.85) 4.or trans-3-(2.14) 1.5) 2.400 (<LOD-.500 (.4.500-.

610-.850-3.20 (1.13) .07) 2.70 (.12-1.07-1.820-2.2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of Cyfluthrin.61) 1.87-8.720 (<LOD-.48 (1.26 (1.00) 1.900 (<LOD-1.00) 1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.28) 2.00 (1.39 (1.74) .720-1.75 (1.19) 961 1184 1015 1340 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .65) 1.07-2.91) 1.16 (1.10) size 1976 2524 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD 75th .15) 3.770) < LOD 2.22-1.970 (.880 (.87) 1.55 (2.15) 2.08 (.13) 1.500-.56-5. population from the National Health and Nutrition Examination Survey.87-3.91 (1.660) .15-3.760 (.34-4.20-2.31 (.47-2.2-Dichlorovinyl)-2.91-11.530 (<LOD-.35 (1.520 (<LOD-. Survey Geometric mean (95% conf.640) .880 (<LOD-1.07-3.34-3.570 (<LOD-.3) 2.33-1.08 (.41) 1.670) .56-2.30-3.87 (1.45-2.780) .87) 1.31) 1.780) 90th 1.530 (.35) 1.11) .580) .68) 3.67 (2.36) 2.15-3.02-1.27-2.560 (.88) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 1.65 (2.850) 1.74) 2.98 (1.55 (2.60 (1.31 (2.00-5.89) 2.780 (<LOD-.880-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.11) 691 680 518 689 595 954 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.30-6. 166 Fourth National Report on Human Exposure to Environmental Chemicals .22) 1.540) .47 (1.S.700 (.36 (1.37 (1.60) 2.47-2.42) 1.580 (.570 (. and trans-Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.800-1.60) 2.29) 1.39) 1.720-1.440-.700 (.410-.15-3.730) .57) 3.750) .480-.19) .45 (1.570-.740) .55 (2.700-.33 (1.15 (1.80) 1. trans-Cypermethrin.33-2.86 (2.12 (.Pyrethroid Pesticides Urinary trans-3-(2.930-1.07) 2.56 (1.27-2.44) 2.00) 5.42 (.22-2.850) .81 (2.19 (1.11) 478 576 675 825 823 1123 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .470 (.64 (1.470-.40-2.48-2.800-1.57 (1.

Drexler H. Angerer J. George DA. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. Wieseler B.109(3):213-217. Environ Health Perspect 2001. Heudorf U. Berger-Preiss E. Barr DB. J AOAC 1985. Sugiri D. Int Arch Occup Environ Health 2004.Pyrethroid Pesticides References Becker K. Int J Hyg Environ Health 2002. et al. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine.134(1-3):141-145. Angerer J. Butte W. Third National Report on Human Exposure to Environmental Chemicals. Fourth National Report on Human Exposure to Environmental Chemicals 167 . Hoppe HW. Ranft U. Kuhn K.209(3):293-299.68(6):1160-1163. Idel H. A longitudinal approach to assessing urban and suburban children’s exposure to pyrethroid pesticides. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides.77(1):67-72. Schulz C. Int J Hyg Environ Health 2003.62:101-108.209(3):221-233. Biological monitoring of workers after the application of insecticidal pyrethroids. Angerer J. Leng G.114(9):14191423. Heudorf U. Lu C. Angerer J. Centers for Disease Control and Prevention (CDC). Levsen K. Int Arch Occup Environ Health 2003. Hadnagy W. Ball M. Bartell S. Toxicokinetics of pyrethroids in humans: consequences for biological monitoring. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Hardt J. Pyrethroid exposure of the general population-is this due to diet? Toxicol Lett 2002. Atlanta (GA). Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. Bravo R.205(6):459-472. Idel H. Heudorf U. Indoor pyrethroid exposure in homes with woollen textile floor coverings. Idel H. Kolossa-Gehring M. Heudorf U. Ranft U. Angerer J. 2005. Pearson M. Bull Environ Contam Toxicol 1999. Leng G. Angerer J. Schettgen T.76(7):492-498. Berger-Preiss E. Int J Hyg Environ Health 2006. Leng G. Drexler H. Permethrin and its two metabolite residues in seven agricultural crops. Int J Hyg Environ Health 2006. Sugiri D. Environ Health Perspect 2006.206(2):85-92. Seiwert M.

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

* 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 169 .2-Dibromovinyl)-2.Pyrethroid Pesticides Urinary cis-3-(2. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. Survey Geometric mean (95% conf. < LOD means less than the limit of detection. 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. population from the National Health and Nutrition Examination Survey. which may vary for some chemicals by year and by individual sample.S.1 and 0.2-dimethylcyclopropane carboxylic acid Metabolite of Deltamethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.1.

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

5/26/09 Ortiz-Perez MD. Angerer J.inchem. Atlanta (GA). Lopez-Guzman OD.77(1):67-72.org/documents/ehc/ehc/ ehc97. Kolossa-Gehring M. Int J Hyg Environ Health 2006. Int J Hyg Environ Health 2006. Environmental health assessment of deltamethrin in a malarious area of Mexico: environmental persistence. Environ Health Perspect 2005. Schulz C. Heudorf U. et al.113(6):782-786. Heudorf U. Environmental Health Criteria 97. Angerer J. Batres LE. Environ Health Perspect 2001. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides. Fourth National Report on Human Exposure to Environmental Chemicals 171 . [online] 1990. Centers for Disease Control and Prevention (CDC). GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. et al. Hoppe HW. Seiwert M. toxicokinetics. Torres-Dosal A. International Programme On Chemical Safety (IPCS).htm. Int Arch Occup Environ Health 2004. Third National Report on Human Exposure to Environmental Chemicals.109(3):213-217. Drexler H. and genotoxicity in exposed children. Grimaldo M. Angerer J. Carranza C. Heudorf U. Available at URL: http://www. 2005. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany.209(3):293-299.Pyrethroid Pesticides References Becker K. Deltamethrin. Butte W. Ball M. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine. Angerer J.209(3):221-233.

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. 2006).52315-07-8 CAS No. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. urinary 3-phenoxybenzoic acid levels at the 95th percentile were about threefold lower than the levels at the 95th percentile in the 2001-2002 NHANES subsample (Berger-Preiss et al. 2005. Following residential spraying with deltamethrin for malaria protection in Mexico. Finding a measurable amount in urine does not mean that the level will result in an adverse health effect. (2004) reported geometric mean levels of 3-phenoxybenzoic acid that were approximately sixfold higher than levels for adults in the NHANES 2001-2002 subsample (CDC. 2005). 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. Saieva et al. 2005). In a small group of indoor pest-control operators. 2005. 2005). In an analysis of 217 urine specimens from a nonrandom sample of United States residents. 52918-63-5 use and house dust levels (Lu et al. the presence of 3-phenoxybenzoic acid in urine not only reflects the metabolic transformation of any of the six pesticides listed above. Baker et al. 2004).. CDC. The mean peak levels in these children were 83-fold higher than the geometric mean for children in the NHANES 2001-2002 subsample (CDC.. 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 .. 68359-37-5 Cypermethrin Deltamethrin CAS No. A study of 396 German children (Becker et al.. CDC. representative NHANES 2001-2002 subsample (CDC. Fenpropathrin Permethrin CAS No. CDC. a temporal variation in levels was observed and considered to correspond to seasonal spraying of pesticides. 2003). In the New York City study. 2003. 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. the postapplication median urinary levels of 3-phenoxybenzoic acid were 24-fold higher than those for adults in the NHANES 2001-2002 subsample (CDC. 2005). Biomonitoring Information Urinary levels of 3-phenoxybenzoic acid reflect recent exposure to the parent pyrethroid pesticides.Pyrethroid Pesticides Cyhalothrin CAS No. 2003. In 57 volunteers entering areas previously spot-sprayed with various pyrethroid pesticides.. 2005). In one study of 145 urban residents in 80 private homes in Germany. 39515-41-8 CAS No. but can reflect direct exposure to 3-phenoxybenzoic acid formed in the environment from the degradation of these pesticides. 2002. median urinary levels of 3-phenoxybenzoic acid were slightly less than median levels in the NHANES 2001-2002 subsample (Leng et al. Hardt and Angerer. 66841-25-6 General Information The chemical 3-phenoxybenzoic acid is a metabolite and an environmental degradate of the six pyrethroid pesticides listed above. Thus. 2005). 2006. Becker et al. Biomonitoring studies of 3-phenoxybenzoic acid provide physicians and public health officials with reference values so that they can determine whether other people have been exposed to higher levels of pyrethroids than levels found in the general population. 52645-53-1 Tralomethrin CAS No. Median levels of urinary 3-phenoxybenzoic acid were 67-fold higher in 307 pregnant New York City women who used indoor pesticides compared with the median levels for adults in the NHANES 2001-2002 subsample (Berkowitz et al.. 2005)...S.

810) 1.276-.330) .190-.280 (.253-.63 (3.62-6.340) 1.250 (.04-5.48-2.45-5.60) .940) 1.190-.360) .820) .434) .78) 1.364) .36) 1.53) 1.430-.320) .510-.320 (.S.28) 1. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.49 (1.41-2.362) .260 (.298 (.586) .233-.340) .25 (2.35 (2.328 (.730 (.370) .470-.227-.34-6.30 (1.04) .63-3.69 (1.870 (.750-1.850) .440) .290 (.46) .12 (.601) .33 (1.314) .238-.680 (.560-.336 (.320) .530-.311 (.550-.49-2.200-.27-2.1) 3.295) .330) .1.230 (.350-.450 (.250-.1) 3.260-.352-.300 (.292 (.260 (.260 (.640 (.740 (.490) .25-4. population from the National Health and Nutrition Examination Survey.46) 2.820) .230-.29-1.297 (.246-.34) 8.314 (.Pyrethroid Pesticides Urinary 3-Phenoxybenzoic acid Metabolite of Cypermethrin.420) .270 (.428-.570-.38 (2.315 (.33 (2.01 (1.271-.840-1.62-8.373) .292-.72 (1.48-2.71 (1.265-.25 (2.73) 1.374) 99-00 01-02 99-00 01-02 99-00 01-02 .277-.390) .78 (1.387) .507 (.325 (.760 (.26) 2.78) 1.570-1.51-6.630) .200-.800 (.320) .830-2.89-71.250 (.220-.16-1.190-.32-21.300) .21 (2.210-.78) 6.49-2.230-.590-.44) 5.27-11.35) 1.740 (.33) .230 (.250 (.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 .39) 2.300 (.384) .18 (1.590 (.42-2.41) 3.160-.32 (2.16) 483 580 682 831 833 1128 99-00 01-02 99-00 01-02 .300 (.700-1.226-.02-6.345) Selected percentiles ( 95% confidence interval) Sample 95th 4.32 (1.50 (2.35) 2.05) 1.800) 1.210-.230-.288 (.76 (1.710 (.850) .25-1.710 (.200-.520 (.990) .650 (.41 (1.240 (.960 (.406) .25-7.8) 3.427) .75 (1.92-3.1) 3.1 and 0.53-3.321 (.430-. interval) .23 (2.16) 1.780) 4.320) .54) 1.35 (1.30 (.454 (.45 (2.05) .49 (1.700 (.12) 4.18 (2.38 (2.247-.355) .560-.353 (.830) 90th 1.52-4.93 (1.43) 3.27-2.610) .510-.595) .03 (3.600 (.52-5.62) 5. Deltamethrin.270) .79) 3.560-1.13) .35) 2.273 (.90) 1.14-6.620-1.16) 974 1193 1024 1346 99-00 01-02 99-00 01-02 99-00 01-02 .65 (1.34 (2.750) .340) 75th .288-.55 (1.41-3.26-2.56-5. Survey Geometric mean (95% conf.240 (.190-.69) 3.180-.160-.26) 2.750) . Fourth National Report on Human Exposure to Environmental Chemicals 173 .12) .267 (.266-. and Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.30) 3.490-.64) 697 680 524 701 603 957 Limit of detection (LOD.369) .670 (.51-3.530-.81 (1.65-2.86 (1.13 (.83-11.417 (.

930) 1.240-.67 (1.272) .275 (.330) .00) 5.03-1.570) .590) .335-.49-2.04 (.48 (1.380-.720 (.200-.610 (.540 (.423 (.310) .22 (1.160-.640 (.07) 2.83 (1.96 (1. population from the National Health and Nutrition Examination Survey.300-.178-.00) 1.73) 1.272 (.92) 483 580 682 830 833 1128 99-00 01-02 99-00 01-02 .500) .670) .401) .510 (.230-.43) 1.278) .550 (.61-2.250 (.94 (1.280 (.62) .480-.261-.250 (.40 (1.740) .41) 1.304) Selected percentiles ( 95% confidence interval) Sample 95th 3.560 (.357) .860-1.35) 1.400) .200-.11 (.670) 3.580 (.530-.43-64.13-1.73-4.200-.81 (1.35) .290-.380 (.270-.362 (.190-.264 (.240-. Survey Geometric mean (95% conf.190 (.40) 2.274-.630) .19) 2.63) 1.49) 3.51-7.35-3.530-.55 (1.328) .225-.17 (.91) 9. interval) .49) 1.677) .350 (.700-1.60-4. Deltamethrin.37) 1.13 (.490-.67) 1.36 (1.960-1.63-3.25) 2.88-5.810) 1.490 (.440-.590) .329) .54 (1.13-1.534) .730) .74) 3.15-2.370 (.590-1.43 (1.202-.25-5.05-3.270 (.437) .09-2.350) .321-.84 (1.650) .62) 1.860-1.44) 2.220 (.36-6.460-.760) .49 (1.55) 3.173-.43 (2.440-.300-.86 (1.490 (.190-.240-.21-4.246 (.387) .720) 90th 1.230-.90) 3.91) .06-3.240-.02-1.750-1.330 (.19 (2.271-.370-.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 .09 (.25-2.52 (1.04 (3.39) 1.238-.91 (2.91-4.230) .365) 99-00 01-02 99-00 01-02 99-00 01-02 .309 (.400-.930) .234 (.280 (.240 (.330) 75th .52) 2.240 (.229-.Pyrethroid Pesticides Urinary 3-Phenoxybenzoic acid (creatinine corrected) Metabolite of Cypermethrin.226-.16-4.240 (.309) .210 (.07-5.270 (.372) .730) .410) .253) .72 (1.860 (.17-1.03 (.274 (.550 (.410-.48) 697 680 524 700 603 957 174 Fourth National Report on Human Exposure to Environmental Chemicals .41-4.75-8.550 (.09) 3.640 (.35 (1.64-5.312 (. and Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.420-.37 (1.19-6.446) .460-.330) 1.270) .250) .280-.270) .329) .440-.316 (.330) .280) .580) .390-.220-.299-.224-.240 (.227 (.19) 974 1193 1024 1345 99-00 01-02 99-00 01-02 99-00 01-02 .S.150-.00) 1.200-.21 (1.378 (.450 (.311 (.44 (1.280 (.60) 1.83) 1.400-.480 (.95) 1.10 (2.80) 4.32 (2.290) .210 (.210-.67 (1.590) .323 (.53 (1.216-.280) .510 (.510 (.840-1.0) 3.261 (.27) 1.320) .11 (.730-1.09-2.02 (2.290) .

urban cohort. Berger-Preiss E. Lopez-Guzman OD. Ranft U. Olsson AO. Ball M.76(7):492-498. Barr DB. Atlanta (GA). Bartell S. toxicokinetics. Idel H.Pyrethroid Pesticides References Baker SE. Ranft U. Barr DB. Int J Hyg Environ Health 2003. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. et al.206(2):85-92. Biological monitoring of workers after the application of insecticidal pyrethroids.209(3):221-233. A longitudinal approach to assessing urban and suburban children’s exposure to pyrethroid pesticides. Centers for Disease Control and Prevention (CDC). Berger-Preiss E.111(1):79-84. et al. 2005.205(6):459-472. Seiwert M. Hadnagy W. Batres LE.114(9):14191423. Ortiz-Perez MD. Grimaldo M. Hardt J. Lu C. Obel J. Kolossa-Gehring M. Becker K. Angerer J. Liu Z. Environmental health assessment of deltamethrin in a malarious area of Mexico: environmental persistence. Sugiri D. Int J Hyg Environ Health 2006. Berkowitz GS. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. Hoppe HW.113(6):782-786. Godbold J. Levsen K. Sugiri D. and genotoxicity in exposed children. Isotope dilution highperformance liquid chromatography-tandem mass spectrometry method for quantifying urinary metabolites of synthetic pyrethroid insecticides.46(3):281-288. Bravo R. Angerer J. Pearson M. Leng G. Leng G. Exposure to indoor pesticides during pregnancy in a multiethnic. Int J Hyg Environ Health 2002. Lapinski R. Carranza C. Torres-Dosal A. Int Arch Occup Environ Health 2003. Environ Health Perspect 2006. Deych E. Idel H. Arch Environ Contam Toxicol 2004. Indoor pyrethroid exposure in homes with woollen textile floor coverings. Third National Report on Human Exposure to Environmental Chemicals. Environ Health Perspect 2005. Fourth National Report on Human Exposure to Environmental Chemicals 175 . Environ Health Perspect 2003. et al.

176 (.180-.169 (.300) .156-.330) .146 (.390) .190 (.210) .350-.140 (.130) < LOD .170 (.109-.130-. Antimony can exist in one of four valences in its various chemical and physical forms: -3.470 (.130 (.240 (.160) .260 (.190) .130-.280-.390) .290-.180 (.200 (.154) .117-.160) .390-.270 (.154) .130) . from air and drinking water.200 (.160-.430 (.150) .330 (.158 (.210) .320 (.330 (.190) .360 (.230-.120-.220) .143 (.130 (.260) .117-.210-.200) .112-.135) * .150) . It is also used in paints.210 (. Stibine is a metal hydride form of antimony used in the semiconductor industry.330) .190-.070 (<LOD-.161) .390) .310-.170-.260 (.120-.350 (.125 (.220-.280-.280-.250 (. Antimony enters the environment from natural sources and from its use in industry.128 (.280) .140-.120-.200-.144) .180-.260) .210) . to a lesser extent.150-.150) 90th .340 (.490 (.154-.210) .170) .250) .250-. ammunition.290-.137) .220) 95th .120 (.230) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.130 (.115) .090 (<LOD-.240 (.220-.200) . < LOD means less than the limit of detection.105 (.134-.280 (.095-.350-.250-.200 (. ceramics.210) .115-.120-.200-.070 (<LOD-.350) .350) .128 (. +3.120 (.120-.220 (. People are exposed to antimony primarily through food and.180 (.180-.310-.04.130 (.370) .123 (.280-.240 (. fireworks.440) .103) .134 (. It is used in metal alloys.300) .190 (.500) .079-.170-.119-.080) .270) .110-.108 (.132 (.330 (.087-.400) .200 (.184) . and excretion of antimony vary depending on its oxidation state.100 (.210-.310 (.160 (.300-.150 (.300 (.350 (.370-.220-.090-.160) .260-.300 (.390-. 0.390) . and 0.142) * Sample size 2276 2690 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .430 (.140 (. and pewter. coal-fired plants.490) .430 (. population from the National Health and Nutrition Examination Survey. solder.126-.Metals Antimony CAS No.130-. The absorption.119) .150-.510) .190) .460) .130-.190) .260 (.110-.470) .120-.140 (.140) .141-.190-.133) * .220) . Two antimony compounds (sodium stibogluconate and antimony potassium tartrate) have been used as antiparasitic medications.140) .160 (.310 (.320-. 176 Fourth National Report on Human Exposure to Environmental Chemicals .270 (.460 (.350 (.110-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.230 (.170 (.230 (.330) .160-.350-.130-.180) .410) .350 (.150-.142 (.090 (.420) .145) Selected percentiles ( 95% confidence interval) 50th . respectively.320) 787 683 618 554 667 723 768 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.100-.280) .140) . 7440-36-0 General Information Antimony is found in ores or other minerals.260-.570) .164-.157) .560) .098-. often combined with oxygen to form antimony trioxide or with sulfur to form stibnite.270 (.320 (.360-.170-.320-.160) .136) * .400 (. 01-02.160-.095 (. and as a fire-retardant in textiles and plastics.340 (.070-.710) .280-.330-.240 (.340) .110-. and glass.180 (.S.110 (.410-.150) .099 (. see Data Analysis section) for Survey years 99-00.190 (.220) . metal bearings.190 (.230-.180 (.390-.390 (.090-.530) .120 (. Dermal contact with soil.080) . which may vary for some chemicals by year and by individual sample.120) .260) .410) .360) .120-.140 (.310 (.120-.300) .080-.170-.090) 75th .130-.175 (.310) .120-.080 (<LOD-.130 (.150 (.120) .270 (.148-.190-.190-.100 (.130) .280 (.400-.197) .440) .290 (.120) .180) .093 (.280) .470) .200) . castings.120) .137) . 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 (.160) .100) .400 (.300-.310 (.220-.100-. distribution.230) .160 (.230) .460 (. or other substances containing antimony is another means of exposure. water.350 (.270-.330-.145 (.180 (.270) .114) .150-.230-.250-.180-.350) .122 (.400 (.320) Total .170-.220-.07.220-.178) .132 (.320) .190-.140) .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 . and +5. storage batteries.160) .230 (.130 (.330) .088-.190) .120 (.230-.240 (.250 (.460 (.110) .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 .04.310) .240) .200-.190 (.140) . sheet and pipe metal.210 (.280) .200 (.300-.240-.350) .230-.400) .136-. and 03-04 are 0.600) .150-.200) .140) . 0.240-.130 (.160-.207) . interval) .200-. enamels.320-.130) .360 (.220 (.180-.320-.126 (.180 (.360) .400) . and refuse incinerators that process or release antimony.130-.200 (.120 (.500) .250 (.250-.131-.440 (.150 (. Workplace exposures can occur at smelters.108-.

263 (.209-.138 (.075 (.124-.135 (.343 (.208-.280 (.30) .385 (.318-.206-. 1954).146-. 1962).104-.098-.146-.176 (.429) .209 (. abdominal pain.120 (.357) .308-.278 (.250 (.171) .183) .194-.132 (.164-. population from the National Health and Nutrition Examination Survey.107-.417) .148-.317) .103-.185 (.131) .080 (<LOD-.152) .143) 90th .108-.153-.400 (.092-.129 (..170 (.214) .092) .099-.135) .159-.248) .116 (. Pulmonary edema may occur in severe cases of inhalation exposure (Cordasco et al.135 (.152) .338) .109 (.118 (.315) .097-. Fourth National Report on Human Exposure to Environmental Chemicals 177 .124 (.089) .267-.144-.146) .253 (.137 (.242-.185-.143) .181) .120 (. 1995).069-.300) .138-.188-.102-.444) .172-.115) .255-.117-.255) .227-.200-..123) .082 (<LOD-.118 (.143) Selected percentiles ( 95% confidence interval) 50th . The toxicity of stibine after acute inhalational exposure is similar to that of arsine.207) .727) .338 (.192 (. 1986).200-.156-.182 (.208 (.294) Total ...192) .113-.364 (.230) 95th .321) .500) .139 (.213 (.320 (.149-. Acute antimony poisoning may cause a metallic taste.263-.741) .257) .077) .405) .250-.485) .288 (.123 (.115 (.286 (.079 (<LOD-.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 . and ulcers (Werrin.150-.236 (.082) . species.333 (.276 (.272) .278) .414) .148) * .281-.109 (.100 (.239-.081) .233) .179-. resulting in hemolysis with abdominal and back pain (Dernehl et al.081 (<LOD-.250-.167 (.133) .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 .269 (.121 (.130) .266 (.148-.127) . Inorganic antimony salts irritate the mucous membranes.250-.098-.250 (.127 (.109-. 1986).107-.300) .298 (.119-.333-.205-.222 (.230-.112 (.280-.430) .211) .173 (.244-. and eyes.108-.259 (.S.104-.138) * .136) .333 (.114 (.132) .173-.245) .191 (. Human health effects from antimony at low environmental doses or at biomonitored levels from low environmental exposures are unknown.233 (.124-.193) .256 (.217 (.145) .241-.147) .122 (.225) .271-.113-.233-.188) .131-.425) .114 (.333-1.106-.117-.352 (.Metals than for trivalent compounds (Elinder and Friberg.167 (.106-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.111-.164 (.147-.115-.241-.471) .209) .741 (.173 (.235-.139 (.125 (.111 (.119-.352) .178 (.095-.134) .125-.107-.320) . interval) .124) . Histopathologic inflammatory and degenerative changes in the lung.192-.082) .087) .313-.113) .248-.333-.226 (. 1958) and occupational exposures (Briegner et al.150-.102-.220) . skin.159-.203) .189 (.186) .143) .228-.267 (. Acute inhalation of antimony has been associated with irritation of the respiratory tract and impaired pulmonary function (Renes.146-.116-.126-. 1953).228 (.086 (.364 (.140) < LOD .080 (. Dysrhythmias and T-wave changes on electrocardiogram have also been noted after both therapeutic (Berman.429 (.117-.129 (.173) .115 (.391) .126 (.204-.086) 75th .200-.085) .250-.195-.135) .295 (.380 (.095-. 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.130) .121) . diarrhea.108-. and kidney have been demonstrated in high dose animal studies depending on the dose.333 (.129) .143 (. Ming-Hsin et al.209) .310 (.421) .229-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.181) .261) .130 (.176 (. and gastrointestinal symptoms such as vomiting. and route of exposure (Elinder and Friberg.338 (.074 (.076-.099-.247) .167-.130) .391) . 1988.178-.320 (.228 (.103-.129) * .203) .250) .199-.195 (.417) .128-.187) .333-.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 .127) .068-.333) .447 (.061-.176-.310) .318-.138-.161) .121 (.310) .105-.068 (.300 (.268) .195-.140) ..078 (. 1944).480) .120 (.357-.238) .164) .317) .444) .135) .112 (.253-.198) .115-.112-.115 (.320-. liver.225 (.127) .277 (.126) .167 (.238) .317) .238 (.373) .153 (.265 (.131 (. myocardium.076-.265-.159-.371 (.163 (.156 (.149) .196 (.098) .122 (.071-.185 (.181) .084) .224 (.161) .120 (. An elimination half-life of approximately 95 hours has been estimated after occupational exposures (Kentner et al.127) .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.075 (.162-.151) .160 (.096-. 1973).320-.267) .175 (.119 (.438) .154-.108 (.114 (.308) .069-.200) .471 (.193 (.163 (.

EPA. clinical efficacy. Iavicoli I. VI. Trace element reference values in tissues from inhabitants of the European community I. Rev Infect Dis 1988. Levels of urinary antimony in infants appeared to be similar to those reported by CDC (2005) for young children (Cullen et al.. 1997). Pilgrim L. 1986. Lauwerys R. Arsine. Delves HT.46:931-936. Dernehl CU. Sabbioni E. Chest 1973.)1954. Atlanta (GA). Finding a measurable amount of antimony in urine does not mean that the level of antimony causes an adverse health effect. Chen J-R. Pietra R. Suchenwirth R. Bailly R.. 1991. Several investigations of airborne antimony exposures in workers have found urinary levels that are many times higher than those seen in NHANES 1999-2000.13:361-362. 1998). Antimony in blood and urine of infants. Chin Med J 1958.16: 33-39. gov/toxpro2. et al. Shao-Chi C. Semisch CW. Mechanism and treatment of cardiac arrhythmias in tartar emetic intoxication. and 2003-2004. indium. Nau CA.html. Biological monitoring of exposures to aluminum. even when exposure levels were below workplace air standards (Bailly et al.76(2):103-115. stibine. population. Wade A. Dezateux et al. et al. Industrial Medicine 1944. Gebel TW. Stocks J. Yu H-S. Experimental and human studies on antimony metabolism: their relevance for the biological monitoring of workers exposed to inorganic antimony. J Trace Elem Med Biol 2002.e. Alimonti A. 2005. Ming-Hsin H. 1990. New York: Elsevier. 1987). Mayne P.. Bolten C. pp. Cordasco EM. and hydrogen sulfide. In: Friberg L. Review of elements in blood. 1998.64(2):182-185. Kuo-Juie Y. Environ Health Perspect 1998. Arch Dis Child 1997. Dunkelberg. Elinder CG. Biological assessment of exposure to antimony and lead in the glass-producing industry.. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.59:469-474... 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. Stasney J. Ludersdorf et al. Liao Y-H et al. External and internal antimony exposure in starter battery production. HH. Int Arch Occup Environ Health 1987. 2004.atsdr. environmental levels) and health effects is available from ATSDR at: http://www. Element reference values in tissues from inhabitants of the European community.10(3):560-586. O’Regan M. Luedersdorf R. J Occup Environ Med 2004.106:33-39. Antimony trioxide is rated by IARC as a possible human carcinogen. Nordberg GF. eds. Third National Report on Human Exposure to Environmental Chemicals. Fuchs A. Van der Venne MT. Kiberd B. Liao Y-H. Br J Ind Med 1991. which may be due to methodologic. Human biomonitoring of arsenic and antimony in case of an elevated geogenic exposure. 2nd ed. Piatnek DA.76:432436. Roland H. Stone FD. Weltle D. 1995. 26-42. arsenic. 2002. Dezateux C. Ho C-K. Paschal et al. Earlier measurements in general populations (Minoia et al. Schaller KH. Skulsukai G... Matthews T. 1994) have reported values slightly higher than those in this Report.Metals to antimony have been established by OSHA and ACGIH. Mayer P. Minoia C. Briegner H... Cheng-Wei L.521-523. Chia-Yu H. Schacke G. Wu M-T. Leinemann M. or exposure differences. Stead FM. Vouk VB. J Clin Pathol 1998. Centers for Disease Control and Prevention (CDC). Biomonitoring of a worker population exposed to low antimony trioxide levels. Hamilton EI. Mahieu P.. Pozzoli L. Biomonitoring Information Levels of urinary antimony reflect recent exposure. Kentner M. Caroli S. et al. Apostoli P.S. Industrial Medicine and Surgery (Dec.. 1998) or compiled reference ranges (Hamilton et al. Yang C-Y. Gallorini M.51:238-240. and a drinking water standard has been established by the U. Chemotherapy for leishmaniasis: Biochemical mechanisms.158:165-190. 20012002. Kentner et al. Information about external exposure (i. Costeloe K. Buchet JP. A study of 46 elements 178 Fourth National Report on Human Exposure to Environmental Chemicals .48:93-97. Lenert G. and future strategies. Handbook on the toxicology of metals. Delves HT. Sabbioni E. Carelli G.cdc. respectively. Konings J. Petrucci F. Int Arch Occup Environ Health 1995. Urinary antimony was not associated with locally elevated soil levels in a study of more than 200 German residents (Gebel et al. Iavicoli et al. Pulmonary edema of environmental origin. Sci Total Environ 1994. References Berman JD. plasma and urine and a critical evaluation of reference values for the United Kingdom population. Ju-Sun P. Urinary antimony in infancy. and antimony in optoelectronic industry workers. Antimony. Cullen A. Industrial antimony poisoning. Friberg L.67:119-123. gallium.

Chemical food poisoning. Sampson EJ. Sci Total Environ 1990. Industrial Hygiene and Occupational Medicine 1953. Werrin M. Fourth National Report on Human Exposure to Environmental Chemicals 179 .76(1):53-59. 27:38-45. Jackson RJ. Renes LE. Morrow JC. Quarterly Bulletin of the Association of Food and Drug Officials 1962. Pirkle JL. and serum of Italian subjects. Environ Res 1998.95:89-105.Metals in urine. Ting BG. Antimony poisoning in industry. Trace metals in urine of United States residents: reference range concentrations.99-108. et al. blood. Paschal DC.

1) 290 725 1542 03-04 03-04 9.7) 90th 37. Arsine (AsH3) is a reactive. and arsenates (oxidation states of -3.5) 95th 65.9-34.2-61. aluminum.8) 7.8) 17.0 (22. sodium arsenite. 7440-38-2 General Information Arsenic is an element that is widely distributed in the earth’s surface in small amounts.4) 60.90-7.30) 17. were used as treatments for syphilis.5) 41.4-65.50-14.70) 8. 2001).6 (9.7) 24. General population exposure to inorganic arsenic can occur through consumption of drinking water and.5-19.00 (6. though in some locations arsenite may be prevalent (WHO. copper arsenates.3-111) 78.0-19. and gray forms).8) 30.8) 7. grain.4 (48.8) 34. Arsenic trioxide (As2O3. chromated copper arsenate (CCA) has been used to treat outdoor timbers and pressure-treated woods to prevent wood rot.5 (40. semiconductors.6 (32.00-9.2 (51.7) 65. alloys.97) 8. Survey years 03-04 Geometric mean (95% conf. arsenic as elemental metalloids may be used in some ammunition. Arsenic can combine with such non-carbon chemicals as sulfur and oxygen to form arsenides. pesticides. as alloy in metal bearings.9 (8. to a lesser extent. to a lesser extent.77) 6.5 (36. arsenites.1-18.34-10. and indium arsenides are used in the semiconductor industry. such as arsenopyrite (FeAsS) and realgar (As4S4). or rarely as elemental metalloids (yellow.02-8.9) 68.2-20.1) 15.29 (8. arsenocholine.4) 40.10-7.20 (8.9-46.6) 11.90-14.5-41.90 (5.3) 10. Various forms of inorganic arsenic can occur in groundwater from natural sources or as a result of soil application or industrial waste.1 (32.08 (5. gaseous hydride manufactured in small quantities for use in the semiconductor industry.8-61.80-9.9) 21.27) 9.7-83.5 (34.90 (7. population from the National Health and Nutrition Examination Survey. mostly for use in wood preservation (ATSDR. Roxarsone and other organic arsenicals are anticoccidial agents added to poultry feed.0 (11. Arsenic is measurable in most soils.4 (26. Arsenic trioxide is approved to treat acute promyelocytic leukemia. CCA-treated wood has been restricted since 2003 and no longer can be used in residential applications such as decks.6-35.41 (7. referred to as inorganic arsenic compounds. see Data Analysis section) for Survey year 03-04 is 0.4 (24.3-19.4 (7.2 (13.57) Selected percentiles ( 95% confidence interval) 50th 7.30 (6.2 (41.7 (11.19-9.8-77.1-40. psoriasis. Also.12 (6.2) 15. black. Before the 20th century. solders. and foods. particularly arsenic trioxide.80 (5. and as a cosmetic to lighten complexion. meats. a trivalent compound known as white arsenic) is a common natural and commercial form that can be released into the air during volcanic action.0 (15.70-9.90) 16. ocean and fresh waters. and. In the last century.6) 618 722 1074 Limit of detection (LOD. and in lead-acid storage battery grids. interval) 8.30 (7.000 metric tons annually.8 (48. trimethylarsine oxide.5-178) 46. Arsenic and its compounds have had many uses in the past and present as medicines. Since the 1940s.90 (7.Metals Arsenic CAS No.5-52.74.0 (43.0 (14.12-10.7-95. and produce. and monosodium methyl arsenate were used as pesticides but contemporary uses are restricted. +3 and +5). Water sources contain mostly inorganic arsenate.10 (6. it is found in over 200 crystalline or mineral forms.50 (8. and play sets.10) 10.5) 66. retaining walls. mental disorders.13-8.S.9-62.84) 8.10-10. and other metals. In nature.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. and as homicidal poisons.5) 43. Arsenic can also combine with organic substances in nature to form such organic arsenic compounds as arsenobetaine.1) 7.40) 7.2) 46.5 (23. lead. Although it is still widely used in the United States. 180 Fourth National Report on Human Exposure to Environmental Chemicals .2-17.55 (7.90-11. 2005). cacodylic acid.4) 13.80) 6.25-9. Groundwater Urinary Total Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. lead hydrogen arsenate.6 (13. from coal burning.2 (12. Various arsenic compounds were used in paint pigments and for tanning animal hides.8) 33.5 (14.6-141) 53.6 (15.8) 29.1 (38. arsenic compounds.70 (6.90) 75th 16.66-8.9 (17.4 (31.90-8. and arsenosugars.84) 8. The United States no longer produces arsenic from mining but imports about 22.2-93. cancers.90-8.34-9.3-15. Gallium.0-60.6-43.1) 1281 1276 03-04 03-04 03-04 9. the smelting of copper.

arsenic does not show biomagnification in the food chain (WHO.6 (35.35) 7. 2001). 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.9) 618 722 1074 Fourth National Report on Human Exposure to Environmental Chemicals 181 .33-10.75 (5.7-188) 27.64 (7.51) 75th 14.3) 9.00 (6.9) 13.04 (5. Inorganic forms of arsenic demonstrate high acute toxicity.5) 290 725 1542 03-04 03-04 8.66-8.3 (24.31 (6.81-9.01) 7.1 (11. The semiconductor dopants. Ingestion of arsenosugars in kelp and algae can also lead to the excretion of DMA. Though modest bioconcentration occurs in some aquatic life.7 (11.0-18. 2001.3 (27.24 (7.7) 28. and arsenosugars.45) 5.3-62.S.1) 24.47 (6.7-18.88) 7.9-56. shellfish. are used in enclosed ultraclean operations within the semiconductor industry. WHO.10-16.44-11. EPA.4) 54.8-75.93-9.7-17.0-69. 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.47 (7.9) 53..4) 32.2-46...66 (7. interval) 8.3-53. EPA’s maximum contaminant level (Hughes.2-15. After absorption.01) 11. 2003.58-10.4 (42.6 (10.0 (17.5 (9.0) 26. and contact with CCA-preserved wood structures.0 (31.. organic arsenic can be converted back to methylated and inorganic arsenic. Children may have additional exposures from ingestion of contaminated soils (e.8 (11. 2001).2) 15. kelp. U.23-7.33 (6. have caused clinical arsenic poisoning.32 (5. but is poorly absorbed dermally (WHO.3-64.S. 2007.76 (6.30-9. age. WHO. 2001). In aquatic sediments.18 (5. population from the National Health and Nutrition Examination Survey.8 (20. Arsenate is reduced in the body to arsenite (oxidation state +3). inorganic arsenic is widely distributed within the body.8 (12.12-10. Chowdhury et al.88 (5.7-35. so exposure to the general population is extremely limited.. arsenocholine is converted to arsenobetaine and also to small amounts of TMAO (Christakopoulos et al.66-8.8 (27.8-62.40) 8.1) 6. TMAO is also formed in the environment from microbiological action and is a metabolite of arsenic in certain mammals.11 (5.28-7.4 (11.2) 40.7-34. 1988).61 (7. Inorganic arsenic and its metabolites have elimination half-lives of approximately 2–4 days (Lauwerys and Hoet.4 (12. Smoking tobacco is also a source of inorganic arsenic. Direct exposure to DMA and MMA may result from use of the two pesticides.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 (12. trimethylarsine oxide (TMAO).06 (4.0-26.7) 95th 50.75) 13. NRC. mine tailings). 2001).4-64.3-41.4 (40. 2001).0) 12. dose level. as observed in Bangladesh where millions of people have been exposed.93-8. These organic forms of arsenic from seafood are absorbed and quickly excreted in the urine (WHO. 2007..g.1 (14. Smelter workers can have significant inhalational exposures to airborne arsenic trioxide for which air standards have been established.0) 42.7 (25. cacodylic acid and monosodium methyl arsenate.47-6. 2006.6-17. 2001).86-17.04) 7.99-9.1) 7.5) 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. Arsenite is then oxidatively methylated to the monomethylarsonic acid (MMA) and dimethylarsinic acid (DMA) with subsequent excretion primarily in the urine (NRC.25-9.3) 6.50 (6.5) 17.07-9. selenium.44) 6. 2006.0) 14. Fish. Tseng. arsenocholine.10-8.0) 33. and folate status (Chen et al.13) 8. 2001. Gamble et al. Extremely high groundwater arsenic levels.6) 45.59) Selected percentiles ( 95% confidence interval) 50th 7.1) 58. Survey years 03-04 Geometric mean (95% conf. Inorganic arsenic is well absorbed from the gastrointestinal tract and absorbed to a lesser degree through inhalation. In aquatic organisms.96) 12.2) 90th 30. dust.9 (45.8 (21. though some reduction may occur in the gut prior to absorption. gallium arsenide and indium arsenide.1-36. and some other seafood can contain organic forms of arsenic including arsenobetaine. 2007.6 (17.38-10. with trivalent inorganic arsenic (arsenite) being more toxic than pentavalent inorganic arsenic (arsenate) (NRC.1) 8.0) 1281 1276 03-04 03-04 03-04 8.41) 6. 2001).0-38.4 (26.5-17.S.20-9.7 (9.4 (24.8) 27.5-120) 40. Steinmaus et al.8) 22.25 (6. 2001).8-32.

2007. and DNA repair inhibition (Cohen et al. 182 Fourth National Report on Human Exposure to Environmental Chemicals .30) 1. Chronic arsenic exposure in humans is considered to be a cause of skin.30) 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1.50) 621 725 1078 Limit of detection (LOD. which may vary for some chemicals by year and by individual sample.g.80) 1. and diarrhea. Acutely.... Cellular glucose uptake. leading to a decrease in adenosine triphosphate energy production. some of these effects may take years to develop. Bangladesh. can cause peripheral sensorimotor neuropathies. and bladder cancer (IARC. population from the National Health and Nutrition Examination Survey.. NRC. substitution in phosphate metabolism. Raml et al. 2001). hypertension. NRC. respectively. and hyperpigmentation of the skin (NRC.g. Chile). 2007). With chronic exposure.. interference in signal transduction pathways. Although arsenate is reduced in the body to arsenite.0. 2001. Arsenic has many actions demonstrated in cellular studies. 2001).S. and it also will inhibit succinate dehydrogenase. 2004. see Data Analysis section) for Survey year 03-04 is 1. 2000. 2001. and altered gene expression. and peripheral neuropathy may also occur with large doses or after surviving an acute overdose. Cohen et al.60) 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. and production of glutathione may be affected as well. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th < LOD 90th < LOD Sample size 1. arsenic trioxide) includes hemorrhagic gastritis with nausea.10 (<LOD-1. cell transformations. including drinking water sources with elevated arsenic levels (e. Chronic human intake of arsenic at less than acutely toxic doses.20 (<LOD-1. WHO. 2004).EPA. Acute toxicity resulting from the ingestion of large amounts of trivalent arsenic (e. 2001). 2001). food residue.50) 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD 1. 2006. 2006) and newly discovered thioarsenic metabolites may also be as toxic (Naranmandura et al. The organic forms of arsenic occurring in seafood have little known toxicity. arsenite will inhibit cellular pyruvate dehydrogenase by binding to the sulfhydryl groups of dihydrolipoamide. OSHA and ACGIH have established workplace standards and guidelines for arsenic exposure and monitoring. it may have its own separate toxic action by substituting for phosphate in glycolysis and other pathways. Taiwan.. apoptosis.50) 1. 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. < LOD means less than the limit of detection. WHO. U..60) 1. including inhibition of numerous enzymes. Laboratory studies using inorganic arsenic have shown chromosomal aberrations. hematocytopenias. and childhood neurodevelopmental effects in observational human studies. WHO. Bredfeldt et al. hepatotoxicity.10 (<LOD-1. Studies of arsenic at levels typical of U. 1998. and by uncoupling oxidative phosphorylation (NRC. Survey years 03-04 Geometric mean (95% conf.EPA has established drinking water. 2001).S. drinking water have not been associated with increased cancer rates (Schoen et al. Chronic elevated arsenic intakes have been associated with diabetes. gluconeogenesis. Such actions may lead to decreased energy production. Cardiac arrhythmias..Metals +3) shows greater toxicity than arsenite itself (Aposhian et al..10 (<LOD-1. hyperkeratosis. WHO. 2007. fatty acid oxidation. 2001). and endothelial injury (Kumagai and Sumi. 2006. renal failure.20 (<LOD-1. 2006) or when exposure occurs in smokers (Chen et al..10 (<LOD-1. noncirrhotic portal hypertension. lung.S. The U. but additional or confirmatory research is needed (Kapaj et al.. cytotoxicity.20 (<LOD-1. Acute unintentional inhalation of arsine gas can produce hemolysis of red blood cells. vomiting. 2004).S.20 (<LOD-1.10 (<LOD-1.50) 2568 95th 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1. which can lead to dehydration and shock.. peripheral vascular disease. 2006. The risk of lung cancer appears more pronounced when large environmental exposures start in childhood (Smith et al. increased oxidative stress.

. Pellizzari and Clayton..S. 1999..69 (<LOD-3.. 2006). Biomonitoring Information Urinary arsenic levels reflect recent exposures and are moderately to highly correlated with arsenic intakes from drinking water and dietary sources (Ahsan et al... In animal studies. gov/toxpro2. 2000. the median total urinary arsenic in about 200 people was approximately four times higher than that of the U. Calderon et al. Additional information about external exposure (i. Fourth National Report on Human Exposure to Environmental Chemicals 183 ... 1986). Caldwell et al. Meza et al. WHO... Daily variation in creatinine-corrected urinary arsenic is relatively small when intake is constant (Calderon et al. 2001).html. population (Rubin et al. although urinary arsenic levels were not associated with CCA contact (Shalat et al. Shalat et al.95) 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.50) 2568 95th 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2.. 1998. 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.75 (<LOD-2. 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. 2004. Caldwell et al. population in NHANES 2003–2004 (Schulz et al. 2004. 2001).cdc. environmental levels) and health effects is available from ATSDR at: http://www. 2006). 2006). IARC and NTP recognize inorganic arsenic and arsenic compounds as human carcinogens.. but generally only at maternally toxic doses (WHO. 2006....00) 1.75 (<LOD-2. Several studies have shown that urinary arsenic levels are not correlated with low levels of arsenic measured in house dust or in washings taken from hands (Hysong et al. 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. Compared with this Report.33 (<LOD-3. 1999.89) 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2. 2006. 2008.. Levels of total urinary arsenic in the U.70) 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD 2.50) 1.Metals compounds. 2008).. and the FDA has established a bottled drinking water standard..04 (<LOD-3.61 (<LOD-3. 1999).41) 3. 2003. 2007.33 (<LOD-3. 2007..18) 3.S.19) 3. 2006). Valenzuela et al. Pellizzari and Clayton. Consequently. Vahter et al. Josyula et al.atsdr. 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. Pellizzari and Clayton 2006). Though CCA-treated wood contains several thousand times more arsenic than untreated wood. DMA produced bladder cancer in some chronic rat studies (Cohen et al. though air levels of arsenic fume and dust are correlated with urinary arsenic levels at higher occupational inhalational exposures (Jakubowski et al..18 (<LOD-3.80 (<LOD-4. median urinary total arsenic levels in 4052 adults varied with seafood intake. 2005) and Urinary Arsenic (V) Acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.e. 2006. had decreased since the prior 1990– 1992 survey. arsenic has been fetotoxic and teratogenic. Offergelt et al. Shalat et al.. and were about two-fold lower than those for the U.S. population from the National Health and Nutrition Examination Survey.. 1992. Survey years 03-04 Geometric mean (95% conf.S.. 2001). In a Nevada town where groundwater levels were naturally elevated. 2008). In the German Environmental Survey III of 1998. higher mean or median total urinary arsenic levels have been reported among people living in specific western areas of North America (Calderon et al. urinary arsenic levels have been accepted as a good biomarker of dose (WHO. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 2000).

20 (1. DMA and MMA compose most (about 75%) of the total arsenic species measured in urine. 2003).S. methylation capacity.00) 3.83) Selected percentiles ( 95% confidence interval) 50th 1. After recent seafood ingestion.4) 23.28) 1.3-39. arsenobetaine and arsenocholine will greatly increase the level of total urinary arsenic and comprise the highest percentage of the total urinary arsenic level.5) 621 725 1078 Limit of detection (LOD. population from the National Health and Nutrition Examination Survey.55 (1.00 (1.. dermal keratosis. < LOD means less than the limit of detection.30) 10.70 (5. and urinary DMA represented about 67% of the total urinary arsenic (Hopenhayn-Rich et al. in NHEXAS 1995–1996. 2007).50) ... Caldwell et al.20-25.1-94.5) 29..2-35. with DMA.5) 292 728 1548 03-04 03-04 1.9) 13.40-7.6-44.80 (4..30 (1.70) 6.37 (1.9 (6. arsenite..6. Great Lakes region residents had median urinary DMA levels that were slightly less than median levels in NHANES 2003-2004 (Caldwell et al.40) 5. population in the NHANES 2003–2004 subsample. 2008.900 (.g.Metals other areas of the world (Ahsan et al.40) 75th 5.1-25. 2008).3% of a representative sample of the U.20) 3.50-6.70-21.9 (7.7-22.S.20-190) 31.4) 31.7 (21.8) 35.2 (6..6) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites Sample size 2568 03-04 03-04 03-04 * * 1. Some noncancer effects of arsenic (e..19 (.60-3. and duration of exposure are also considered important.68) .80 (.5 (14. DMA has been the predominant metabolite composing the majority of measurable inorganic-related arsenic in the urine (i. China. Detectable levels of MMA reported in NHANES 2003–2004 were found only at the upper percentiles and. population (Ahsan et al.4 (16.66 (1. 2001). and two methylated metabolic products. Caceres et al..20 (4.8 (12.800 (.6.3 (9. The higher percentiles of total urinary arsenic levels in the U. 2005. arsenite. 2008).9-23.0) 4.10) 4. MMA. Chowdhury et al.17-1.00 (. interval) 1.. 1.6 (25.62) 2. In the late 1980s.. Caldwell et al.S. Valenzuela et al. When seafood intake is avoided. 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.800) 1. 4.93) 1.900-1. median levels of urinary DMA were about 40-fold higher than the adult median reported in NHANES 2003– 2004.S. 1996.8. 1990. and 0. Blom et al.3) 95th 35.3) 1284 1284 03-04 03-04 03-04 1.20) 7. respectively.S.20-3.10 (4.70-21.500-1. as evidenced by trace or nondetectable levels of arsenobetaine and arsenocholine in the urine.3 (21. 2000. 2000. In the residents of a Chilean town who consumed water with high levels of arsenic.30) 2.20 (2.50) .70 (3. 2001. and TMAO.48-2. Aposhian et al. Measurable organic arsenic species in this Report are three biologically generated environmental forms. 2005.80-5.4-35.50) 90th 16.8-40.800-1. 2005. see Data Analysis section) for Survey year 03-04 is 0. 2008.0 (26.10) 8. Pellizzari and Clayton.. and other factors such as nutrition. These associations are stronger at higher urinary levels.11-1.45 (1.00-6. and arsenobetaine being the main contributors to the total urinary arsenic levels (Caldwell et al. 1985.00-12. DMA and MMA.800 (..43-1. which may vary for some chemicals by year and by individual sample..90-29.1) 18.7) 13..05) < LOD .00-4..800-4. 2008).30 (2.e.600 (. and peripheral neuropathy) have been associated with urinary levels as low as 50–100 μg/L in chronically exposed populations (ACGIH.20) 18.20 (.6 (11.. WHO. 2008).400-. Arsenate. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Levels of DMA and MMA increase in approximate proportion to the intake of inorganic arsenic. 2000.40-6.700-1.80) 1. a control population of 696 Tacoma residents had median urinary DMA levels similar to those for NHANES 2003–2004 (Kalman et al. In most human studies.6 (13. Sun et al. 2006). population (Sun et al.60) 1.. Also. Tseng et al. Total arsenic measured in the urine includes all species of inorganic and organic arsenic.8 (17.8-50.90-7..2-38. arsenobetaine.700-1.5) 32.31-1.74 (1.0-23. when seafood organic arsenic is subtracted). arsenocholine.7 (13.5 (26. arsenocholine.1-51.80 (3. vasospasm. Individually measurable species resulting from inorganic arsenic exposure are arsenate.3) 35. Urinary Arsenobetaine Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.0 (27. and TMAO were detected in only 7.0) 29.29 (1. Caldwell et al. For residents of Inner Mongolia. geometric mean levels were about 70-fold higher than for the U..4.00-1. 2007) with higher levels of arsenic in the drinking water. population showed a higher contribution of arsenobetaine (Caldwell et al.1) 45. Survey years 03-04 Geometric mean (95% conf.871-1.7) 15. 184 Fourth National Report on Human Exposure to Environmental Chemicals .

50-7.25-7. The 95th percentile of the U..531 (.43) 75th 5.8) 29.51-2. 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.30-1. 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.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 * * 1.25 (.3) 1284 1284 03-04 03-04 03-04 1.05 (.2 (12. 2008). Finding a measurable amount of arsenic in urine does not mean that the level of arsenic causes an adverse health effect. interval) 1.82) Selected percentiles ( 95% confidence interval) 50th 1.16 (.9 μg/L.4-21.65 (1.4) 13.18-1.4 (24.9) 32.2 (13. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.7) 9.7) 17.83) 2.30) 1.6-32.13-39. 2001).80) .80-153) 17.47 (2.877 (.5 (18.51) 5. Urinary Arsenobetaine (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.55) 1. 1998.612-1.3 (10.4) 292 728 1548 03-04 03-04 1.9 (25.12) < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.36) 2.6 (6. 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 (3.21) 5.32-7.68 (1.909-1.959-1.938-1.4-28. 2001).5) 26.3-24.786-1. 2003. Vahter et al.15-4. these levels were much lower than those found in other studies where environmental exposures were highly elevated (Chowdhury et al. 1992. not to imply a safety level for general population exposure. 1986.3) 95th 29.4 (11.28) 1.2 (12.64-29...47 (1.05) 1.5 (18.78 (3.67) 4.29-14.29 (4.6-29.1 (26.2 (4.88) 2.00 (1.833-1.43) 14.67) 1. which is below the ACGIH BEI (Caldwell et al. 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. Sun et al.62-6.76-27. population from the National Health and Nutrition Examination Survey.S.54 (1.78-5.11 (.40) 1.91) 90th 16.58 (3.70) 5..10 (.73-6.6 (9. Information about the biological exposure indices is provided here for comparison.Metals as with DMA. 2008). Fourth National Report on Human Exposure to Environmental Chemicals 185 .72) 12... Survey years 03-04 Geometric mean (95% conf.0-36.5-20.19-2.5) 17.1-18. 2007).S.6) 19.. Offergelt et al.45) 1.88 (5.1-36.53 (.0) 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.81 (4.9 (13.15-1.82) 4. Caldwell et al. WHO.91 (4. 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.4-82.61-6.3 (10.15-1.40 (1.14 (1.50-15.1) 26.79 (1.93 (1. 2006.9) 14.9-18.0 (9. In recent years.400-.39-3.7) 30.44 (1.37-2.901-2.83) 8. population for the sum of inorganic related species was 18.6-46.4) 32..638) 1.

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

interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th < LOD 90th < LOD 95th < LOD Sample size 2568 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.S. Urinary Arsenous (III) Acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.08 (<LOD-4.70) < 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 2.40 (<LOD-1.80) < LOD 621 725 1078 Limit of detection (LOD.S. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.76) < LOD 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 3.Metals Urinary Arsenous (III) Acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th < LOD 90th < LOD 95th < LOD Sample size 2568 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1.95 (<LOD-2. Survey years 03-04 Geometric mean (95% conf.00) 1.20 (<LOD-1. population from the National Health and Nutrition Examination Survey. population from the National Health and Nutrition Examination Survey. Survey years 03-04 Geometric mean (95% conf.00 (<LOD-2.2.44) 2. < LOD means less than the limit of detection.29) < LOD 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. which may vary for some chemicals by year and by individual sample. see Data Analysis section) for Survey year 03-04 is 1. Fourth National Report on Human Exposure to Environmental Chemicals 187 .00 (<LOD-3.

72 (4.00) 4.0) 9.0) 9.03 (3. see Data Analysis section) for Survey year 03-04 is 1.00-3.5) 95th 13.00-7.69 (3.0 (10.00 (6.1-22.00) 75th 6.00) 90th 11.42) 3.6-18.90 (3.60-3.88 (4.2) 10.89 (3.80 (4.5 (11.80) 2.32 (8.00 (7.86-7.61-11.0) 16.20-4.00 (3. population from the National Health and Nutrition Examination Survey.12 (3.0) 11.24) 3.0 (13.00) 12.31) 4.3 (8.7. population from the National Health and Nutrition Examination Survey.94-3.34 (3.00-11.00-4.24-4.65-8.00-4.3 (8.95-4.92-12.17-4.20-12.25 (4.00-7.55 (2.0 (10.0 (9.00) 5.0) 16.74 (2.45) 8.00) 6.00 (3.27 (3.00 (3.0) 95th 16.32-10.67) 8.0) 292 728 1548 03-04 03-04 4.00 (6.00 (6.14) Selected percentiles ( 95% confidence interval) 50th 3.12-4.0 (14.11 (3.7) 12.1 (8.00) 9.73) 6.0) 12.90) 5.71 (3.95-3. Urinary Dimethylarsinic Acid (creatinine corrected) Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.7) 13.0 (13.0-17.00-8.80-3.10) 3.1-18.73 (3.9) 12.7-16.20) 11.0 (8.05) 10.00-9.67) 9.0) 11.34) 3.00 (3.4 (7. interval) 3.60-4.90) 2.00 (5.44) 5.70-3.1-15.11) 4.69 (3.60-7.00-4.62) 4.98) 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 3.8) 7.0 (11.80) 7.17-6.00-15.27 (2.74) 90th 9.00-11.00 (5.33-4.95 (4.69-6.60-6.71) 3.0) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites Sample size 2568 03-04 03-04 03-04 4.00 (5. interval) 3.65-6.29-4.0 (8.37 (3.00-4.85 (3.0-16.33) 3.14) 3.0) 17.0-25.0 (10.70-12.34-4.84-8.0) 621 725 1078 Limit of detection (LOD.80-6.0-16.94) 3.7) 1284 1284 03-04 03-04 03-04 4.44 (2.13-4.0-18.91) 75th 5.00-13.39-3.00-4.4) 621 725 1078 188 Fourth National Report on Human Exposure to Environmental Chemicals .34 (3.27-2.78) 4.00-15.57-5.45 (8.97-3.00-12.00) 3.70) 5.00-22.17 (2.0-19.7 (10.82) 3.9) 13.0) 13.0 (9.00-7.6) 1284 1284 03-04 03-04 03-04 4.45) 3.10) 6.0) 13.S.50 (4.70 (3.27-5.00) 7.22) 4.05) 5.0 (12.70-4.08 (2.0 (10. Survey years 03-04 Geometric mean (95% conf.00-15.18 (6.Metals Urinary Dimethylarsinic Acid Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.03-6.95-6.37 (2.00-11.82-5.00) 4.0) 9.79 (3.00) 3.50-15.69-3.05) 3.32 (4.00 (7.16 (4.6 (9.00 (5.92) 3.06) 5.5) 12.19) Selected percentiles ( 95% confidence interval) 50th 3.84-18.71-4.00 (3.00-4.3 (7.00) 6.00) 6.0-12.30 (7.57 (3.48 (3.9 (7.77 (3.8) 7.00 (3.00) 6.16 (2.00 (4.81 (5.48 (2.0) 17.80-5. Survey years 03-04 Geometric mean (95% conf.9 (11.0 (12.30) 3.49) 10.49-4.00-12.46 (4.15) 4.0 (9.59 (6.00 (5.86 (2.38 (3.9) 11.86-21.16-11.78 (4.28) 2.00-5.9) 5.82-9.09 (7.S.00-7.31-4.6) 292 728 1548 03-04 03-04 3.52) 3.0) 10.71 (4.0-17.61-16.34-4.00-10.50-5.00-3.0) 14.

45) 3.50) 1.00-2.00) 1.53) 1283 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.80 (1.20 (1.30 (1.10 (1.20 (1.96-2.28 (1.85) 1. population from the National Health and Nutrition Examination Survey. < LOD means less than the limit of detection.30) 2.Metals Urinary Monomethylarsonic Acid Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.86 (2.985) 1.35-3.20) 2.00) 2. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th 1.90 (2.40) 2.60-2.86) 3.82-2.30-1. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th 1.00 (2.60 (2.10-1.10 (1.79) 2.40-3.40-3.85) 2.30-2.33 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.53) Sample size 2567 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.70-2.36) 1.82-2.86 (2.00-1.23) 1.00 (<LOD-1.17) 2. which may vary for some chemicals by year and by individual sample.50-2.10 (<LOD-1.62) 2.07 (1.80 (1.00) 1.73-2.18-1.70-2.40) 1.10 (.00-2.93) .50 (1.40-2. Survey years 03-04 Geometric mean (95% conf.07) 2.80-2.61-3.05-1.84-3.80 (1.30) 90th 1.90) 2.00 (<LOD-1.00 (2.S.88-2.30 (1.90 (1.88 (1.9.S.80) 1.00) 1.60) 292 728 1547 03-04 03-04 * * < LOD < LOD 1.88 (1.10) 2.20-1.10-3.20 (1.54) 90th 2.816 (<LOD-.80 (2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.53) 292 728 1547 03-04 03-04 * * < LOD < LOD 1. see Data Analysis section) for Survey year 03-04 is 0.90) 1.18-1.60) 1283 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.20 (1.70) 2.50 (2.60) 1.60) 2.60) 2.46-2.50 (<LOD-1.70-2.36 (1.30-1.77) 1.40) 1.50 (1.31 (1.34) 2.30 (2.40 (2.00 (1.16 (2.80 (1.80) Sample size 2567 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.81) 1. Fourth National Report on Human Exposure to Environmental Chemicals 189 .30) 1.50) 621 725 1077 Limit of detection (LOD.90) 2.22 (1.20 (1.22) 3.37 (1.70-2. Survey years 03-04 Geometric mean (95% conf.900-1.63 (<LOD-1.853-1.30 (1.40 (1.46 (1.28 (1.80) 1.80-2.43-3.00-4.71-2.11-1.30) 1. population from the National Health and Nutrition Examination Survey.75) 621 725 1077 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.20-3.10-1.20 (1.15-1. Urinary Monomethylarsonic Acid (creatinine corrected) Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.57) 95th 2.61) 2.58) 2.40-2.86) 2.31-3.00-1.10 (.10) 95th 2.52 (2.14-1.60 (1.53 (1.33 (1.70-3.53-2.07-3.00) 2.

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

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80-5.93-8.00) 4. Fourth National Report on Human Exposure to Environmental Chemicals 193 .00-3.30 (3.8) 5.90) 4.90-2.2) 6.18 (6.75) 2.70) 1.39) 1.72) 4.34) 2.22-1.71-9. and ceramics.59-11.97 (1.96-2.00) 1.70 (5.15-1.21 (1.47) 4.01-7.95-6.65-5. are high in barium (Genter.52 (4. and 03-04 are 0. soluble forms of barium.54-1. Barium compounds are also used commercially in paint.87-3.88) 4. 7440-39-3 Medically.49) 2.12 (2.50 (1.43) 297 368 290 621 762 725 1262 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 1.34 (2.4) 7.54) 2.00) 1.39) 4.62 (1.74-2.12.14-1.06-2.20-1.29-1.38 (1.49-9.27 (1.72) 75th 3.65-8.46) 1.S.50 (1.39 (1.64-3.87 (5. water.21-2.04-2.90 (4.06-1. and food.33 (1. 2001).61 (3.60 (1.77-3.22) 6.50 (4.55-3.35 (2.93 (4.51) 2.41-3.51) 7.57 (5.56) 1.35-4.56) 4.93-2.85) 1.80-7.62) 1.30) 3.75-3. Small amounts of barium can be released into the air during mining and other industrial processes.50) 2.60-6.26) 2.27) 2.40) 3.20 (4.8 (6. depilatories.73) 3.41-1.61 (2.32) 8.24 (4.53) 1.10) 5.11-1.70-2.76-3.52 (1.14 (6.8) 9.70-6.70-5.48-4.81-2.10 (2.73 (6.30-1.69 (1.00 (1.24-1.80 (5.77 (3.21 (1.05% of the earth’s crust.80) 6.80) 7.80 (2.45 (1.95 (4.90-13.80-3.20-1.30 (5.03 (1.63) 1.80 (1.80 (2. population from the National Health and Nutrition Examination Survey.77) 1.40) 7.20-6.36 (4.90-9. interval) 1.60-3.36) 5.49) 4.15-11.40 (5.76-7.76-2.86 (4.50) 4.25-1.71) 95th 6.31-2.71) 1.60) 3. Urinary Barium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.41) 1.82) 1.48 (6.10) 3.86-4.30 (2.61 (5.26-1.70) 7.31 (2.50 (2.57-7.60) 4.61 (1.50-6.30-2. such as barium chloride.20-1.66) Selected percentiles ( 95% confidence interval) 50th 1.14-6.40-13.80 (1.11 (3. it combines with other chemicals such as sulfur or carbon and oxygen.19) 2.55-7.50 (1.00-8.30-2. Certain foods.74-3. Ingested soluble barium General Information Elemental barium is a silver-white metal which comprises approximately 0.60-10.43) 2.37 (4. 0.40 (1.Metals Barium CAS No.54-8.20-1.g.15 (6. rubber.10-5. bricks.91) 6.20-5.67) 6.78-2.30) 5.54 (2.65-1.70-3.78) 1. tiles.86) 6.56 (6.00-76.85 (2.05-2.19-1.73 (5.40 (1.62 (1.73) 1.29-5.82) 2.80) 1.70) 1.47-1.32-7.30-1.09 (2.73-5.50 (3.54-1.50 (4.20-8.76 (3.36 (1. barium sulfate and barium carbonate).49 (1.30) 2.48) 1.30) 5.98) 1.50-1. The general population can be exposed to low amounts of barium in air.00 (2.47-1.48) 1.60) 1.38 (1.88) 1. see Data Analysis section) for Survey years 99-00.30-3.87) 7.16) 5.51) 1.12) 7.51 (1.00) 6.35) 5.22-1.70 (1.86 (4.43 (5.04-6.59) 3.18-1.26) 5.35 (1. and 0.30-5.35-1.82-6.50 (1.53-5. whereas others are practically insoluble (e.49) 11.39-1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.90) 1.90 (1.11 (2.72) 1.15 (1.40 (4.26-7..54) 1.49-1.85) 1.1) 9.65) 1.88) 7.44-2.49) 8.40 (5.80 (1.10 (3.27 (1.61 (1.46) 1.44-5.94-6.16 (1.40 (1.70-8.50 (5.70) 4.30) 8.42 (1.24-1.12-1.63 (5.60) 1.20 (1.34 (1.35-1.28) 90th 5.12 (2.65) 1. were relatively well absorbed following inhalation (60-80% of a dose) or ingestion (11-32 % of a dose).08 (6. respectively.87 (6.90) 2. In single dose animal studies.70-2.32-1. Some barium salts are freely soluble in water.43 (1.87-7.28-1.31.71 (2.50) 1.18) 3.02 (7.20) 2.43 (1.90 (6.63 (2.62) 1.50) 2. glass.30 (1.36-1.86-5.10) 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 1.50 (1.39 (1.78) 1.63) Total 1.54 (6. Workers employed by industries that make or use barium compounds can be exposed to barium dust.80-2. 01-02.90) 2.70) 3.64) 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 2.50 (6.4) 9.53) 2.60 (2.40) 7.63 (8.01 (4.87-9.34 (1.4) 6.48-4.70) 5.11 (3.43) 6. fireworks.15) 5.37) 1.37-1.50-6.10 (4.07 (2.60-6.66 (4.45) 7.54) 1.29) 5.12.38) 8.35 (3.38) 2.63 (1.81-2. barium sulfate is used as a contrast medium for taking radiographs of the gastrointestinal tract.25-11.76) 1.92) 2.40 (5.68 (1.56 (1.63) 1.25 (1.71) 2.91) 2.53) 692 683 618 540 667 723 765 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.09 (1.99-5.30 (5.56 (2.99 (4.56 (1.30) 5.74) 3.21-8.20-8.46-1.78-3.17-1.10-4.81-3.9) 5. Barium compounds are used by the oil and gas industries to make drilling muds.65) 3.37-8.20 (3.15 (2.44 (1.50 (4.60-2.88 (5.91 (2.57) 3.36-1. Barium salts have also been available as rodenticides.12) 6.84) 5.30) 4.65 (5.87-14.15-1. such as brazil nuts.20-8.37) 5.50-1.64 (1.61-8. In nature.08-8.

38) 4.69-9.881 (.49 (1.59 (1.00) 4.47) 10.56) 4.48 (1.57) 2.0) 6.14-2.34 (1.96-6.32) 2.00) 1.47 (5.59) 1.63-4.02-5.18 (1.60 (1.60 (2.03) 2.48 (1.45-8.21 (1.60 (2.56 (1.Metals was eliminated primarily in feces and to a lesser extent.38-1.10) 6.64 (1.31-1.65 (2.10 (6.16-1.50) 1.47) 1.99 (4.29 (3.75) 2.20) 4.01 (4.16) 11.11-2.45) 1.36-2. in urine.48-1.49-1.51) 6.905 (.65 (5. paralysis.60 (5.39-1. Urinary Barium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.31 (1.70) 1.76) 2.45 (3.62) 2.57-5. 1985.26) 4.82) 1.98 (2.64 (1.45-1.24-1.99 (2.59 (1.58 (4.96) 4.54 (2.73-4. 1994.77) 1.80) 3.40 (1.62 (2.66 (1.703-1.60 (1.2) 5.20-2.48-3.43) 1.52-4.915 (. a benign condition that may occur among barite ore miners.59-7.45-1.68) 3.51-3.08-1.76-3.33-1.27) 692 682 618 540 667 723 765 1132 1074 Non-Hispanic blacks Non-Hispanic whites 194 Fourth National Report on Human Exposure to Environmental Chemicals . vomiting. 1984.50 (4.97 (5.46) 1.62 (1.52) 1.74) 1.57 (6.56-3.73) 2.54) 1.50) 2.82) 1.92) 2.38 (1.62 (4.31) 5. and cardiac dysrhythmias.38) 1.30) 2.03) 3.72) 6. water solubility.97-4.710-1.64 (1.68 (3. chemical form.84 (3.38 (4.S.55 (1. Chronic high doses in animals resulted in kidney damage (McCauley et al.87) 1.81-6.32 (2.97 (4.46-22.0) 7.86 (2.41 (2. Wones et al. Perry et al. Symptoms following acute high dose include perioral paresthesias.96) 4.29-1.02) .26-1.03-1.64) 7.56 (1. interval) 1.84-5.23-2.70) 4.55-5. are not absorbed when administered.28-11.96) 7.96 (4.68 (2.55-6.77) 5.2 (3.31-1.67-6.27 (2.51 (3.27) 7.99) 1.75) 2. 1986).52-10.96 (4.29-7.24-6.92 (4.40 (1.76) 1.03-1.58) 4.29-4.4) 5.25 (1.55 (5.51 (1.41) 4.91-2.76 (3. NTP.89) 90th 4.36-1.32 (1.29-3.39-1.42) 1.34-1.43-6.77) 1.22-4.56) Selected percentiles ( 95% confidence interval) 50th 1.39 (2.52) 7.0) 5..12) 2.34-3.23-1.04) 5.00-1. weakness.47-8.51) 4.29) 1.68-3.55 (1.19-2.00 (3. 1990).00) 6.921 (. Toxicity from soluble barium salts is rare.. population from the National Health and Nutrition Examination Survey.91 (3.26-1. hypertension.25) 4.33 (1.34) 1.31 (4.45) 95th 6.89 (2.58) 75th 2.68 (3.80-6.38 (4.68-3.01) 1.28-7.88 (6.42) 1.70) 10.48-5.83) 3.28-1.79-5.34-5.39) 4.891 (.40 (1.11) .44-2.27-3.64 (1. The health effects of exposure to barium compounds depend on the dose.76) 2.24-11.42 (4.36 (5.46 (2. and route of exposure.46) 3.39 (3.13-3.5) 1083 1334 1281 1097 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.32 (1.45 (1.36 (3.20 (1.27-1.47) 1.74) 1.38) 1.97) 1.57-10.60) 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 2.88 (2.64) 7. such as those used in medical radiographic procedures.8) 4. but can occur after intentional or accidental ingestion of barium carbonate in rodenticides (Genter.75) 1.38 (1.75-22.3 (6.02 (3.39-5.46) 2.75) 1.28) 5.81-7.44 (1.80) 4. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.880-1.20-8.24-6.84-2.31-1.35-1.39-10.22-1.59) 2.00 (5.33 (1.19-1.16 (1.24-1.36 (1.22-2.37 (1.53 (2.40-1.37-2.69 (5.68) 1.04) 1. diarrhea.48) 2.00) 4.28-6.29 (1.04 (2.38-7.06) 2.3) 6.54) 2.47) 4.28 (1.02) 4.48 (1.47 (2.24 (3.832-1.754-1.71 (5.777-1.15-4.49-1.51) 4.06) .25-11.32) 2.22-1.24) 3.72 (2.26-1.79) 1.19-1.57-7.36-1.58) 1.963 (.2) 6.10-1.33) 6.01 (5.13-2.33-4.39 (2.49-1.50) 1.52 (3..81-6.86-7.33 (5.03) 1.26-1. Following intravenous injection in animals. 2001).61 (4.33) 1.05-1.09) 6.10-2. about 75 % of a dose of soluble barium was eliminated within 3 days (Reeves.76 (2.00 (2.24-3.77) 1.91) 2.41 (1.58 (2.58-6.86) 5.73-2.24 (5.54 (1.37 (1.45-6.50) 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 1.37) 2.4 (5.26-4. Barium blocks cellular efflux of potassium resulting in profound hypokalemia.36 (1.63) 1.00 (3.30 (1.44-2.41 (1.52) 2.77) Total 1.11) .77-5.20-1.29-4.59) 1.23-5.96) 4.51 (1.39 (2.90-2.83) 2.97-3.36 (3.49 (1.85-5.38-5.55) .41) 5.72) 4.37-1.74 (5.84) 2. Chronic accumulation of inhaled barium dust in the lung tissue may cause baritosis. Barium is not rated for human carcinogenicity.00-7.55 (4.35-1. Human health effects from barium at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 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. 1989).19-1.53-21.61) 2.10) 3. Insoluble barium salts.08-2.91 (3.30 (1.75-3.18 (1.35-3.76 (4.53) .78 (2.

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

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. 0. In medicine. and 03-04 are 0.S. population from the National Health and Nutrition Examination Survey.130 (<LOD-. which may vary for some chemicals by year and by individual sample. soil.140 (<LOD-. < LOD means less than the limit of detection. and dental bridges. 7440-41-7 General Information Pure beryllium is a hard gray metal. coal.130 (<LOD-.13. bertrandite and beryl. nuclear. Low-level beryllium exposure in the general population can occur through breathing air. less than one percent of the inhaled dose was slowly absorbed into the blood and eventually incorporated into the skeleton. In studies of laboratory animals. and from breathing tobacco smoke. electrical.13. near some hazardous waste sites.Metals Beryllium CAS No. and volcanic dust. inhaled insoluble beryllium sulfate was retained in the lungs and nearby lymph nodes. Exposure to beryllium occurs mostly in the workplace. respectively. eating food. 196 Fourth National Report on Human Exposure to Environmental Chemicals . beryllium is used in instruments. and can be found in mineral rocks. x-ray machines. A half-life of 450 Urinary Beryllium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. aircraft. the lightest of all metals. 01-02.150) < 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 . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.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 . or drinking water containing the metal.13. Burning coal and oil can produce small amounts of beryllium dust that can be released into the air. and refined beryllium is used in mirrors and special metal alloys for the automobile. Beryllium compounds are commercially mined. are mined for commercial recovery of beryllium. Beryllium is also used in the production of sports equipment such as golf clubs and bike frames. and 0. computer. Two types of minerals. see Data Analysis section) for Survey years 99-00. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th < LOD < LOD < LOD 90th < LOD < LOD < LOD 95th < LOD < LOD < LOD Sample size 2465 2690 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . Survey years 99-00 01-02 03-04 Geometric mean (95% conf. and machine-parts industries.

More information about external exposure Urinary Beryllium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.273) < LOD < LOD < LOD < LOD 340 368 290 719 762 725 1406 1559 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . S. IARC has classified beryllium as a human carcinogen. which produces pneumonitis.281 (<LOD-. Chronic beryllium disease. EPA. is a granulomatous interstitial lung disease that is caused by chronic beryllium inhalation and the resultant immunologic response. population from the National Health and Nutrition Examination Survey. including contact dermatitis and subcutaneous nodules. 1990). 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 . Human health effects from beryllium at low environmental doses or at biomonitored levels from low environmental exposures are unknown. Air levels greater than 100 µg/m3 can result in erythema and edema of the lung mucosa. Workplace air standards and guidelines for external exposure have been established by OSHA and ACGIH.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. or berylliosis. NTP considers beryllium to be a known human carcinogen.346 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Genetic factors modify individual sensitivity to beryllium and susceptibility to developing chronic beryllium disease (McCanlies et al. 2002). Fourth National Report on Human Exposure to Environmental Chemicals 197 . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.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 . Maier. based upon excess lung and central nervous system cancers in studies of workers. 2003.231 (<LOD-. Skin exposure can result in delayed hypersensitivity reactions.Metals days has been calculated for beryllium elimination from the human skeleton (IPCS. respectively. 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.S..

patient population and literature reference intervals for urinary trace elements. 2000. Gallorini M. Apostoli P. urinary levels for general populations have been either undetectable or had different detection limits than in this Report (KomaromyHiller et al. Urinary beryllium--a suitable tool for assessing occupational and environmental beryllium exposure. Weston A. Finding a measurable amount of beryllium in urine does not mean that the level of beryllium causes an adverse health effect. 1998).157:388-398. Morrow JC. 3/27/08 Komaromy-Hiller G. 0. Hamilton et al.html. Sabbioni E. A study of 46 elements in urine. 2001). Sci Total Environ 1990. which approximate this Report’s limit of detection. 1990.S. blood.. Maier L. Howerton K. Comparison of representative ranges based on U. Genetic and exposure risks for chronic beryllium disease. Clin Chest Med 2002. et al.74:162-166. Available at URL: http://www. 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. Centers for Disease Control and Prevention (CDC). less than 0. In other studies. Minoia C. Review of elements in blood. McCanlies EC. Pietra R. Trace metals in urine of United States residents: reference range concentrations. Sampson EJ. Sabbioni E. Hamilton EI. Sci Total Environ 1994. environmental levels) and health effects is available from ATSDR at: http://www. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. (1994) noted that analytical methods used in several general population studies appeared to have limits of detection that were insufficiently low (i. Ting BG. VI. References Apostoli P. et al. Paschal et al. Int Arch Occup Environ Health 2001. Van der Venne MT. International Programme on Chemical Safety (IPCS).1 μg/L).. Levels of beryllium in urine for the U. Pozzoli L.inchem. 1990. Atlanta (GA) 2005. Costa R. Element reference values in tissues from inhabitants of the European community. Am J Epidemiol 2003.15 μg/L in workers exposed at the recommended threshold limit value (Apostoli and Schaller. Beryllium [online].atsdr. population were generally undetectable in NHANES 1999-2000.158:165-190.org/documents/ehc/ehc/ ehc106. Clin Chim Acta 2000.cdc.12 to 0. Environmental Health Criteria. Trace element reference values in tissues from inhabitants of the European community I.23:827-839. and serum of Italian subjects.e.. Pirkle JL. population are lower than levels in workers.e. Environ Res 1998. Third National Report on Human Exposure to Environmental Chemicals. 198 Fourth National Report on Human Exposure to Environmental Chemicals .95:89-105. Ash KO.Metals (i. 106. 20012002.13 μg/L.296(1-2):71-90. HLA-DPB1 and chronic beryllium disease: a HuGE review.S. it is likely that urinary beryllium levels in the U. Given these results.htm. They reported urinary beryllium levels ranging from 0. Schaller KH. and 2003-2004. Minoia et al. Andrew M. Paschal DC. Biomonitoring Information Urinary beryllium levels represent recent and accumulated exposure. and the 95th percentile for males in NHANES 2001-2002.. and the fact that most NHANES participant levels were undetectable.gov/toxpro2.S. Kriess K. Apostoli and Schaller (2001) stated that detection limits in earlier studies were inadequate to estimate nonoccupational exposures.76(1):53-59. Jackson RJ. plasma and urine and a critical evaluation of reference values for the United Kingdom population..

400) < LOD .20) 1.300-.500-.500-.700-1.300) .300-.300 (<LOD-.50-1.00) .80) 1.300) .500-.600 (.300) .500) .500) .400-.600 (.441) * .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 * * * * * * .300 (<LOD-.300-.00-1. and nonferrous alloys. coatings and plating.3.400 (.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 .60 (1.60) 1. and 03-04 are 0.600 (.700) .50) 1.10) 1.500 (.00 (. 01-02.30) .400 (.3.400 (.00 (1. U.200 (.20) 1.900 (.800-1.70) 1.10 (1.500-.300-.600) 90th 1.400 (.378 (.80) 1.20-1.500 (.300) .500-.200-.40 (1.S.700) .400-.800) .600) .300-.500 (.00 (.30-1.600-.400 (.S.50-1.400) .500-.00 (. EPA.300 (.10 (1.400-. Since 2001. Cadmium also may be emitted into the air from zinc.400) < LOD .600) .300) .304 (.400 (.427) * .412 (.500) .800-1.400-.300-.300-.300 (.376-.10 (1.700) .10) 1.20) 1.400) .500-.400 (.900-1.300) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.344) .300-.00 (.400 (.600) .600) .500-.10 (1.300 (.362-.20) 1.50-1.600 (.30) 1.60 (1.900-1.20-1.300) .40 (1.10) 1.452) .600-.400) .300) .900-1.700) .600 (.10) 1.382 (.420 (.300) 1.700) .40 (1.200-.333 (.30-1.326 (.500) .10 (1.50 (1.60-1.60) Total * . Other uses include pigment production.60 (1.255) .20) 1.70) 2742 2268 2085 1842 2219 2292 2716 3806 3478 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.359-.60 (1.200-.60) 1.00-1.300) .gov/minerals/pubs/commodity/cadmium).00 (.400 (.400-.500-.289-.20 (.00-1.30-1.20-1.400-.300-.30 (1.275-.200-.800 (.50-1. plastic stabilizers.700 (.40-1.300-. Blood Cadmium Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U.00-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.600 (.300-.00-1.378-. population from the National Health and Nutrition Examination Survey.300-.300) .300) .10 (.30) 1. Important sources of airborne cadmium in the environment are burning fossil fuels such as coal or oil.700) .426-. and incineration of municipal waste materials.10 (1.400-.40) 1.449) Selected percentiles ( 95% confidence interval) 50th .300 (. 7440-43-9 General Information Cadmium is a soft.300-.400) .400) .513) .395 (.304-.460) .300-.20 (1.200) .500 (.10) 1.00 (.300-.600 (.500-.300 (.200 (.200 (.70) 1.400-.400 (.400) .400 (. as zinc sulfide) and to a lesser extent.00 (.300-.393 (.200 (<LOD-.368-.00-1.50) 1.300 (. interval) .500-.20) .700-1.400) .300 (. Fourth National Report on Human Exposure to Environmental Chemicals 199 .367-.300-.20) 95th 1.313 (.600) .70) 1.300-.400-.266-.40 (1.400) .470) * .400 (.403 (.20) .398) < LOD < LOD < LOD < LOD < LOD < LOD .900 (.800) 1.600) .400) < LOD .400) .Metals Cadmium CAS No.20-1.700-1.00-1.300 (.60) 1.500 (.00 (.309-.usgs.00-1.300 (. 0.300-.421 (.400) .300) .235 (.300) .00 (.600 (.500 (.600) .400-.50 (1.40 (1.40 (1.14.300-.300) 75th .400-. or copper smelters (U.500-.500-.386-.361-.424) * . malleable.900-1.900-1.900-1.20) 1.800) .600 (.30-1.400) .500-.20) 1.10 (1.200) . The predominant commercial use of cadmium is in battery manufacturing.400) .200-.30-1.70) 1. < LOD means less than the limit of detection.700) .304 (.300 (.800 (.500 (.300 (.200 (<LOD-.500) .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 .20-1.500) .30) 1.468 (.600-1.400 (.500 (.600 (.10) 1.900-1.900-1.366) * * .300 (<LOD-.600 (.10) 1.600) .500-.40 (1.500 (. bluish-white metal that is obtained chiefly as a by-product of processing zinccontaining ores (principally sphalerite.00 (.20-1.400) .50 (1.700) 1.296-.425 (.600) 1.400 (. lead.600 (.90) 1.400) . during refining of lead and copper from sulfide ore.40) 1.500) .20) 1. and 0.60 (1.300 (.80 (1.283 (.300 (.600 (.400 (.10) 1. respectively.337) .300-.S. cadmium use has declined in response to environmental concerns (http:// minerals.00 (1.20-1.500-.400 (.00) .500-.500-.216-.00-1.403) .50) 1.400) < LOD < LOD < LOD .900-1. see Data Analysis section) for Survey years 99-00.600-.600 (.50 (1.300 (<LOD-.300-.600) .300 (.900-1.40-1.400 (.331) .700) . which may vary for some chemicals by year and by individual sample.

372) .140 (.462 (.326) .219 (.17 (.06-1.310 (.519) .813 (. Diamond et al.189) .220) .06. drinking water is a source for cadmium intake.229) .277 (.450 (. copper) and protein. The kidney is a critical target and shows the earliest sign of cadmium toxicity.351-.763-. 01-02.253-.219 (.289-.199 (.960) 1.466 (.187 (.060-.540) .339) .240-.12 (.733-.22 (1.13 (.20 (1.03) .330-. zinc.310) .700-.329 (.151-.886-1.390-. 2003).633 (.481) .230 (. wheat.198) .191-.209 (. Cadmium is absorbed via inhalation and ingestion.980 (.282 (.222) .607) .126) .177-.366-.25) 1. and 03-04 are 0.203 (. To a lesser extent.233) .300) .559 (.623) .203) ..320) .210 (.972 (. Renal tubular and glomerular damage.475 (.115-.191 (.211 (.492 (.400-.430) .114-.890-1.S.366-.860) 1.195-.230) 75th ..20) 1.989-1.090) .820) 1.28-1.06.360) .490) 1.216 (. 0.061 (<LOD-.173) .234 (.240) . Horiguchi et al.25 (1.960 (. including many food crops such as cereal grains. 200 Fourth National Report on Human Exposure to Environmental Chemicals .193-.855-1.510) .445 (.839 (.200-.189-.490) .220-.714-1. however.479) .400-.192-.232 (.820 (.283 (.200 (.717-. 2003).110-.238) .10 (1. and 0.450 (.06-1.233) .507) .15) 1.302 (.963-1.17) .04 (.101) .128 (.817 (.700-.440 (.090) .237-.249) .362) .519) .263) .220 (. **All results are corrected for molybdenum oxide interference in the ICP-MS method.977) .239 (. Inhalation of cigarette smoke is a predominant source of exposure in smokers.550 (.219 (.500) .870) .580) .201 (.284) .741-1.790 (.51 (1.30-1.299) .520-.09-1.74) 1.214-.458 (.255) .160-.226) . Cadmium absorption may be increased with iron deficiency (Berglund et al.260-.38) .190-.843-1.135-.393-. whose body burdens of cadmium can be approximately twice that of nonsmokers.366) .800-.179-.206) .02-1.733) .109 (.892 (.57) 1.394-.260-. Kikuchi et al. cadmium accumulates in the liver and kidneys where it is bound to metallothionein. 2003).806) .081) .246) .184-.875) .270 (. a factor that may contribute to the higher absorption of cadmium by women (Diamond et al.077 (.260 (.232) .313) . individual values vary and are affected by factors such as dietary intake of essential nutrients (iron.280 (.387) .790 (.447 (.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 .13-1.980) .800 (.890 (.249-.43) 1.551 (.261-.112-.836-1.980-1.230) .17 (.255) .092 (. 2004a.01-1.279 (.210) .327 (.388-.165-.226) Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 * .858 (. calcium.160) .247) .261-.202-.610) .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 .210 (.730-.175 (.336) .190-.316 (.880) .196-.713) .426 (. 2003.243-.633-1. potatoes.194-. With chronic exposure.510-.148-.748-1.680 (.980-1. rice.211-.52 (1.493-.41 (.22 (.227 (.390-.231) .455 (. and various seeds.** Survey Geometric mean (95% conf.38) 1.255) .452 (.200 (.34) 1.306 (. The gastrointestinal absorption of dietary cadmium is about 5% in adult men and 10% or higher in women (Diamond et al..157) .167-.157-.01 (.545 (.810-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. population from the National Health and Nutrition Examination Survey.817 (.26) size 2257 2690 2543 Total years 99-00 01-02 03-04 50th .210) .19) 1.191-.148) . 1999.080 (.48 (1.229) .818 (.24) 1.700-.20 (1.686-.121 (.220-.430-.295) .120 (.210 (.078 (.705-.498-.918-1..141 (.180 (..17 (.32 (1.207-.15) . For nonsmokers who are not exposed to cadmium in the workplace.38) .640) .092) .135 (.990) .272-.067-.061-.257-.308) . see Data Analysis section) for Survey years 99-00.192-.530) .500) 90th .107-.238-.150-.160) .257) .322 (.290-.190-.241) .300 (. ingestion through food is the largest source of exposure.13) . 1994).820-1.530 (.539) .204 (.350 (.354) .183-.251) .82) 1.Metals 2000).087-.273 (.12-1.206 (.235) .28) 1.262) .28 (1.433-.181 (.193 (.210 (.065-.136) .456-.480) .15 (.130 (. About one-third to one half of the total body burden accumulates in the kidney tissues (Nordberg and Nordberg.875 (.445 (.170-.229-.06.412) .72) 1.440 (.221) .596) .175 (.753-.20 (1.551) .285-.423-.38) 1.170-.381-.589 (.077 (. Cadmium in soil is absorbed by plants.153-.270 (.265) .202 (.200-.04 (.892-1. The estimated half-life of cadmium in the kidney is from one to four decades (ATSDR.208-.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.980) .221 (.265 (.169-.160 (.47) 1.476-.440-.36) 1.886) .281 (.067-.436-. 2001).150) .06) .109-. respectively.470-. Urinary Cadmium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.940-1. an inducible metal binding protein.223 (.220) Selected percentiles ( 95% confidence interval) Sample 95th 1.848 (.170 (.01) .919) .134) .100-.171-.20-1.178-.766 (. interval) ..189-.482) .210 (.390 (.07-1.83) 1.

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.221 (.336-.247-. Most studies of relatively low level environmental exposure to cadmium have demonstrated associations between higher urine or blood cadmium levels and an increased prevalence of various biomarkers of renal tubular effects (Alfven et al.559-..270 (.207-.09 (.288) .261 (.131-.263-.077-.097) .331 (.078 (.222-.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 .321) .191) .507-.412 (.176 (.500-. 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.421 (.722-.107) .783 (. However.693 (.423 (.308 (.245 (.438) 90th .16) .091) .075-.161-.666-.239-.729 (.304-.163 (.316 (.647-.700 (. 2003.663 (.177) .712 (.232) .716-.085-.091 (.917 (.288 (.725-1.490 (.199-.135) .414-.173-.274) 1.432 (.484 (. 1996.096) .191-.04) size 2257 2689 2543 Total years 99-00 01-02 03-04 50th .247-.873 (.767) .228-.828) .473 (. 2004).700) ..240) .071 (.687 (.813-.479 (.063-.304) .173 (. 2004b). Jarup et al.223) .727-.340) .07) .927-1.253 (.210) .687-.219 (.256-.318 (.381-.084 (. 2002. Horiguchi et al.078-.338 (.175-. 2002..516-.192) .136-.112) .00 (.434 (.789 (.199 (.210 (.234) .297) .204-.998) .818) .229) .719 (..113-.101) .185) .104) .126 (.143-.303) .884) .533) .691-.545) .418) .210 (. 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.182) .156 (.209) Selected percentiles ( 95% confidence interval) Sample 95th .247-. 2002.941 (.536 (.091 (.100 (.234-..329 (.12) 1.802 (..431) ..382) .207) .472) .292) .296 (.200 (. Noonan et al.181 (.470) .833-1.157-.630-.826-1.148 (.919 (.278) .104) .181 (.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 .476) .391-.404 (.830) .538) .876-1.16) 1.38) .827) .818) .350) .856) .255-.607) .690-.308) . 2000.106) .769 (.352) .551) .216-. 1999).688-.075 (<LOD-.197-.235) .560-.147-.146-.157-.074-.221-.208-.083-.591 (. 1999).300-.183 (.187-.909-1.267 (.325 (.178-.187) .678 (.236-.170 (.184-.283 (.154 (.481 (.143) .678-.343-.182) . At lower environmental exposures.225) .263 (.159 (. Fourth National Report on Human Exposure to Environmental Chemicals 201 .158-.150-.518) .168-.289) .175 (.198) .690-.289) .779 (.098) .185 (.123-.190 (.S. two studies in Japan did not find an association between cadmium in urine and renal biomarkers (Ezaki et al.423-.241) .830-1.364) . most often a result of occupational exposure (Roels et al.184-.196 (.13) .234 (.181-.686 (.189-.093 (. During the 1950’s and 1960’s.220 (.783) .826-1.929) .159 (.05) 1.266) .211 (. population from the National Health and Nutrition Examination Survey.225) ..07 (.137-.757) .414 (.491-.00 (.168-.219) Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 * .140-.085 (.940 (.784) .219 (.267 (.377-.650-.183) .206-.190 (.716) .140-.143-.163) .718 (. 1999).931 (.266-.261-.631) .201-. a condition known as “itaiitai” (“ouch-ouch”) affected postmenopausal women living in a cadmium-polluted region of Japan.501 (.10) 1.614) .850) .137 (.335 (.136-.281) .Metals manifested by irreversible proteinuria and progressive reduction in glomerular filtration rate.388-.487 (.156) .232) .293-.208 (.051-.708-1.690 (.147 (.123-.209) .311) .440) .218) .17) .415) . 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.645-.280 (.288-.166 (.940-1.227-.962) .979 (.438-. can result from high dose chronic exposure.250) .194-.622 (.176 (.856 (.446) .174-.170-.273 (. 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.08) .754) .224 (.156-.184) .144-..147-.668-.111-.441-.696-.238-.282 (.562-.906) .426-.985 (.387-.154-.084-.202 (.433-.242) .950) .205 (.162 (.740 (.215 (.444-.233 (.252 (.090 (.02 (.667) .086 (.122 (.** Survey Geometric mean (95% conf.261) .212 (.653) .281) .865 (.917) .06 (.387 (.067-. interval) .418-.181) .238) .178) .175 (.806-1.398-. **All results are corrected for molybdenum oxide interference in the ICP-MS method.268 (.850) .617 (.839) .440) .240) .531 (.757 (.404) .130-.182) .795) 1.191 (.874-1.792 (.382-.674-1.253) .813-1.537-.226) 75th . Olsson et al.541) .171-.470) .316) .767 (..094) .168 (.449) . Staessen et al.

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

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Wennberg M. Stelitano A. Roels H. Merlino MV. Wang JX.21(3-4):251-262. Salpietro CD. Lybarger JA. Environ Res 2006. Cadmium carcinogenesis. et al. Thijs L. 204 Fourth National Report on Human Exposure to Environmental Chemicals . EPA). Staessen JA. Bergdahl IA. Japan. Occup Environ Med 2002. Schwenk M. Staessen J. Mutat Res 2003. lead. Lauwerys R. Time trends in burdens of cadmium. age. Nordberg M. Arch Environ Health. Lijnen P. Hazard Summary.39:2507-2515. Olsson IM. Tawara K. New York: Plenum Press.84 (Section A):4455. Okubo Y. 151-168. et al. Environmental exposure to cadmium. Cadmium compounds. Friberg L. J Perinat Med 2002. Hoet P. Revised 2000 [online]. Bruiglia S. lead.S. Zhang YL. Kido T. et al. Kuznetsova T. Environ Health Perspect 2002. Ren Fail 1999.3:26-41.209:301305. Campagna D. 2001. Lundh T. Environ Health Perspect 2002. Effect of environmental exposure to cadmium on pregnancy outcome and fetal growth: a study on healthy pregnant women in China. Ottosson H. dietary intake. Effects of exposure to low levels of environmental cadmium on renal biomarkers. Nishijo M. 2000.30(5):395-399. and mercury in the population of northern Sweden. Honda R. or cadmium in controlling occupational and environmental risks of nephrotoxicity. Tanebe K.110:151-155.533(12):107-120. Public health implications of environmental exposure to cadmium and lead: an overview of epidemiological studies in Belgium. Sager PR. Renal effects of cadmium exposure in cadmium nonpolluted areas in Japan. Zhu HD. Mueller PW. Suwazono Y. created 1992. 2004. Schultz C. Usefulness of biomarkers of exposure to inorganic mercury. Biological monitoring of toxic metals.gov/ttn/atw/ hlthef/cadmium. forearm bone density. Lancet 1999.html. Kobayashi E. Skerfving S. Biological monitoring of cadmium. Kathman SJ. Tanebe K. Nogawa K. Sarasua SM. 4/8/09 Waalkes MP. In: Clarkson TW. Available at URL: www. iron status. et al. Toyama. Ginucchio G. Saito S. Lundh T. Roels HA. Nakagawa H. J Cardiovasc Risk 1996. Liu QF.epa. J Environ Sci Health B 2004. lead. United States Environmental Protection Agency (U. Nakagawa H. Nakagawa H. Nordberg GF.110:1185-1190. Zhao YC. Effects of maternal exposure to cadmium on pregnancy outcome and breast milk. Oskarsson A.353:1140-1144. Roels HA. Cadmium in blood and urine – impact of sex.100:330-338. Gangemi S. and risk of fractures: prospective population study. et al. Honda R.59:394-397. Buchet JP.Metals Nishijo M. Relationship between newborn size and mother’s blood cadmium levels. Environ Res 2000. Cadmium concentration in maternal and cord blood and infant birth weight: a study on healthy non-smoking women. Emelianov D. et al. Minciullo PL. Fan YG. Int J Hyg Environ Health 2006. Stegmayr B. and former smoking – association of renal effects.59(1):22-25. Bensryd I. Revised and new reference values for arsenic. cadmium. Gallmans G. Wilhelm M. Nordberg GF. Noonan CW. and mercury in blood or urine of children: Basis for validation of human biomonitoring data in environmental medicine. pp. Jansson J-H. Vangronsveld J. eds. Lison D.

90) 4.97-7.34 (4.70) 5.46) 7.5) 12.00-10. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.03-4. Inorganic cesium compounds are used in photomultiplier and vacuum tubes.7 (9.4 (10.4) 95th 11.50 (4.24) 4.5-16.37) 5.71-5.68 (7.40) 7.66 (7.6 (9.77 (9. see Data Analysis section) for Survey years 99-00.83-4.03 (4.90-8.89) 5. Most human exposure to cesium occurs through the diet.22 (4.3) 9.26 (3.64) 5.08-5.30-10.35 (4. infrared lamps.87-7.7 (11.20) 5.17 (6.6) 11.55-11.40-7.25) 4.1-12.40 (4.64) 4.40-5.81) 4.90 (6.1 (10.70 (6.80) 7.71-8.64-5. nausea.14.1) 11.68) 9.5-14.02 (4.27) 4.26) 4. and cardiac arrhythmia (ATSDR.20 (6.74 (4.8-13.0) 11.49 (4.4) 10.05) 5.9 (11.59-5.3) 10.14.80-13.12 (4.3 (8.10-7.91 (7.72) 4.80 (4.97) Sample size 2464 2690 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 4.50-7.80 (4.86 (7.0 (10.94 (4.74) Selected percentiles ( 95% confidence interval) 50th 4.0) 12.91-8.26) 7.49 (5.93 (4.55 (7.71-9.14 (4.6 (11.67 (4.2-13.86-12.50 (4.7-14.30 (6. soil. scintillation counters.9 (11.00-4.59-5.63-4.56 (4.7) 10.40) 5.90-10.4) 12.12-11.1) 9.40-11.73-11.60) 7.42-7.39-4.4 (9.8) 12.01-8.1 (9.76-6.61-6.94-4.25-5.1) 9.81 (4.71 (8.3) 10.3) 10.2) 12. Case investigations of ingestions of large doses of cesium chloride have reported decreased appetite.9 (10.13 (7.77-8.40-5.90-10.00-8.77 (9.98 (7.0) 11.30 (6.97 (7.00) 7.90-10.10 (6.6) 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. interval) 4.5) 10.59-5.9 (11.8 (10.1) 11.05) 5.07-11.50 (7.2) 11.50) 5.08 (6.5-13.60 (7.64-10.9) 11.50 (6.37) 7.35-5.43-8.36 (3.83) 6.7) 11.70 (8.20) 7. the body half-life is estimated to be 70-109 days based on 137Cs exposures.Metals Cesium CAS No.9) Total 4.6 (9.16-6.3-15.40-11.4 (9.60-5.52) 7.53 (6.56) 5.95) 5.8) 12.1) 10. and 0.10-5. 7440-46-2 General Information Cesium is a silver-white metal that is found naturally in rock.15-8.90) 9. 2004).95-4.80 (4.64 (4.60-7.13 (5.8) 9.7 (9.00-8.84 (4. Whether cesium compounds are carcinogenic is unknown.3-13.2-13.23) 9.95 (3.70 (4.5-14.43 (5.33 (6.12-5.7) 884 683 618 568 667 723 821 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.38) 5.08) 7. However.77 (4.87 (4.59 (5.20-8.47-8.49) 75th 7.60-6.90 (4.90) 5.82-4.10-8.9) 8.07) 4.05-5. Urinary Cesium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.92-13.7 (10.9) 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. photographic emulsions. For absorbed cesium salts.71 (4.86-11.4) 9.90-12.84-5.40-5.47-4.4) 10.7 (10.29 (4. semiconductors.60-6.87 (4.7 (10.80-10.99-11.2-12.20-4.9) 12.34) 9.99-11.80 (8.73-5.89) 4. population from the National Health and Nutrition Examination Survey.72-7.17) 4.40) 5.62 (5.10 (6.20 (4.59) 7.61) 7.23-4.2-14.30) 5.13-8.74-5.70 (6.12) 5.6) 10.97) 4.21 (4.0) 9.1-12. and as polymerization catalysts.5 (8.01) 7.53-11.56-11.27-5.45-8.70 (9. diarrhea.79 (4. 0.16-6.57-5.70) 7.39) 7.62 (5.09-5.87) 5.90-12.20-5.60) 7.60-12.8 (11.9 (11. cesium hydroxide is corrosive and irritating at high concentrations.99) 7.8) 9.6 (9.31-8.54) 4. Human health effects from cesium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.88 (8.80 (8.70) 5.05-5.0) 12.8) 11.10 (8.60-7.3) 10.70-5.81) 9. although cesium was generally of low toxicity when given to animals.90) 5.63 (4.03 (4.0) 10.4-13.7) 10.00 (7.70 (8. Fourth National Report on Human Exposure to Environmental Chemicals 205 .4) 11.80 (8.26-11.81) 4.01-6.2 (9.40-5.2. Radioactive 137Cs has been used medically to treat cancer.50 (4.35 (4. and clay.0-15.80-11.30-5.94) 4.2-13.45-5.99) 9.1-13.0) 12.2 (9.84) 8.42) 6.56 (4.81-14.32 (3.25 (3.21) 90th 9.70-8.7 (9.10-9.89-5.1 (11.20-7.10 (8. Little is known about the health effects of this metal.04 (4.60 (8.3) 12.71) 4.32) 4.96 (6.84) 5.50) 9.17-6. Workplace guidelines for cesium hydroxide are available from ACGIH and NIOSH.08 (7.82) 5.33-5.3 (8.7) 11.3-13.5 (10.49) 4.29) 4.27 (7.9 (10.36 (6.55 (4.00) 6.87 (4.5) 9.33 (5.04) 7.00-9.80-10.44 (8.6 (11.7 (8.69-6.60) 5.0 (9.64) 5.20) 4.42) 7.54-11.6 (9.62) 4.20) 8.0-13.32-5.S.00) 4.36) 3.80-6.09) 5.30) 7.8) 11.8) 12.80-10. 01-02.63) 6.70 (5.98 (7.94 (4. respectively.08-5.84-9.22-4.52-9. and high-power gas-ion devices.13 (8. and 03-04 are 0.90) 7.99-6.4) 12.8 (10.

29) 4.13 (3.56) 3.44-9.50 (6.06) 5.19-3.35-11.72 (4.14 (6.30) 10.72) 4.93-7.11 (5.63-6.42 (5.31-4.5) 7.63 (7.58) 8.74) 3.65-3.60 (3.93-9.96-4.99-9.56 (4.64) 5.16-5.51 (3.05-4.79) 6.22-11.8) 6.08 (5.87) 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 5.17) 9.35-7.97-5.51 (4.08-7.48) 7.48-6.23 (7.51) 4.06) 4.08) 4.14) 4.44 (8.66 (5.24-10. 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.70 (7.04) 5.47) 7.31-6.51 (3.92 (5.00) 6.6) 6.3) 11.13-9.21-4.28 (4.51 (4.99) 4.19-6.66-6.70) 6.84-9.7) 10.38-12.33 (5.78 (3.54 (3.38-7.41 (4. Finding a measurable amount of cesium in the urine does not mean that the levels of cesium cause an adverse health effect.2 (8.71) 6.82) 7.44) 3.00-8. Minoia et al.09) 4. Urinary Cesium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.47) 4.66 (6.10) 7.21-5.27) 4.95) 10.01-8.96) 4.13) 7.29-3.73-4.36-10.62) 5.21-3.39) 5.54 (5.68) 4.78) 4.77 (6.68 (4.64) 9.12-6.97) 8. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.53) 3.43 (4.50 (5.77-5.27 (6.95 (3.65-4.2 (8.95) 8.55-5.58) 3.90 (7.63 (6.91 (5.15) 95th 8.87-4.78) 4.28 (5.61 (7.14-4.07) 8.40) 6.S.30 (4.28) 7.38 (3.35 (3.85-4.64-6.13-9.08 (6.98 (6.9 (9.11 (5.18 (7.25) Selected percentiles ( 95% confidence interval) 50th 4.98 (7.15 (7.16) 5.78 (3.14) 4.05) 3.31 (4.06 (3.43-11.67 (6.79) 4. Urinary cesium levels were similar in a group of forest fire fighters and residents living near the fire area (Wolfe et al.53) 6.18-7.75 (6.9 (10.84-7.37-3.04-11.0) Total 4.41-4.99-9.03) 5. 2005.55 (3.64 (4.91-6.81 (4.35 (4.60-10.07-4.50) 4. Two small studies of European populations reported urinary cesium levels similar to U.74-11.26-6.59-8.76-9.0 (7.15-4.96-4.98) 5.68) 6. population from the National Health and Nutrition Examination Survey.41) 4.8 (9.5) 9.S.30) 10.44 (4.16-8.60-20.17 (6.00-4.2) 11.42 (4.24 (3.83-7.63) 6.27 (6.0) 7.20-4.07 (5.88-10.96 (4.75-11.5) 9.81 (4.74 (4.37) 4.22) 6.07) 8.00-10.46) 6.59) 4.86 (4.58-5.47 (4.67) 5.Metals Biomonitoring Information Urinary cesium levels reflect recent exposure.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 3.91-7.9) 10.42-4.20-4.91) 5.94 (5.65 (6.30-4.30-4.05-3.29-3.00-9.14-7.3) 9. Using clinically submitted specimens.8) 10.02 (5.56) 4.41 (8.53 (6.80) 6.30 (7.96) 4.08) 4.40-5..22 (3.3-15.20-8.27 (8.38) 10.91-9.49) 3.14-6.57) 3.08 (3.00 (8.18-6.50-5..54 (4.74 (5.10-4.95-6.46 (8.95 (5.4) 10.28) 8.68-11.8) 5.39 (5.50) 8.55) 4. Komaromy-Hiller et al.50) 4.41-7.20-4.38 (3.72-5.79-5.43-6.04-5.61-3.79) 9.12) 3.29) 4.50) 4.71 (7.00-5.91 (5.24-4.58 (6.43 (8.87 (5.36-3.6 (9.60 (5.54 (4.85) 4.42-6.26 (3.91) 4.3 (9.68) 3.90-8.58 (4.76-6.03-5.04) 6.73 (3.36-6.67 (5.34 (5.S.75 (7.40) 7.63 (4.43 (4.10 (3.41) 9.74) 75th 5.35) 3.48) 90th 7. population.77 (7.18) 8.84-9.08) 3.66 (5.10 (5.89-4.87) 5.03-6.83-6.3) 1226 1334 1281 1238 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 3.82-4.45 (4.99 (3.91) 5.43) 8.27-4.70) 7.3 (8. (2000) found urinary cesium levels that were slightly lower than those reported for the U.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 .50 (7.63-6.00-5.27-6. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.83) 8.10 (3.99-4.47) 6.44-5.77 (4.09 (4.46-4.7) 10.26 (4.08-3.17-4.33-3.6 (9. interval) 4.45-6.3 (10.90-8.79 (5.41 (5.62-8..53 (4.90-3.94) 7. 1990).85) 5.64) 4.15-11.03) 6.88-4.77) 4.05 (4.46 (7.1) 11.31 (4.60) 3.30 (3.84-7.12 (3.95) 4.52-5.5 (9.7-12.09) 8.56) 4.16-8.02-4.42-4.33-8.84-11.98) 5.39) 8.17) 4.20) 5.25) 4. and were also roughly similar to those in this Report.29) 5.95-12.06 (5.05) 6.47) 6.64 (8.47 (7.92) 3.05-3.56-10.46-8.51 (7.21 (2.43 (3. 2004). population results shown in this Report (Alimonti et al.33 (5.97-4.

Metals References Agency for Toxic Substances and Disease Registry (ATSDR). Uncertainty of inductively coupled plasma mass spectrometry based measurements: An application to the analysis of urinary barium. blood. Wolfe MI. Comparison of representative ranges based on U. 2000. Mincione G. Sewell CM. New Mexico. et al. Forte G. Fourth National Report on Human Exposure to Environmental Chemicals 207 . Ronchi P. et al. Howerton K.atsdr. Gatti A. Pietra R. 4/8/09 Alimonti A. Available at URL: http://www.95:89-105. Paschal D. Voorhees RE. cesium. et al. Wood CM. Sci Total Environ 1990. and serum of Italian subjects. antimony and tungsten. Centers for Disease Control and Prevention (CDC).cdc. Clin Chim Acta 2000.14:120-128. Third National Report on Human Exposure to Environmental Chemicals. Assessment of urinary metals following exposure to a large vegetative fire. A study of 46 elements in urine.2004 [online]. Toxicological profile for cesium. Atlanta (GA) 2005. Ash KO. Komaromy-Hiller G. Trace element reference values in tissues from inhabitants of the European community I. J Expo Anal Environ Epidemiol 2004. Sabbioni E. Minoia C. Pozzoli L.html. Costa R.296(1-2):71-90.19:3131-3138.S. patient population and literature reference intervals for urinary trace elements. Spezia S.gov/toxprofiles/tp157. Gallorini M. Rapid Commun Mass Spectrom 2005. Apostoli P. Mott JA.

900) .520-.740-.930) .470 (. It is emitted into the environment from burning coal and oil and car and truck exhaust.390) .520 (.890) .388-.680 (. 01-02.465) .760) .430) .640) .460) .32 (1.26) 1.48) 1.310 (.670-.800-.940-1.580 (.22 (1.410 (.290-. blue-colored pigments.543) .340-.338-.330-.03 (.560 (.434 (.950) .630 (.400-.68 (1.300-.640) .03) . Medical uses include joint and dental prostheses and radioactive cobalt in cancer chemotherapy. and magnetic recording media.64) 1.56) 1.47) 1.26) 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.32-2.410-. diamond-polishing wheels.308-.570 (. hard metal or in combination with other elements.469-.870-1.523) .370-.620) .393-.25-1.05 (.790) . 7440-48-4 General Information Cobalt is a magnetic element that occurs in nature either as a steel-gray.570) .331-.374 (. and in synthesizing polyester and other materials.870 (.620-.770) .600) .428-.490-.670 (.32 (1.372) .333-.22-1.45 (1.316 (.570) . The cobalt used in U.650 (.09 (. and fertilizers.301 (.01 (.840) .730) 1.550-.375 (. shiny.410 (.461 (.850-1.23-2.367 (.680) .07.564) .790-.450) .424) .410 (.417) .550 (.510) 1.380 (.371 (.300 (.14-1.850) .42) 1.17 (.22) 1.540-.460) .39) 1.520-.410) .06 (. and kitchenware.398) .16) 1.386) .470) .463-.05 (.414) . Cobalt is used as a drying agent in paints.19) .09) .590-.05) 1.530-.16-1.350 (.15-1.480 (.950-1.416) .59 (1.14) .348-.750 (.500 (.28 (1.15 (1.450) .50 (1.336-.581) .21) 1.830-1.540) 1.900) .26-2.07 (.330 (.620-. 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.334) . Cobalt compounds are also used in manufacturing battery electrodes.348-.28-2.360-.630-.340-.460 (.390 (.50) 1.530 (.540-.960-1.S.305-.410-.419) Selected percentiles ( 95% confidence interval) 50th .760 (.379 (.17 (1.580 (.520-.660-.630 (.12) 1.394) .660) .920) 1.26-1.360-.16 (1.60 (1.520 (.430) .390-.900-1.900-1.660) .430 (.740-.399) .890-1.670 (.820 (.950 (.03) 1.16 (.16) 1.690-.710) .520 (.880-1.700) . seawater.340) .610 (.890) 95th 1.930 (.294 (.450-.16-1.418 (.370-.700) .420) . 0.46 (1.480 (.460 (.320 (. Cobalt occurs naturally in airborne dust.340) .380 (.259-.29 (1.540-.440-.17 (1.590) .680 (.610) .81) 1.47 (1.350-.740 (.316-. industry is imported or obtained by recycling scrap metal that contains cobalt.398 (. and 03-04 are 0.53) 1.640) .670 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. large appliances. population from the National Health and Nutrition Examination Survey.490-.06-1.01-2.03-1.360-.04-1.370) .570-.520) .920-1.500) .92) 1.03) 1. Among its many uses are manufacturing superalloys used in gas turbines in aircraft engines.450) .313) .430 (.359 (.530) .75 (1.07-1.590 (.24 (.33-1.420 (.870 (.333-.520) .26) Total .350) 75th .850) 1.14) 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 .850-1.330) .350-.65) 1.430-.810-.450-.364-.32) 1.800) .17-1.02-1.930-1. Cobalt compounds are used as catalysts in producing oil and gas.583) .01 (.435 (.28 (1.380 (. and 0.940-1.373-.285 (.33 (1.410 (.600-.690-.519 (.47) 1. steel-belted radial tires.355-.03 (.08) .810) .750 (.570-.860 (. respectively.590-.16 (1.36) 1.910-1.81) 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 .S.502) .430 (.410) .431) .04 (.370-.327-.820 (.369 (. and soil.48) 1.28 (1.515 (.680) .379 (.67) 1.650 (.380-.04-1.270-.23) .08-1.07.52 (1.377-.550) 90th .452 (.670-.520-.310-.950-1.Metals Cobalt CAS No. automobile airbags.431) .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 .01-1.405-.352 (.270-.750 (.319) .890-1.390 (.410 (. varnishes.880 (.487) .291-.373) .410-.610-.460) .980-1.12) 1.710) 1.343 (.08.980) .20 (1. interval) .450) .24 (1.480-.950 (.47 (1.280-.340 (.37-1.380-.04-1.499 (.420) .900) .460-.404) .750-.13) 1.496) .73) 1.427-.710 (.810) .580 (.690 (.800-.650-.790 (.454 (.270-.350-. and inks.07-1. hard metal (alloys of cobalt and tungsten carbide).620-.00) .06 (.520 (. It is also a component of porcelain enamel applied to steel bathroom fixtures.600 (.370 (.890-1.44) 1. 208 Fourth National Report on Human Exposure to Environmental Chemicals .99) 1. see Data Analysis section) for Survey years 99-00.32) 1.610) .820 (. Usual human exposure is from food sources.09 (.940 (.540-.04) 1.390 (.339 (.

738 (.522) .513) .328 (.378 (.29 (1.542 (.306 (.495 (. population from the National Health and Nutrition Examination Survey.435-.707) .547 (.353 (.239-. but with a minor fraction (10-15 %) exhibiting a half-life of several years (Mosconi et al.821 (.259) .04 (.369 (.365-.442-.429) 1.515 (.259-.452-.561) .635 (.691 (.850-1.257 (.04-1.595) .990) .310) .337) ..281) .358 (.523 (.975 (.533 (.753) 1.335 (.581) .289) .348) .353-.378-. 1979).313-.469-. Once absorbed and distributed in the body.938) .394) . in the feces.419) .313-.10-1. Elimination reflects a multi-compartmental model dominated by compartments with half-lives on the order of several hours to a week.29 (1.543) .362) .434-.838 (.560-.895-1.976 (.554 (..279) .259 (.25 (.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 .297-. 1972).268 (.694) .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 .297) .467-.313-.728 (.339-.355) .19) .333-.342-.409) .392 (.16 (1.786-.644 (.293 (.847) . Urinary Cobalt (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.537 (.257-.368 (.33) . respectively.740-1.278 (.844 (.638-1.842) .704-.750-.393-.848 (.29 (1.324-.25 (.273 (. Lung retention of relatively insoluble cobalt compounds such as cobalt oxide may be prolonged.463-.00 (.781-1.632-. an essential human nutrient.457-.372) .329 (.433) .344-.36) 1. 1972).44 (.960 (.386 (.237-.804) 1.488) .352 (.425) .425-.10) Total .03-1.407) . Human studies with 60Co administered as soluble cobalt chloride have reported oral absorption ranging from approximately 1 to 25 % (Smith et al.324) .17) .352) . using hard metal cutting tools.00 (.30 (1.361 (.360) .304-.349) .280-.00) .234 (.331-.343-.60) 1.963) .303-.11-1.365) .306) 75th .49) 1.333 (..301-.444 (.274-.396) . refining or processing alloys.06 (.905) .879-1.313 (.250) .487-.757-1.505) .608 (.251-.861-1.380-.826-1.723 (.391 (.302-.333-.334) .290 (.738 (.500-. Exposure in the workplace may come from electroplating.368) .16 (.895-1.391) Selected percentiles ( 95% confidence interval) 50th .00 (.29) .606 (.829-1.291 (.333-.12 (.508-.83) 1.744) 1.362 (.256-.630-.55) .955) .727 (. Cobalt constitutes 4% by weight of vitamin B-12 (cobalamin).290 (.990-1.408 (.28) 1.750) .611) .700 (.384) .277-.461) .286) .616-.248-.777-.248-.428-.660-.247 (.955) .24) .911-1.352 (.594) . Workplace standards and guidelines for external air exposure to cobalt and several of its compounds have been established by OSHA and ACGIH.10) .582-.932-1.301) .381) .857-1.73) 1.523 (.481) 90th .426 (.282-.963) . Smith et al.591 (. Recent inhalation exposure to soluble cobalt compounds can be monitored by measuring cobalt in urine or blood (Lison et al.439) . A nutritional requirement for cobalt other than that contained within dietary cobalamin has not been established.296-.417) .821-3.326-.737 (.02 (.36) 1.851 (.964 (.09) 1.599) .60) 1.850 (.337 (.50) 1.378-.00-1.552 (.50 (1.626-.11-1.327-.449-.378-. cobalt is excreted predominantly in the urine.534-.243-. 1994).343 (.00) .471-.500 (.457) . with pulmonary clearance half-lives of from one to two years (Hedge et al.388 (. and to a lesser extent.361-.402 (.03 (..12-1.388 (.313-.215-.400 (.368) .689 (.938-1. Cobalt is absorbed by oral and pulmonary routes. 2003).829) .468) .50) 1.756 (.792 (.396) .503-.327 (.785) .404-.57) 1..669) .983) .304) .471 (.563-.417 (.949) .753-.296) .683-.309) .792-1.275-.271 (.861 (.393 (.554 (.479) .733-1.316 (.421) .328 (.314 (.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 .647) . interval) .937 (.363) .529 (.600-.361-.562) .328) .278-.917) .27) 1.33) 1.513 (.760-1.329-.640) .471-.548 (.362-.35) 1.449) .275-. A portion of cobalt retained for long periods is concentrated in the liver.300) .952 (.10 (.476-.667-1.323) .457 (.774 (.679-.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 .983-1.585) .872 (.487-.14 (.667-1. 1994.435 (.609) .830 (.781) 95th 1.475 (.700 (.16 (.15 (.703-.611) .479-.15) 1.833-1.319-.346 (.282 (.Metals fabricated from cobalt alloys (Lhotka et al. or using diamond-polishing wheels that contain cobalt metal.562) .824 (.500-.376 (.898 (.900-1..382-.630-.929) .361 (.673-.615) .574-.S.00 (.23 (1.294-.550-.27) 1.438) .513-.272-.728) .736-.298 (.662) .317 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.455 (.29) 1.462) .290 (.313-.387) .54) 1.407 (.634-.963-1.534 (.598 (.963-1.708) .279 (.593) .16) .35) .

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

Dunning SP.21(2):189-195. A report of two cases from mineral assay laboratories and a review of the literature. Mutat Res 2003.48:172-173. Ghat IS. Fujimura N. Barnaby CF. Kato M. Pradhan C. Health Phys 1979. Meyer zum Buschenfelde K-H.55(4):269-276. Oksa P. Hoet P. Sabbioni E. Edmonds CJ. Iversen BS. Alessandrelli M. Sabbioni E. Am J Ind Med 2003. Cobalt and antimony: genotoxicity and carcinogenicity. Biological monitoring of cobalt exposure based on cobalt concentrations in blood and urine. Swennen B.533:135-152. Kristiansen J. Ziaee H. Peltier A. Clin Orthop Relat Res 2003.87(5):628-631. Occup Environ Med 2001. Int Arch Occup Environ Health. 1985. Lhotka C. Steffan I. Moulin JJ.242:1412-1415. Respiratory health of cobalt production workers. Heki S. Goto S. Sci Total Environ 1994. Stanescu D. Goldberg MA. Lung cancer risk in hard-metal workers.Metals effects of cobalt. Thomassen H.(1-3):133-139. Hypothyroidism and thyroid hyperplasia in patients treated with cobalt JAMA 1955. J Occup Med 1992. Lauwerys RB. Unwin P. Romazini S. Metal ion levels after metal-on-metal proximal femoral replacements: a 30-year follow-up. J Rheumatol 2001.51(7):447450. Science 1988. Lauwerys R. Goto S. J Trace Elem Med Biol 2006. Biological monitoring of workers exposed to cobalt metal. Co-sensitivity between cobalt and other transition metals. 3rd ed. Blunn G. J Bone Joint Surg Br 2005. Linna A.36:732-734. Industrial Chemical Exposure: Guidelines for Biological Monitoring. Mosconi G. Angerer J.44:124-132. Contact Dermatitis 2003. Exposure assessment in the hard metal manufacturing industry with special regard to tungsten and its compounds. et al. Robinson C. et al. Radulescu M. De Boeck M. Boca Raton (FL): Lewis Publishers. Kriss JP. Cleland D. Weber A. Daniel J. Shirakawa T. Sci Total Environ 1998.” Contact Dermatitis 2001. Cobalt excretion in urine: results of a study on workers producing diamond grinding tools and on a control group. Schank M. MacDonald SJ. et al. Lison D. et al. Br J Ind Med 1993. Dunstan E. Szekeres T. Cobalt-specific T lymphocytes in synovial tissue after an allergic reaction to cobalt alloy joint prosthesis. and cobalt metals. Kraus T. Occup Environ Med 1994. X. Palmroos P.150(1-3):167-171. Carnes WH. Cresti R. Buchet JP. Wild P. Schaller KH. Christensen JM. Chess DG. Kiilunen M.22:359367. Fourth National Report on Human Exposure to Environmental Chemicals 211 . Pisati G.157:117121. Urinary cobalt as a measure of exposure in the wet sharpening of hard metal and satellite blades. McMinn DJ. et al. and hard metal dust. Leghissa P. Arch Intern Med 1990.406:282-296. Meier R.204:147-160. Iavicoli I.148:241-248. Cannon SR. Lison D. Zobelein P. Sci Total Environ 1997.69(3):193-200. Lison D.34:620-626. Bozec C. Epidemiological survey of workers exposed to cobalt oxides. White MA. Diepgen TL. Int Arch Occup Environ Health 1997. Zweymuller K. Kuska Y. Hoher T. Chest 1989. Dickel H. Buchet JP. Salama A. Am J Epidemiol 1998.95:29-37. 2001.150. The effect of the diameter of metal-on-metal bearings on systemic exposure to cobalt and chromium. Occupationallyinduced “isolated cobalt sensitization. Toxic trace element reference levels in blood and urine: influence of gender and lifestyle factors. Laippala P. Zhuber K. Vitali MT.28(5):1121-1128. Lauwerys R. et al. Bunn HF. Thabe H. Hammon E. cobalt salts. Health Phys 1972. J Orthop Res 2003. Cobalt cardiomyopathy. Falcone G. salt. Hedge AG. Thakker DM. DeSantis V. Bacis M. Ichikawa Y. oxides.45:246-247. Lisi P. Four-year study of cobalt and chromium blood levels in patients managed with two different metal-on-metal total hip replacements. Rorabeck CH. Metal-on-metal versus polyethylene in hip arthroplasty: a randomized clinical trial. Salvatori S. Kusaka Y.88(4):443448. Sabbioni E. Schramel P.58(10):631-634. J Bone Joint Surg Br 2006. Molders J.216:253-270. Roto P. Uitti J. Lasfargues G.20(1):25-31. Kirsch-Volders M. McCalden RW. Sci Total Environ 1994. The release of metals from metal-onmetal surface arthroplasty of the hip. Linnainmaa M. Bourne RB. Swennen B.50(9):835-842. a study of 13 elements in blood and urine of a United Kingdom population. Regulation of the erythropoietin gene: evidence that the oxygen sensor is a heme protein. Smith T. Gross RT. HoffmannB. Outcome of occupational asthma due to cobalt hypersensitivity.150:177-183. Zedda S. Weyher I. Long-term clearance of inhaled 60Co. Jarvis JQ. Absorption and retention of cobalt in man by whole-body counting. Trace element reference values in tissues from inhabitants of the European Union. Occupational asthma from cobalt sensitivity in workers exposed to hard metal dust. Tilley S. Sanghrajka AP.

50-3.50 (2.20 (3.40-1.80-2.00-1.30) 1.30-4.90) 5.10-3.10) 2.30-2.20) 90th 3.00) 1.25 (1.40-2.942 (. malleable.70 (5.40) 1.50-4.50-1.30) 95th 5.68-1. 01-02.80 (2.g.30-1.S.40-1.20) 3.70-2.50) 75th 2.20 (1.40-4.30-1.50) 1.01 (1.40-3.22 (1.50 (1.80-3.34-1.30 (1.90) 3.70-2.60) 2.23 (1.80-3.20-2.30 (2. bronze).899-.62) 1.86) 1.30) 2.70) 3.40 (1.30) 2.60) 1.900 (.40 (5.10-3.37 (1.70 (2.60) 4.19 (1.40) Total 1.32-1.50 (1.60 (1.90-4. ceramic glazes.60) 3. Aerosolized lead is either inhaled or ingested after it is deposited on surfaces and food crops.40 (1.50) 4.50-5.87 (1.50 (2.10 (1.10) 1.70 (3.50) 2.30 (4. blue-gray metal that occurs naturally in soils and rocks.50 (3.36-1.00) 2.50) 7.10 (2.50-2.10-3.60 (2.20) 2.30-2.40) 2.70) 3.900 (.60) 1. Lead is most often mined from ores or recycled from scrap metal or batteries. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.10 (3.51 (1.10 (2.50) 1.10-1. Before the 1980’s.20 (3.00 (5.20-4.75) 1.80 (5.20 (3.60-2.00-2.50 (4.70-1.49-1.60-2.69) 1.66 (1.40-6.78 (1.80 (4.80) 2.00 (4.40-1.80 (1.60) 4.90-4.50-1.00 (3. plastics.50-6.20) 4.20) 1.30 (1.36-1.10-4.90 (3.66) 1.80 (3.60-1.81) 1.30 (2.900-1.40-1.60) 1.90) 2.60 (3.40 (3.50-3.50-4.70) 3.40) 2.62-1.10-2.90 (2.50-1.70 (2.60) 3.90 (3.90) 2.80 (1.986) .60 (2.43 (1.43 (1.00) 1.20 (3.30-6.40-1.10-2.70 (1.00) 3.60) 3.50) 5.60 (1.70-1.50-5.50-2.75 (1.20 (2.50 (1.80-4.51) 1.50 (2.80 (5.30) 5.10-1.50) Sample size 7970 8945 8373 Age group 1-5 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 2. Elemental lead can be combined with other elements to form inorganic and organic compounds.40 (1.43-1. and 0.93-2.10-2.70) 4.90) 1.30 (3. ammunition.00) 1.00) 2.40) 1.50 (2.70) 1.48) 1.65 (1.52-1.60) 4.80 (4.96-2. Since lead has been eliminated from gasoline.10) 2.10 (1.80 (2.90-4.30 (2.90) 3.00) 2.00 (1.70 (2.80) 1.10-1.17) .43) 1.75-2.50-2.55-1.28.60 (2. leaded glass.30-1.70-5. 7439-92-1 General Information Elemental lead is a soft.80) 3.69 (1.60) 2.00-4.20) 3.00-5.50) 5.30 (1.14-1.40-3. population from the National Health and Nutrition Examination Survey. lead was added to gasoline and residential paints and used in soldering the seams of food cans.70-6.14-1.80) 2.45 (1.30 (4.80) 1. Lead has a variety of uses in manufacturing: storage batteries.10 (1.60 (1.46 (1.90 (1.60 (2.Metals Lead CAS No.40-5.10) 3.40) 3.90) 2.30) 2742 2268 2085 1842 2219 2293 2716 3806 3478 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.30-1.20-3.40-2.90 (4.80 (1.20 (3.10 (4.3.40 (2.37 (1.80) 1.40 (1.10) 1.40 (2.00) 2.60 (1. dense.10) 4. such as lead phosphate and tetraethyl lead. interval) 1.50 (4.946 (.20 (3.50-1.10-3.30 (2.30 (4.00) 1.40-1.32-1.40-2.20 (2.70) 1.30-2.50-1.90 (2.91) 1. the main source of lead exposure for the general U.878-1.10-4.37-1. solders.60-6.70) 4.10-2.50 (1.52-1.89) 1.50-2.72) Selected percentiles ( 95% confidence interval) 50th 1.30 (2.90-2.00-6.80-3.20) 4.10) 3.60-4.09) 1.70) 2.60) 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 2.69 (1.50) 4.69) 1.80-3.30-2.80 (2.90 (3. Lead was used in plumbing for centuries and may still be present.40 (4.80-4.45-1.00) .90 (1.80) 1.39-1.20 (1. In the past.40) 2.20-3.75-1.70) 4.77 (1.90) 2.55 (1.00) 3.20-3.10-8.53) 1.20 (1. adult lead exposures tend to be limited to Blood Lead Geometric mean and selected percentiles of blood concentrations (in µg/dL) for the U.70-1.12-1.00) 4.20) 3.10) 3.02) 1.50 (3.25 (1.20-2.10 (2.40) 4.40-3.60 (2. see Data Analysis section) for Survey years 99-00.50) 1.80-4.60 (1.60) 5.80-5.60 (2. and 03-04 are 0.90) 1.31) 1.70-3.70-2.20) 3.90) 1.20 (1.40) 2.90-2.70 (3.95) 1.50 (2.60) 2.80 (1. respectively.90) 2.43) 1.20-6.60) 3.90-2.60) 1.60 (1. population was aerosolized lead emitted from combustion engines that used leaded gasoline.40) 1.20 (4.60-4.40) 5.60 (3.30-1.00-1.87) 1.62 (1.20-3.00) 6.36) 1.30-1.90-4.00-4.10-6.10-6. 0.60-3.60 (3.00) 4.20) 5.60 (3.60) 4.00) 1.20-1.60) 5.50) 3.60) 1.20 (1.55-1.00 (1.50) 1.70) 1.90-6.800-1.30 (1.70 (1. antique-molded or cast ornaments.80) 1.71-1.00-4.00 (2.60 (1. metal alloys (e.70 (1.30 (2.90 (3.60 (4.70) 1.83 (1.25) 1.40-6.50) 2.20 (3.10) 1.56 (1.10) 5.70) 4.3.60) 2.80 (1.00 (6.10-2.20) . brass.04-1.20-1.70) 1.60-1.80) 3913 4339 4132 4057 4606 4241 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1. 212 Fourth National Report on Human Exposure to Environmental Chemicals .30-5. and for radiation shielding.14-1.80 (1.80) 2.90-3.70-4.90-2.60-1.S.39) 1.00) 5.60) 2.00 (4.90 (3.52 (1.70 (1.30 (2.80) 2.30) 2.60-1.10-2.

lead-contaminated dust in indoor firing ranges. population from the National Health and Nutrition Examination Survey. 2000).20) 1.10-1. 1991).680) . respectively.616) .900) .75) 4.02 (. battery and radiator manufacturing) and recreational sources.800-1.700) 1.59) 1.941) .41) 2.00) .700-.642 (.06) . and contact with soil.80) 2.20 (2.659 (. Fourth National Report on Human Exposure to Environmental Chemicals 213 .13-3.620 (.40-5.540-.40) 2.33 (2.40 (2.900-1.90 (1.700 (.960-1.50-2.840 (.677 (.22) 1.558 (. 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.90 (2.80 (2.40-1.30-1.900) .680-.785) .752 (.30) 2.10-1.700 (.50-2.688 (.749) . pewter utensils and drinking vessels.10 (1.00 (1.691-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.800 (.00) 1. Less common sources of incidental or unique lead exposure are numerous: lead-glazed ceramic pottery.640-.900) .30) 1. the primary source of exposure in children is from deteriorated lead-based paint and the resulting dust and soil contamination (Manton et al.700 (.10) 2.700-1.731 (.710-1.604 (.960 (.12) 90th 2.60 (1.50-2.10-3. or water contaminated by mining or smelting operations. In the blood.00 (1.62-4.86) 1.14-1.808 (.600-.40 (2.21 (2.1.700) .75) 3.960-1.10-1.80) 1.857) .60-1.625-.20 (1.00) 2. dust.23) .30 (3.600-.10 (1.91) 2.62) Total .04 (.64) 2.13) .04) 2. stained glass framing.701) .60 (1. CDC.00-2.900 (.10-1.80) 3.40 (1.00 (1.27 (1.40) 1.955-1.40) 1.745-.19 (1.40-1.915-1.40) 2.10-3.708-.14 (1.03 (1.600 (.800 (. which is the site of approximately Urinary Lead Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.940 (.931) .00) .800) .600-.900-1.11) 2.00) 2.30) 2.10) .70) 3.900-1.90) 1.00-1.00-2.80) 2.S.900) .90-4.04 (.30-1.59-2.753 (.815 (.80-2.800) .613) .572-.80) 1.80) 3.90 (1.17 (1.90-2.50) 1.70 (2.600) .70) 2.90-2.800 (.1.35 (.89) 2.610 (.72) 1.818) .60 (2.30 (1.920 (.671-.60-2.70-2.700 (.00-1.30) 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 1.14 (1.20-1.60-3.20 (1. older plumbing systems with leaded pipes or lead soldered connections.20-1.30) 2.637-.70) 3.690) 75th 1. and 0.29 (2.680-.556-. interval) .10 (.40) 1.800) .60-3.33. lead-based painted surfaces undergoing renovation or demolition.30-2.40) 2. However.90-2.700-.20 (1.49 (1.40-2.50-3.g.10-5.900) .00 (1.20) .11 (1.990) 2.50 (1.591 (.60 (1.70) 1.20 (2.10 (.640 (.90-3.00) .60-2.535-.40 (2.10-3.651) .00-2..641-.04-2.630 (.Metals occupational (e.70-3.90-2.49) 340 368 290 719 762 725 1406 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 . see Data Analysis section) for Survey years 99-00.80 (1.50 (2.80) 2.78-2.660) .29) 2.66 (2.833-1.70 (2.50) 1.579-.10-1.20) .40 (1. Small amounts of environmental lead also may result from burning fossil fuels (ATSDR.50-1.30) 1.52 (1.90 (2.82 (2.50 (2.10 (. lead-containing folk remedies and cosmetics.738) . Approximately half of the absorbed lead may be incorporated into bone.52-1.850 (.674) 1.40 (1.20-2.40 (2.718) .910-.90 (2.506-.730 (.30) 1.30) . 01-02.30) 1.700 (.10) . Lead is absorbed into the body after fine lead particulates or fumes are inhaled.620) 1.580-.70) 1.600-.03-2.920 (.90 (1.40) 3.600 (.590 (.97) 4. or after soluble lead compounds are ingested.990) 1. 0.573 (.20) 1.650) 1.729-.10) 2.564 (.23-4.810-1.70 (2.605) .848 (.628) 1.700-.822-1.40 (1.800-1.10) 1.70) 1.923 (.00-1.30-1.560-.636 (.02) 1.80-3. Children may also be exposed to lead brought into the home on the work clothes of adults whose work involves lead.44-2.986) .40) 1.800-.862) .00) .935) 1.700 (.766 (.800) .09) 1.00 (.60 (1. imported children’s trinkets and toys.50) 1.31 (1. absorbed lead is bound to erythrocytes and then is distributed initially to multiple soft tissues and eventually into bone.30) 1.86 (1.40-3.31-3.710-.30-3.80-2.90) 2.553-. bullet fragments retained in human tissue.80) 1.970-1.80 (1.589-.700-.50 (1.579-.625 (.24-1.480-.900 (.00 (2.10 (1.20-2.20 (2.540 (.32 (1.795 (.500-..526-.80) 2.600-.73 (1.40) 2.90) 2.773) .50) 2.900 (.90-3.820-1.30-1. 2007. and 03-04 are 0.66 (2.50) 2.40) 1.20-1.828) Selected percentiles ( 95% confidence interval) 50th .52-1.800) .700-.595-.82 (1.40-1.90) 2.680) Sample size 2465 2690 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.07-1.900) .833 (.20 (1.60) 2.661-.800-.20 (3.80) 2.20 (1.30 (2.20) 1.18-1.800 (.27) 1.10 (1.50 (2.40 (1.50) 3.600) .790 (.30-5.51) 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.78-2.07 (.04) .20) .86-2.40-1.33-2.78-2.20) .70 (1.20 (1.570-.86) 95th 2.695 (.757-.70 (2.900-1.

342-.06 (1.41-1.617-.19) 1.677) .79 (1.56 (1.988 (.28-1.44 (1.22) .10) 1.03 (.828-1.655) 75th 1.89-2.15) 1.07) .96 (1.605-. 1991.988-1. hair.97) 1.39-1.774 (.404 (.870 (.06 (.53-1.50-1. BLLs near 10 µg/dL can affect blood pressure in adults and neurodevelopment in children (Bellinger.608 (.18) 1.97) 1.621 (.10 (1.938-1.04-3.671 (.62-1.50) 1.44 (1.14 (1..63) 1.03) .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 .571-. kidney injury.24 (1.510-.18) 2.645-.02) 1.31 (2.07 (. In 1991.623 (.03) 2.61) 1.559-.43-1.607-.18) .15-2.Metals 90% of the body lead burden in most adults.404-.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 ..561-.957-1.94-2.579-. and nails (Leggett.997-1.679-.588-.659-.31 (1.701) .05 (1.09) 1.658 (.74 (1.34-1.992-1.97-18.25-1.914-1.33 (1.841-1. 1996).52) 1.657) 1.44) 1.696 (.64-2. 1995.S.632 (. Additional mechanisms include generating reactive oxygen species and altering gene expression (ATSDR.702) .731-. population from the National Health and Nutrition Examination Survey.588-.47) 1.08) .82) 1.551-.41) .593 (.15) 1.655-.78-4.11 (1.893) .64) 95th 2.981-1.963-1.375 (. Schwartz.639 (.383-.00 (1.529-.18) 1.87) 1. The toxic effects of lead result from its interference with the physiologic actions of calcium.746) . encephalopathy.721 (.615 (.655) .17 (.625 (.428) .50-2.17-1.00) .639 (. seizures.725) .11 (1.06) 1.755 (.992-1.633 (.88) 1.586-. through the inhibition of certain enzymes.11 (. 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.639 (.50-2.606-.918 (.603-.990 (.50-2.64 (1. and iron. Equilibrated blood lead levels (BLLs) after chronic intake are associated with certain toxic effects.933) .65 (1.683-.569 (.404 (.52 (1.70 (1.742) Selected percentiles ( 95% confidence interval) 50th .707 (.73) 2.61) 1.31) 1.962 (. based on prospective population studies.55 (1.61) 3.94 (1.48 (1.700-.98) 2.14) 1.654) .01) .608-. and paralysis.20-3.679) 1.933-1.85) 1.667-.975-1.408-.971 (.781-1.43) 2. CDC.43) 1.03) 1.75-2.22-1.698) .47 (1.917-1.718) 1.65-2.763) . O’Flaherty. For instance.33-1.15-3.793-1. with lesser amounts eliminated via the feces. Lead is cleared from the blood and soft tissues with a half-life of 1 to 2 months and more slowly from the skeleton.03) 1.37-1.37-1.742) .838) .914 (.53) 1.61) 1.667-. 2004.701 (.645-.49 (1.682) .688) . 1993.673) .19-5.77) 2.56-3.15-2.28) 2.734) .66) 2.594-.40-1.88) 2. scant amounts are lost through sweat.898) .45 (1.85 (1.09-1.635 (.98 (1.753) .436) . 2003.03) 90th 1.946-1.02-1.649 (.765) .380-.876-1.38 (2.43 (2.541-.97 (1.75 (2.61) 1.72-2.469 (.720 (.612-.12-1.05-1.78 (2.571-.92) 2.62) 2.00 (.01 (.681-. zinc.43 (1.686) .36-2.11) 1.89-5.88-2.718) . abdominal pain.739) .03) .702-. Approximately 70% of lead excretion occurs via the urine.22) 1.592-.85-2.00 (1.71 (1.938 (.38 (2. interval) .623 (.11-1.432 (.26) 2.609 (.73-2.04) 2.722 (.08) .22) 1.71-2.668-.31) 1.38 (2. 1995).46 (1.69 (1. The skeleton acts as a storage depot.26) Total .79) 2.461) .725) .400) .594-.03 (.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 .644 (.644) .601-.20) .676) . Nash et al.72-2.33) 2.796-1.693 (.615 (.83 (2. Lead can cross the placenta and enter the developing fetal brain.20) .79) 1. 1993).720 (..652 (.722 (.496 (.703) .887 (.07-1.67-4.812-1.828) .851) .62-3.08-2. and through binding to ion channels and regulatory proteins.85-2.10 (.05 (.730) 1.25-1.58) 1.62-2.98-2.641 (. Staessen et al.68 (1. BLLs and associated toxic effects differ in children and adults.702) .22-2.03-2.83) 1. Large amounts of lead in the body can cause anemia.583-.677 (.72) .979 (.460-.708 (.587-.603 (.622 (.46 (2.648 (.639) .710) . with a half-life of years to decades.03) 2.86 (1.66 (1.810 (.790) .06) .03 (.758) .05-1.59-3.63) 4.47 (2.51 (1.55 (1.603-.712 (.33) 1.31 (1.11) .03 (1.677-.604-.18 (1.709 (.64) 2.09-1.0) 3.492-.50 (1.862-.638 (. and approximately 40 to 70% of lead in blood comes from the skeleton in environmentally exposed adults (Smith et al.508) .56) 3.977) 1.29 (1.853-1.88) 2.27 (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 1.918-1.681-.882-1.535) .51) 1.914 (.11 (.56-2.00 (1. 2007). Survey years 99-00 01-02 03-04 Geometric mean (95% conf.926 (.670) 1.920-1.09-1.66 (1.88 (1.900 (.667) .28) .800-.940 (.23 (1.35) 2.618 (.698) .41 (1.

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.9 µg/dL) and percentage of children with BLLs greater than 10 µg/dL (1. Many animal studies have established the multiple neurotoxic effects of lead (ATSDR. However. At low environmental exposures. the geometric mean BLL was 3. Results of studies of adults with either occupational or environmental lead exposure have shown consistent associations between increased BLLs and increased blood pressure (Nash et al. and organic lead compounds not classifiable with respect to human carcinogenicity. 2006). 1995) and associations between increased bone lead concentrations and blood pressure (Hu et al. Schwartz et al.. adult population has similar or slightly lower BLLs than adults in other developed nations (CDC. adults in the 19992000 NHANES sample (Apostoli et al. including minority race or ethnicity.S. 2003). premature delivery. 2009). with overt encephalopathy.. Overall.S. environmental levels) and health effects is available from ATSDR at: http://www. Data submitted through state public health programs from 2006 showed that 1.5 per 100. subtle or nonspecific neurocognitive effects have been reported at BLLs as low as 20-30 µg/dL (Mantere et al. Pirkle et al.3 million children tested had BLLs of 10 mg/dL or higher (http://www.cdc. which is an 84% decline.Metals µg/dL or higher as the level of concern in children. Jones et al (2009) showed that the prevalence of BLLs of 10 µg/dL or greater decreased from 8. Korrick et al. High dose occupational lead exposure. 1999). 2002. NTP considers lead and its compounds reasonably anticipated to be human carcinogens.6% in NHANES 1988-1991 to 1. 2002a). particularly in the skeleton. 2003. 1996.S.xls). the prevalence rate has declined annually since 1994 (CDC. Staessen et al. 2000).S..gov/toxpro2.. and spontaneous abortion (Baghurst et al.atsdr. 1994). and low family income (CDC.g. though there is greater individual variation in urine lead than in blood and greater potential for contamination. Payton et al. urban residence. adult residents.07 µg/dL (Becker et al. 1991. In occupationally exposed adults.. the national prevalence rate for adults with BLLs 25 mg/dL or higher was 7.. A general population survey of adults in Italy tested in 2000 found BLLs slightly more than double those reported for U. higher than 100-200 µg/dL). Borja-Aburto et al. 2000)... and peripheral neuropathy generally occurring at much higher levels (e.000 adults.. both the geometric mean (1. The U.4% of children had BLLs of 10µg/dL or higher (CDC.6%) were lower than those from NHANES 1991-1994. A general population survey of adults Germany in 1998 reported a geometric mean blood lead concentration of 3. 1998). Low level environmental lead exposure may be associated with small decrements in renal function (Kim et al. A decrease in BLLs is evident also in adult NHANES results reported over past decades (CDC. 1984. 1996. 2003. 1996.. Lanphear et al. 2006). 2003.cdc. Recent studies have suggested that neurodevelopmental effects may occur at BLLs lower than 10 µg/dL (Canfield et al..S. almost double the geometric mean of 1.7 µg/dL and 4. Urine levels may reflect recently absorbed lead... when the geometric mean BLL was 2. Bellinger 2005. Jones et al. 2007). 2001). Information about external exposure (i.. 2005b). Telisman et al. CDC.html. adults in the 1999-2000 NHANES sample. 1999). residing in housing built before the 1950’s. For example.21% of approximately 3. reduce sperm count. 2005a)... Temporal declines in children’s BLLs have been found in other developed countries (Wilhelm et al.75 µg/dL in U.0 µg/dL in females (Soldin et al.. lead in women may be associated with hypertension during pregnancy. More recently.. and decrease fertility (Alexander et al. approximately 11.. Muntner et al. Both drinking water and ambient air standards for lead have been established by the U.. 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.e. BLLs greater than 10 µg/dL continue to be more prevalent among children with known risk factors. Schwartz. IARC considers inorganic lead compounds probable human carcinogens. 1995.000 higher-risk children and adolescents who were tested from 2001 to 2002 at an urban medical center had higher BLLs than the NHANES sample.. 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. EPA. Biomonitoring Information Blood lead measurement is the preferred method of evaluating lead exposure and its human health effects. Fourth National Report on Human Exposure to Environmental Chemicals 215 . 1987. seizures.S.2 µg/dL in males and 3.. may alter sperm morphology. respectively. BLLs reflect both recent intake and equilibration with stored lead in other tissues. usually with BLLs greater than 40 mg/dL. 2005b. Surveillance data reported by U. Workplace standards and guidelines for lead exposure and monitoring have been established by OSHA and ACGIH.4% in NHANES 1999-2004.. In NHANES 1999-2002 in children 1-5 years old.gov/nceh/lead/surv/database/State_ Confirmed_byYear_1997_to_2006. 2002).

McMichael AJ. Ewers TG. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans.htm. et al. 4/14/09 Alexander BH. MMWR Morb Mortal Wkly Rep 2006. Atlanta. Lead and hypertension in a sample of middle-aged women. Kaufman JD. Caldwell KL. Recommendations from the Advisory Committee on Childhood Lead Poisoning Prevention. JAMA 1996. 2005. Farias P. 4/14/09 Centers for Disease Control and Prevention (CDC). Vimpani FB. Jacobson JL. Mantere P.113(4):1016-1022. Pediatrics 2004.101(7):598-616. Lepom P. Ganzi A.89:330-335. IARC Monogr Eval Carcinog Risks Hum 2006. Cox C. Int J Hyg Environ Health 2002. Semen quality of men employed at a lead smelter. Am J Public Health 1999. 1991 [online].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. 4/14/09 Centers for Disease Control and Prevention (CDC). Available at URL: http://www. Brody DJ. Kuehnemann TJ. Pediatrics 2009. Jones RL. Public Health Rep 2000. Available at URL: http://www. Managing Elevated Blood Lead Levels Among Young Children. Third National Report on Human Exposure to Environmental Chemicals. Blood lead and chronic kidney disease in the general United States population: 216 Fourth National Report on Human Exposure to Environmental Chemicals . Age-specific kinetic model of lead metal in humans. Batuman V. Apostoli P. Cox C.275:1177-1181. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Hänninen H. N Engl J Med 2003. Rotnitzky A. The relationship of bone and blood lead to hypertension. Hunter DJ.cdc. Kim R. Payton M. Environ Res 2000.gov/nceh/lead/publications/ books/plpyc/contents. Seiwert M. Manton WI.cdc.1542/peds:2007-3608. Scand J Work Environ Health 1984.73:409-420. 1999-2002. Roberts RR. Lanphear BP. Neurotoxicol 1987. 4/14/09 Centers for Disease Control and Prevention (CDC). Ronchi L. Dietrich K.26:359-371. Hernberg S.54(20):513-516. Available at URL: http://www. Jusko TA. Bavazzano P. Cognitive deficits with blood lead concentrations < 10 µg/dL in US children and adolescents.htm. Neri A.gov/nceh/lead/ CaseManagement/caseManage_main. A prospective follow-up study on psychological effects in workers exposed to low levels of lead. Bellinger D.10:43-50. Blood lead reference values: the results of an Italian polycentric study.87:1-471.gov/mmwr/preview/mmwrhtml/ mm5532a2. Hu H. Pirkle JL. Meyer PA. Atlanta (GA).82:60-80. Neurodevelopmental effects of postnatal lead exposure at very low levels. Speizer FE. Preventing Lead Poisoning in Young Children. 1988-2004.atsdr. Kaus S.348:15171526. 2005b. Reese YR.275(15):1171-1176. Robertson EF. Am J Epidemiol 1999. Blanco J. Baj A. Cory-Slechta DA. Hertz-Picciotto I. A longitudinal study of low-level lead exposure and impairment of renal function: the Normative Aging Study. Becker K. et al.287:1-11.55(32):876-879. Baghurst PA.123:e376-e385. Checkoway H. Available at URL: http://www.53:411-416. Bellinger D. Lead.cdc. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Aug 2007 [online].htm.gov/toxprofiles/tp13. Ga. Centers for Disease Control and Prevention (CDC). Intellectual impairment in children with blood lead concentrations below 10 µg/dL. 2002 [online]. Stanek KL.205:297-308.htm. MMWR Morb Mortal Wkly Rep 2005a. Sparrow D. Vupputyuri S. Rojas LM. Weiss ST. Canfield RL. Teratogen update: lead and pregnancy. Adult blood lead epidemiology and surveillance—United States. Aro A. Wigg NR. Homa DM. Angle CR. Lanphear BP. Chiodo LM. Trends in blood lead levels and blood lead testing among US children aged 1 to 5 yeas.8(3):395-401. Luukkonen R. Borja-Aburto VH. Sparrow D. Hu H. Schulz C. Auinger P.150(6):590-597. Neurotoxicol Teratol 2004.cdc. CDC. Krause C. 4/14/09 Centers for Disease Control and Prevention (CDC). Korrick SA. Coresh J. Jacobson SW. Environ Health Perspect 1993. References Agency for Toxic Substances and Disease Registry (ATSDR).cdc. Blood lead levels measured prospectively and risk of spontaneous abortion. Blood lead levels—United States. Occup Environ Med 1996. Inorganic and Organic Lead Compounds. Muntner P. Weiss ST. Wager C. et al. Hu H. van Netten C. et al. Leggett RW. Muller CH. Toxicological profile for lead. Rios C.115:521-529. 2003-2004. et al. Available from URL: http://www. doi:10. Birth Defects Research (Part A). Rotnitzky A. Sci Total Environ 2002. Henderson CR. JAMA 1996.html. Korrick S. gov/mmwr/preview/mmwrhtml/mm5420a5. The Port Pirie cohort study: lead effects on pregnancy outcome and early childhood development. Atlanta (GA). Acquisition and retention of lead by young children.

Rubin R. Kinetics of lead disposition in humans. Am J Epidemiol 1994. Schwartz J. Wilhelm M. dimercaptosuccinic acidchelatable lead. Semen quality and reproductive endocrine function in relation to biomarkers of lead. Use of endogenous.118:16-29.153(5):453464. Brody DJ. Kaufmann R. Exposure of the U. et al.106:745-750. Revised and new reference values for arsenic. Schwenk M. cadmium. Flegal AR. Hu H. Am J Epidemiol 2001. Association of blood lead. J Hum Hypertens 1995. Sherwin R. Amery A. 50:31-37.Metals results from NHANES III. Roels H. Clin Chim Acta 2003. Soldin SJ. et al. Kidney Int 2003. Lead. JAMA 2003. Blood lead concentrations in children: new ranges. blood pressure.104(1):60-66. Smith DR. Cvitkovic P. Soldin OP. Gavella M. Int J Hyg Environ Health 2006. Lustberg M. Sparrow D. Pirkle JL. Gunter EW. Telisman S.108(1):45-53. and copper in men. Nash D. Physiologically based models for bone-seeking elements. and mercury in blood or urine of children: basis for validation of human biomonitoring data in environmental medicine. cadmium. Environ Health Perspect 1996. population to lead: 1991-1994.327:109-113. Magder L. Environ Health Perspect 1998. Lauwerys RR.209:301305. Schwartz BS. Blood lead. and hypertension in perimenopausal and postmenopausal women. Rocic B. Environ Health Perspect 2000. Lee GS.289(12):1523-1531. O’Flaherty EJ. Low-level lead exposure and renal function in the Normative Aging Study. IV. Paschal DC.140:821-829. Lee BK. Pizent A. Hanak B. Payton M. Fourth National Report on Human Exposure to Environmental Chemicals 217 . Low-level lead exposure and blood pressure. stable lead isotopes to determine release of lead from the skeleton. zinc.9:303-327. Lee SS. Stewar WF. Hickman T. blood pressure and cardiovascular disease in men. Schulz D. Kaufmann RB. Toxicol Appl Pharmacol 1993. Hwang KY. Osterloh JD. and tibia lead with neurobehavioral test scores in South Korean lead workers.63:1044-1050. Staessen JA. Jurasovic J. Arch Environ Health 1995. lead. Weiss ST.S.

40-2.S.363-. merbromin).700-. Woods et al. Elemental mercury is a shiny.2.877 (.689-.672) .60-2.00) 3.50) 5. Elemental mercury is released into the air from the combustion of fossil fuels (primarily coal). 1998.40 (3.50-2.70-2. which can bioaccumulate in aquatic and terrestrial food chains.00-1.00 (1.50) 2.50-1.g.714-.50) 1.400-.700) .800 (.500 (.40-2.70 (1.. to form inorganic mercury compounds or salts.40-3.90-3. 1994. such as chlorine (e. 1999 . and is distributed to most tissues.. Survey years 03-04 Geometric mean (95% conf. and mercury compounds are still used as preservatives (e.903) Selected percentiles ( 95% confidence interval) 50th .10-3..40 (4.500 (.12) . or oxygen.700-.600 (. and mining and smelting.00 (.927) . synthetic organomercury compounds were once used in pharmaceutical applications. elemental mercury is absorbed mainly by inhaling volatilized vapor. mercuric chloride). 1980..400 (.00 (.50-3. The ingestion of methyl mercury.400-.30-6.800-1.20-4.30-5.800-1.703-. and dental amalgam.700) .70 (3.574) .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 .900) 75th 1. IARC. Inhalation of elemental mercury volatilized from dental amalgam is a major source of mercury exposure in the general population (Halbach.372) .80 (1.90 (1.00) 1.900) .60) 2085 2293 3478 Limit of detection (LOD.g. Also. phenylmercuric acetate) or topical antiseptics (e.800 (. sphygmomanometers and barometers.30) 1. which create an episodic potential for volatization and inhalation of mercury vapor. interval) .700-.30 (1.600) 1.776 (.500-.30) 5.900) 1.80 (3.800-1.00 (2. Kingman et al.20) 2. Poorly absorbed from the gastrointestinal tract.60-6. with the highest concentrations occurring in the kidneys (Barregard et al.60 (1.Metals Mercury CAS No.40) 3. In addition. Inorganic mercury exists in two oxidative states (mercurous and mercuric) that combine with other elements. 1993).80 (1. see Data Analysis section) for Survey year 03-04 is 0.80) 3. silver-white liquid (quicksilver) obtained predominantly from the refining of mercuric sulfide in cinnabar ore.800-1.814 (. water can be contaminated by the direct release of elemental and inorganic mercury from industrial discharges.655-.80 (1.900 (.300-.70 (4.900) 1. Accidental spills of elemental mercury.80) 1.30 (2. predominantly from fish and other seafood.60 (2.90) 3.20 (2.30) 4132 4241 03-04 03-04 03-04 .00 (2.30-4. thimerosal.30-2.860-1.00 (2. constitutes the main source of dietary mercury exposure in the general population.80) 4. Some cosmetic skin creams from countries other than the U.900) 1.30) 3. an organic form of mercury.70 (1.418-. 218 Fourth National Report on Human Exposure to Environmental Chemicals .00) .300) .490 (. The kinetics of the different forms of mercury vary considerably.90) 95th 4.40) 1.20-4.60-5.10) .90 (1.800 (.02) .919) .30) 1.500) . elemental mercury is used in rituals practiced in some Latin American and Caribbean communities.90) 90th 3.60-6..40-1.563 (. 2002).40 (3.500-. Apart from methyl mercury. Other major uses include electrical equipment (e. Hursh et al. Imported folk and alternative medicines occasionally are contaminated with inorganic mercury. have often required public health intervention (Zeitz et al.800 (.. inorganic. and organic forms.50) 4.979 (.300 (.60) 1.60-3.60) 1.800-1.326 (.00 (. electrical lamps.. solid-waste incineration.419 (.700-.40-1.g.00) 4.700 (. 7439-97-6 General Information Mercury is a naturally occurring metal that has elemental (metallic).90 (4. may contain inorganic mercury.781 (. Inorganic mercury compounds such as mercuric oxide are used in producing batteries and pigments and in synthesizing many organic chemicals.40 (4.60 (1.484) .285-. thermometers.20-3.00) 1. population from the National Health and Nutrition Examination Survey.700-.886) .00-5.797 (. After elemental mercury is absorbed. Atmospheric elemental mercury can be deposited on land and water.00 (.753-1.472-. sulfur. Metabolism of mercury by microorganisms in aquatic sediments creates methyl mercury. Elemental mercury is used to produce chlorine gas and caustic soda for industrial applications.S.30) 3.70) 911 856 2081 4525 03-04 03-04 .g... thermostats and switches). it is oxidized in Total Blood Mercury—2003-2004 Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U. 2007).

667 (.300 (.90 (4.30-2.00) 6..00) 4.200 (. 1994)..60 (3.00-2.14.06 (.20-3. Smith and Farris.10 (. 1999-2002.265-.70) 4.299-..20 (2.600) .820 (.800 (.900 (. 2004. 1990). Suzuki et al.800-1.70-6. the transfer Total Blood Mercury−1999-2002 Geometric mean and selected percentiles of blood concentrations (in µg/L) for males and females aged 1 to 5 years and females aged 16 to 49 years in the U. 1992).318 (.50) 1.726-1.30-4. 1998). Methyl mercury enters the brain and other tissues (Vahter et al.00 (3.500-. After exposure to elemental mercury. Vimy et al. Smith et al.10) .40-2.. 1998).00-6.10) 1. 1971).40) 2.900 (.400-.738-.00 (2.200-..475) .. McDowell et al. 1994) and then undergoes slow dealkylation to inorganic mercury.80-3. 1999). Vahter et al.200-.00 (2.Metals the tissues to mercurous and mercuric inorganic forms..50 (1.70-5.40 (1. 1984. Jonsson et al.10 (.297-. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.20) . excretion of mercury occurs predominantly through the kidney (Sandborgh-Englund et al.824) 1.919) .23) .377 (. 1973).10 (3.944 (.50-3.500 (.20-2.20 (.35 (1. 1991.30-4.300) .700-1. 2005).30-6.50-2...300 (. and a useful marker of exposure in epidemiologic studies (Grandjean et al.00) 1.500-.900-1..70) 4. Miettinen et al..30-11.10-1. Transplacental transport of methyl mercury and elemental mercury has been demonstrated in animals (Kajiwara et al.500-1.10-3.900 (. interval) Selected percentiles (95% confidence interval) 50th .407) .70-3. 1995.800 (.697-.0) 4.300) .50) 2.90) 2. 16-49 years) Mexican Americans Non-hispanic blacks Non-hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .60 (1. Inorganic mercury and methyl mercury are distributed into human breast milk in relatively low concentrations.700 (.40) 5.60 (3.40-2. The half-life of inorganic mercury in blood is similar to the slow-phase half-life of mercury after inhalation of elemental mercury.825-1.14 and 0.70) 1. Geometric mean Survey years (95% conf.600 (.369) 1.300 (.30-5.329 (..40-1.S.73) 1.90 (3. and the newborn’s levels decline gradually over several weeks (Bjornberg et al.269-.500-.70-3.871-1.27) . National Health and Nutrition Examination Survey.30 (.30-3.60 (2.00 (1.00) 1..800) 1.30) 1.600) .800) . The slow-phase half-life may be several weeks longer in persons with chronic occupational exposure (Sallsten et al.200-.664-1.374) .700-. Lesser penetration of inorganic mercury occurs through the bloodbrain barrier than occurs with either elemental or methyl mercury (Hattula and Rahola.50) 3.29) . 1994.30 (1.00-2.377) .500-.833 (.00-3. 1992 and 1999.01) .00-2. and peak urine levels can lag behind peak blood levels by days to a few weeks (Barregard et al.80 (1.268-. Excretion occurs by renal and fecal routes. 2003).395) .70 (1.10 (1.900-1.541-..00) 2.80) 579 527 370 436 588 806 Limit of detection (LOD.3) 4. 2003).940) Race/ethnicity (females.800) 75th . Human pharmacokinetic studies indicate that methyl mercury declines in blood and the whole body with a half-life of approximately 50 days...20-3.800 (.307 (.30) 3..90) 90th 1.700-. Less than 15% of inorganic mercury is absorbed from the human gastrointestinal tract (Rahola et al.30) 1. 1993).30 (1.90 (1.300) .800-1.70-5.200-.90 (4.50) 1.200-.40) 1.70 (1.60) 3. 1992. a measure of accumulated dose (Cernichiari et al.300) .700) 2.50) 95th 2.700-1.60 (1.. population.30-6. 1996).10 (1.800) . Mercury levels in the cord blood are higher than in the mother’s blood (Stern and Smith..10 (1.00) 7.70 (1.10) .06-1.90) 3..500 (.10 (5.700 (.00) .90) 2.90 (1.700 (.256-. for both acute and chronic exposures.90) 5.30-6.700 (.02 (.20) 1.00 (2. 1969.200 (.60) 1. Fourth National Report on Human Exposure to Environmental Chemicals 219 . with most elimination occurring through in the feces (Sherlock et al. Methyl mercury is incorporated into growing hair..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 .40 (1.500-.20-3.30 (1.800-1. 1996. 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. Sandborgh-Englund et al. thereafter.00-1. 1975.60 (1. The fraction of methyl mercury absorbed from the gastrointestinal tract is about 95% (Aberg et al.50 (2.50-12. 1993).20) .800) 1.300) .7) 4. Myers et al.317 (.300) . urinary mercury levels decline with a half-life of approximately 1-3 months (Roels et al..343 (.60) 1.60) 2.200-.20-11.80 (3.300 (.80) 1.

and progressive constriction of the visual fields.600 (. insomnia.600 (. Sakamoto et al..600 (. and sleep disturbance (Bidstrup et al. sensory impairments.. 2000. 2005.600-.600 (.500-. 2000.600-. dysarthria.800) .600 (.700) . 2000).. typically after a latent period of weeks to months. Oskarsson et al. Smith et al. Sakamoto et al. hearing impairment.700 (. Bellinger et al.. Rice. and pinkish discoloration of the hands and feet (Tunnessen et al.600) . anorexia.700) 2007 2240 3406 Limit of detection (LOD. Acute..700 (. population from the National Health and Nutrition Examination Survey. particularly irritability. the existence of a causal relation is unresolved (Chan and Egeland. 2005). ataxia.42.700-. 1963)..600 (. Although recent investigations have suggested a possible link between chronic ingestion of methyl mercury and an increased risk for cardiovascular disease. altered physical growth.500-.. Overt poisoning from methyl mercury primarily affects the central nervous system.600) * 03-04 03-04 03-04 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . irritability. and cerebral palsy (NRC.600) . The health effects of mercury are diverse and can depend on the form of the mercury to which a person is exposed and the dose and the duration of exposure. pain in the extremities.600 (. dysarthria.600) . Vupputuri et al. causing parasthesias. 1970.500-..500 (. Mercury levels in breast milk also decline in the weeks after birth (Bjornberg 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 ..500-. see Data Analysis section) for Survey year 03-04 is 0.500-. which may vary for some chemicals by year and by individual sample. cerebellar ataxia.500 (<LOD-.S. 2002. 2003).800) 4015 4132 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD .600-. Low-level exposure from dental amalgams has not been associated with neurologic effects in children or adults (Bates et al. hypertension. and neurocognitive and behavioral disturbances. Large amounts may cause irritant or corrosive effects on the gastrointestinal tract (Sanchez-Sicilia et al. 1993).600) .700-.500-. < LOD means less than the limit of detection. 1998.700 (. Stern 2005. Factor-Litvak et al.500 (<LOD-. 1995.700-.. 2006. gingivitis.700 (. the most prominent effect is on the kidneys where mercury accumulates and may lead to renal tubular necrosis.600) .800) 792 842 2060 4453 03-04 03-04 * * < LOD < LOD < LOD < LOD .500 (.500-. 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. At levels below those that cause acute lung injury.. limb deformities..600-.800) .500) .600 (.600) . 1996). depression. fatigue. 2006. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 1951. The constellation of findings may include anorexia. Drexler and Schaller. Once absorbed. 1995.. high-dose exposure to elemental mercury vapor may cause severe pneumonitis..700 (.Metals may be more efficient for inorganic mercury (Grandjean et al.. 220 Fourth National Report on Human Exposure to Environmental Chemicals .500-. Occupational exposure to elemental mercury vapor has been associated with subclinical effects on biomarkers of renal dysfunction (Cardenas et al. and a drinking water Inorganic Blood Mercury Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U. Acrodynia is a sporadic and predominantly pediatric syndrome historically associated with calomel (mercuric oxide) in teething powders and occasionally other inorganic forms of mercury. 1983). short-term memory loss. 2004. DeRouen et al. maculopapular rash.. Workplace standards for inorganic mercury exposure have been established by OSHA and ACGIH. Rissanen et al.. High-level prenatal exposure may result in a constellation of developmental deficits that includes mental retardation.700 (. Smith et al. Inorganic mercury exposure usually occurs by ingestion. Survey Geometric mean (95% conf. 1987). 2004). 2004).600) .. Salonen et al. 2004. In recent epidemiologic studies.600) .600) . interval) Selected percentiles ( 95% confidence interval) Sample 95th . overt signs and symptoms of chronic inhalation may include tremor.500-.

(2000) studied 1216 blood donors in the Czech Republic (896 men and 320 women.52) 2.33 (2.509) .63-2. adult women in several ethnic subgroups (Hightower et al.330-. the median concentration of blood mercury was 0.29) 1.39-3.78 µg/L for adults and 0.60-2. 1998).200 (.89) 3.99-6..406-.480 (.28) 1.gov/mercury and from ATSDR at: http:// www.58 µg/L for 4645 adults.495 (.330 (.416 (.76-3.68 (2.440 (.23) 2. Total blood mercury levels increase with greater fish consumption (Dewailly et al.S.. the developing fetus may be the most susceptible to the effects of ongoing methyl mercury exposure (NRC.447 (. 2009).570) . Mahaffey et al. environmental levels) and health effects is available from the U. Among the three racial/ethnic groups.epa.770-1.358 (.16 (1. 2009).18) 2.01 (.05) 1.66) 3.14.430 (.420 (..330-.14) 90th 2.60 (1.480) 75th 1. although non-Hispanic black females had higher levels than non-Hispanic white or Mexican American females.254 (.e.840) 1.65) 1. These distinctions can help interpret mercury blood levels in people.382-.gov/toxprofiles...340-.08 (1. et al.S.250) .24) 1.433 (.460) . military veterans (mean age 52.304) .530) . In NHANES 19992002.940 (. who participated in a 1998 representative population survey (Becker et al.78-2..580) ..14-2.46 µg/L for children.77-2...549) . Benes et al.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 .85-2.430 (. 1995. slightly higher total blood mercury levels were found in U. 2001. 2003). total blood mercury geometric mean levels in females aged 16-49 years did not change. IARC considers methylmercury to be a possible human carcinogen and elemental and inorganic mercury to be unclassifiable with regard to human carcinogenicity.430) .610-1.16 (. and the age-related changes differed across the groups (Caldwell et al. 2004.350-. average age 33 years.30) 3.890 (.530-.213-..96 (1.930-1. 2001.00 (.492) Selected percentiles ( 95% confidence interval) 50th .S.509) .46) 3.408) . Urine mercury levels increase as more occlusal surfaces of teeth are filled with mercury-containing amalgams (Becker et al. 2000).09 (2. 2006).19 (1. 1997. Information about external exposure (i.476 (. Sanzo et al. 1998).441 (. Biomonitoring Information In the general population.400 (.410-.413-.88 (1.360-. aged 18 to 69 years.396-. see Data Analysis section) for Survey year 03-04 is 0.90) 2.54 (2.9 years).60) 619 713 1066 Limit of detection (LOD.313-. particularly methyl mercury.76-3.03-4.24 (2. A cord blood mercury level of 85 µg/L (lower 95% confidence bound = 58 µg/L) is associated with a 5% increase in the prevalence of an abnormal Boston Naming Test (NRC.96 (1. 2003).700 (.534) . Urinary mercury consists mostly of inorganic mercury (Cianciola et al.07 (. range 40 years to 78 years) had an average total blood mercury concentration of 2. Survey years 03-04 Geometric mean (95% conf. total blood mercury levels declined slightly in non-Hispanic black and Mexican American children.08 (1.31) 2.19 (2.840-1.960 (.76-4.61) 1.31) 1266 1272 03-04 03-04 03-04 .360-. 2002). the total blood mercury concentration is due mostly to the dietary intake of organic forms. Schober et al. EPA. EPA at: http://www.67-3.330-.870-1. During the same survey periods. These men had no occupational exposure to mercury but previously had received dental amalgams at military facilities (Kingman et al.530) . Clinically observable signs of ataxia and paresthesias may occur when blood mercury levels increase to approximately 100 µg/L after methyl mercury poisoning.00) 1. From 1996 through 1998.160-.460 (. However.20 (1.280-.13-2.360 (.34-3.55 µg/L. Over the NHANES 1999-2006 survey periods. and increased slightly in non-Hispanic white children (Caldwell..442-.S. 758 children.463) .. Kingman et al.93 (1.8 years. population from the National Health and Nutrition Examination Survey.05) 3. Urinary Mercury—2003-2004 Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.S.97) 2. total blood mercury increased with age. Fourth National Report on Human Exposure to Environmental Chemicals 221 .88-3..420 (.555) .67-2.870-1.290-. Grandjean et al.23) . interval) .840-1. average age 9.405-.88) 287 722 1529 03-04 03-04 ..26 (1.700-1.370) .cdc.Metals standard for inorganic mercury has been established by U.520) .atsdr.42) 95th 3. A cohort of 1127 U.12 (. In Germany the geometric mean for blood mercury was 0.

1992).28 (.30) 2.508 (.64-2.44) 1.S.784) 1.400) .51-2. population from the National Health and Nutrition Examination Survey.1 µg/L for each surface with a dental amalgam (Kingman et al. military veterans with dental amalgams.476 (. Urinary Mercury (creatinine corrected)—2003-2004 Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.358) .62 (1.11) 1.687) .875-1.455-...32-2..384 (.. Biomonitoring data will also help scientists plan and conduct research on exposure and health effects.06 (. 2006). Survey years 03-04 Geometric mean (95% conf.800-1.391) ..00 (.400-.455) . Czech (Benes et al.969-1. 2006.79) 1.417) .970 (.11) 2.599) .545 (.11-2.217 (.246-.07) 1.463 (. Langworth et al. The ACGIH (2007) currently recommends that urinary inorganic mercury in workers not exceed 35 µg/g of creatinine.485 (.443 (.76 (1.39) 1.333-.588) .404-.Metals 2000).362 (.297 (.225-.13-2. Information about the biological exposure indices is provided here for comparison.768 (.307-. 1988.306 (. 2009).343 (.87) 2. mean urinary mercury was 3.67 (1.301-.196-.525 (. 2005).40-1.255 (.32 (1.522-. among workers with urinary mercury concentrations of 25-35 µg/L or greater (Barregard et al.455-. Levels in U.785-1. representative sample of women aged 1649 years reported in NHANES 1999-2006 (Caldwell.486) Selected percentiles ( 95% confidence interval) 50th .365 (.16) 1.S. not to imply a safety level for general population exposure. An expert-panel report recently prepared for the U.90) 618 713 1066 222 Fourth National Report on Human Exposure to Environmental Chemicals .696 (.S. et al.309-.667-1.347) .630) . Department of Health and Human Services noted that several studies have observed a modest.77 (2.566) . Blood mercury levels of women and children in NHANES 19992006 were also below levels established as occupational exposure guidelines (Caldwell. women of childbearing age have generally been much lower than these levels (CDC. Urinary mercury levels in recent German (Becker et al.532 (.18-1.31 (1.00) 90th 1.464 (.78-4.87 (1.09) 1.03) 2.964-1.13 (1. In the study of U.619-..385-.990) .88-2. 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. ACGIH recommends that the blood levels due to inorganic mercury exposure in workers not exceed 15 µg/L.35 (1.01) 2.21) 1. and on average.447-.67 (1. et al.208-.652) .46-2.392-.265-.61) 1. the urine mercury increased by approximately 0.472-.04-3.86) 95th 2. 2002).280-.23-2.S.376-.276 (.620-.30) 1.616) .909 (. reversible increase in urinary N-acetyl-glucosaminidase.447 (. 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.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 .06 (. Urine mercury and the number of dental amalgams were correlated.537) .88-2.587 (. and Italian (Apostoli et al.56) 1266 1271 03-04 03-04 03-04 .480) .275) .40 (1..54 (2.. interval) . 2009).25 (.498) 75th . a biomarker of perturbation in renal tubular function.714-1. Biomonitoring studies provide physicians and public health officials with reference ranges so that they can determine whether people have been exposed to higher levels of mercury than are found in the general population.41-2.63) 1. 2003).00) 286 722 1529 03-04 03-04 .65 (1.365 (.368) . DeRouen et al.535) 1.391-..79 (1. 1998).289) .12-3..88 (1. 2002) adult population surveys were similar to those in a U.S.

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.92) 3.61) 1.31-1. interval) Selected percentiles (95% confidence interval) Survey years 50th .Metals Urinary Mercury−Females Aged 16-49 Years Old.09-1.624-.04-10.85-3.50-4.526-.831) .610-.16) 5.578-.17) 95th 5.39) Sample size 1748 1960 Age group (females) 16-49 years Race/ethnicity (females.14-2.657 (.99 (2.615 (.670) 75th 1.50 (1.721 (.580 (.24-1.665) Mexican Americans Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .27 (1.799) .742-1.45 (1.450-.553-.S.23-1.790) .631-.87-4.930) .59-5.685 (.39-3.809) .97) 2.68-3.13-4.636-.426-.05 (2.910) .569-.699) 1.81 (3.592 (.63) Sample size 1748 1960 Age group (females) 16-49 years Race/ethnicity (females.909-1.21-3.709) 75th 1.710 (.69 (1.06 (.56) 4.92) 2.14-1. 1999-2002 Geometric mean and selected percentiles of urine concentrations (in µg/L) for females aged 16 to 49 years in the U.637) .656-.77) 2.620 (.45-3.42) 90th 2.691) .420-.53) 595 531 381 442 594 826 Fourth National Report on Human Exposure to Environmental Chemicals 223 .89 (2.03 (.69-3. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.724 (.650) 1.47) 1.84 (2.45) 2.03-2.27-1.540 (.557-.83-3.740 (.502-. National Health and Nutrition Examination Survey.658 (.23-1.97 (1.61-6.579-.832-1. interval) Selected percentiles (95% confidence interval) 50th .850-1.42-3.95 (2.892) . population.18 (3.91-7.62 (3.508-.51) .632 (.48 (2.45-2.81-6.85) 4.664) .92) 4.664) Mexican Americans Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .30 (2.540-.S.600 (.56 (1.30-2.516 (.582-.806) .47) 1. population.32-3.21 (2.665) .710 (.387-.55-3.57-4.97) 2.45) 95th 3.831) .09-1.560 (.41 (2.35 (1.76 (1.22 (. 1999-2002.97) 2.03) 1.650 (.3) 5.21 (1.56) 3.46) 3.686) .68 (3.65) 1.00 (2.709) .560-.410-.04-1.41 (1.772 (.606 (.14.07-2.30 (1.810) .51 (3.00 (3.616-.500-.10-4. Urinary Mercury (creatinine corrected)−Females Aged 16-49 Years Old.46-4.99-2.72) 1.744) 1.24) 6.79) 1.655 (.70 (2.62 (1.25) 2.870) .501-.46 (1.91 (2.622-. Geometric mean (95% conf.650 (.30 (2.522 (.50 (2.710) 1.79) 3.31 (1.719 (.22-3.65-4.580-.824) .41-6.18) 3.99 (3.846) .16-5.45) 2.13 (2.723 (.54) 595 531 381 442 594 826 Limit of detection (LOD.774) .55) 90th 3.475-.14 and 0.44) 3.966) .98 (5.76) 2.52) 3.62 (4.37 (1.15 (2.520-.43-1.42) 2.14) 3.77) 1.605-.596 (.84 (2.15-1.76-5.37) 1.706 (.03 (.07) 1. 16-49 years) 99-00 01-02 .28 (1.10-2.53-3. National Health and Nutrition Examination Survey. Geometric mean Survey years (95% conf.41 (1.520-.32 (1.68) 3.05 (3.565 (.94) 1.00) 2.32) 2.38) 4.639 (.99) 1.760 (. 1999-2002.27 (2.35) . 16-49 years) 99-00 01-02 .07-5.833) .

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Yoshinaga J. 1999-2000. Stern AH. Friberg L. Hall LL. Whittle K. Allen PV. Public health consequences of mercury spills: hazardous substances emergency events surveillance system. The contribution of dental amalgam to urinary mercury excretion in children. Patil LS. Elevation of mercury in human blood from controlled ingestion of methyl mercury in fish. A review of the studies of the cardiovascular health effects of methylmercury with consideration of their suitability for risk assessment. Methyl mercury pharmacokinetics in man: a reevaluation. Longnecker MP.110:129-132. Sinks TH. Amurrio A. Tunnessen WW. Matsuo N.97(2):195-200. Goldberg J. Smith JC. Blood mercury level and blood pressure among US women: results from the National Health and Nutrition Examination Survey 1999-2000. Am J Physiol 1990. Daniels JL. et al.115(10):1527-1531. Osterloh J. Topping G. Blood mercury levels in US children and women of childbearing age. Orr MF. Burbacher T. Vorwald AJ. Fisher HL. Dorronsoro M. Imai H. Mooney TF. Sandler DP.2:117-131.79:786789.37:245-252. Leroux BG. Most B. Toxicol Appl Pharmacol 1994. Smith AE. Bernardo MF. Bolger PM.258(4 Pt 2):R939-945. Kaye WE. Environ Res 2005. Baser M. Sherlock J. The kinetics of intravenously administered methyl mercury in man.98(1):133-142. Smith PJ. et al. DeRouen TA. Amiano P. Smith JC. Hum Toxicol 1984. Turner MD. Vahter M. Newton G. Langolf GD.124:221-229. Public Health Nutr 2001.Metals Sanzo JM. Pediatrics 1987. Vupputuri S. Vimy MJ. Environ Health Perspect 2002. Aguinagalde FX.111(12):1465-1470. Lind B. Effects of occupational exposure to elemental mercury on short term memory. JAMA 2003. et al. 1993-1998. Farris FF. McDowell M. Maternal-fetal distribution of mercury (203Hg) released from dental amalgam fillings.40:413-419. Smith RG. Leitao JG. Zeitz P. Hongo T. Environ Health Perspect 2003. The hair-organ relationship in mercury concentration in contemporary Japanese. Speciation of mercury in the primate blood and brain following long-term exposure to methyl mercury. Br J Ind Med 1983. Shen DD. Takahashi Y. Environ Health Perspect 2007. Estimation and validation of mercury intake associated with fish consumption in an EPIC cohort of Spain. Environ Res 2005. Acrodynia: exposure to mercury from fluorescent light bulbs. Azpiri MA. Jones RL.31:687-700. 226 Fourth National Report on Human Exposure to Environmental Chemicals . McMahon KJ. Mottet NK. Arch Environ Health 1993. Schober SE.48(4):221229. Effects of exposure to mercury in the manufacture of chlorine. Lorscheider FL. Toxicol Appl Pharmacol 1996. Am Ind Hyg Assoc J 1970. Stern AH. Guo S. Woods JS. Suzuki T. An assessment of the cord blood: maternal blood methyl mercury ratio: implications for risk assessment. Toxicol Appl Pharmacol 1994. Martin MD.4(5):981-988. Hislop D. Nakazawa M.289(13):1667-1674.128(2):25125-25126.

1-59.3) 54.2) 52.7-91.0-53. Excretion occurs predominantly via the kidneys.3) 65.7-51.7) 46.7 (58. and paints.7) 57.2-91.4 (80.1-52.0-85.2) 150 (128-187) 130 (120-141) 119 (112-130) 119 (105-138) 115 (104-128) 101 (97.8-108) 87.8) 48.8 (82.0 (46.7 (44.9) 62.9) 67.8) 46.6) 53.9 (33.Metals Molybdenum or ore deposits.3-75.7 (71. inks.4) 42.0-65.4) 76..5) 85.2 (56.1-51.4-75. hydrogenation catalysts.4) 41.0 (43.7-96.9 (34.9 (73. Molybdenum is a nutritionally essential trace element that enters the body primarily from dietary sources.0 (41.4) 49.0-77.2-79.6) 71.9 (44.1 (38.2) 40.2 (49.3) 47.0) 54.0) 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 (73.2 (40.1-48.9 (40. molybdenum is a cofactor for three enzyme classes— sulfite oxidase.6-55.7) 45. Compounds of molybdenum are also used as corrosion inhibitors.5 (41.6 (52.7) 78.8-46.2-59.3) 37.7 (37.9-83.6) 51. 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.2 (69.2) 37.7-92.3-91. More recently.8) 40.2-37.5-41.1) 60.7-50.5.6-62.2-70. 0.0) 60.1-88.0) 62.8-94.6) 71.3 (38. Gastrointestinal absorption of molybdenum averages 8893% for dietary intakes of 22-1490 µg/day.4 (48.3 (46. 1996). interval) 45.9) 34.8.3) 41.4) 52. and in pigments for ceramics.7-84.7-73.5) 80. 2001).7) 77.6 (55.2-53. WHO.1) 59.3-108) 215 (161-278) 169 (145-194) 148 (136-163) 154 (132-180) 158 (130-177) 127 (114-139) 1121 1335 1281 1136 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 47.0-100) 63.8 (85.5 (37.S. 7439-98-7 General Information Elemental molybdenum is a silver-white.8-49.3-44.3 (84.6-58.7 (73.0-71.7) 75th 84.8-106) 88.3 (73.3 (37.4-52.6-96.6 (40. population from the National Health and Nutrition Examination survey.9 (32. 1997).2) 178 (147-259) 169 (138-197) 138 (127-152) 146 (112-171) 145 (129-159) 118 (105-125) 126 (114-134) 114 (103-124) 105 (98.7-39.7 (50.1 (34.6 (55.4 (79.1) 57.5 (67. lubricants.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 (99.5-91.0 (76.6-82.7) 78.1-55.4 (34.9-109) 97.5-68.1 (71.5-65.0-38.6-42.1-52.0-56.3 (55.5 (41. urinary excretion over six days CAS No.5-66.9 (52.2 (63.7-68.2) 79.0-62.6-46.9-82.7) 51.9-55.5 (48.5 (49.2 (38.0-101) 82.0-110) 90.5-124) 108 (92.8 (67. see Data Analysis section) for survey years 99-00.7-41.6) Selected percentiles ( 95% confidence interval) 50th 50.2 (55. The recommended dietary allowance for adult men and women is 45 µg/day (IOM. 01-02.5-46.8) 75.5) 44.5 (74.0 (48.3 (79.4-82.2 (61. 2001.9-55.8) 39.7 (36.0) 97.2 (83.5 (43.1) 126 (106-147) 109 (94. and 1.2) 48.7 (45.0) 84.0 (42.2-42.3-115) 152 (120-217) 177 (142-207) 152 (141-169) 206 (150-274) 166 (147-170) 156 (135-175) 187 (146-223) 152 (134-180) 130 (119-142) 780 683 618 546 667 723 760 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limits of detection (LOD.0) 39.5-52. aldehyde dehydrogenase.3 (71.7-122) 93.7-60.1) 82. respectively.8) 44.2) 53. which exert homeostatic regulation over molybdenum balance.1) 35. and xanthine oxidase (Kisker et al.9 (78.5) 80.1-63. Fourth National Report on Human Exposure to Environmental Chemicals 227 .7 (51.6) 93.8 (42.4) 45.0 (81.5) 47.3 (64.1) 46.3) 90th 135 (125-146) 124 (117-130) 111 (105-118) 95th 180 (154-216) 165 (145-176) 138 (133-146) Total 45.6-72.5) 60.3 (53. hard metal widely used to add strength and hardness and retard corrosion in metal alloys.3 (47. semiconductor and battery industries have begun to use molybdenum.9-56.4) 56.7-105) 69. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.1 (91. At a daily oral molybdenum dose of 24 µg.6 (43.3) 85. chemical reagents in hospital laboratories.7-47.9-85.9 (37.4-61.7) 86.3) 83.8-90.2 (49.2-59. and 03-04 are 0. In humans.0) 55.5 (81.0 (42.4 (48.7) Sample size 2257 2690 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 78.3-47.6 (40.3 (55.2) 41.8. and the average dietary daily intake of molybdenum is approximately 100 µg/day (IOM.4 (72.5-52.1-44.

4) 89.9 (39.9-96.8) 62.8) 38.9) 173 (130-243) 159 (129-170) 132 (107-158) 85.4-185) 106 (94.2) 37.2 (40.5 (41.5) 214 (154-1040) 185 (165-219) 160 (129-257) 112 (78.8) 45.4) 44.3 (71.3 (83.3) 44.2 (57.5 (65.9-87.9 (35.2-47.0-41.7) 115 (93.2 (33.8-47.3) 40.8) 79.3) Sample size 2257 2689 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 85.0) 36.0) 88.6 (38.1) 65.7-43.4 (67.5 (65.1) 40.4-106) 85.6-45.6) Selected percentiles ( 95% confidence interval) 50th 41.2) 55.4) 48.3-45.1-127) 90.8-42.4 (56.1-112) 78.7-44.8-118) 81.4-41.5 (59. dust and other fine particles produced during refining or shaping of molybdenum or molybdenumcontaining alloys are inhalational pathways of exposure.1 (33.1 (42.9) 92.5-48.4 (40..2) 43.3-102) 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 40.4-107) 85.3 (53.3-141) 109 (81.4 (37.7 (77.4) 47.6-61.1) 43.7-100) 77.4-118) 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 .9 (40.7) 45.5-97.5 (35.3) 43.3-43.2-40.8 (36.1-43.2) 42.2-121) 107 (92.5 (39.3-52.0-56.6-61.7) 112 (95.3) 37.2 (40.2) 58.3 (71.8) 61.8) 71.2-65.7) 57.1 (30.5 (41.1-100) 86.3) 64.5 (40.8 (75.0 (35.3) 61.1-67.4 (59.2 (50.9 (73.1-43.2) 39.4) 40.3 (37. Biomonitoring Information Molybdenum is an essential element for health.1-81.2 (43.4) 122 (107-133) 109 (99. interval) 43.S. U.0 (80. and clinical or epidemiologic evidence of adverse effects is limited.6) 39.6) 48.2-96.4) 60.4 (53.1-41.1 (37.3) 56.5 (37.1 (44.9 (64.3 (55.7-137) 129 (109-155) 112 (97.1-109) 89. A long term inhalation bioassay of molybdenum trioxide in mice yielded “some evidence” of carcinogenicity (NTP.3-46.5 (79.5) 71. Human health effects from molybdenum at low environmental doses or at biomonitored levels from low environmental exposures are unknown.3-44.5) 90th 108 (97.3-115) 98. 2001).8-84.7) 41.7) 62.6-41.4 (55.9) 44.2 (37. 1961.5-60.4) 58.1 (38.S.. and molybdenum has not been systematically evaluated for carcinogenicity by IARC.9) 31.5 (37.0-46.0) 44.0) 38.6-78.7-52.3-68.5-99.2-80.0) 95th 144 (125-171) 130 (120-149) 120 (107-135) Total 42.Metals was 18% of the ingested dose.8) 39.3 (36.9 (49. EPA.0) 53.9-117) 57.5-69.8-67.5) 60.6) 39.3 (58.1-39.3-56.0) 72.2-103) 131 (112-179) 123 (107-155) 118 (100-139) 152 (122-181) 136 (117-169) 122 (115-142) 1121 1334 1281 1136 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 42.2) 39.9-68.6 (71.5 (35. and urinary levels reflect intake from all sources.5) 72.2 (52.2) 37.7-93.9 mg/kg/day and established a tolerable upper intake level of 0.1) 37.7) 75th 63.7 (75. urinary excretion over six days rose to 50% and 67%. 1999).5) 63.9-45.3 (51. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.9) 40.6 (36.8-46.0-120) 85.0) 39.1-40.9-45.8-66.0-133) 119 (88.5 (50.1) 37.4-39.5 (39.6 (57.3) 57.4-76.9-41.5 (78.1 (82.0-38. population from the National Health and Nutrition Examination survey.5 (80.3 (36.1-39.7) 53.1 (49.8 (56.4) 61.5 (36.7-62.1 (40.5-44. Based on studies finding adverse reproductive effects in rats and mice.7-40.2-96.9-61. In industry.2-49.8 (90.9 (36.1) 101 (83.4) 77.1) 56.3) 41.5-45.4-120) 101 (84. 1993). at daily oral doses of 95 µg and 428 µg.1 (39.1-79.0) 62. respectively.8) 37.7-38.2) 38.3-59.6) 36.5-35.5 (40.2) 42.0) 33. Chronic exposure to very high levels may result in higher serum uric acid levels and a gout-like illness (Koval’skiy et al.0-46. but available epidemiologic data are scant.5-92.5-70. Levels of molybdenum Urinary Molybdenum (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.8) 38.7 (30.9-40.7-120) 87.9-118) 91.0-103) 103 (90.6-88.9 (79.4) 116 (101-126) 104 (88.2 (40.9-71.8-47.1-38.1-45.4 (44.3 (37.5-50.7) 42. 1997).2-41.6-76.6 (59.2 (73.4 (78.8 (37.9-42. 1995).03 mg/kg/day in humans (IOM.5-62.5 (83. Molybdenum is generally considered to be of low human toxicity.1-34.6) 43.8 (57.9 (39.9 (64.5 (38.1 (38.0 (74.2-46.0 (58. of the ingested dose (Turnlund et al.6 (36.5 (54.9) 79.4-66.5) 73.2 (69.5-46.6 (42.5 (34. the Panel on Micronutrients of the Institute of Medicine identified a no observed adverse effect level (NOAEL) of 0.6-63.7 (66.6-63. One case-control study suggested a possible link between occupational exposure to molybdenum and lung cancer (Droste et al.4-42.2 (36.1 (54..5-119) 90.9) 41.8-52.0) 39.8-65.

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

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

. 1969. metallic... Animals exposed to cholorplatinate salts used in industry have demonstrated severe hypersensitivity with asthma-like symptoms and anaphylactic shock (Parrot et al. Information about external exposure (i. or recommended for the metal form by NIOSH (Czerczak and Gromiec.Metals doses or at biomonitored levels from low environmental exposures are unknown. The carcinogenicity of other platinum compounds remains uncertain.g. intravenous medicinal use. or organometallic). 1975a.e. inorganic salt. Most absorbed platinum accumulates in the kidneys and is excreted in urine (Moore et al. cutaneous. The pharmaceutical cisplatin is an animal carcinogen and reasonably anticipated to be a human carcinogen as determined by NTP. Fourth National Report on Human Exposure to Environmental Chemicals 231 . Platinum metal is biologically inert. 1975b).S. inhalational. 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. oral). and duration of exposure. Workplace air standards for external exposure are established for soluble salts of platinum by OSHA and ACGIH.. When ingested or inhaled. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.g. 2000). Saindelle et al. halogenated salts) encountered in occupational settings can cause platinum salt hypersensitivity with symptoms that include bronchitis and asthma after inhalational exposure and contact dermatitis after skin exposure. platinum metal and insoluble salts are very poorly absorbed (<1% of a dose) and cleared from the body within a week after a single dose... Platinum metal and insoluble salts can produce eye irritation. 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. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. whereas soluble platinum compounds (e.. population from the National Health and Nutrition Examination Survey.g. 1969). Toxicity is determined by the type of compound (e. route of exposure (e.

123(3):451-454. Int J Hyg Environ Health 2004. In: Bingham E. Int Arch Occup Environ Health 1997.55(2):138-140. Part 1: monitoring of urinary concentrations. Gieler U. Parrot JL. 1991 [online]. Schierl et al.org/documents/ehc/ehc/ehc125. Begerow J.. Available at URL: http://www. 2004). Urinary platinum levels associated with dental gold alloys.. Several studies have shown that background concentrations in general populations were usually less than 0. Stilianakis NI.4(1):27-36. Fries HG. Biological monitoring of hospital pharmacy personnel occupationally exposed to cytostatic drugs: urinary excretion and cytogenetic studies. Pethran et al. 2000. International Journal of Hygiene and Environmental Health 2003. Schulz C. Wilhelm et al. Stara J: Preliminary studies on the toxicity and metabolism of palladium and platinum. Cohrssen B. 2003. Schierl. Occup Environ Med 1998. Angerer J. Seifert B. 2004) or less than 0. Hauff K. Hall L.htm. Kelly J.inchem. Patty’s Toxicology. Czerczak S. 289-380. Hysell D. International Programme on Chemical Safety (IPCS). Herr et al. Schierl R. Wilhelm M. Arch Environ Health:1969. Br J Pharmacol 1969. Farago ME. 206:15-24. Gromiec JP. 1997. Pethran A. et al.76(1):5-10.htm. Jankofsky M. Carelli G. palladium. One study found that traffic-control officers had no greater urinary platinum concentrations than office-based control subjects (Iavicoli et al. Blanks R. Iavicoli I.. Campbell K. Levels of platinum in urine for the U. J Expo Anal Environ Epidemiol 2003. Hebert R. Herr et al.01 µg/L (Becker et al. Influences on human internal exposure to environmental platinum.61(7):636-9. eds.9:152-158.Metals the International Programme on Chemical Safety at http:// www. Schierl R. Gold-platinum dental restorations were correlated with increased urinary platinum concentrations. New York: John Wiley & Sons. van de Weyer C.207(1):69-73. osmium. and in blood and urine in the United Kingdom. Platinum concentrations in urban road dust and soil.19:685-691. Kavanagh P. Biomonitoring of traffic police officers exposed to airborne platinum. Ruff F: Platinum and platinosis. Bocca B. Finding a measurable amount of platinum in the urine does not mean that the level of platinum causes an adverse health effect. Int Arch Occup Environ Health 2003. and gold excretion of patients after insertion of noble-metal dental alloys.35:313-321. Boos KS. 232 Fourth National Report on Human Exposure to Environmental Chemicals ..S. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Saindelle A. et al.70(3):205-208. Turfeld M. Biomonitoring Information Urinary platinum levels reflect recent exposure. pp.. Schierl R.. Huber R. ruthenium. Kuster W. Schierl R.56(3):283-286. 2004. Kulka U. 5th ed.10:63-71. Petrucci F. Environ Health Perspect 1975b. Kaus S. Biomarkers 1999. Herr CE. et al. Pethran A. Platinum. Kazantzis G. 1999... Seiwert M. Environ Res 1975a. References Becker K. 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. Urinary excretion of platinum from platinum-industry workers. Moore W Jr. Ensslin AS. 1998). Rommelt H. Saindelle A. Stara J: Biological fate of a single administration of 191Pt in rats following different routes of exposure. Revised and new reference values for some trace elements in blood and urine for human biomonitoring in environmental medicine. Raab W. 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. and platinum. Arch Environ Health 2001. Neuendorf J. which elevate urinary platinum by five to twelve-fold (Begerow et al.. Ruff F: Histamine release by sodium cholorplatinate. rhodium. population were below the limit of detection (0. Uptake of antineoplastic agents in pharmacy and hospital personnel. 3/31/08 Moore W Jr.13(1):24-30. Occup Environ Med 2004. Schulz C. Crocker W.. Allergy and histamine release due to some platinum salts. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Ewers U. 2001).04 µg/L) in this Report. palladium. Thornton I.005 µg/L (Iavicoli et al. Environmental Health Criteria 125. 2003. Platinum-industry and precious-metal workers had urinary concentrations about one-thousand times higher than general populations (Schierl et al..inchem. Hysell D. Nowak D. et al. Alimonti A. Senofonte O. Duneman L:Long-term urinary platinum. Powell CH. 1998). 2003.org/documents/ehc/ehc/ ehc125. Nickel. Analyst 1998. Fruhmann G. Grimm CH. 2003).

520) .206) .290 (.260-.156-.150-.290) .260 (.300) . 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.146 (.210-.370 (..239) .180-.400) 95th .480) .202) .170 (.188) .290 (.400) .360 (.156) .192) Selected percentiles ( 95% confidence interval) 50th .400) .172 (.360 (.170-.500) .290) . and 03-04 are 0.420) .148-.180) 75th .170) .167-.450 (.410-.350-. In the United States.260 (.230 (. Human health effects from thallium at low environmental CAS No.201 (.Metals Thallium depilatory cosmetics.410-.170-.176 (. It is still used in relatively small amounts in pharmaceutical and electronics manufacturing.197-.420-.330) .155 (. In the past.410 (.230) .220) .290 (.250-.160-.460 (.280 (.470) .220 (.250-.450 (.450 (.270 (.02.200) .240) .180) .137-.480) .172) .480) .360-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.350-.270-.390) . it has not been specifically mined or refined in the United States since 1984.220-.250-.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 .02. 7440-28-0 General Information Elemental thallium is a blue-white metal found in small amounts in soil and in sulfide-based minerals.330-.460) 861 675 618 561 657 723 801 1114 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.02.300-.185-.290 (.147-.170-.260-.290-. thallium was obtained as a by-product of smelting other metals.430 (.470 (.260 (.300 (.147-.390 (.156) .330-.480) .157-.420) . thallium is produced in a fine particulate form that can be absorbed through inhalation or ingestion.320) . Elimination from the body tissues occurs slowly through urine and feces (Blanchardon et al.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 .243) .184 (.430-.400) .290 (.280-.210 (.370 (. the latter being the current major industrial consumer of thallium in this country.175) .159 (.200) .400) .170 (.330-.340-.330) .181-.360-.350-.390-.270 (. representing distribution into other tissues.190-.160 (.330-.430 (.290 (.410 (.300) .172 (.430-.200) .360 (.170-.310 (.490) .160-.290-.180-.350 (.420) .430 (.510) .460) .390) . Fourth National Report on Human Exposure to Environmental Chemicals 233 .160 (.330) .163) .230-.197 (.330-.340-.220) .360) .240-.520 (.410 (.400-.220 (.410 (.218) .196) .690) .390-.170-.178) .159 (.153-.470 (.360-.270) .380) .320 (.250) .360-.370) . 01-02.280 (.144 (.173) .370 (.450 (.270) .183) .220) .185 (.250 (.340-.180 (.210 (.370-.173) .410-.250-.440 (.400 (.420-.200) . population from the National Health and Nutrition Examination Survey.360 (.490 (.173-.200 (.370-.170 (.160 (.240-.440 (.202 (. see Data Analysis section) for Survey years 99-00.420) .190 (.190 (.340) .171 (.183) .150-.250-.190 (.230) .170-.390) .179-.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 .220) .330-.230) .200 (.340 (.630) .480) .590) .640) .400-.180-.145-.420-.201 (.350-. respectively.240) .220 (.400-.165 (.350) .380-.370 (.410) .182-.440) .220 (.340) .430) .390-.430 (.450) .145-.410 (.202 (.440-.400-.370 (.420-.240) .260-.320-.196) .490) Total . From these and other sources.430-.160-.177) .170-.180 (.180-.400 (. 0.190 (.450 (.230-.460-.250-.180 (.380 (.187-.220) .217 (.200 (. however.280 (.520) .310-.200-.260-.220) .590) .520) .167-.470) .160-.390-.200-.420 (.420) .150-.310) .220 (.440 (.280-.500) .430) .S.200 (.380 (.147-.450 (.350-. In addition.200-.159 (.440) .162-.320) .160 (.270 (.310 (.270 (.560) .150-.135-.390) .160 (.370 (.200 (.240-.215) . Thallium disappears from the blood with a half-life of several days.200) .150-.190 (.410-.200 (.500) .300 (.290) .149 (.280) .340-.191 (.370-.260-. and 0.300) .270-.290) 90th .410-.440) .370) .310 (.400 (.145 (.140-.400-.330) .250-.280) .350) .440 (.490) .217) .490) . 2005). interval) .450 (.270 (.154-.450 (.370 (.290) .190 (. Thallium exposure occurs primarily from industrial processes such as coal-burning and smelting.420) .500 (.450 (. thallium readily crosses the placenta and also distributes into breast milk.410 (.390 (.218) .230) .320) .510 (.260) .420) .300 (.400 (.134-.150-.133-.470) .400 (.300) .350 (.170) .380-.350-.280) .250 (.370-.200-.170) .225) .250-.210) .200) .167 (.410-.230-.330-.160-.550 (.270-.360-.158) .

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

Seventy-eight percent of the urine specimens in that study contained greater than 1 μg/L. Long term retention and excretion of 201Tl in a patient after myocardial perfusion imaging. Minoia C.5 μg/L.. blood. 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. Schaller et al. 2005) and are shown with results from NHANES 2003-2004 in this Report. Trace metals in urine of United States residents: reference range concentrations. 1985). White MA. with concentrations ranging up to 76. 7/15/09 Blanchardon E. Paschal et al. White and Sabbioni. Finding a measurable amount of thallium in urine does not mean that the level of thallium causes an adverse health effect. J Soc Occup Med 1985.95:89-105.1 mg/m3 (Marcus.113(1):47-53. Sci Total Environ 1990. Environ Res 1998. population) are thought to correspond to workplace exposures at the threshold limit value of 0. Manke G. 2005. 1998). 1992 [online]. Sabbioni E. Minoia et al.35(1):4-9. Ewers U.. Intake and health effects of thallium among a population living in the vicinity of a cement plant emitting thallium-containing dust. Cassot G. 2005. Trace element reference values in tissues from inhabitants of the European community I.47(3):223-231. Wiegand H. Fourth National Report on Human Exposure to Environmental Chemicals 235 . A study of 46 elements in urine. and serum of Italian subjects. et al. (1981) studied 1. Apostoli P.. 1990. Nearby residents were exposed by eating garden plants that had been contaminated by the thallium. Radiat Prot Dosim.216:253-270. Trace element reference values in tissues from inhabitants of the European Union. Raithel HJ.Metals (CDC.76(1):53-59. et al. Pietra R. Pozzoli L. 1998. Brockhaus et al. Investigation of a working population exposed to thallium. Valentin H. Morrow JC. References Agency for Toxic Substances and Disease Registry (ATSDR). Celier D. Martin J-C. A study of 13 elements in blood and urine of a United Kingdom population. Third National Report on Human Exposure to Environmental Chemicals. Centers for Disease Control and Prevention. Buhlmeyer G. Challeton-de Vathaire C. Atlanta (GA). et al. Boisson P. Marcus RL. 1980.265 people living near a thallium-emitting cement plant in Germany. Jackson RJ. Dolger R. Investigations of thallium-exposed workers in cement factories. Ting BG. Sabbioni E. Urinary concentrations of 100 μg/L in asymptomatic workers (500 times higher than median levels in the U.gov/toxprofiles/tp54. 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. 1981. Schmidt M. Int Arch Occup Environ Health 1980.html.48(4):375-389. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.S. Toxicological profile for thallium.atsdr. These urine levels are generally comparable to levels observed in earlier studies of general populations (Brockhaus et al.. Sci Total Environ 1998.cdc. Available at URL: http://www. Pirkle JL. Brockhaus A. Gallorini M. Paschal DC. X. Kramer U. Sampson EJ. Int Arch Occup Environ Health 1981. Soddemann H. Schaller KH.

470) .090-.180-.500 (.060-.078-.093) .270 (.130-.180 (.090) .100-.130) .110 (.280-.096-.066-.460 (.190-.113 (.090-.062 (.580) .470) . and 03-04 are 0.260) . which are used in rock drills and metal-cutting tools.150-.070-.092 (.800) .190-.650) .100 (. Although workers occupationally exposed to tungsten carbide may develop serious lung disease (“hard metal disease”).056-.350) .300 (.Metals Tungsten CAS No.260-.330) .530 (.204) .068) .070) .210 (.290) .430-.050-.520) .060 (.330-.082-.370 (. and as catalysts in the petroleum industry. their illness may stem from exposure to cobalt mixed with tungsten carbide rather than to tungsten alone.140-.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 .670) .180) . Occupational exposure is from dusts released during grinding or drilling of hard metals.270-.080) 75th .130 (.460) .520) .090-.390 (.620) .380-.460 (.380 (.087-.380-.092 (.220) .060 (.070-.090) .050-.120-.230) .450 (.250-.180) .107 (.140 (.050-.130) . bronzes in pigments.120) .300) .110 (.109) .810) .210 (.320 (.140-.110 (.100) .420-.070 (.073) .430 (.370-.062 (.087) .460 (.101-.360) .095-.060-.330) .058-.360-.250) .310-.180-.130-.170-.110-.360-.090-. 0. respectively.120) .480) Total .140 (.170) .180 (.290 (.410-.120-.550 (.120) .320 (.240 (.S.090 (.093 (.190 (.510-.110 (.360 (.081 (.060-.130-.100) .116) .105) .300) 95th .400 (.080) .130) .110) .120) .065-.210-.04.073-.140 (. Little information is available on the toxicity of tungsten.220) .560) .350) .080-.160 (.370) .070) .090 (.120-.360 (.113 (.560) .04.200) .060 (. Tungsten compounds are used as lubricating agents.250) . which is used in the steel industry.096 (.230-.060-.071-.520) .400-.060 (.380) .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 .100 (.270 (.070) .160 (.310 (.620) .430-.340) .370-. Most background environmental exposures to tungsten are from the soluble forms such as tungstate salts that may occur in drinking water.530 (.080 (.056-.100) .320-.070-.400 (.160 (.077-.151) .350) .170) .074-.080) .400 (.080 (.260-.070-.250) .200 (.770 (.080 (.060 (.091) .220-.290) .210) .088 (.101 (.370 (. 236 Fourth National Report on Human Exposure to Environmental Chemicals .110) .620 (.290-.160-.092) .130) .270 (.570 (. and 0. 01-02.230 (.210 (.410) 790 680 618 562 649 723 802 1117 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.084 (.070-.070) .270-.071 (.500) .230-.170 (.250) .086 (.350 (.340-.210 (.113 (.550) .220) .060-.460) .123-.560) .430 (.470-.150 (.070 (.350-1.080-.290-.080 (.080 (.090-.320-.410 (.120-.330 (.122) .310-.090 (.160) .510-1.120 (.073 (.590) .100-.160-.110 (.070 (.104) .340-.210 (. Human health effects from tungsten at low environmental doses or at biomonitored levels from low environmental exposures are unknown.120-.090-. see Data Analysis section) for Survey years 99-00.450-.240-.100) .080) .130) .082 (.120) . Tungsten is used mainly for producing hard metals.300-.270-. interval) .550) .360 (.170 (.260 (.370 (.160 (.320) .250) .490 (. population from the National Health and Nutrition Examination Survey.440) .830) . and for producing ferrotungsten.160-.158 (.082) .250-.130-.190-.340-.180-.090-. and it has not been classified with respect to its carcinogenicity by either IARC or NTP.170) .100) .150 (.310-. filaments for incandescent lamps.570 (.097-.420-.064-.800) .630) .00) .300 (.330-.550) .220 (.126) .430) .050-.095-.310-.250) .280 (.130 (.069) .120-.110-.160-.310-.470 (.470 (.076 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.260-.270-.510 (.560) .100 (.180-. Evidence is lacking for the carcinogenicity of tungsten.790) .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 .150) . Urinary Tungsten Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.060 (.140 (.160 (.090) .190) .950) .113 (.400 (.170) .111-.137 (.105 (.180) .100 (.120) .084-.100-.530 (.690) .065 (.290-.230) .069-.230-.260 (.400) .110-.390) .073-.560 (.200-.084) .53) .190 (.150 (.280 (. mainly as scheelite (CaWO4).430 (.300 (.135) .180) .04. 7440-33-7 General Information Tungsten is a steel-gray to tin-white metal that occurs naturally in the earth’s crust.082 (.160) .380-.080-.093-.132) .490) .133) .076 (.380 (.190-.100) Selected percentiles ( 95% confidence interval) 50th .140) 90th .380-.090) .230-.060-.500 (.310) .640 (.090-.088) .

086) .083-.067 (.555 (. population in the NHANES 1999-2000 slightly higher values than those found in NHANES 1999.150 (.108) .057-.161) .133) .130 (.261-.116-.301) .107-.069 (.200-.317) .081 (.093) .119 (.075) .095-.375) .197) .091 (.167-.237) .059 (.143-.078 (.426) .074) 75th .231 (.091) .634 (. 1998).073 (.144 (.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 .084) .286-.880) .211 (.169) .431) .197 (.143 (.083) .358) .340 (. interval) .120) .056-.188-.333-.329 (.087 (.144-.154) .087) .245-.069 (.091 (.28) .341 (.085 (.089 (. 1997).360 (.739) .109-.133) .106 (.275 (.081 (.065-.070 (.538) .150-.270 (.306) .104-.215 (.347 (.Metals Workplace air standards for external exposure have been established by ACGIH and recommended by NIOSH.085-. Using neutron activation analysis to 2000.452-.136-.797) .079) .139) . 2005).120) .240-. Biomonitoring Information median urinary levels were as much as 15-fold higher than median levels in the U.071 (.258-.S.353 (. 2001).125) .164 (.082 (.063-.381) .100 (. 2001-2002.359 (.353 (.065 (.379 (.078) .083) .053-.091) .065 (.111 (.331-.727) .186 (.061-.267-.174 (. 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.146 (.131-. population.056-.383 (.279 (.086) . population (CDC.080 (.216-. Nicolaou et al.214) .439 (.465) .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 .062 (.222) .079 (.231-.148) .439 (.354) .085) . 2003.054-.201) .086) .285) .067 (.184 (.105 (.074 (.410-.145 (.253) 95th .198-.250 (.667) .077) .287) .068-.459) .138) .060-.386) .482 (.554) .117 (.667 (.084 (.300-.124-.158) .167) .190) .105 (.462) .317-.S.302-.224) .484 (.439) Total .063-.071 (.197-.582) .215) .267) .075-.077) .084 (.385 (.392) .412 (.071) .293 (.057-.151 (.098 (.121-.317 (.081-.179-.294 (.217-.067-.070 (.100) .083 (.198) .061-.216 (.058-.255-.465) .064-.083 (.096) .302-.078-.099-.150-.080-.152-.138 (.237) .333 (.300) .431) .089) . Workers involved in grinding operations that released tungsten metal into the air had elevated urinary levels that Levels of urinary tungsten reflect recent exposure.426) .068 (. (1987) found possibly due to methodologic.090-.065) .121 (.075) .250 (. or exposure that a control group of non-metal workers had mean levels differences.078) .333) .158) .453) .146) .279 (.308) .075 (.301) .122 (.359 (.165) .055-.431) .436-1. measure urinary tungsten.605) .258 (. and 2003-2004 (Paschal et al.308) .284) .122-.484) .098-.153) .082) .075-.133) 90th .326) .146 (.436) .199 (.180-.071-.136-.148 (.103-.074-.154) .126-.063-.080 (.414) .176-.174) .079 (.329-.344-.071) .283) .250-.072-.300 (.209-.098-. A study of 14 unexposed adults yielded values that were similar to the 95th percentiles in this Report.216 (..116 (.364 (.077-.075 (.066 (.124 (.065-.315-.059-.094) .090-.167-.108-.136-.092) .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 .061-.094-.088) .079) .187) .054-.333 (.497 (.078 (.117) .072 (.077-.233-.122-.073 (.S.253 (.060 (.119-.086-.100) .300-.093-.176-.074-.064-.206-.059-.071) .098-.279 (.071 (.201 (.080-.255 (.088) .208-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.109 (.168 (.063-.181 (.253-.500) .179-.153-.333) .299 (.094) .205-.130-.136 (.095) Selected percentiles ( 95% confidence interval) 50th .265 (.217-.060-.084) .091) ..354-.333 (.125 (.823) .158) .339 (.214-.155-. population from the National Health and Nutrition Examination Survey.167) .072-..216-.116) . Patients with medically-inserted tungsten found at increased levels in drinking water.069-.272-.301) . In whereas the tungsten-worker group had mean urine levels a Nevada community where tungsten was measured and 35 times higher.278-.197) .082) .222-.158 (.063 (.065-.237-.079) .139-.049-.333 (.200-.203-.157) .073 (.073 (.218 (.138 (.169 (.091) .066 (.136-. similar to those in this Report (Schramel et al.216-.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 .170-.(Kraus et al.079) .333-.081) .063 (.339 (. A were more than 900 times higher than the overall geometric nonrandom subsample from NHANES III demonstrated mean of the U.059-.139 (.255 (.074) .098) .199 (.

Paetzel C. J Trace Elem Electrolytes Health Dis 1987. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Sampson EJ. 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. Angerer J. Link J. Pirkle JL. Environ Res 1998. tin and tungsten) in urine samples by inductively coupled plasma-mass spectrometry. Kraus T. Ting BG. The determination of metals (antimony. palladium. Third National Report on Human Exposure to Environmental Chemicals. Manke C. platinum.62:380-384. tellurium. References Bachthaler M. Catheter Cardiovasc Interv 2004. et al. and hair (Bachthaler et al. National Center for Environmental Health. Cancer Clusters. Centers for Disease Control and Prevention. Churchill County (Fallon). Atlanta (GA).cdc. Urinary tungsten levels in many patients were hundreds-fold higher than observed in this Report. Occup Environ Med 2001.Metals blood. Nevada Exposure Asssessment. Available at URL: http://www. Schramel P. Schaller KH. mercury. thallium. Trace metals in urine of United States residents: reference range concentrations. Pietra R. Paschal DC. Schramel P. Angerer J. Multielement determination of metals in biological specimens of hard-metal workers: a study carried out by neutron activation analysis.. 2004).htm. Mosconi G. bismuth.(2):73-77. Nicolaou G. Exposure assessment in the hard metal manufacturing industry with special regard to tungsten and its compounds. urine.gov/nceh/clusters/Fallon/study. Lenhart M. [online] 2003. 2005. Zobelein P. 4/15/09 Centers for Disease Control and Prevention. Sabioni E. Feuerbach S. Weber A.69(3):219-223. Jackson RJ. Cassina G. lead. Int Arch Occup Environ Health 1997. cadmium. Seghizzi P.76(1):53-59. Wendler I. Morrow JC. 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.58(10):631-634. 238 Fourth National Report on Human Exposure to Environmental Chemicals .

008-.046 (.007) .008-.019-.008 (.008-.005-.011-.045) .036 (.009-.021 (.007-.069) .006-.006-.007 (.009) .017-.023-.009) .009 (.011-.020-.020-.023 (.054) .016) .030-.S.017-.035) .012) .008 (.033 (.008 (.054-.016) .026-.026 (.035-.009 (.007 (.007-.041 (.060 (.008-.010-.033) .012 (.008 (.022 (.005-.006-.016 (.024-.038) 340 368 289 719 762 725 1405 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .009) .016-.013-. human exposure occurs primarily by inhaling dust and other small particles.007) .010-.007 (.007-.009-.008) .006 (.020 (.008-.008 (.013 (.007-.015 (.031 (.007-.015) .021-.036-.014 (.040 (.028-.031 (.011) .017) .017) .056) .009-.008) Sample size 2464 2690 2557 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .017) .007 (.023) .040-.017) . Uranium has many commercial uses.050) .027-.009-.053) .008 (.010 (.009) .011-.016-. see Data Analysis section) for Survey years 99-00.008-.062) .006-.007-.007-.053 (.015) .010) .008 (.010-.037) .040 (.006-.044 (.012-.007 (.031-.025-.011 (. DU has been used by the military in armor-piercing ammunition and as a component of protective armor for tanks.014 (.011) .017) .027 (.012) .031 (.033 (.046) .040) .018 (.005.009-.008 (.072) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.017 (.012-.012-.039-.029-.022) .066) . Fourth National Report on Human Exposure to Environmental Chemicals 239 .026) 95th .008) .011) .026) . population from the National Health and Nutrition Examination Survey.009) .024-.018) .020-. milling.006-.010) * .028 (.008-.028-.015 (.011) .007 (.009 (.011-.046 (.007) .022-. 235U (about 0.007 (.005-.063) .039) .014 (.014 (.009 (.009) . and as an aid in electron microscopy and photography.010) .010) .045) .015 (.013) .038 (.052 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.009 (.010) * .007-.158) .010-.011-.033-.012 (.004.023-.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.021-.008 (.279) .012) .010 (.026 (.009) .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 .038) .010-.018) .055 (.020) .007 (.014 (.048) .030) .010) .027) .024-.007 (.065) .008) . It usually occurs as an oxide and is extracted from ores containing less than 1% natural uranium.011-.034-.023) .028 (.012) .035) .031 (.037) Total .010 (.017-.023 (.009-.022-.018) .008 (.023) .010) .027-.010) .027) .011-.037-.008-.015-. including nuclear weapons.042) .023 (.008 (.008 (.027) .023-.017-.006-. Thus.023-.006-.049) .027 (.042 (.006-.009 (. Natural uranium is a mixture of three isotopes: 238 U (greater than 99%).009 (.007) .036) 883 683 618 568 667 722 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.005-.016) .032 (.050) .007-.008 (.019-.009) * . interval) . and 234U.008) . in some ceramics.011) .007-.056) .024 (.006 (.009 (.065) .007-.007 (.022-.007) .012 (.72%).034) .013 (.027) .088) .013 (.007) 75th .027 (.009-.018-.036) .019-.034-.073) .009-.021) .043 (.010 (.007-.026-.051) .015 (.012 (. 7440-61-1 General Information Uranium is a silver-white metal that is extremely dense and weakly radioactive.016) .026) . In workplaces that involve uranium mining.006-.028 (.006-.008) .009) Selected percentiles ( 95% confidence interval) 50th .027 (.029-.007-.039) .008 (.046 (.006-.017-.008 (.018) .006 (.021) .020-.037 (.067) .012-. or processing.046-.006 (.009 (.012-. respectively.020) .048 (.037) .009) .008 (.013-.040-.041 (.013 (.016) .005-.009-.030 (.020-.047 (.013 (.043) .036) .007-.010 (.009-.017-.010-.016-. the primary exposure sources for nonoccupationally exposed persons are dietary (especially root vegetables) and drinking water.007-.031 (.049) . 0.007-.019-.011 (.018 (.004. Variable concentrations of uranium occur naturally in drinking water sources.007 (.017 (.016) .127) .067) . and 0.021 (.011) .037) . and 03-04 are 0.009) .014 (.012 (.036 (.054) .009) .019 (.012-.013 (.036-.026 (.030 (.012 (.006-.021) . Since the 1990’s.114 (.013-.009 (.010) .030 (.008 (.046 (.009) .007-.013 (.013) 90th .009) .Metals Uranium CAS No.011) .029 (. nuclear fuel.010) . 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.021 (.040) .064 (.007-. 01-02.027-.

028 (.007 (.039) .008 (.017 (.015) .006) .026 (.050 (.008) .004-.007 (.006-.051) .019) .026 (.025 (.010-.030 (.008) .009) .033 (.010) .033 (.009-.013 (.010 (.011 (.033 (. which can occur occasionally from high occupational exposure.016) .034 (.016) .006-.006-.007 (.009) .063) .007 (.053) .021-..006-. Soluble forms of uranium salts are poorly absorbed in the gastrointestinal tract..029 (.012 (.019 (.012) .018-.008 (.042) .012) .007-.030-. where limited absorption occurs (less than 5%).014-.007-.008) .009 (.020-.034 (.030 (. 240 Fourth National Report on Human Exposure to Environmental Chemicals .005 (.020 (.009) .037 (.017) .009 (.009 (.146) .024) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.006-.012 (.008 (.010 (.026 (. In cases of retained DU shrapnel.006-. kidneys.011) * .006) .005-.034) .007 (.029) .007 (.027 (.024) .051) .018 (.013 (.013 (.007-.006-.028) .011-.007 (.012 (.017) .012-.006 (.016-.015 (.051) . After inhalation.009-.034 (.006 (.015-.006 (.080) .030) .053) .027-.013 (.024) .013 (.007 (.027 (.024-.044) .024) .023-.013 (.011) .008) .006-.016) .005 (.047) .015 (.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) .022 (.007 (.012 (.015-.007 (.035 (.010) .009) .009) .029) .1%-6% of an ingested dose may be absorbed.033) .010 (. liver.025-. Human health effects from uranium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.006-.017-.028) . the shrapnel acts as a source of chronic.009-.020) .017-.022) .043 (.010 (.006-.016-. interval) .020-.009) .006-.022-.008-.018-.067) .025) 95th .008-.020 (.014 (.005-.014-.010-.011) . Inhaled uranium-containing particles are retained in the lungs.008-.029) . 2003).008-.010) .030-.006-.008) .024-.011-.010) .015-.007-.270) .016) .027-.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 .024 (.024-.007-.005-.018-.Metals impact.051 (.004-.006-.008) .027) .010-.013) . After exposure to soluble uranium salts.007) .034 (.013 (.007 (.028) . the half-life of insoluble uranium in the lungs is several years (Durakovic et al.010-.039) .027-.009-.006-.011-. which represents distribution and excretion.016) .006 (.014 (.014) .011-.006-.061) .020-.015-.030) .021 (. Health effects from uranium exposure result from chemical toxicity to the kidney.008-.007 (.032) . and bones can accumulate uranium with the largest amounts being stored in bones (Li et al.006-.022-.005-.007 (.029) .056) .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 .017-.020 (.008-. Radiation risks from exposure to natural uranium are very low.050) .007 (.039) Total .019-.008 (.042-.019-.007 (.007 (.022 (.007 (.007) .028-.006 (.011 (. low level exposure.015) .042) .034 (.011) .077) .007-.028) . 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.010 (.011-.016-.007-.024 (.016-.012-.017-.006-.010-.025-.058) .010-.008) .008) .021 (.009 (. the initial half-life of uranium is about 15 days (Bhattacharyya et al.008 (.050) .006) .016) .009-.006-.029 (.024 (.015) .006-.024) .016) .007 (. Depending upon the specific compound and solubility.031 (.019-.011-.028 (.019-.006-.005-.008 (.007-.015 (.020-.009-.013 (.006) .006-.014) .032) .027-.041) . 0.006 (.016 (.022-.008 (.021) .030 (.012) .025 (.008 (.008) 75th ..019) .100 (.039) . 1992).011-.021 (.027 (.014) 90th .018-.019 (.048) .011-. with much slower elimination from bone.013) .035 (.006) .019-.007 (.009) Selected percentiles ( 95% confidence interval) 50th .009) .034-.006-.048) .011-.007-.008 (.008) .019 (.033 (.016) .013 (.025-.010-. After long term or repeated exposure.045 (.058) .014) .034-.007 (.009 (.013-.026-.054) .022 (.015) .015-.017) .009) * . Uranium is eliminated in feces and urine.010) * . population from the National Health and Nutrition Examination Survey.015 (.008) .012 (.009) .010) .010-.005-.005 (.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 .012 (.010-.007-.007) .013 (.008 (.021 (.010-.010-.007 (.006-.014-.074) .S.005-.009) .012 (.010) .025-.005 (. about 50% of the absorbed dose is eliminated in the urine within the first 24 hours.009) .018) .017 (.040 (.059 (.026) .008) . 2005).018-.027) .029 (.009) .031-.006-.

S. 2006). 28 soldiers who may have been exposed to DU by inhalation. In two studies of a Finnish population with high natural uranium concentrations in their drinking water.65 μg/L). 41 (1). Pullat VR.. et al. 2004). the geometric mean urinary uranium concentration was 0.S. Drinking water and other environmental standards have been established by U.. 1992. 2004). Nuclear Regulatory Commission (NRC) has set an action level of 15 μg/L urinary uranium to protect people who are occupationally exposed (U. 2001-2002. EPA.S.. McDiarmid M. Mil Med 2003.e. but in whom no shrapnel was embedded. with emphasis on quality control. Carmichael AJ.011 μg/L (McDiarmid et al. Uranium content of blood. (May et al... 2002. A previous nonrandom subsample from NHANES III (n = 499) (Ting et al... Thomas RG. Kent (England): Nuclear Technology Publishing. Metivier H.S. eds.110 to 45 μg/L (Ejnik et al. 2006). Recent studies of veterans have been conducted to examine concerns about DU exposure during military conflicts. 1994.1996.cdc. Galletti. Pillai KC. 2002). Information about external exposure (i.. Guidebook for the treatment of accidental internal radionuclide contamination of workers. in that the levels were below their respective detection limits (Byrne et al. The U. population.168(8):600-605. Atlanta (GA).. In a study of 105 persons exposed to natural uranium in well water. 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.62:562-566.. although slightly increased during and after deployment. 2004).78:143-146. Health Phys 1992.162 μg/L) (Orloff et al. Workplace air standards and guidelines for external exposure to soluble and insoluble uranium compounds have been established by OSHA and ACGIH. Six workers in a depleted uranium program showed concentrations of 0. 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. In a much larger study of 446 Gulf War veterans who were concerned about past exposure to DU. 2003. 1978). Radiation protection dosimetry. Breitenstein BD. 2006). Byrne AR.61 μg/g creatinine. Older studies have demonstrated urinary uranium concentrations that are consistent with levels in the U. Volf V. IARC and NTP have no ratings for uranium human carcinogenicity. Muggenburg BA. and no consistent effects on multiple endpoints of kidney function were found.55 μg/L (median 0. 1-49. Fourth National Report on Human Exposure to Environmental Chemicals 241 .S. had a mean urinary uranium concentration of 0. Centers for Disease Control and Prevention (CDC). 1999) and other small populations have shown urinary concentrations that are similar to those in NHANES 1999-2000. Determination of the isotopic composition of uranium in urine by inductively coupled plasma mass spectrometry.atsdr. In the same study. In 17 U. 2006. environmental levels) and health effects is available from ATSDR at: http://www. or wound contamination. Hamilton MM. Komaromy-Hiller et al.. 2000). Zimmerman I. McDiarmid et al. 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. 1991.html. respectively..066 μg/g creatinine (Gwiazda 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.S.gov/ toxpro2. A cohort of 46 U. Vol. Horan P. References Bhattacharyya MH.107:143-157. 2006). Squibb K. Biomonitoring Information Levels of urinary uranium reflect recent and accumulated exposure. Boyd P. soldiers who had been injured and had embedded DU shrapnel for as long as eight years. ingestion. Ejnik JW. Tolmachev et al. In: Gerber GB. 2005. NRC. Hamilton et al. Eighty-five percent of those levels were above the 95th percentile of the NHANES 1999-2000 population. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. during. urine and hair of exposed and non-exposed persons determined by radiochemical neutron activation analysis. Benedik L.1992. Durakovic A. Urinary uranium measurements in 103 Canadian military personnel showed mean urinary levels slightly less than geometric mean in this Report (Ough et al. 2000). Health Phys 2000. Dietz LA. Karpas et al.Metals injury associated with elevated urinary uranium levels (Kurttio et al. Dang HS. Sci Total Environ 1991.. soldiers evaluated before. 2004).. urinary levels of uranium were as high as 9. Stradling GN.. and 2003-2004 (Dang et al. pp. (Kurttio et al.... Determining the normal concentration of uranium in urine and application of the data to its biokinetics. Finding a measurable amount of uranium in urine does not mean that the level of uranium causes an adverse health effect.078 μg/L (ranging up to 5. the median urinary concentration was 0. Third National Report on Human Exposure to Environmental Chemicals. the median urinary uranium concentration was 2.

Kurttio P. Bennett LG. et al. Saha H. McDiarmid MA. Jackson RJ. Gwiazda RH. Cremisini C. Human exposure to uranium in groundwater. Pirkle JL. Englehardt SA. Roth P.158:165-190. Mistry K. concentration and daily excretion of uranium in urine of Japanese. Kuwabara J. Sampson EJ. Am J Kidney Dis 2006. patient population and literature reference intervals for urinary trace elements. Sabbioni E. Metcalf S. Jarrett JM.79(1):11-21. Kane R. Health Phys 2006. Review of elements in blood.94:319-326. NRC). Salonen L. Environ Health Perspect 2002. Karpas Z. U. Saha H. Nuclear Regulatory Commission (U. Hollriegl V.86:12-18. Orloff KG.85:228-235. Van der Venne MT.91(2):144-153.Metals Galletti M. Ough EA. Health Phys 2003.87:51-56. Paretzke HG. Gucer P. July 1978. Smith D. Military deployment human exposure assessment: urine total and isotopic uranium sampling results. J Toxicol Environ Health A 2004. Tolmachev S. Ash KO. Li WB. Makelainen I. Comparison of representative ranges based on U. Auvinen A.S. VI.S. et al. Roiz J. and inexpensive method for determination of uranium in urine and fresh water: comparison with LIF. Komaromy-Hiller G. Environ Res 2004.71(6):879-85. et al. May LM. Squibb K.44:29-40.82(4): 527-532. Komulainen H. Engelhardt SM. et al. Karpas Z. Nuclear Regulatory Commission (NRC) Guide 8. Hancock RG. Washington (DC): NRC. Hamilton EI. Health Phys 2002. Kidney toxicity of ingested uranium from drinking water. Costa R. Katorza E. et al. D’Annibale L. Heller J. Lewis BM. plasma and urine and a critical evaluation of reference values for the United Kingdom population. Scott K.47(6):972-982. Shelly T.81:45-51. Health Phys 2004. Pekkanen J. Clin Chim Acta 2000. Kurttio P. Squibb K. Health Phys 1996. U. Environ Res 1999. Noguchi H. Uranium daily intake and urinary excretion: a preliminary study in Italy. Oeh U.S. Biological monitoring and surveillance results of Gulf War I veterans exposed to depleted uranium. McDiarmid MA. Salonen L. et al. Element reference values in tissues from inhabitants of the European community. Int Arch Occup Environ Health 2006. Radiat Environ Biophys 2005.296(1-2):71-90. Cordero S. Lorber A. Uranium and thorium in urine of United States residents: reference range concentrations. Wahl W. Pinto V.67(8-10):697-714. Kalinsky V. Paschal DC. An examination of uranium levels in Canadian forces personnel who served in the Gulf War and Kosovo. 242 Fourth National Report on Human Exposure to Environmental Chemicals . McDiarmid M.S. Biologic monitoring for urinary uranium in Gulf War I veterans. rapid. Oliver M. Wilson PD. Oberbroekling KJ.22–Bioassay at uranium mills. Howerton K. Ejnik J. Health Phys 2004. Halicz L. Sci Total Environ 1994. Ting BG. Renal effects of uranium in drinking water. Andrews WS. Inductively coupled plasma mass spectrometry as a simple. Detection of depleted uranium in urine of veterans from the 1991 Gulf War. Harmionen A. Marko R. Charp P. Auvinen A. Marino R. Biokinetic modeling of uranium in man after injection and ingestion.110(4):337-342.

60) 8. leather tanning.70-3. lettuce) can be the main sources of intake for humans (FDA.55) Sample size 2820 2522 01-02 03-04 01-02 03-04 01-02 03-04 4.75-3.0) 11. matches.0-17.50) 5.93-4.20 (7.0-17.10 (6.20 (2.0 (12. milk.80) 75th 6. Drinking water.0) 14.10-4.96 (3.10-11.50) 3.0 (9.0) 15.50) 11.60-6.40 (3.0) 10.05.EPA.40) 6. see Data Analysis section) for Survey years 01-02 and 03-04 are 0.0-17.76) 4.90 (5.03) 3.80-6.00-6.70 (3.30 (2. 2007).40) 4.10 (7.0 (11.05 (2.88) 3.50-3.67-5.0) 19.30-6.40-11.0) 16.40) 90th 10.20-12.56) 3.0) 12.60 (4.0) 13.5 hours and has a small estimated volume of distribution (Crump and Gibbs.0) 9.30-7.11) 4.00-6.10 (5.12) 3. and certain plants with high water content (e.09) 3.20) 3.0) 10.65) 3.20-11.60) 5.g. potassium.70 (3.80) 7.0-18.35 (3.75 (3.00) 4.90 (5.68) 4.0) 8.30 (5.10-11.20-3.10) 5.0 (9.81) Selected percentiles ( 95% confidence interval) 50th 3.90-6.20 (5. Large doses of perchlorate have been used as a medicine to treat hyperthyroidism and to diagnose disorders related to thyroid or iodine metabolism.10) 3.. 2005).54 (3.70) 3.0 (12.50 (5.S. Perchlorate is stable under most environmental and physiological conditions.90 (2.93 (4. and limited applications in pharmaceutics.45-4.22 (2.70-9.90 (5. 2005).51 (3.0) 13.0-17.20) 4.30-7. 7601-90-3 General Information Perchlorate is an inorganic chemical containing one chlorine and four oxygen atoms.90-3.39-4.89-3.0) 15.0 (9.19-4.62 (3.0 (8.0-20. Survey years 01-02 03-04 Geometric mean (95% conf.0 (11.40 (5.30) 6.00) 7.0) 8.29-3.0) 708 617 681 652 1228 1092 Limit of detection (LOD.18-3.40-13.0 (8.80) 12.80-15.66) 3. It is normally found and produced as the anion of a sodium.70 (3. and reducing agents.00) 3.30 (2.20 (8.30-17.Perchlorate Perchlorate (Urbansky.0 (12.46) 3.81-16.40 (8.07-4.10-7.70-12. In addition.0-17.0 (8.90-10.60 (7.40-4.93-3.0 (11.0) 9.38) 5. Other manufactured uses include fireworks.10) 5.70-7.0) 14.08-3. fabric dyeing.0) 13.20) 7.90-11.01 (2.70-3.0 (11.90 (4.10-12. 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.50-7.0 (9.0 (11.0) 9.0 (11. Perchlorate has been characterized as a mobile and persistent ground and surface water contaminant.40 (4.0) 13.44-4.80 (6. laboratory analysis.50-4.0 (11.70-11.0) 13.0 (8.0) 13.21 (2.10 (6.00) 5.20 (6.90-3.0 (11.0-18.0 (11.40 (3.40) 3.20-4.0) 95th 14.11) 3.16) 3.80-8. 1998). Inhibition of iodine uptake by competition for the sodium/iodide symporter in the thyroid can be estimated in humans by measuring radioiodine uptake CAS No.40 (5.76 (3.40-6. interval) 3..0-17.00-5.20 (2.0) 14.10 (2.10) 12.0 (10.50) 6. Perchlorate is excreted unchanged from the human body with an estimated elimination half-life of about 7.S. 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.60) 3.70-6.0) 9.20 (4.80-4. but has strong oxidant properties in the presence of concentrated acids.0-29.80 (3. 2006) and accumulate in nitrate-rich mineral deposits mined for use in fertilizers Urinary Perchlorate Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.05 and 0.40-4.60 (4.0) 9.50 (3.30-19.22-5. 2001-2002 performed on surplus samples (variable unavailable of NHANES website) Fourth National Report on Human Exposure to Environmental Chemicals 243 .50-4.50 (8.0-15.40 (4.20-4.80 (7.0-14.60-7.0-23.30) 6.70-5.26 (2.49-3.0) 374 314 828 721 1618 1487 01-02 03-04 01-02 03-04 4.0) 1335 1229 1485 1293 01-02 03-04 01-02 03-04 01-02 03-04 4.90-11.74-3.0 (9.20 (4.80 (3. or ammonium salt.0) 10.90 (3. and electroplating. 2002).50-11.32 (3.90-9.84) 14.0) 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 3.79 (2.40 (5.0 (11.19 (3.90-9.0 (13.0-15.0) 9.40) 3.10) 3.0-18.00) 3.0-19.80) 3.0) 11.90) 5.50) 5.0 (9.0) 13.S. small amounts of perchlorate can form naturally in the atmosphere (Dasgupta et al. population from the National Health and Nutrition Examination Survey.87-3. Animal and human studies have shown that perchlorate can inhibit thyroid hormone production (NAS.40-7. certain catalytic metals.31) 2.0 (12.40) 2. Perchlorate was added to the U.47-4.80-4.80-12.90-12.02 (3.40) 3.30 (5.0 (9.0) 11.51 (3.90) 6.0) 13.0 (8.40-5.

age.10 (4.70-5. In the U.60 (3.87) 2.30) 3. it is known that maternal and congenital hypothyroidism adversely effects neurological development and decreases learning capability.83 (5.22-4.6) 12.84) 2.42 (3.60-8.S.21 (2.0-14.60) 3.91) 4.40 (4. Survey years 01-02 03-04 Geometric mean (95% conf.70 (2.00) 3.0) 12.90-11.20 (2. Lamm and Doemland.70 (4.54 (2.0) 13.52-9. suggesting its tumorgenic effect is a result of a chronic increase in thyroid stimulating hormone indirectly resulting from iodine uptake inhibition.4 (11.30 (6.74) 7. 2006.60-3.6-17.1 (11. Ecologic studies from screening programs with elevated perchlorate in the regional drinking water have indicated no increased prevalence of abnormal neonatal screening tests for this disorder in these regions (Kelsh et al.26 (3.80-3.87-3.30 (5.0) 1335 1220 1483 1284 01-02 03-04 01-02 03-04 01-02 03-04 3.37-13.20) 3.0) 7.99-3.40) 5. Li et al.60-11.44-6.93-5. congenital hypothyroidism is a condition for which nearly all newborn blood is screened. In these small short-term experimental studies on males and studies of male perchlorate workers with doses or estimated exposures thousands-fold higher than known environmental exposures. 2007).60-15.00-3. 2005).10-7.00-11..4) 13.19-6.99 (5.03 (2. 2002).10 (4. but without effects on serum levels of thyroid stimulating hormone or thyroxine (Braverman et al.45) 3.80 (4.22-6.87 (5.20 (6.02-4.90-2.10) 6.10 (6.43) 6.10-3.60-8.10 (1.56-3.40) 3.0 (8.0) 12.0) 14.73) 3.00 (4.50 (6.0) 4.70-15.00 (2.46-4. Though it produces follicular cell thyroid tumors in animal studies at goitrogenic doses.12-2. However.61 (5.00) 4.61-10. in a representative sample of U.0) 6.4 (8. and the presence of other substances known to affect thyroid function (e.08 (3.93-8.02) 3..93) 3.46-13.95 (2. 2005). 2005.81-3.4-16.90 (2.39 (3. chronicity of exposure.98) 3.35) 3.37 (4.29-6.0 (8.64) 5.50) 5.90-20. urinary perchlorate at environmental exposure levels were inversely associated with thyroxine levels and positively associated with levels of thyroid stimulating hormone (Blount et al.0) 10.51-4.97-5.60) 10..3 (10.3) 12.76-3.0-44.33-6.24 (4.58) 2.33-12.50-9.90 (2.0) 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 .S.20-3.60) 8.44) 3.0 (10.S.45-2.09 (7.1) 8.41) Sample size 2818 2504 01-02 03-04 01-02 03-04 01-02 03-04 5.90-3. 2002.82 (5.46 (3.47) 2.1-22. dietary iodine intake.90 (7.93-5.20-10. thiocyanate.07 (2.40 (3.71 (5.4 (10.35 (4.33 (7. 2001.90) 5.10) 3. medications).40 (7.30) 75th 5.75) 3.60-11.87 (7.34-3.30 (3.05 (4.7 (11.0) 9. 1999.20-9.S.90-9.2) 8.50) 2..5) 8. 2005). 2002.25) 5.5 (13.25) 5.67) 5.54 (3. interval) 3.20 (3.0 (11.g.39) 2.0-14. population from the National Health and Nutrition Examination Survey.70 (2.4 (11. During gestation and infancy. menopausal status.1-16.Perchlorate inhibition (RUI). Short term human studies of the effect of perchlorate on RUI have been used for risk estimation (Greer et al.12 (6.10 (2.0-19.80 (7.22-4.51 (3.00-2.15-12.00) 9.76 (3.S. 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.04-3.35 (2.EPA.52 (8.80 (7. levels and sufficient in most participants (Tellez et al..00 (6.10) 4. 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.80) Selected percentiles ( 95% confidence interval) 50th 3. NAS.50) 2.50 (3.1-14.25) 5. Many factors may be important in consideration of perchlorate action on the thyroid: dose.16-3.20-3. gender.30-10.61-5.18-3. Also.77 (3.3) 11. nitrate.72 (3.93-7. levels.0 (9.1-13.14 (2. 2000).30-5.70-3.0) 13.3) 8.0) 12.89 (2.10) 13.60-5.24-2.50) 6.39-4.20 (7. U..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. 2005. women with urinary levels of iodine less than 100 micrograms per day.20) 8.56 (3.32) 5.70) 10.19-10. Greer et al.70) 2.0 (11.4) 8..30-5.41-9.90-15.26) 4.66) 3..20-4.96) 2.36 (8.40-10..0-17. Lawrence et al.8 (11.0) 11.20 (4.22 (2.60-6.87) 7.S.80-3.08) 3.04-3.60-5. 2003.S.50-3.90 (4.EPA.53 (2.40) 17.29) 2..09) 3.64-3. Steinmaus et al.0 (9. up to 68% RUI has been demonstrated.1 (8. perchlorate is negative in most genotoxic assays (U.89-3.40 (3.0) 374 313 827 715 1617 1476 01-02 03-04 01-02 03-04 3.50-5.0) 12.30) 5.2) 8. although iodine intake was higher than U.50) 95th 12.3-14.0) 9.30) 90th 9.50) 9.86) 4.0 (11.59) 3.25 (3.0 (9.6) 20.70-4.

Long-term environmental exposure to perchlorate through drinking water and thyroid function during Fourth National Report on Human Exposure to Environmental Chemicals 245 . newborn thyroid function.11(3):295. Dasgupta PK.46(5):509. Blount BC. Lau EC. Sesser DE. J Occup Environ Med 2003.htm. Erratum in: Environ Health Perspect 2005. Also.gov/toxpro2. 2007). Osterloh JD. Environ Sci Technol 2006.. Lawrence J. Health Implications of Perchlorate Ingestion. most of the population is considered to be below the U. National Academy of Sciences (NAS). Page Last Updated: 05/28/2009.. Additional information about exposure and health effects is available from the U. et al. epa. Urinary perchlorate and thyroid hormone levels in adolescent and adult men and women living in the United States. 2005. Pirkle JL.115(9):1333-1338. Thyroid 2001. Pino S. Howd R. Benchmark calculations for perchlorate from three human cohorts. Deyhle GM. He X.S.113(11):A732. Dyke JV. May 2007. Chacon PM.45(10):1116-1127. When these NHANES 2001-2002 urinary levels of perchlorate are used to calculate daily oral intakes for the U. (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. The effect of short-term low-dose perchlorate on various aspects of thyroid function. Perchlorate Exposure of the US Population. Buffler PA.10(8):659-663. Has perchlorate in drinking water increased the rate of congenital hypothyroidism? J Occup Environ Med 1999. Perchlorate in the United States. Greer SE. Thyroid 2000. Magnani B. Blount BC. Rutherford GW.90(2):700-706. Compared to a previous study of pregnant women in three Chilean communities with varying perchlorate levels in the drinking water. The effect of perchlorate. Li FX. Crump KS. Pino S.gov/safewater/ccl/perchlorate/perchlorate. J Clin Endocrinol Metab 2005.42(2):200-205. and environmental perchlorate exposure among residents of a Southern California community.40(21):6608-6614. Li Z. 2005). Low dose perchlorate (3 mg daily) and thyroid function. Health effects assessment for environmental perchlorate contamination: the dose response for inhibition of thyroidal radioiodine uptake in humans. 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. 6/2/09 Greer MA..S. Impact of smoking and thiocyanate on perchlorate and thyroid hormone associations in the 2001-2002 national health and nutrition examination survey.cdc. References Blount BC.114(12):1865-1871. Daaboul JJ. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Finding a measurable amount of perchlorate in urine does not mean that the level of perchlorate causes an adverse health effect. Primary congenital hypothyroidism. Doemland M. Lawrence JE. Mauldin JP. Blount et al. Preliminary Estimation of Perchlorate Dietary Exposure Based on FDA 2004/2005 Exploratory Data. Lamm SH. Crump KS.Perchlorate be unlikely to occur without overt perturbation of thyroid homeostasis. 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. Gibbs JP. Kelsh MA.fda. Richman K. Kirk AB. Landingham CB. EPA reference dose (Blount et al. Braverman LE. et al. Biomonitoring Information Urinary perchlorate levels reflect recent exposure. Jackson WA.17(4):400-407. Washington (DC): National Academy Press. population.S. Steinmaus C.gov/Food/FoodSafety/ FoodContaminantsAdulteration/ChemicalContaminants/ Perchlorate/ucm077653. Environ Health Perspect 2002. Caldwell KL.atsdr. Braverman LE. Cross M. Osterloh JD. Abarca CR. thiocyanate. J Expo Sci Environ Epidemiol 2007. et al.html.html and from ATSDR at: http://www. Environ Health Perspect 2005.EPA at: http://www. J Occup Environ Med 2000. Lamm S. CFSAN/Office of Plant & Dairy Foods.113(8):10011008. Barnard JC. Valentin-Blasini L. Braverman LE.41(5):409-411. Lamm SH. The levels seen in NHANES 20032004 show a similar pattern to NHANES 2001-2002. Miller MD. Pleus RC. Tellez RT. Available at URL: http://www. Pirkle JL. Goodman G. Analysis of relative source contributions to the food chain. Neonatal thyroxine level and perchlorate in drinking water. Lamm SH. 2001-2002. et al.110(9):927-937. Skeels MR. Food and Drug Administration (FDA). National Research Council of the National Academies. Valentin-Blasini L. and nitrate on thyroid function in workers exposed to perchlorate long-term. 2005). Erratum in: J Occup Environ Med 2004. Byrd D. Environ Health Perspect 2007. 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. Environ Health Perspect 2006.

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

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

. Bookstaff et al. Prevedouros et al. In some cases. U. 1990).. by high protein binding in plasma and other proteins.. may metabolize or degrade to PFOA (Dinglasan et al. kidney..S. 2006a.. see Data Analysis section) for Survey year 03-04 is 0. Excepting PFOS and PFOA... there is limited information on the sources. Serum Perfluorobutane sulfonic acid (PFBuS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U. 2003). PFOA has been reported to cause liver. but probably include dietary sources (Kannan et al. Keller et al. 2006.5 years and for PFOS. PFCs have been identified in surface coastal and ocean waters (Yamashita et al.. Survey Geometric mean (95% conf.. The PFCs often measured in human serum are listed in the table. The ammonium salt of PFOA has been tested at high doses in mammalian animal studies and produced altered weights of the liver. 1993). 2004). which may vary for some chemicals by year and by individual sample. endocrine and immune effects. 2004. in a wide variety of marine and land animals (Kannan et al. 2005. 2003). Kannan et al. The elimination half-life of PFOA in humans is roughly estimated to be 3. the 8-2 telomer. in part. and in offspring. Taniyasu et al.... including immunologic effects and tumor induction. human toxicokinetics.Perfluorochemicals PFOS greater than 2000-fold over aquatic levels). Both PFOA and perfluorodecanoic acid have been shown to reduce androgen levels in laboratory animal studies (Biegel et al. 2007a). heptadecafluoro-1-decanol. EPA. 2005. 1995. 248 Fourth National Report on Human Exposure to Environmental Chemicals . 2004. PFOA is mostly excreted in the urine in animal studies. PFOA preparations used in many studies may also contain a small percentage of other chain length perfluoroalkyl acids (i. peroxisomal proliferation. pancreas. Human health effects from PFCs at low environmental doses or at biomonitored levels from low environmental exposures are unknown.. Lau et al.. 2007).. 2004).. but still can have long residence times in the body. C6.e. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. C7). < LOD means less than the limit of detection... 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. Tittlemier et al. Some of the effects in animals may be mediated through peroxisomal proliferation. Unlike many organohalogen contaminant chemicals.. 2004) and may be attributable to the ability of PFCs to affect intracellular lipid binding proteins.. For instance.. Vanden Heuvel et al. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th < LOD 90th * 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 485 538 962 Limit of detection (LOD.4. 2005. 2005). but limited observations in humans suggest that only one-fifth of the total body clearance is renal (Harada et al. population from the National Health and Nutrition Examination Survey. growth retardation and delayed sexual maturation (Kennedy et al.8 years (Olsen et al. thymus and spleen. PFOS and PFOA levels in archived bird eggs from Sweden have increased thirtyfold from 1968 to 2003 (Holmstrom et al. hepatotoxicity. Lau et al. Olsen et al. the perfluoroalkyl acids (PFOA and PFOS) do not tend to accumulate in fat tissue.. 2000. Guruge et al. approximately 4. C5. and β-oxidation of lipids (Kudo et al. 2005).S. 2003. but the relevance of peroxisomal pathways in humans is unclear (Kennedy et al. All sources of human exposure are uncertain. The liver toxicity of several PFCs is evident by vacuolization and lipid accumulation in both rodent and monkey livers (Seacat et al. or effects of other PFCs. and in human blood and semen (Calafat et al.. 2005). 2004. 2004. It is unclear if environmentally degraded telomer products are a major source of other PFCs.. 2003a and 2004a). environmental fate. 2002.. PFOA (and probably other perfluoroalkyl acids) exist in the anionic state at physiologic and environmental pHs and their distribution in the body is determined.

400 (<LOD-. A study of workers chronically exposed to primarily PFOA showed no biochemical evidence of hepatotoxicity or hormonal changes (adrenal. < LOD means less than the limit of detection.800 (.500 (. 2007b.800 (.. 2003a.400 (<LOD-. 2003.S.600 (. Roughly similar levels of PFCs in serum have also been measured previously in other samples of the U.900 (.800 (. U. perfluorohexanesulfonate (PFHxS). 2004b). 2004.. 2003. developmental and teratogenic effects were demonstrated in offspring.500) .500-3.. 2007a.800) 1. 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. thyroidal).. Biomonitoring Information Serum levels of PFCs (particularly PFOA and PFOS) tend to reflect cumulative exposure over several years. Serum Perfluorodecanoic acid (PFDeA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.. the potential to estimate risks to humans from animal doses is uncertain.500) . or increased cancer rates (Alexander et al.500 (. Late gestational exposure to PFOS in animal studies has also demonstrated early neonatal lethality. PFOS.700) . interval) Selected percentiles ( 95% confidence interval) Sample 95th . 2007b).500) . 2007a.00) .400-1.00) . Fourth National Report on Human Exposure to Environmental Chemicals 249 . and there was no clear evidence of excess all-cause or diseasespecific mortality.10 (. EPA. PFOA.10) * 03-04 03-04 * * < LOD < LOD < LOD .00 (.500-1..S. Effects on serum liver enzymes in limited observational studies of human occupational exposures are unclear.. 2003. Lau et al. 2003). 1999.800 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 2003a). At high but non-toxic maternal doses of PFOS. reproductive. 2004a. PFOS.108 times higher than background serum levels in humans (Butenoff et al.00) . and humans. monkeys.400) .500) . 2005).300 (<LOD-.900 (. 2003a.Perfluorochemicals and testicular tumors in high dose animal testing (Biegel et al. Slightly higher levels of PFOS and PFOA in males than females have been noted in several other studies (Calafat et al. Serum PFOS levels associated with toxicity in test animals were 310-1550 fold higher than 95 percent of the levels found in a study of adults (Olsen et al.. U. 2004).50) .40) .300 (<LOD-. 2003a). In comparing three separate reports on adults.300-1. population. hepatotoxicity.. animal and human serum PFOA levels have been compared: serum levels associated with toxic effects in animals are 66-11.400-1.500) 90th . population from the National Health and Nutrition Examination Survey.20) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD .10) .. 2007. PFOA.500-.800) 1.500 (<LOD-1.500-1. 2004).600 (. 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.. Twelve different PFCs were measured in the sera of NHANES 2003-2004 participants.. Thibodeaux et al. and other PFCs have not been classified as to human carcinogenicity by IARC or NTP. Two recent cross-sectional human studies observed a negative correlation of birth weight with serum levels of PFOA (Apelberg et al. 2001.. Fei et al. which may vary for some chemicals by year and by individual sample.... Olsen et al.S.80) 640 1454 03-04 03-04 * * < LOD < LOD . Due to marked intergender differences in the elimination of PFOA in rats and substantial differences in the half-life of PFOA in rats.600 (.600-2. Cook et al.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 . 2003a. 2007). Olsen et al.400-.. see Data Analysis section) for Survey year 03-04 is 0. and changes in thyroid hormone concentrations (Grasty et al.300 (<LOD-.700 (. elderly and children. 2005). However....400-.20) . Survey Geometric mean (95% conf. Harada et al. possibly related to lung immaturity (Lau et al. At doses causing maternal toxicity. development in offspring was stunted and hypothyroxinemia was observed.500-1.400 (<LOD-. In such studies. Olsen et al. 2004. Animal studies of PFOS have demonstrated weight loss.10) . EPA. and no substantial age trends were seen within adults ages 20-69 (Olsen et al.3. 2003). Kennedy et al.400-1.400-1.. the median PFCs values tend to be roughly similar in these age categories (Olsen et al.900 (.80) 485 538 962 Limit of detection (LOD.500-1. 2003).400-1.S. 1992.

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

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

30 (2.70-5.27) 1.60 (1.30 (1.90 (1.70) 2.900 (. see Data Analysis section) for Survey year 03-04 is 0.91) 2.10 (.56-1.5) 8.40 (1.77-2.00-6.60 (1.70 (2.20 (6.60-3.50) 6.70) 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 1.80 (1.800-1.40 (2. see Data Analysis section) for Survey year 03-04 is 0.70-2.01 (1.50-3.50 (1.92 (1.00 (1.834-1.852 (.40-1.70-6.80 (4.40 (1.00 (2.984 (.14 (.60-8.12) .586-.40) 1.00) 1.20 (1.17-1.600-.20) 1.00 (1.80-8.60-2.689 (.20) 485 538 962 Limit of detection (LOD.40 (1.20-1.70-2.73-2.721-1.17 (1.816-1. population from the National Health and Nutrition Examination Survey.80) 1.10) 4.80-8.72) 1.90 (1.70-7.10) 5.60-2.80) 3.50 (6. population from the National Health and Nutrition Examination Survey.90) 90th 5.00-1.10) 8.80-3.30) 03-04 03-04 .697-1. Serum Perfluorononanoic acid (PFNA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.00 (1.90 (4.963 (.00-7.03) 1.40) 4.50-6.90) 1.70) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 1.40-3.80 (1.50 (6.09 (.80) 5.30) .30 (1.10) 1053 1041 03-04 03-04 03-04 . Survey Geometric mean (95% conf.00-1.1) 485 538 962 Limit of detection (LOD.1.50 (4.42 (1.40) 1.50 (1.20) .70) 3.30 (3.54) .30 (7.60-4.0) 8.00 (.20) 2.00 (1.S.10 (1.Perfluorochemicals Serum Perfluorohexane sulfonic acid (PFHxS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.50) 2.20-1.40 (1.10 (4.00 (.10) 6.80-4.90) 1.10) 1.72 (1.10) 6.70 (1.826-1.20 (1.90-10.80-6.0) 1053 1041 03-04 03-04 03-04 1.60 (6.900-1.20) 03-04 03-04 2.50 (1.20-1.10 (.14) Selected percentiles ( 95% confidence interval) Sample 95th 3.44 (2.80-12.50-10.10) 1.861 (.80-7.20-1.10 (4.912-1.70) 1.60-4.40) 640 1454 03-04 03-04 1.70) 2.900-1.900-1.30 (1.90) 1.26) 2. Survey Geometric mean (95% conf.50 (4.800 (.700 (.20 (1.80-2.30 (2.87-2.04) .3 (9.809) 1.S.80-3.05-2.20-3.60) 2.30-12.00) 3.30) 3.00 (5.900-1.900) 1.10-5.40-1.20 (1.10) 75th 3.93 (1.30 (1.20 (6.80-7.900-1.70) 13.80-4. 252 Fourth National Report on Human Exposure to Environmental Chemicals .60) 3.30-9.40) 2. interval) .60-2.86 (1.10-9.00) 2.30) 3.10) 4.700-1.90) 8.70) 1.00) 1.30) 3.80) 90th 2.90) 3.40) 640 1454 03-04 03-04 2.60-3.900-1.30-6.90-2.70-10.10 (.900 (.60-7.60) 1.62-2.90 (1.20-2.50) 2.60) 9.10) 75th 1.16) .67-2.90-19.90 (1.60 (1.40) .10-9.16) Selected percentiles ( 95% confidence interval) Sample 95th 8.90 (4.30 (6.5) 5.50 (1.20) 1.30-2.90 (2.00-8.966 (.6) 7.80-4.80) 4.51) 1.50-6.835-1.3.50 (2.08) 2. interval) 1.

8-22.47 (4.07-4.80-9.1) 57.60 (7.90-4.9 (19.5) 1053 1041 03-04 03-04 03-04 14.6 (44.8 (37.21-3.4 (17.5-33.4) 20.7-49.0) 43.91) 3.4-42.30-8.0-16.6 (35.40) 75th 5.4) 21.50) 4.40-10.60-6.7-33.8) 32.1 (24.4) 75th 30.1.3 (44.60 (6.S.1-33.8) 46.53) 3.89 (3.1) 15.5) 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 21.2 (28.8-30.50-4.2 (18.00 (3.6) 18.6) 35.65-4.5 (28.90 (7.5-21.85-4.99-3.9 (13.3 (35.6-24.0) 21.2-22.50-13. population from the National Health and Nutrition Examination Survey.3) 42.2) 45.40) 3.30-3.70-9.90) 6.0) 485 538 962 Limit of detection (LOD.3-61.8 (45.2 (27.60 (4.27) 4.20) 5.S.0) 36.1-25.2) 30.6) 9.60) 03-04 03-04 3.30 (3.20-9.82) 4.9) 22.4) 640 1454 03-04 03-04 23.0 (20. Survey Geometric mean (95% conf.2-57.9 (17.30-6.60-13.9) 22.7 (35.5) 57.8) 27.2 (16.9 (22.8-22.5-62.0) 21.60 (6.50 (4.35) 3.8 (34.0) 03-04 03-04 19.5 (28.79) 4.5) 18.10 (3.6) 7. Serum Perfluorooctane sulfonic acid (PFOS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.3) 485 538 962 Limit of detection (LOD.50-6.3) Selected percentiles ( 95% confidence interval) Sample 95th 54.20 (4.90-12.1) 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 4.30 (3.3-22.60 (5.5-23.4-17.9) 27.80-12.2) 30.40 (4.7 (13.5) 9.11 (2.10 (3.2 (21.2 (19.5) 19.6 (42. interval) 3.10-3.40 (6.70 (5.7-53.3) 41.40) 90th 7.84-3.70) 6.0-70.6) 42. interval) 20.7-30.7 (35.8-22.70) 4.7-69.10 (6.90 (5.18 (3.9-19.0-20.0-66.47-4. Survey Geometric mean (95% conf.70) 3.20) 7.20-4.4 (19.95 (3.70-7.00 (5.5) 7.Perfluorochemicals Serum Perfluorooctanoic acid (PFOA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.6-45.70-5.8-35.60 (3.1 (23.40-17.4) 56.40) 5.5) 8.5) 32.6-50.7 (7.6) 62.8-81.50 (3.60-14.80 (6.70-7.80-4.27) Selected percentiles ( 95% confidence interval) Sample 95th 9.60) 8.7 (43.67-4.40-6.1 (19.70 (5. see Data Analysis section) for Survey year 03-04 is 0.20) 5.3) 28.4 (23.1-52.80 (5.8-78.4.6) 1053 1041 03-04 03-04 03-04 3.40-6.30) 7.1-35.4 (19.20) 7.7 (19.90 (7.00 (5.3 (35.9-38. Fourth National Report on Human Exposure to Environmental Chemicals 253 . population from the National Health and Nutrition Examination Survey.1-24.30-11.7-23.50) 7. see Data Analysis section) for Survey year 03-04 is 0.6 (19.80) 8.90 (7.20-5.00) 3.80 (7.37 (2.20 (4.30-5.60-9.4-25.6) 21.40-14.96 (3.20) 4.3 (17.0 (27.9) 9.10) 5.70-10.20) 10.70 (3.4 (28.30 (5.30) 6.0) 90th 41.80 (6.7) 39.90-4.9-23.2) 640 1454 03-04 03-04 4.1-36.7 (43.0) 23.3 (28.

300) * 03-04 03-04 * * < LOD < LOD < LOD < LOD .200-. which may vary for some chemicals by year and by individual sample.300) . interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th < LOD 90th * 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .300) .S. Serum 2-(N-Ethyl-perfluorooctane sulfonamido) acetic acid (Et-PFOSA-AcOH) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.300 (.300 (.300-.300) . Survey Geometric mean (95% conf.300 (. < LOD means less than the limit of detection.300-.300 (. < 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.200-.300 (. see Data Analysis section) for Survey year 03-04 is 0.300 (.300-.300) . which may vary for some chemicals by year and by individual sample.300) .400) 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD . 254 Fourth National Report on Human Exposure to Environmental Chemicals .300 (.300) . see Data Analysis section) for Survey year 03-04 is 0.200-.200-.500) .300 (. Survey Geometric mean (95% conf.500) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .200-.500) .300 (.500) 485 538 962 Limit of detection (LOD.500) < LOD 485 538 962 Limit of detection (LOD.400) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th 90th .300 (.400 (<LOD-.300 (.4. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.200-. population from the National Health and Nutrition Examination Survey. interval) Selected percentiles ( 95% confidence interval) Sample 95th .500) .300-.200 (<LOD-.S.300 (.300) .200-.2.200-.300 (. population from the National Health and Nutrition Examination Survey.300 (.200-.Perfluorochemicals Serum Perfluorooctane sulfonamide (PFOSA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.200-.

Survey Geometric mean (95% conf.700) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD . interval) Selected percentiles ( 95% confidence interval) Sample 95th .10) .30) 1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.600 (<LOD-1.700 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.10-1.00 (.00 (. which may vary for some chemicals by year and by individual sample.10-1.10 (. population from the National Health and Nutrition Examination Survey.600 (<LOD-1.00) < LOD .900-1. population from the National Health and Nutrition Examination Survey.10-1.900-1.700 (<LOD-.10 (.70) 1.20) 1.90) .3.10-1.20-1.700 (<LOD-.700) .900-1. Survey Geometric mean (95% conf.900-1.300 (<LOD-1.800) . see Data Analysis section) for Survey year 03-04 is 0.700 (<LOD-.700) 90th 1.80) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD .00 (.700) 1. < LOD means less than the limit of detection.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) 1.10-1.10 (1.400 (<LOD-1. Fourth National Report on Human Exposure to Environmental Chemicals 255 . Serum Perfluoroundecanoic acid (PFUA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.60) 485 538 962 Limit of detection (LOD. see Data Analysis section) for Survey year 03-04 is 0.00 (.S.700) 1.700 (<LOD-2.800) . < LOD means less than the limit of detection.10) .30 (1.800 (<LOD-.30) .10) * 03-04 03-04 * * < LOD < LOD .40) 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD .900) .40) < LOD < LOD .30 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.40) 1.900 (.50 (1.10) 1.60) 640 1454 03-04 03-04 * * < LOD < LOD .900) 485 538 962 Limit of detection (LOD.80) 1.900-1.400 (<LOD-.00-1.30) 1.900-1.30 (1.300 (<LOD-.500 (<LOD-.900) 1.S.600 (<LOD-.700 (<LOD-.700 (<LOD-.600) .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 .600 (<LOD-1.10 (.50 (1.20 (1.900-1.300-2. which may vary for some chemicals by year and by individual sample.900 (<LOD-1.6.80) 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 .

2007b. Needham LL. Cook JC. et al. Reidy JA. Cord serum concentrations of perfluorooctane sulfonate and perfluorooctanoate in relation to weight and size at birth. Environ Sci Technol 2007a. Dinglasan MJ. Falandysz J.7(4):371-377.104(2):322-333. population: Data from the National Health and Nutrition Examination Survey (NHANES) 1999–2000. and perfluorinated contaminants in livers of polar bears from Alaska. Evans TJ.38(17):4489-4495. Toxicol Sci 2001. Kuklenyik Z. Biegel LB. Yoshinaga T. Bignert A. Sasaki S. Aguilar-Villalobos M. sex and geographic factors on levels of perfluorooctanesulfonate and perfluorooctanoate in human serum over the last 25 years. Halden RU. Corsolini S. et al.and perfluorinated acids. Birth Defects Res B Dev Reprod Toxicol 2003. Needham LL. Guruge KS. Keller JM. Mandel JH. The toxicology of perfluorooctanoate.39(23):9101-9108. Caudill SP. Characterization of risk for general population exposure to perfluorooctanoate. Kudo N. Taniyasu S. Calafat AM.46(2):141-147. Mortality of employees of a perfluorooctanesulphonyl fluoride manufacturing facility. Frame SR. Kuklenyik Z. Perfluorinated chemicals and fetal growth: A study within the Danish National Birth cohort. Kawashima Y. Herbstman JB. et al. Katakura M. Environ Sci Technol 2004. The influence of time. Calafat AM. Bandai N.39(1):80-84. Serum concentrations of 11 polyfluoroalkyl compounds in the U. Rodricks J. 256 Fourth National Report on Human Exposure to Environmental Chemicals . Edwards EA. O’Connor JC. Environ Health Perspect. Peterson RE. Saito N. Hurtt ME.S. Tully JS. Kuklenyik Z. Fluorotelomer alcohol biodegradation yields poly. Cook JC. Environ Sci Technol 2004.60(10):722729. Day RD.113(2):209-217. Harada K. Environ Sci Technol 2006a. Androgenic deficiency in male rats treated with perfluorodecanoic acid. et al. Fillmann G. Yamashita N. Polyfluoroalkyl chemicals in the U.60(1):44-55. Chemosphere 2006b. Toxicol Appl Pharmacol 1995.39(3):363-380. Taniyasu S. Cook JC. Kennedy GL Jr.38(10):2857-2864. Kannan K. Yoshinaga T. Loganathan BG. McLaughlin JK. Olsen J. Burris JM. Needham LL. Suzuki E.115(11):1677-1682. Butenhoff JL. Mabury SA. Witter FR.Perfluorochemicals References Alexander BH.179:99-121. Inoue K. Rev Environ Contam Toxicol 2003. et al. Ingall GB. Frame SR. Moore RW. Kannan K. J Occup Health 2004. Environ Health Perspect 2007. Tully JS. Jarnberg U. Environmental and toxicity effects of perfluoroalkylated substances. et al. Caudill SP. Koizumi A. Calafat AM.68(6):465-471. Olsen GW. Grey BE. Watanabe T. Mechanisms of extrahepatic tumor induction by peroxisome proliferators in male CD rats.63:490496. Hurtt ME. Inoue K.S. Tarone RE.34(4):351-384. Olsen GW. Regul Toxicol Pharmacol 2004. brominated. Gaylor DW. et al. J Environ Monit 2005. Prenatal window of susceptibility to perfluorooctane sulfonate-induced neonatal mortality in the Sprague-Dawley rat. Saito N. Seneviratne HR. Environ Res 2005. Liu RC. Seacat AM. Perfluorooctanesulfonate and related fluorochemicals in human blood from several countries. Environ Sci Technol 2005. Environ Sci Technol 2005.99(2):253-261. Mandel JH.40:21282134. Reidy JA. Kumar KS. Wong LY. Reidy JA. Butenhoff JL. Rogers JM.134(1):18-25. Olsen GW. Grasty RC. Lau CS. Hekster FM. Kannan K. Yun SH. Calafat AM. Holmstrom KE. Biegel LB. Kuklenyik Z. Morikawa A. Perkins RG. Perfluorinated organic compounds in human blood serum and seminal plasma: a study of urban and rural tea worker populations in Sri Lanka. Calafat AM. population: data from the National Health and Nutrition Examination Survey (NHANES) 2003-2004 and comparisons with NHANES 1999-2000. Environ Health Perspect 2007.41:2237-2242.1968--2003. Hurtt ME. Induction by perfluorinated fatty acids with different carbon chain length of peroxisomal beta-oxidation in the liver of rats. Temporal trends of PFOS and PFOA in guillemot eggs from the Baltic Sea. and ex vivo studies. Apelberg BJ. Environ Sci Technol 2005. Reidy JA. Moore JA. Murray SM. Fei C. de Voogt P. Perfluorinated compounds in the plasma of loggerhead and Kemp’s ridley sea turtles from the southeastern coast of the United States. Arendt MD. Crit Rev Toxicol 2004. Yamashita N. Perfluorochemicals in pooled serum samples from United States residents in 2001 and 2002. Induction of Leydig cell adenomas by ammonium perfluorooctanoate: a possible endocrine-related mechanism. Kamiyama S. Mohotti KM. in vivo. Perfluorinated chemicals in selected residents of the American continent. Chlorinated. Ye Y. Occup Environ Med 2003. Bookstaff RC. Harada K.Koizumi A. Wijeratna S. Toxicol Appl Pharmacol 1990. Mandel JS. Toxicol Appl Pharmacol 1992.115(11):1670-1676. Needham LL.115(11):1596-1602.124(2):119-132. Effects of ammonium perfluorooctanoate on Leydig cell function: in vitro. O’Connor JC. Laane RW. Chem Biol Interact 2000. Renal clearance of perfluorooctane sulfonate and perfluorooctanoate in humans and their species-specific excretion.39(23):9057-9063.

Yamashita N. Dietary exposure of Canadians to perfluorinated carboxylates and perfluorooctane sulfonate via consumption of meat.51(8-12):658-668.111(16):1900) Olsen GW. Olsen GW.gov/opptintr/pfoa/pfoara. Environ Sci Technol 2006. J Children’s Health 2004b. I: maternal and prenatal evaluations. Fourth National Report on Human Exposure to Environmental Chemicals 257 . Lundberg JK. Mandel JH.41(9):799-806. Butenhoff JL. A survey of perfluorooctane sulfonate and related perfluorinated organic compounds in water. and food items prepared in their packaging. Prevedouros K.82(1):359. Lau C. Seacat AM. Olsen GW. et al. Gamo T.54(11):1599-1611. Environ Sci Technol 2003. Environ Health Perspect 2003a. Buck RC. Ehresman DJ. The developmental toxicity of perfluoroalkyl acids and their derivatives. Barbee BD. Thomford PJ. U. and humans from Japan. 2003.111(16):1892-1901. Burris JM. Taniyasu S. Church TR. Burlew MM. Mar Pollut Bull 2005. Exposure to perfluorooctane sulfonate during pregnancy in rat and mouse.74(2):369-381. Lundberg JK. perfluorooctanoate andother fluorochemicals in human blood.45(3):260-270. Korzeniowski SH.113(5):539-545. Butenhoff JL. Burris JM. J Occup Environ Med 1999. Church TR. Mair DC. Hansen KJ. Reagen WK. Peterson RE. Taniyasu S. Hansen KJ. fish. Environmental Protection Agency (U. Lau C. Butenhoff JL. fast foods. Butenhoff JL.Perfluorochemicals Kudo N. Olsen GW. Yamashita N. Half-life of serum elimination of perfluoroo ctanesulfonate. EPA). Kannan K. Biol Pharm Bull 2003. Induction of triglyceride accumulation in the liver of rats by perfluorinated fatty acids with different carbon chain lengths: comparison with induction of peroxisomal betaoxidation. Sources. et al.68:105–111. fate and transport of perfluorocarboxylates. Coordinate induction of acyl-CoA binding protein.. 2003a. Miller JP. Perfluorooctanesulfonate and other fluorochemicals in the serum of American Red Cross adult blood donors. Chemosphere 2007b. Ehresman DJ. Butenhoff JL. et al. 2007a. J Ag Food Chem 2007. Church TR. Olsen GW.) Tittlemier SA. Hansen KJ. Olsen GW. Seymour C. Butenhoff JL. Rogers JM. Subchronic toxicity studies on perfluorooctanesulfonate potassium salt in cynomolgus monkeys.perfluorohexanesulfonate. Serum perfluorooctane sulfonate and hepatic and lipid clinical chemistry tests in fluorochemical production employees. Kannan K. Hansen KJ. Chemosphere 2004a. Thibodeaux JR.S. (Erratum in: Environ Health Perspect. birds. Helzlsouer KJ. Huang HY. Environ Health Perspect 2005. Hanson RG. Froehlich JW.68(1):249-264. (Erratum in: Toxicol Sci 2004. Grey BE.40(1):32-44. Hanson RG. Richards JH. Olsen GW. fatty acid binding protein and peroxisomal beta-oxidation by peroxisome proliferators. J Occup Environ Med 2003b. Rogers JM. Ellefson ME. et al. and perfluorooctanoate in retired fluorochemical production workers. Nesbit DJ. Cao XL et al. Toxicol Sci 2003. Available from URL: http://www. Pepper K. Historical comparison of perfluorooctanesulfonate. fish. Zobel LR. Horii Y. et al. van Belle G. Seacat AM. Petrick G. Quantitative evaluation of perfluorooctanesulfonate (PFOS) and other fluorochemicals in the serum of children. Exposure to perfluorooctane sulfonate during pregnancy in rat and mouse. Hanari N. Burris JM.1177(2):183-190.2(1):53-76.55:3203-3210. A global survey of perfluorinated acids in oceans. et al.115(9):1298-1305. Mandel JH. Thibodeaux JR. Grey BE. Olsen GW. Washington.74(2):382-392. htm. Preliminary Risk Assessment of the Developmental Toxicity Associated with Exposure to Perfluorooctanoic Acid and its Salts. 1/15/06 Vanden Heuvel JP. Epidemiologic assessment of worker serum perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) concentrations and medical surveillance examinations. Burris JM.epa. Case MT. Toxicol Appl Pharmacol 2004. Moisey J. II: postnatal evaluation. Serum concentrations of perfluorooctanesulfonate and other fluorochemicals in an elderly population from Seattle. Toxicol Sci 2002. Preliminary evidence of a decline in perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) concentrations in American Red Cross blood donors. Horii Y. Hansen KJ. Burris JM.26(1):47-51. Mandel JH. Stanton ME. Cousins IT.S.37(12):2634-2639. Rogers JM. Larson EB. Sterchele PF. Kawashima Y. Toxicol Sci 2003.198(2):231-241. Biochim Biophys Acta 1993. Olsen GW. Environ Health Perspect. Mandel JH. Bronson R.

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

Environ Health Perspect 1982.3. Evaluation of a recombinant yeast cell estrogen screening assay. Connor C. McDonnell DP. dibutyl phthalate (DBP). Coldham NG. 1986). Massey RC. and Sertoli cell abnormalities in the male animals and. 2001. but similar findings were not present in young Swedish men with comparable or higher median levels of urinary metabolites (Jonsson et al. Pharmacokinetics. 2002).cdc. Clark K. These differences may contribute to species-specific differences in toxicity (ATSDR. Biomonitoring Information Urinary levels of phthalate metabolites reflect recent exposure to the parent phthalate diester. and extent of metabolite conjugation to glucuronide (Albro et al. Information about external exposure (i. Dave M. Also.. Available at URL: http://www. 2004. Peck and Albro. Springall C. Matthews HB. Rhodes et al. 2002. 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. 2001. van der Broek PH.Phthalates and metabolites have been tested.nih. The monoester metabolites are thought to mediate toxic effects for some of the phthalates. 2004. McKee et al.. Sauer MJ. 2005.cdc. Castle L. Lovekamp-Swan and Davis.. Food Addit Contam 2001. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 2000a. Population estimates of concentrations of specific phthalate metabolites may differ by age. Toxicological profile for di(2-ethylhexyl)phthalate update [online]. Phthalate urinary metabolite levels in men evaluated at an infertility clinic were associated with several measures of sperm function and morphology (Duty et al. NTP-CERHR. 227-262. 2005)..html. 2006).atsdr.gov/ toxprofiles/tp9. interactions with macromolecules and species differences in metabolism of DEHP.gov/ reports/index.. Springer. Metabolism of di(2-ethylhexyl) phthalate. Dirven HA. Silva MJ. A biomarker approach to measuring human dietary exposure to certain phthalate diesters. 2004. Environ Health Perspect 1997. peroxisomal proliferation may not be a relevant pathway in humans (Rusyn et al.niehs.. 1985.. Variation occurs from person to person in the proportions or amounts of a metabolite excreted after similar doses (Anderson et al. 4/20/09 Agency for Toxic Substances and Disease Registry (ATSDR). atsdr. 1982).. Vol. Corbett JT.html. which may be a pathway to the development of liver toxicity and cancers in these animals. 2000c.805:49-56. 4/20/09 Albro PW. testicular atrophy. 2004). at very high levels. 2001). Drug Metab Rev 1989. phthalates have been shown to induce peroxisomal proliferation in rodents. 2000b. phthalates produced anti-androgenic effects by reducing testosterone production and. 2007). 1982. J Chromatogr B 2004. Assessment of critical exposure pathways. 2004. 2002). Calafat AM. Automated solid phase extraction and quantitative analysis of human milk for 13 phthalate metabolites. Cousins IT.18(12):10681074. Kessler et al. pp.atsdr.html. but there are known species-related differences in the hydrolysis of diester phthalates. 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. Slakman AR. Herbert AR. 2007. Jordan S. Needham LL. at higher doses.gov/toxpro2. Albro PW and Lavenhar SR.e. 2003. Jongeneelen FJ. Hauser et al.. Part Q: Phthalate Esters.. References Agency for Toxic Substances and Disease Registry (ATSDR). Determination of four metabolites of the plasticizer di (2-ethylhexyl) phthalate Fourth National Report on Human Exposure to Environmental Chemicals 259 .New York. Mackay D. efficiency of intestinal absorption. reducing estrogen production. In animals. and benzylbutyl phthalate (BzBP) during the fetal period produced lowered testosterone levels. However.. environmental levels) and health effects is also available for some phthalates from ATSDR at: http://www.. effects that may be mediated by inhibiting testicular and ovarian steroidogenesis. The proportions of each metabolite for a given phthalate may vary by differing routes of exposure (Liss et al.. Scotter MJ. 2006).html). gender. Hauser et al. Hoppin et al. variation also occurs in the same person during repetitive monitoring (Fromme et al. Anderson WA. Toxicological profile for di-n-butyl phthalate update [online].45:19-25.cdc. ovarian abnormalities in the female animals (Jarfelt et al. 105:734-742. High doses of di2-ethylhexyl phthalate (DEHP). and race/ethnicity (Silva et al. The Handbook of Environmental Chemistry.gov/toxprofiles/ tp135. 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. Available at URL: http://www. 2003... Silvapathasundaram S.21:13-34.. Schroeder JL. In Staples CA (ed).

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

6) 29.6 (66.6) 35.4) 38.2-39.3-18.1) 31.7-17.3 (13.4 (27.2-19.6) 14.3 (30.5-18.4) 108 (96.4 (59.4-24.2 (10. and 03-04 are 0.4 (29.8-133) 89.4-62.0 (27.2 (14.4 (10. 2004..2-16.7-35.9-47.6 (13.5-35.5) 55.0 (15.2 (11.4 (10.5-36.5 (47.0) 70.9 (12.3) 13.1.4) 12.5-97.2-183) 101 (78. NTPCERHR.6-116) 122 (102-142) 101 (85.2 (19.2) 17.6 (32.9-14.4 (48.8-72.1 (58.6-132) 103 (84.9) 18.9 (28.9 (11.5-33.2-31. can produce developmental and reproductive toxicity in rodents.8) 33.0) 23.9-49. Biomonitoring Information The median levels of MBzP in NHANES subsamples from 1999-2000.4 (31.0) 90th 67..9-27.5 (67.6 (12. 262 Fourth National Report on Human Exposure to Environmental Chemicals .0 (14.0) 33. Food crops take up BzBP.6-39.4) 81.1) 13.8) 28.1) 12.7-82.8-41.0 (43.8-17.1-214) 166 (116-191) 145 (110-213) 88.6 (21.3 (22.1 (14.5) 15.3-161) 99.1) Selected percentiles ( 95% confidence interval) 50th 17.4) 75th 35. some personal care products.5) 214 (108-399) 235 (183-330) 255 (146-365) 125 (93.5) 16.4) 33.4) 49. BzBP can be released into the environment during its production and.8-16.1 (10. particularly male animals (McKee et al.9 (22.0-55.8) 63.2 (43.6) 35.1-61.S.4-16.5 (26.2-33.3 (54.2-116) 122 (102-143) 101 (84.7 (11.3) 23.5 (76.7) 23.9-16. population from the National Health and Nutrition Examination Survey.7-16.5-62.2-17.8-17.3.0 (30.4-120) 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 13.8-76.3-88.5) 15.6 (13.8) 14.9-62.0-130) 101 (86.0 (26.6-92.2 (47.6) 37.4 (13. respectively.1-18.2-38.6-17.5 (61.7-16.7-58.2) 78.8-35.1-16.3) 94. 2000).1 (32.5 (57.3 (12.1 (13.8-121) 79.6-29.1-16.1-120) 52.5) 27. vinyl tile.2-20.4) 80.7 (51. and diet is the major source for general population exposure.3) 37. sealants.3-75.3 (33.2) 66.9) 14.6) 24.6-79.1 (13.1-38.2) 33. residents (Blount et al. because it is not bound to products in which it is incorporated.5-40.5-41.6) 13.9) 11.8 (86.6) 50.5-84.8 (80.1) 67.6) 16.9 (70. 2001-2002.7-15.2) 12.6) 67.2) 69.3) 15.7-14.7 (12.5 (13.0 (12.6 (13.4-92.3 (29.9 (16.7 (13.6-150) 94.9 (39.4-15.9) Sample size 2541 2782 2605 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 39.S.4-25.0) 32.3) 54.1 (20.6-38.5 (27.3 (12.7 (80.9-87.4 (63.9-190) 86.3-91.8 (28.6) 25.1 (55. including MBzP.2) 14.2) 15.2) 13.1) 32.8 (14.8-18. interval) 15.3 (12.3-18.5 (55.6) 95th 103 (94. High dose BzBP and its monoester metabolites.9-28.4) 14.3-12.5-94.9 (21.8-14.6 (53.0) 34.9) 12. it can be released into the ambient air during use or disposal of the products.6) 14.7-172) 103 (74.8-48.Phthalates Benzylbutyl Phthalate CAS No.9) 15.1) 29.4) 129 (98.8 (71.3-27.2-40.3 (29.3 (44.1-15.2 (19.8-13.7) 38.8 (50.0) 20.4-127) 80.6 (13. 0.7 (70.1-35.8 (38.5) 23.0-26.0 (33.0 (11.6) 13.5 (66.0 (23.2-16. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.3-34.5) 82.6 (41.1-15.9) 49.3-130) 122 (88.9-30.5-36.4 (53.5) 30.8 (71. 01-02.0 (34.3-125) Total 15.9 (13.7-25. and 0. 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) 40.4) 51.9) 43.8.4) 71.8 (30.6) 63.9) 13.3) 13.8-16.0 (55.5-145) 138 (106-241) 143 (127-179) 120 (99.6-72. People exposed to BzBP will excrete mono-benzyl phthalate (MBzP) and small amounts of mono-n-butyl phthalate in their urine.0 (30.0 (15.1-116) 122 (93.0-85.1-90.8-14.8 (10.2-155) 91. 85-68-7 General Information Benzylbutyl phthalate (BzBP) is a solvent and additive used in products such as adhesives.2) 22.3-43.3-122) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.1 (19.8 (12.8 (21.3-21.8) 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 16.4) 35.1-43.3) 63.3-74.2 (25.7-16.6-92.6-43. and 2003-2004 were generally similar those reported in U.3-82.9 (12.6-18.9) 14.8) 24.4 (53.2-115) 113 (91.7 (82.6) 15.4 (32.1-39.8-64.4) 35.0) 24.0) 16. see Data Analysis section) for Survey years 99-00.1) 14.7 (53.2) 32.4 (68.5) 65.0-106) 58. and to a lesser extent.1 (14.4) 65.5-25.2) 14.7-170) 169 (134-198) 152 (99.7-119) 99. IARC considers BzBP not classifiable with respect to human carcinogenicity.7-13. 2000). car care products.1) 68.8 (53.7 (15.4) 98.0 (20.5-14.1) 76.8-98.4 (32.

6-12.4) 13.0-51.0-90.6) 13.4-14.2 (27.2-49.3) 14.3) 13.8) 24.4-60.8-42.3 (35.8-69.5) 20.1-27.4-79.4-116) 73.S.4) 328 393 342 752 742 729 1461 1647 1534 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 12.6 (14. 2002.1 (13.2-21.73-12.9-28.4) 50.9) 12.8) 13.8-13.1 (23.8-27.0) 49.8-14.3) 36.7 (11..0 (49.7-20.5 (11.9 (43.. 2003).6 (51.4 (11.4 (60.7) 46.3 (13.3 (60.9-23.5-79.2) 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 12.7 (21.9) 64.8 (69.3 (38.7 (19.5-31.8 (64. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.1) 23.3) 90.0 (38.6 (19.0 (41.9) 100 (80.3 (39.7 (14.6-15.4 (46.9) 12.7-12.1-29.4) 15.8) 26.0) 13.9 (22.7) 25.8-85.7) Sample size 2541 2782 2605 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 40.4-93. 2007).4 (63.8-15.9 (12.5-99.4) 104 (89.3) 16.3) 55.4 (26.8) 71..1 (34.4) 90th 50.5-16.8) 108 (75.7 (11.4) 25.0 (13.8) 33. 2004).5) 13.2 (56.5-13. Weuve et al.5-76.9-104) 62.8) 16.0 (11.8-34.4-90.9 (10..1) 80.2) 67.3 (12.1-12.1 (46.9-13..6 (11.2-15.2-13.8 (46. In NHANES 1999-2000.2) 11.6 (30.2 (41.7) 38.8 (12.9 (10.8 (50.2 (40.9) 24.1 (21.8) 46.7 (54.4 (11.9-40.3 (23.69-11.5) 78. 2002). 2006). Hoppin et al.1) 12.9 (24.6 (15.4) 51.3) 29.1-12. in young Swedish men (Jonsson et al.5-26.9) 42.3) 37. population from the National Health and Nutrition Examination Survey.8-64. In an annual sample of German university students.5) 41.5 (12.8 (10.1-14.6) 30.2) 11.0-48.5 (48.6) 12.2-26.1 (19.9-62.7-90.9 (15.7-15.6 (30.4 (34.6-26. and females compared to males (Silva et al.7-29.7-19.8) 56.7 (59.6) 75th 25.5-23.8 (11.5 (49. 2007).4-17.7 (11.4-42.6-20.9-16. 2005).6) 25.4) 12.2-51.0 (33.6 (24.7 (23. interval) 14.4) 60.4) 21.2) 32.0) 12.1 (15.8) 68.Phthalates York City (Adibi et al.9-69.0) 15.5 (56.5-58.6-13.4) 28.3) 89.1 (11.4 (11.5) 16.0 (41.9-83.4-19. 2005.3) 18.3) 13.9 (15.1 (21.6) 58.1) 35. in men attending a Boston infertility clinic (Duty et al.1-120) 77.0 (12.8-60.4) 13.7 (55.1) 39.4-18.7-31.6 (22.6-81.5) 17.4 (13.6-47.7-61.6-86.2-12.5) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Fourth National Report on Human Exposure to Environmental Chemicals 263 .7-14.1) 24.4-14.8) 53.4 (25.7-69.9-14.8-39.8) 34.1 (21.6 (34.4-102) 70.5) 46.5) 10.9-13.6) 53.1 (18..9 (51.8) 80.5-42.9) Total 14.6 (11.7-19.9) 11. the adjusted geometric mean levels of urinary MBzP were significantly higher in several subgroups: children compared to adolescents and adults.8-173) 195 (121-305) 229 (99.3-38.3) 13.0 (10.7-56.5) 23.8) 33.4-23.1-58.1 (25. 2003).2-57.1-35.5) 95th 77.8) 53.7 (13.3) 12.0) 11. 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.7) 19.9 (39. 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.0-53.4-99.2-15..4-142) 134 (116-176) 136 (85.7) 56.9 (29.4-15.5) 14. Hauser et al.9) 52.3) 14.9 (24.7) 11.0-27.6 (36.6 (57.5 (35.1) 27.1 (14.6 (11.0-15.3-11. and in a small sample of German residents (Koch et al.4) 44.3-16.0-109) 65.3 (15.0 (12.4) 17.9-115) 57.5-61.2) 15.6-116) 74.5-29.9 (55.0) Selected percentiles ( 95% confidence interval) 50th 13.5-26.4 (33.3) 67.7-15.0 (62.8) 54.5-57.8 (49.3) 73.1) 17.4 (10.4 (74.1 (43..9) 11.1 (41.0) 24.7 (18.4 (69.7 (13.6) 12.9 (9.8 (30.4 (12.2) 11.1 (13...3 (24.1) 142 (99.8 (57.7-20.1 (53.2-17.4) 14.9) 12.7 (12.7-397) 70.9 (54.95-14. Urinary Mono-benzyl phthalate (MBzP) (creatinine corrected) Metabolite of Benzylbutyl phthalate (BzBP) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.3-64. 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.1) 24.5 (10.8 (13.8-80.1-125) 86.1 (21.5 (9. adolescents compared with adults.5 (10.5-213) 49. DC reported median urinary MBzP levels that were about twice the levels of adults and females reported in NHANES 1999-2002 (CDC.3) 21.6) 38.7-14.9 (12. 2004.1-79.8-13.2 (69.3-73.4-27.2-78.0 (67.6) 73.8) 15.0) 60. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.5-58.8-48. A small study of African-American women in Washington.8) 11.5 (42.0-26.7-123) 77.3-34.1 (9.8-16.4 (21.2-13.8-15.2) 26.2-117) 95.6-40.6-99.8-14.7 (38.0) 24.2) 12. median urine levels of MBzP were about one-half the median levels in NHANES subsamples from 1999-2002 (Wittassek et al.5-38.8-13.

Rylander L. Phthalate monoesters levels in the urine of young children. Brock JW. Singh NP. David RM. Chen Z. et al. Third National Report on Human Exposure to Environmental Chemicals. Caudill SP. et al. Environ Res 2003. Centers for Disease Control and Prevention (CDC). et al. Silva MJ. Prenatal exposures to phthalates among women in New York City and Krakow. Environ Health Perspect 2006. Hagmar L.93:177-185. Hoppin JA. Brock JW.nih. Available at URL: http://cerhr. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Environ Health Perspect 2002. Hum Reprod 2007. Butala JH. Int J Hyg Environ Health 2007. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. Davis BJ. 2005. Perera FP. Rossbach B. Camann DE. Sampson EJ. Reidy JA.S.68:309-314. J Androl 2004. Ryan L. et al. Hauser R. Poland. Wiesmuller GA. Levels of seven urinary phthalate metabolites in a human reference population.112(3):331-338. et al. Urinary levels of seven phthalate metabolites in the U.18(1):122. et al. Malek NA. Wittassek M. Brock JW. Gans G. Angerer J. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Helm D. McKee RH. Caudill SP.16(4):487-493. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. Environ Health Perspect 2003. Eckard R. Silva MJ.22(3):688-695. Pirkle JL.gov/ chemicals/phthalates/bb-phthalate/bbp-eval. Silva MJ. Bull Environ Contam Toxicol 2002. Dobler L. 2000 [online]. Jonsson BAG. Hu H.Phthalates References Adibi JJ. Research Triangle Park (NC). NTP-CERHR. Monograph on the Potential Human Reproductive and Developmental Effects of Butyl Benzyl Phthalate (BBP). Barr DB. Baird DD. Hilborn ED. Calafat AM. Epidemiol 2005. Silva MJ. Jedrychowski W. Schettler T.html. Caudill SP. Reprod Toxicol 2004. Calafat AM.niehs. Needham LL.114(9):1424-1431. Environ Health Perspect 2004. 112(5):A270]. Barr D. Jacek R. Needham LL. Weuve J. Green RA. Duty SM. Urinary phthalate metabolites and biomarkers of reproductive function in young men. Duty S.110(5):515-518. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. et al. Drexler H. Exposure to phthalates in neonatal intensive care unit infants: urinary concentrations of monoesters and oxidative metabolites. Hodge CC.111(14):1719-1722. Reproducibility of urinary phthalate metabolites in first morning urine samples. Sanchez GN. Internal phthalate exposure over the last two decades—a retrospective human biomonitoring study. Giwercman A. 4/20/09 Silva MJ. Atlanta (GA). Richthoff J. Environ Health Perspect 2000. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. Blount BC.25(2):293-302. Ryan L.108(10):979-982.210(3-4):319-333. Koch HM. 264 Fourth National Report on Human Exposure to Environmental Chemicals . Koch HM. Meeker JD.

73-5.17) 4.6 (9.30 (4.26 (2.59) 3.50) 5..1 (13.50-10.6) 17.3 (16.6) 16.20-9.3 (11.50-4.0 (11.3) 3.10) 2.3-43. 2000).3-48.9 (16.5-29.30-3.1) 16.10) 8.9) 15..20-6.3-19. Biomonitoring Information Median concentrations reported in the NHANES 19992000.50-6.37) 6.97-7. mostly as MnBP (Anderson et al.0) 20.43) 6.90 (4.30-7.00-4. Fourth National Report on Human Exposure to Environmental Chemicals 265 ..3) 33.10-9.50) 90th 12.00) 10.1) 22.50) 7.20) 4. 2000.91) 4.7 (18. 2005.10 (4.30-6.71 (2. Studies of children found age-related differences in urine MBP levels.25) 01-02 03-04 01-02 03-04 01-02 03-04 4.0) 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. and in a small sample of Japanese adults (Itoh et al. residents (Blount et al.40-9.97) 4.6) 17.0) 13.6) 16.30) 2.30) 5.4-27.00-6.5 (17.S.4-12.4) 22.40 (2. they have been referred to as monobutyl phthalate (MBP). 2001).20-2.10) 3.0) 24. 2003)..8 (9..80 (5. Survey Geometric mean (95% conf.02) 4.50) 18.0) 12.20 (3.70 (5.60 (8.7 (9.3-20.72-3.3-18.3-30.7-18.4) 12.40) 5. OSHA has established a workplace air standard for external exposure to DBP.40 (7.60 (5.10-2..70) 3.48 (2.07 (3.6-26.5-16.7-20.82-3.73 (2. and also in some printing inks.1-12.66) 2. Median MBP levels in two European studies were about two to six times higher than median levels in this Report (Jonsson et al. referred to as DBP) are industrial solvents or additives used in many personal care products such as nail polish and cosmetics.70) 5. see Data Analysis section) for Survey years 01-02 and 03-04 are 1.5) 25.6-20.6 (11. population from the National Health and Nutrition Examination Survey.1-25.2 (8. 2005).1-17. interval) 2.4) 5.80-5. in a small sample of pregnant women in New York City (Adibi et al.40-17.2-33.0 (19.S.0-25.90) 12.7 (17.84) 4.97) 2.70-8.6-14.6 (10.56 (5.3-24..46-5.24-8. Compared with the median for 6 to 11 year olds in NHANES 1999-2004 (CDC.96) 3.8) 677 652 703 699 1216 1088 Limit of detection (LOD.80 (3.4 (20.17 (2.30) 6.80) 75th 5.33 (2.10-9.7) 15.20 (7.55) 2. Koch et al.46 (3.00) 7.7 (7.19-3.50-2.7-31.5 (10.7 (17.2) 5.00 (5.3) 18.70 (2..1-20.85-6. When total DBP metabolites have been measured.0) 9.00) 4.4 (14.94) Selected percentiles ( 95% confidence interval) Sample 95th 17.6 (13.90-4.30-13.90-4. about 65% to 80% of a dose is eliminated in urine within 24 hours.3 (13.10) 11.50) 8. In addition.67 (5.63) 3.6) 26.6-34.70-4.5 (11. 2005).60 (2. pharmaceutical coatings.60) 3.3 (13.5-16.46) 2.40-4.0 (13.0-38.20 (6. 2001-2002 and 2003-2004 subsamples were similar to MBP levels reported in U.6 (13.56-4.40-5. DBP can produce reproductive toxicity in male rodents (McKee et al.0-18.0 and 0.70-4.40-12. Following oral administration of DBP to humans.5) 22.2-14.7) 4.50) 2.1 (8.40 (2. 2004.00-9.6-18.9-23.90-7.50 (3.6 (14.7) 7. 2004.00 (7. Small amounts of mono-3-carboxypropyl phthalate are also produced from di-n-butyl phthalate.5-24.56 (3.80 (2.30-11.30 (3.80 (5.00-6.00) 4. 84-69-5 General Information Dibutyl phthalates (both di-n-butyl and di-isobutyl phthalates. 84-74-2 Di-isobutyl Phthalate CAS No.20-12.90 (6.44-2.8) 40.7) 18.20) 7.10 (4.68 (2.80-5.2-22. in men attending a Boston infertility clinic (Duty et al.3 (18.81 (3.5) 12.30-6. and insecticides.5 (27.2 (11..11-3.28-5.5) 14.60-6.30) 10. People exposed to dibutyl phthalates will excrete mono-n-butyl phthalate (MnBP) and mono-isobutyl phthalate (MiBP) in their urine.40-3.9) 10. CDC.0) 393 342 742 729 1647 1534 01-02 03-04 01-02 03-04 2.6) 12.7-31. NTP-CERHR.6 (29.7) 14.5) 23.0) 1371 1250 1411 1355 01-02 03-04 01-02 03-04 01-02 03-04 3.0-14.2 (12. 2003).40 (6.90 (3.9 (16.8) 21.49-2.30) 10.5) 18.22 (3.22) 3. Hauser et al.10 (3. Neither IARC nor NTP has evaluated dibutyl phthalates with respect to human carcinogenicity. 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.00-11. 2007).40-4.7 (16.3 (16.9-14.40 (3.3 (19. exposure to benzylbutyl phthalate (BzBP) will also result in small amounts of mono-n-butyl phthalate appearing in the urine.5) 18.56) 3. NIOSH and ACGIH have established guidelines for workplace air exposure to di-n-butyl phthalate.30-2.5 (20.6 (14.20-12.6 (10.90 (4.60 (4.5) 19. 2005).50 (6.80 (2.30 (1.Phthalates Di-n-butyl Phthalate CAS No.00) 6.40-3.0 (13.46 (2.90-2.3.1) 25.10) 9.55 (3.6) 10.

82) 4..34 (3.66) 10.41 (2. 2005).1-24.28 (4.74 (4.65-4.47-12. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.07-5. Differences in urinary MBP population estimates by gender have also been shown (Silva et al.37) 3.81) 4.76-3. the students’ median values for MiBP levels remained relatively unchanged.2) 8.26-2.4) 23. An analysis of NHANES 2001-2002 showed similar age.9 (11. respectively.8) 10.8 (10.03 (5.22 (2.00-3.29-3.1-15.11) 5.54) 2..9-26.0-18.47 (3.91-6.3) 13.3) 28.62-12.92 (7.33 (2.7) 19.6 (15.15) 3.83 (2.38 (6.76-3.25) 5.0) 7. Studies measuring urinary MnBP have reported variable median values compared to the NHANES 2001-2002 and 2003-2004 subsamples.15-4.68 (2.72-7.6-19.52) 3.0) 11.42) 2.52-3.58-3.6 (12.13 (2.43) 3.81) 9.80 (3.46) 3.18) 3.65 (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.43) 3.89 (3.3 (17.59 (4.18 (1.75 (4.0) 3.03-7.8-18. Survey Geometric mean (95% conf.8-18.76-15. Weuve et al.9) 12.6) 13.57 (3.84 (4.64-7.7) 11.07 (2.00 (3.39-3.68) 5.32 (7.95) 2. interval) 2.45) 3.3) 18.99-4. Finding a measurable amount of MnBP or MiBP in urine does not mean that these levels or the parent compound cause an adverse health effect.78) 9.53-3.11 (5.18 (4.6 (9.64-10.46-11.1) 4.33-9.5) 13.00-3.18) 4.2 (11.79-8.39) 5..43) 3.5 (11.66 (8.80) 7.7 (11.20-3.6) 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 2.32) 7.2 (10.1 (10.29-8.56-4.67-5.35) 3.20 (2.31) 2.S.02 (7.88 (2.78) 8.73) Selected percentiles ( 95% confidence interval) Sample 95th 12.5 (9.47-5.3) 13.64-7. 2005). Between 1998 and 2003.65-11.7-28. 2004).51) 5.98 (2.1 (11.08-2.36-7.and gender.8 (9.97-2.94) 6.31) 2.9-40.38-10.54 (4.1-25.20 (2.04) 3.1) 11.56-15.2-13.27-12.74-3.7 (9.89-5.66) 4.02-10.33) 3.6) 11.3 (13.2) 9. Urinary Mono-isobutyl phthalate (MiBP) (creatinine corrected) Metabolite of Di-isobutyl phthalate (DBP) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.1) 13.31 (7.24) 3.3) 16.05) 2. population from the National Health and Nutrition Examination Survey.81 (3.9 (9. up to four and 13 fold.21) 10.17-12.69-7.85 (2. samples from German university students had consistently higher median urine levels of MnBP and MiBP..19 (2.53-5. 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.04-5.10-5.20-2.7) 1371 1250 1411 1355 01-02 03-04 01-02 03-04 01-02 03-04 3.58-4.0 (8.52-20.21 (5.75 (6.11-2.0) 15.46 (2.79-6.8-13.6-19.7 (21.1) 677 652 703 699 1216 1088 266 Fourth National Report on Human Exposure to Environmental Chemicals .Phthalates for neonates was lower (by about half) and the median for toddlers was higher (by about sixfold) (Brock et al.17 (2.72) 5.04) 7.5-19. ranging from more than one-tenth the NHANES median (Itoh et al.01-2.00-7.51) 15.33 (3.86) 6.78-8.14 (4.53-4.79 (4.08) 75th 4..2) 24.1) 10.28-13. 2002.36-2.99) 7. 2007).03-11..9 (15.1) 7.82 (4. 2007).18-4..26 (2.57-4. In an analysis of NHANES 1999-2000.17) 90th 8.52 (2.51) 2. 2006).6 (10.7) 3.76 (3.1) 15.18-10.6 (8.32 (3.0 (10.1-12.69) 4.86-4.4 (12.81 (6.57 (3.56) 5.7) 10.54 (2.0) 393 342 742 729 1647 1534 01-02 03-04 01-02 03-04 2.20 (7.96 (3. to about two to fourfold higher (Fromme et al.4) 15.94 (5.95-3.00) 01-02 03-04 01-02 03-04 01-02 03-04 4.related differences in the adjusted geometric mean levels of urinary MiBP and MnBP (CDC.0 (12.09-2.56) 2.7 (13.55-6.95) 10. Over this time.68) 3.4) 7.13-6.5) 15.9-16.80-3.6 (8.2-15.73 (5.94-12. than adults in NHANES subsamples during the same time period.20-4.66) 2.31 (2.93-6.84 (8.69 (2.62 (6. while MnBP declined (Wittassek et al.44 (3.61-3.8 (8.30) 2.89) 6.30 (6. 2004).69) 6.4-16.8-36.

4) 20.3) 24.6) 166 (127-279) 159 (110-290) 191 (150-243) 165 (121-227) 148 (106-185) 134 (110-158) 143 (117-161) 95.7-127) 328 393 342 752 742 729 1461 1647 1534 12-19 years 20 years and older 99-00* 01-02 03-04 Gender Males 99-00* 01-02 03-04 99-00* 01-02 03-04 22.2-21.0 (45.3) 18.7-124) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites 99-00* 01-02 03-04 Limits of detection (LOD.2 (58.1-27.1) 25.2-114) 73.2-93.1) 23.6-40.1 (26.1) 31.0) 38.6 (55.7) 42.4 (19.5 (28.1 (16.9) 46.6-29.5) 34.7-106) 69.0-51.2-49.4 (35.1) 23.7-121) 97.1 (19. Fourth National Report on Human Exposure to Environmental Chemicals 267 .2-33.0-24.2 (79.6-31.4 (71.2 (21.5-47.7-26.1) 30.1 (54.3 (36.0) 120 (98.7 (51.6-49.7 (28.6) 35.7-20.2) 90th 98.0 (18.5) 17.0 (23.4-159) 107 (84.7 (16.4.5 (59.5) 19.8) 23.4 (21.6-69.9-87.1) 23.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.1 (18.9-42.7-92.1-80.2-23.0 (72.4-31.3) 26.3 (51.9-22.6 (32.0 (15. see Data Analysis section) for survey years 99-00.2 (25.1 (19.4 (23.1-75.5-47.8-29.9) 36.4 (84.7 (33.9 (17.7-42.1 (36.6) 46.8-22.3-40.3 (23.3-21.7 (18. 1.1-51.5-53.2) 38. concentrations of mono-isobutyl phthalate and mono-n-butyl phthalate were measured together and expressed as a combined value.2-159) 92.2 (17.1 (28.3 (42.3) 21.0-26.1 (41.7) 52.0 (78.9) 18.1 (34.1.7) 124 (98.9-53.3-60.0 (36.5 (29.8 (57.0) 31.1 (17.4) 22.9 (79.3 (37.4) 52.5) 21.0 (20.6-44.9) 26.9-28.2 (21.4 (25.4 (72.3 (23.3 (56.7-91.6 (61.3-79.5) 85.1) 36.8) 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. referred to as monobutyl phthalate (MBP).4-60.5 (59.5) 20.1) 17.3-24.6 (65.0) 20.1-22.7 (22.0 (30.3 (60.7-42.7 (43.5) 26.8 (19.5) 40.8-123) 101 (90.6-48.7 (64.3-67.7 (18.2 (59.5) 31.2 (20.9) 29.2) 20. interval) 24. *In the 1999-2000 survey period.6) 80.3) 40.1) 47.0-24.7-53.9.0-19.0) 27.5) 95.5) 78.6-36.1-24.5) 36.3-85. and 0.6-143) 127 (99.1) 20.3-136) 137 (107-162) 119 (90.0) 21.1 (58.5) 36.1 (51.1-82.6) 20.3-76.0-21.4) 59.3) 23.5) 24.0-32.1 (21.7 (24.7) 28.4 (35.2-32.2 (75.2-24. respectively.2-87.9) 71.8-119) 90.9-22.1 (62.7) 74.7-116) 95.4 (36.4 (35.6 (44.1) 19.2) 68.9-79.0-73.7-111) 64.4-44.5-44.9 (79.1-92.8) 48.5) 47.2 (78.0) 84.3 (30.8-25.8-132) 95.5) 65.2) 42.5-117) 95.0-58.7 (19.1 (31.3-96.1-122) 122 (104-137) size 2541 2782 2605 Total years 99-00* 01-02 03-04 50th 26.3 (17.6-24.7 (70.1 (19.6-20.5-43.1 (19.0) 30.6) 38.8-165) 167 (143-197) 138 (110-184) 144 (115-168) 142 (111-161) 107 (89.6-33.7-117) 118 (108-143) 93.6 (48.9-101) 77. 01-02.6 (26.0 (17.9) 21.8) 75th 51.2 (74.4) 64.4 (35.9-114) 116 (97.2 (19.2 (18.2) 26.2) 62.1) 46.S.2-63.9-33.9-92.7-24.5) Age group 6-11 years 99-00* 01-02 03-04 99-00* 01-02 03-04 41.8) 58.6) 21.0 (25.3-145) 85.5-60.4-42.5-27.5 (30.6) 39.7-34.6) 17.5-42.8) 43.7) 92.8) 62.3 (30.6 (19.5) 37.9 (17.2) 32.7-34.4-18.1-20.9 (20.6 (90. Survey Geometric mean (95% conf.4-20. population from the National Health and Nutrition Examination Survey.2-22.4-25.4) Selected percentiles ( 95% confidence interval) Sample 95th 150 (121-169) 108 (94.6 (22.0) 117 (104-131) 112 (84.9) 75.5 (74.0 (31.6) 71.6-113) 108 (90.8-42.3) 36.6 (16.6-29.0-19.6-37.7 (38.4-26.2-56.5-121) 106 (94.4 (38. and 03-04 are 0.3) 19.1-29.

6-22.4-24.7 (54.2-22.4-103) 117 (83.4-164) 96.4-131) 81.7) 20.6-42.2-22.4 (31.9-56.9) 24.2) 21.6 (57.8 (17.7 (16.0 (50.4-61.3) 21.6 (31.2-21.5-30.8) 75th 38.5-15.6-53.4 (53.0 (43.0 (27.8 (33.2-28.4 (16.6) 23.8) 30.9-68.7-78.8 (18.5 (15.8 (50.4-34.0-41.3) 67.8 (16.9-84.6-27.2-86.8 (18.1) 35.4-76.6 (74.1) 21.6) 64.6-128) 96.0 (34.9 (30.2 (19.0) 81.1-18.4) 19.5-64.7-26.5) 60.3 (21.9 (58.7-20.5) 82. 268 Fourth National Report on Human Exposure to Environmental Chemicals .3) 19.2) 65.5-16.3-20.9) 14.5 (18.6) 38.9) 30.4 (17.4 (17.5 (14.0) 55.9 (19.3 (48.2 (16.2) 159 (102-263) 147 (93.0) 28.3-21.8) 34.1 (15.6-155) 91.6 (61.6) 24.9-49.8) 20.1) 20.0-19.0) 108 (71.3 (19.5) 134 (93.5-41.6) 65.0 (19.1) 50.7-19.3 (17.5 (64.0 (52.6) 24.6-16.0 (71.6) 83.1 (29.9 (64.0 (16.2-61.1) 61.3) 52.1) 37.4 (13.8 (25.7-19.7 (73.4) 51.3) 33.6-26.3-49.1 (46.2-16.0 (20.8-235) 137 (108-198) 88.9) 28. population from the National Health and Nutrition Examination Survey.2 (38.2-85.1-21.6-74.4) 53.6 (72.1) 42.7-80.3-114) 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 17.5-142) 89.6-19.8-23.4) 15.9-100) 86.4-72.0-38.9 (20.9 (16.6) 34.1) 44.7 (43.Phthalates Urinary Mono-n-butyl phthalate (MnBP) (creatinine corrected) Metabolite of Dibutyl phthalate (DBP) and Benzylbutyl phthalate (BzBP) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.6) 14.8 (22.1-23.0-47.2) 31.7-21.3-32.9-36.7-23.3-23.1-99.4 (23.8) 23.9-105) 85.8) 22.8-43.9) 39.4 (18.9 (30.4-135) 71.6) 39.4 (47.8) 13.8 (18.4) 15.6-50.5-70.3 (42.8) 17.0 (26.5) 17.6) 18.3-81.7) 36.2-27.9-34.7 (14.5 (81.6) 37.3-26.2-22.1-99.1-128) 97.1-62.9 (73.4 (19.4 (20.0) 53.7 (19.9 (56.9 (35.3) 35.0-90.1) 17.3-78.5) 21.9-14.6 (17.3-21.3) 59.1) 22.7 (60.9) 20.4 (50.2 (35.4 (31.0) 59.1) 53.5 (18.0) 35.0-17.6 (27.2-108) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites 99-00* 01-02 03-04 *In the 1999-2000 survey period.8) 17.6-24.3 (69.4 (50.3 (60.1 (32.6) 31.6-23. Survey Geometric mean (95% conf.3 (55.6) 25.7-51.5) 84.4) 20.4 (45.3) 33.0 (70.3 (24.2-73.9) 91.9) 52.3 (28.6-23.0-75.5-18.8) 19.4) 16.3-40.1-115) size 2541 2782 2605 Total years 99-00* 01-02 03-04 50th 21.4-65.4 (33.0) 70.5-23.4 (68.5-142) 81.8) 20.6 (25.7 (28.9-38.4 (37.4 (31.6-24.5-21.1 (61.0 (18.2) Age group 6-11 years 99-00* 01-02 03-04 99-00* 01-02 03-04 41.5) 90th 68.7-28.0-92.7 (20.8) 63.2) 59.0-113) 104 (83.7 (12.3-106) 74.1) 20.3 (52.S.7 (60.4) Selected percentiles ( 95% confidence interval) Sample 95th 97.3-18.9 (37.4 (56.3 (16.0) 25.2-179) 84.0 (61.8) 40. interval) 22.0 (69.7-39.5 (30.8-32.5-76.7) 19.3 (76.9 (35.9 (39.0) 41.1-32.7) 42.8) 17.6-44.6-44.3) 20.6-28.5-37.2-18.3 (52.2 (83.8-24.0-60.6-92.3 (46.3 (17.6-139) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00* 01-02 03-04 99-00* 01-02 03-04 21.7 (81.8) 34.2-106) 64.9) 62.2) 74. concentrations of mono-isobutyl phthalate and mono-n-butyl phthalate were measured together and expressed as a combined value.8) 28.7 (57.3-17.0) 94.3) 18.1 (34.0) 19.3-71.3 (71.9) 19.3-39.9-68.4 (16.6 (29.9 (30.0 (18.4) 62.1 (21.0 (15.8 (13.6 (41.9) 49.4) 21.8 (65.6 (19.8) 35.6 (25.5) 39.5-22.4-47.5) 91.0) 75.9 (21.3 (17.7 (27.2-48.8-24.3) 19.2 (19.7-42.6-43.0) 29.3) 17.3-38.0) 26.6-32.1 (56.9-26.1-83.7-37.2) 16.9-70.6-119) 63.

Environ Health Perspect 2004. Angerer J. Needham LL. Helm D. Green RA. Richthoff J. Hodge CC. Scotter MJ. Weuve J. Reprod Toxicol 2004. NTP-CERHR. Calafat AM. Koch HM. Malek NA. McKee RH. Levels of seven urinary phthalate metabolites in a human reference population. Caudill SP. Brock JW.112(3):331-338. Itoh H. Internal phthalate exposure over the last two decades—a retrospective human biomonitoring study. Environ Res 2003. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Silva MJ. Singh NP. Centers for Disease Control and Prevention (CDC). Koch HM. Wiesmuller GA.nih. et al. Dobler L.25(2):293-302. Sanchez GN. Brock JW.93:177-185. Phthalate monoesters levels in the urine of young children. Duty S. 2005. Duty SM.niehs. Hu H.S. Barr D. Drexler H. Environ Health Perspect 2006.108(10)979-982. Bull Environ Contam Toxicol 2002. Yoshida K. Third National Report on Human Exposure to Environmental Chemicals. Meeker JD. Boehmer S. Int J Hyg Environ Health 2005. Hilborn ED. Caudill SP. J Androl 2004. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. et al. Needham LL. Barr DB. Jonsson BAG. Butala JH. Schettler T.208:237-245. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review].210(3-4):319-33. Rossbach B. et al. Environ Health Perspect 2000. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. Hum Reprod 2007. Castle L. Int J Hyg Environ Health 2007.114(9):1424-1431. et al. Poland. Fourth National Report on Human Exposure to Environmental Chemicals 269 . Monograph on the Potential Human Reproductive and Developmental Effects of Di-n-Butyl Phthalate (DBP).18(1):122. Drexler H. Hauser R. Food Addit Contam 2001. A biomarker approach to measuring human dietary exposure to certain phthalate diesters.210:21-33. et al. Silva MJ. Eckard R. Anderson WA. Camann DE. Wittassek M. et al. Prenatal exposures to phthalates among women in New York City and Krakow. Caudill SP. Occurrence and daily variation of phthalate metabolites in the urine of an adult population. Jacek R.Phthalates References Adibi JJ. et al. Massey RC. Pirkle JL. Reidy JA. Exposure to phthalates in neonatal intensive care unit infants: urinary concentrations of monoesters and oxidative metabolites. Available at URL: http://cerhr. Hagmar L. Perera FP.18(12):10681074.22(3):688-695. Epidemiol 2005. Silva MJ. Calafat AM.68:309-314. Masunaga S.html. 4/20/09 Silva MJ. et al. Chen Z. Gans G. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. Rylander L. Springall C. 2000 [online]. 112(5):A270].16(4):487-493. Jedrychowski W. Ryan L. Int J Hyg Environ Health 2007. Giwercman A. Silva MJ. Koch HM. Bolte G. Angerer J. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Urinary phthalate metabolites and biomarkers of reproductive function in young men. Research Triangle Park (NC).gov/chemicals/ phthalates/dbp/dbp-eval.111(14):1719-1722. Sampson EJ. Blount BC. Urinary levels of seven phthalate metabolites in the U. Atlanta (GA). David RM. Fromme H. Environ Health Perspect 2003. Ryan L. Evaluation of the effect ofa governmental control of human exposure to two phthalates in Japan using a urinary biomarker approach.

500) < LOD < LOD .20) . and polyvinyl chloride.500-. see Data Analysis section) for Survey years 99-00.500 (.300 (.400 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.300 (.00 (<LOD-1.70) .200 (<LOD-.500) < LOD 1.10) .500 (.500 (.500 (.500) .400-.00 (<LOD-1.70) .S. and 0.400) 1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.400-. 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.200-.400-. 0.400 (.200-.3.300-.400) < LOD 1. Neither IARC nor NTP has evaluated DCHP with respect to human carcinogenicity.300-.Phthalates Dicyclohexyl Phthalate CAS No.900-1.400-.10 (<LOD-2.400 (<LOD-. including nitrocellulose.00 (<LOD-1.10 (<LOD-1. resins.400-.500 (.300 (.600) .70 (1. 01-02.500) 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 .400) 1. People exposed to DCHP will excrete mono-cyclohexyl phthalate (MCHP) in their urine.00) .70 (1. which may vary for some chemicals by year and by individual sample. population from the National Health and Nutrition Examination Survey.500 (. polyvinyl acetate.500) .50) .400 (<LOD-. respectively.200-.500) .500) .80) . < LOD means less than the limit of detection.300-.300-.700) .300) < LOD .400 (<LOD-.300 (<LOD-.300-.300-.600) .90) .300-.200-.400-.500 (.9.700) .200-.300) < LOD .400 (. Urinary Mono-cyclohexyl phthalate (MCHP) Metabolite of Dicyclohexyl phthalate (DCHP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. 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. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.300-.300-.300-. In this Report.2.300) 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 .00-3.700) .500 (.500) < LOD * * * Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1.400 (.500) < LOD < LOD . 84-61-7 General Information Dicyclohexyl phthalate (DCHP) is used to stabilize some rubbers. Survey Geometric mean (95% conf. and polymers.300 (.500) 1.400) < LOD < LOD .600) .400) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.300 (. only levels at or above the 90th percentile could be characterized.400-.600) .400 (.400 (.600 (.600) .500 (.300 (.10 (.200-.300 (.400) size 2541 2782 2605 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .400 (<LOD-. 270 Fourth National Report on Human Exposure to Environmental Chemicals .50) .400 (.500) 1.10 (<LOD-1.500) 1.00-2. and 03-04 are 0.600) < LOD . 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.

690) < LOD 2.74) .33) .910 (.240-.330 (.350-.67 (1.450 (.880 (.740) < LOD < LOD .940 (.260-.490) .270) < LOD .510 (.380 (.420-.910 (.06) .500-.500) 3.330 (.17) .470) 3.530-.590 (. Survey Geometric mean (95% conf.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.770-1.670-1.05) .660) .560) 1.690 (.220 (<LOD-.82 (1.54-6. Fourth National Report on Human Exposure to Environmental Chemicals 271 .630 (<LOD-.S.800-1.690) < LOD < LOD . population from the National Health and Nutrition Examination Survey.53) .610 (.620) < LOD .170-.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 .290-.500) size 2541 2782 2605 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .530) 1.360-.710) .470 (.400-.36-1.53) .770) < LOD 2.910 (.450 (.00 (<LOD-3.22 (<LOD-1.16) .740) .16 (<LOD-3.54 (<LOD-2.790-1.54) .310) < LOD .530 (.690-1.12-1.830) 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.500 (.660) < LOD < LOD .420-.420-.910 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th 3.43 (1.380-.770-1.510-.18) .670 (<LOD-.10) .250 (.370 (<LOD-.82) .770 (.770-1.310-.14 (<LOD-3.690) < 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 1.44) .400-.590 (<LOD-.33 (<LOD-3.00) .480 (.34) .950 (.06) .630 (<LOD-.410 (.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.500) 328 393 342 752 742 729 1461 1647 1534 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .11) .530-1.390 (.

. 2007). DC (Hoppin et al. 2003) and African-American women in Washington. colognes. Neither IARC nor NTP has evaluated DEP with respect to human carcinogenicity. and also in men attending a Boston infertility clinic (Hauser et al. 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. 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.2-102) 95..3-110) 211 (160-278) 197 (159-243) 225 (187-270) 190 (164-219) 191 (171-214) 205 (176-238) 75. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.2.S.7 (70.4 (62. 0. shampoos. respectively.9. In contrast. 2002).7) 71.9-92.5) 81.1 (71.8-111) 85. deodorants. 84-66-2 General Information Diethyl phthalate (DEP) is a solvent used in many consumer products.Phthalates Diethyl Phthalate CAS No. Biomonitoring Information MEP levels in the NHANES 1999-2000. 01-02. and 0. and 03-04 are 1. particularly those containing fragrances. a sample of young Swedish males entering the military had median urinary MEP levels that were somewhat higher than males in the NHANES subsamples. 2001-2002. Workplace air guidelines for external exposure to DEP have been established by ACGIH and NIOSH. see Data Analysis section) for Survey years 99-00. and hand lotions. 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.9 (61. population from the National Health and Nutrition Examination Survey. 272 Fourth National Report on Human Exposure to Environmental Chemicals . soaps.3 (74. People exposed to DEP eliminate mono-ethyl phthalate (MEP) in their urine.1-93. Products that may contain DEP include perfumes.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.3 (82.4..

Median MEP levels found in a small sample of German residents (Koch et al.2 (66. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. 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. with adjusted geometric mean levels of urinary MEP that increased with age (CDC.0 (66.5-114) 101 (87. population from the National Health and Nutrition Examination Survey..S. 2005). 2003) were slightly lower than levels found in NHANES 2001-2002.0-156) 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 .6 (65.6 (77. Finding a measurable amount of MEP in urine does not mean that the levels of MEP or the parent compound cause an adverse health effect.9 (82. This age-related trend is opposite the direction seen for other phthalates. 2002).9-110) 96.7-110) 81. 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.Phthalates 2002 (Brock et al.3-105) 87.0-117) 142 (119-169) 152 (126-184) 168 (141-201) 179 (161-199) 181 (164-200) 197 (174-223) 79.. In an analysis of NHANES 1999-2000. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.5-113) 122 (93. Analysis of NHANES 2001-2002 showed similar findings. Other population estimates also differed by sex and race ethnicity (Silva et al. interval) 163 (149-178) Selected percentiles ( 95% confidence interval) 50th 141 (129-157) 148 (133-162) 153 (137-177) 75th 360 (307-422) 388 (330-435) 452 (386-504) 90th 905 (753-1180) 969 (805-1180) 1110 (889-1290) Total 167 (150-185) 181 (163-202) Sample size 1950 (1670-2310) 2536 1840 (1450-2200) 2782 2040 (1640-2540) 2605 95th Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 92. 2004).. 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.

Baird DD. Caudill SP. Environ Health Perspect 2003. Needham LL. Third National Report on Human Exposure to Environmental Chemicals. Camann DE. et al. Poland. Drexler H. et al. Hauser R. Hum Reprod 2007. Singh NP. Rossbach B. 274 Fourth National Report on Human Exposure to Environmental Chemicals . Hodge CC. Hilborn ED. Duty S. Hoppin JA. Caudill SP. Bull Environ Contam Toxicol 2002.110(5):515-518. Barr D. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Prenatal exposures to phthalates among women in New York City and Krakow.S. Barr DB.Phthalates References Adibi JJ. Reproducibility of urinary phthalate metabolites in first morning urine samples. Silva MJ. Phthalate monoesters levels in the urine of young children. Environ Res 2003. Centers for Disease Control and Prevention (CDC). Ryan L.112(3):331-338. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Davis BJ. Jedrychowski W.93:177-185. 112(5):A270]. Malek NA. Brock JW. Urinary levels of seven phthalate metabolites in the U. Atlanta (GA). Perera FP. Jacek R. Silva MJ. Silva MJ.22(3):688-695. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. Brock JW. et al. Environ Health Perspect 2002.111(14):1719-1722. 2005. Angerer J. Meeker JD. Environ Health Perspect 2004. Koch HM.68:309-314. Reidy JA.

1989. mono(2-ethyl-5-oxohexyl) phthalate (MEOHP).23 (2.3) 13.50 (7.00) 9.2 (10.0) 23.30 (6.57 (3.9-48.9 (13.80-9.70-4.10-4.10-3.00) 5.70-5.9) 15.1 (11.40) 4.21 (2.60) 4. see Data Analysis section) for Survey years 99-00.40) 1.5 (24.8) 17.15 (1.9) 13.3 (10.84-4. MEHP is primarily formed by the hydrolysis of DEHP in the gastrointestinal tract and then absorbed.6) 9.60 (5.31-4. packaging film.7 (17.40) 75th 7.90) 4.19-3.50) 9.90) 7.6) 14.00) 1.40) 8.03-2.10-5. 1982.6-28.80-4. mono-(2-ethyl5-hydroxyhexyl) phthalate (MEHHP) and mono-(2-ethyl5-carboxypentyl) phthalate (MECPP).63-4.60) 90th 14.8) 15.40-9.9-57.50 (7.90-8.10 (2.85 (3.70-3.50-14.5 (30. and blood product storage and intravenous delivery systems. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.4-40.37-4.50-5.70-2.60) 7.0) 23.5) 23. 2002.70 (7.00) 1.10-2.6 (11.9-28.00 (4.5-28.30 (3.25-3.70 (3.40 (6.5 (31.S.5-27.50-6.90) 1.5) 43.2.96) 4. Following ingestion.92-2.7) 19.5 (11.49 (3.30 (4.8 (17. DEHP present in medical devices and parenteral delivery systems results in the diester rather than the monoester form being directly introduced into the blood.9) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.50 (2.0-18.0) 11.4) 15.10) 3.0-19.10-5.82) 3.82 (3.91-3.2) 4.50 (8.60) 8.20 (1.0 (13.5 (25..8-47.10 (4.2 (11.4-20. and 0. and in humans.6 (16.3 (24.0 (17.80-4.80-8.20 (4.30-8.92-2.50-6.40 (4.50-8.2) 42.07-4.1) 19.8-36.9) 13. After parenteral administration. respectively.3-25.35) 4.0 (14. as glucuronide conjugates (Albro et al.42) 3.4) 33.6) 39.80) 6.1-48.60 (6.2) 6.0 (19.90) 4.2) 29.7) 22.40) 11.40-11.1 (8.10-11.8 (19.4) 13.87-2.6 (20. Peck and Albro.9 (7.6-60.50-11.89-3.40 (2.80) 9.80 (8.90-3.40 (4.77 (2.40-12.2-17.21 (2.3) 28.10) 3.2-28.60) 10.90) 3.40) 2.6) 5.5-17.3-57.0) 23.60-11.2-39.83) 2. Albro and Lavenhar.5 (18.3) 52.10) 2.50-5.00 (5.80-3. Urinary Mono-2-ethylhexyl phthalate (MEHP) Metabolite of Di-2-ethylhexyl phthalate (DEHP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.30-11. Four metabolites were measured in this Report: mono-(2-ethyl-5-hexyl) phthalate (MEHP).50-16.3 (19.1 (8.68 (3.84) 3. and 03-04 are 1.1-27.40) 4.2) 23.40-1.16-3. ATSDR.80-27.00 (7.10) 3. DEHP has been removed from or replaced in most toys and food packaging in the United States.69) Selected percentiles ( 95% confidence interval) 50th 3.7-58.9 (17.Phthalates Di-2-ethylhexyl Phthalate CAS No.7) 8.60) 4.0) 35.0-84.6 (41.70) 7.2 (7.96-5.70-5.70 (1.0) 39.70 (2.92) 4.3-26.6-38.4) 20.5-36.4) 22.3-49.70) 2.5) 40.4-42.10) 2. 01-02. Concentration