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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2'.2'.2'. Paradichlorobenzene) 1.4'.4'-Tetrabromodiphenyl ether (BDE 47) 2.3.2-Dichloroethene trans-1.2'.6.4'-Tribromodiphenyl ether (BDE 28) 2.5-Pentabromodiphenyl ether (BDE 99) 2.2-Dichloroethane (Ethylene dichloride) 1.4'.3-Dichlorobenzene (m-Dichlorobenzene) 1.2-Dichloropropane 2.1.2’.4’.5'.2-bis[4-Hydroxyphenyl] propane) 4-tert-Octyl phenol (4-[1.6-Pentabromodiphenyl ether (BDE 100) 2.3'.4. 2009 Acrylamide Adducts Acrylamide Glycidamide Total and Speciated Arsenic Arsenic.4.What’s New in this Report What’s New in this Report In this Fourth Report. 75 new chemicals are added for the 2003-2004 survey period and are listed in Table 1.5-Dimethylfuran Ethylbenzene Hexachloroethane Methyl-tert-butyl ether (MTBE) Nitrobenzene Styrene 1.4. The process for selection is described at http://www.2'.1.4-Dichlorobenzene (p-Dichlorobenzene.and p-Xylene o-Xylene 2 Fourth National Report on Human Exposure to Environmental Chemicals .4.5'-Hexabromobiphenyl (BB 153) Volatile Organic Compounds (VOCs) Benzene Chlorobenzene (Monochlorobenzene) 1.4-Tribromodiphenyl ether (BDE 17) 2.2'3.html.3-Tetramethylbutyl] phenol) Triclosan (2.4. Table 1.3.4.2-Trichloroethane Trichloroethene (Trichloroethylene) m.2-Tetrachloroethane Tetrachloroethene Tetrachloromethane (Carbon tetrachloride) Toluene 1.2'.3.4.6'-Hexabromodiphenyl ether (BDE 154) 2.4.5'-Hexabromodiphenyl ether (BDE 153) 2.1-Trichloroethane (Methyl chloroform) 1. Chemicals reported for the first time in the Fourth National Report on Human Exposure to Environmental Chemicals.gov/exposurereport/chemical_selection.5.5.1.2'.2'.1-Dichloroethane 1.5.5'-Tetrachlorobiphenyl (PCB 44) 2.4'.4’.2-Dichloroethene Dichloromethane (Methylene chloride) 1.cdc.5'-Tetrachlorobiphenyl (PCB 49) 2.3’.2-Dichlorobenzene (o-Dichlorobenzene) 1.4.4'-Pentabromodiphenyl ether (BDE 85) 2.4.2'.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 (2.4.5’.4'-Tetrabromodiphenyl ether (BDE 66) 2.1.6'-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 2.5.4.4’-Trichloro-2’-hydroxyphenyl ether) Non-dioxin-like Polychlorinated Biphenyls 2.2-Dibromo-3-chloropropane (DBCP) Dibromomethane 1.4'.6-Heptabromodiphenyl ether (BDE 183) 2.3.1-Dichloroethene (Vinylidene chloride) cis-1.2.4'.

4-dichlorophenol and 2. urinary 2.1). five results that all have the value 90. and polycyclic aromatic hydrocarbons (PAHs) for one or more of the 1999-2002 survey periods.5-dichlorophenol for the 1999-2002 survey periods.g.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.g. Data for other pesticides are included only for 1999-2000 and 2001-2002. Only slight differences should be noted when one compares the recomputations to previous releases of the Report. the presence of an interference) that produced results of inadequate quality. Percentiles for all three NHANES survey periods (1999-2000. 2003-2004 data for these other pesticides will be provided on this website as soon as they are available. 2003-2004 data for the organochlorine pesticides and the dialkyl phosphate organophosphorus insecticides are included in the Report.. Some results reported previously have been changed or removed due to improvements in analytical measurement or recognition of an analytical issue (e. Fourth National Report on Human Exposure to Environmental Chemicals 3 . 2001-2002.. and these data will be included in the next release of the Report. 2003-2004) have been re-computed by use of this improved procedure. Affected analytes were serum beta-hexachlorocyclohexane for the 2001-2002 survey period. Explanations for each change are provided in Appendix B. Details of this procedure are provided in Appendix A.

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

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

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

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

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

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

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

Tareke et al.9 (60.5 (79. and an average daily intake is estimated as 0.4) 57.6-75. acrylamide has produced upper airway irritation following inhalation of high levels. it was discovered that acrylamide is formed when starch-rich foods.1) 53. Commercially. Smaller scale applications of polyacrylamides include additives to paperboard used for food packaging. Elimination occurs mainly in the urine as mercapturic acid conjugates.0) 57.1-61.7-64. 2002). 2005).0 (53.4) 57.9) 58.. Acrylamide is not thought to accumulate in the body at environmental doses.4 (54.1 (47.7) 75th 79.9-105) 86. Fourth National Report on Human Exposure to Environmental Chemicals 11 .3) 70.1 (88.8 (52.9 (54.2-118) 98.2-67.5 (52.6) 90th 141 (124-155) 03-04 03-04 03-04 03-04 03-04 03-04 03-04 59.5) 58.S. widely distributed in tissues.Acrylamide Acrylamide CAS No. in permanent press fabrics.2 (58.5-85.9-61.1-64.8-57. 1994). 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. Recently.7) 58. the main source of exposure is from the diet. 1990.4-60.0-104) 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 61.3) 86. In 1997. 2004.7-64. such as potatoes and some grains.0.0-66. FDA. pulp and paper production.2 (75.7 (55.5) 66. mineral processing.3 (53.7-60.4) 100 (89.3-2. and peripheral neuropathy following chronic Acrylamide Geometric mean and selected percentiles of hemoglobin adduct concentrations (in pmol/g hemoglobin) for the U.5 (44. 2006).8 (57.7 (58.4 (54.. environmental releases of acrylamide can enter aquatic systems and soils where it degrades within days and does not bioaccumulate (U.0-58..8-55.6 (56. These estimated intakes are hundreds of times lower than occupational exposures. FAO/WHO.1 (73. Survey Geometric mean (95% conf.1) 46. and in some cosmetics. EPA.6) 90.2-93.S. and from dermal contact with products that contain residual acrylamide.4 (53.6-65.1-57.4-89.9) 57. In humans.1 (83.7 (65.4-83.9 (69.4-76.7) 54.6-108) 61. or to glutathione conjugates (Calleman et al. 217 million pounds of acrylamide were produced commercially in the U. ocular and dermal irritation from direct contact with acrylamide containing materials.4) Selected percentiles ( 95% confidence interval) Sample 95th 192 (168-217) size 7101 Total Age group 3-5 years 6-11 years 12-19 years 20-59 years 60 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 54. and well below doses known to cause nerve damage or carcinogenicity in animals.0 μg/kg for adults (FAO/ WHO.4 (59.3) 63.2 μg/kg/day (U. In the general population.9) 75. but are generally above the U. 2006. and is either metabolized to the reactive epoxide.1) 55.0-108) 152 (139-175) 126 (111-142) 108 (86. 2005).6) 73. are heated at temperatures used for frying and baking.S. smoking. Fennell et al. and cosmetics (NTP-CERHR.5 (74.6-66. in some sealing grouts.2) 57.1-64.6) 50.0) 85. Natural substances in the food are converted to acrylamide. 2005.0 (69.5-80.S.2-91.9-52. soil conditioners. 2005). People may be exposed to acrylamide from foods.0 (67.0-49.1) 101 (95. 79-06-1 General Information Acrylamide is a small organic molecule existing as a white crystalline powder in its pure state. gels.2-77. and in the synthesis or compounding of dye materials. 2004).2) 57.S.0 (57. Since acrylamide has limited volatility and high water solubility.2-70. Polyacrylamides are useful water-compatible polymers used in water treatment.7 (63.3-71. 2005).6 (81. EPA reference dose of 0.6 (51.9) 63.1) 62. (NTP-CERHR. and binding agents.8 (81. interval) 61. as an absorbent in disposable diapers.2-114) 163 (147-191) 96. drinking water.3 (55. population from the National Health and Nutrition Examination Survey.2-59.8 (91.2 (62.6) 71.7) 96.4-60. 2005). acrylamide is synthesized and used in the production of polyacrylamide polymer. see Data Analysis section) for Survey year 03-04 is 3.4 (51.1 (52.6-104) 82. although additional exposures from cosmetic products could add a similar amount (NTP-CERHR. EPA. glycidamide.7) 73. Animal studies indicate that acrylamide is well absorbed. but can covalently bind to form adducts with proteins.0-115) 156 (120-203) 146 (129-163) 149 (125-179) 218 (172-271) 197 (172-223) 1792 1874 2994 Limit of detection (LOD.6-61. Estimated intakes in children are about twice that of adults (DiNovi and Howard.

NTP-CERHR.6 (90. 2005.9-77.9-62. reproductive effects (reduced litter size. 2004. Vesper 2005) and smoking (Bergmark.4) 46. EPA.2 (56..2 (63.7) 74.2) 65.1-60. 2005. 2008).9-64. respectively) are markers of integrated acrylamide exposure over the preceding few months.3) 85.7 (84. AHA levels have been shown to increase with dietary intake (Hagmar et al. In addition.6-64. EPA.Acrylamide occupational exposures..9) 87.9) 65. EPA at: http://www. 2006). and to increase DNA reactivity when glutathione availability is reduced (Klaunig et al.S. Rice.8) 45.1 (66.7) 61. Adducts are formed when either acrylamide or glycidamide react to form a permanent covalent bond with hemoglobin in the blood.0) 94. U... dominant lethality).8 (44.0-62. although different analytic methods can affect results.. Survey Geometric mean (95% conf.0. Younger children may have slightly higher levels possibly due to increased intake of acrylamide-containing foods relative to body size (Dybing et al. uterine.. Maniere et al. 2003. 2005.2 (72. 2009).. 2006). male germinal cell injury.8 (51.1 (57.1-70. 2008).0) 118 (103-126) 121 (112-134) 113 (94.3-78. probably through its epoxide metabolite..who.4 (81.5 (59. 2005)...4 (57.int/ ipcs/food/jecfa/summaries/summary_report_64_final.7) 60.7-64.9-138) 143 (130-159) 96. see Data Analysis section) for Survey year 03-04 is 4..5-64. Hagmar et al.7 (87. and other sites) (FAO/WHO. 1997. Biomonitoring Information Acrylamide and glycidamide hemoglobin adducts (AHA and GHA.1) 56.5) 75th 85.7 (57.9-76.4-103) 79.1 (56. 2006.2-90.5 (42.S.2) 55. U.4) 53.9) 59. After exposure ceases.7 (61. 2002. 2005. glycidamide (NTP-CERHR.8-49.9 (81. The degree of formation of the more toxic glycidamide and levels of GHA can be influenced by polymorphisms in several of the enzymes that metabolize acrylamide (Duale et al. Schettgen et al. Axonal degeneration. gov/iris/ and from the Food and Agriculture Organization of the United Nations and WHO at: http://www.0 (80. and neuronal DNA reactivity (Doerge et al. presynaptic nerve terminal binding (LoPachin.0 (70.3-101) 95.1) 62. 12 Fourth National Report on Human Exposure to Environmental Chemicals .. 2004). Puppel et al.6-62.9 (57.3) 59. Additional information is available from U.6-90.4 (51. Acrylamide is clastogenic and can produce dominant lethal mutations.7-62.3) 59. 2005. fetal death.2-68.5 (56. levels of AHA adducts decline but may remain detectable for several months (Hagmar et al.. 2005). adrenal. population from the National Health and Nutrition Examination Survey.6 (66. 2002.0 (52. thyroid.0 (75. Glycidamide has been shown to react with DNA (Doerge et al.2-91.1) 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. 2005.9) 75.0-93. 2005) and sperm DNA adducts (Xie et al..5) 90th 130 (120-141) 03-04 03-04 03-04 03-04 03-04 03-04 03-04 71.5-92..8) 60.4 (61. Glycidamide Geometric mean and selected percentiles of hemoglobin adduct concentrations (in pmol/g hemoglobin) for the U.3) 59.S.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. 2005. 2005) have been demonstrated in animals.1 (70. Vesper et al. 2006) have been demonstrated after acrylamide dosing.9-78.5) 71. 2005.4-65.8-61.9 (58. 2001).2) 87.. to increase the unscheduled synthesis of DNA in tumor susceptible tissues (Klaunig et al.5) 118 (110-129) 121 (108-140) 136 (124-149) 152 (135-170) 159 (129-204) 172 (157-194) 1841 1954 3044 Limit of detection (LOD. 1997. scrotal.1 (82.4-59.1) 60.1-62. Mucci et al.8-48.5-94.epa.7-86.S.4 (56. Several of these studies have shown that smokers have adduct levels that are three to fourfold higher than non-smokers. 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..4-98. interval) 59. and cancer (mammary. Puppel et al.5 (83.5-66. Schettgen et al. 2005). 2005).5) 87. Klaunig et al. most non-smokers had levels less than about 100 pmol/gram hemoglobin. 2005.4) 83. Animal studies have shown that acrylamide can cause nerve damage (neuropathy).1-56.4 (90.3 (56..pdf.7) 90. 2005. 2005.. altered gene expression in testicular tissues (Yang et al.. IARC classifies acrylamide as probably carcinogenic to humans.

He F. DiNovi M and Howard D. 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. Hagmar L. Churchwell MI. Hagmar et al. symptoms of numbness or tingling in the extremities did not occur in exposed workers whose AHA levels were below 510 pmol/gram hemoglobin. Beland FA. 1999). Granath F. Perez et al. Duale N. Mutat Res 2005.580(1-2):157-165. and 39% of workers with levels above 1000 pmol/gram hemoglobin had these symptoms (Hagmar et al.. et al. 054472. References Bergmark E. Costa LG.cfsan.gov/chemicals/ acrylamide/Acrylamide_Monograph. Available at URL: http://cerhr. and Research Strategies. 2004 Acrylamide in Food Workshop: Update Scientific Issues.. Twaddle NC. smoking habits and gender.int/ipcs/ food/jecfa/summaries/summary_report_64_final. Godard T. Calleman CJ.pdf. NIH Publication No.. Available at URL: http://www. 1994). The Updated Exposure Assessment for Acrylamide.niehs. J Agric Food Chem 2008. Uncertainties. Guffroy M. Survey data on acrylamide in food: individual food products. 1993. 8-17 February 2005.561:21-37. da Costa GG. Fennell TR. Calleman CJ. Joint FAO/WHO Expert Committee on Food Additives. Tornqvist M. CFSAN/Office of Plant and Dairy Foods. July. Chem Res Toxicol 1990. Rosen I. Laurentie M. Center for the Evaluation of Risks to Human Reproduction (NTP-CERHR). Italy. Relationships between biomarkers of exposure and neurological effects in a group of workers exposed to acrylamide. 2/3/09 Perez HL. Wilson KM. Monograph on the Potential Human Reproductive and Developmental Effects of Acrylamide. April 13-15. Toxicol 2005. Magnusson AL. Mucci LA. McDaniel LP. Doerge DR. Paulsen JE. et al. Spicer R.. Simultaneous analysis of hemoglobin adducts of acrylamide and Fourth National Report on Human Exposure to Environmental Chemicals 13 . Fennell TR. Axmon A. Costa LG. Becher G. Rome. Human exposure and internal dose assessments of acrylamide in food. 2/3/09 Klaunig JE. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. morphological and molecular endpoints in animal models. Tornqvist M. 2005. Hemoglobin adducts of acrylamide and acrylonitrile in laboratory workers. 2/3/09 Hagmar L. Chicago. Chem Res Toxicol 1997 Jan. Cheong HK. 2006. Differences in hemoglobin adduct levels of acrylamide in the general population with respect to dietary intake. et al. Paulsson B. Nordander C.fda.3:406-412. Available at URL: http://www. Haugen M. 2004. Adv Exp Med Biol 2005. 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.85:447-459.43:365–410. Bergmark E. Adv Exp Med Biol 2005. Aprea P. et al. 2001. [Epub ahead of print] Dybing E. 2009 Jan 8.Acrylamide In occupational settings.html#u1004. Health effects of occupational exposure to acrylamide using hemoglobin adducts as biomarkers of internal dose. Toxicol Sci. National Toxicology Program. 6013-6019. Doerge DR. Acrylamide intake through diet and human cancer risk. Scand J Work Environ Health 2001. 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. Bergmark E. et al.27(4):219-226. In another study. February. Bridson WE. Bruze M. Toxicol Sci 2005. Bergmark E. Osterman-Golkar S. He F. gov/~dms/acrydata. DNA adducts derived from administration of acrylamide and glycidamide to mice and rats.561:49-62. Bjellaas T.580(1-2):119-129. Tian G. Alexander J. Snyder RW. 64th Meeting: Summary and Conclusions (FAO/WHO). Andersen M. Calleman CJ. Illinois. smokers and nonsmokers.126(2):361-371. DNA damage and DNA adduct formation in rat tissues following oral administration of acrylamide. Summer SCJ. AHA levels were several fold to several hundredfold higher than levels in non-exposed non-smokers (Bergmark et al.120(1):45-54. Acrylamide is metabolized to glycidamide in the rat: evidence from hemoglobin adduct formation. Wirfalt E. Food Chem.who..580(1-2):131-141. Mechanisms of acrylamide induced rodent carcinogenesis.Toxicol Appl Pharmacol 1994.56. Farmer PB. Kautiainen A. Malmberg B. Determination of hemoglobin adducts in humans occupationally exposed to acrylamide. Maniere I. 2001). Yang JS. Churchwell MI. Wu Y. Mutat Res 2005. Metabolism and hemoglobin adduct formation of acrylamide in humans. Acrylamide neurotoxicity: neurological. Biomarkers of human exposure to acrylamide and relation to polymorphisms in metabolizing genes.pdf. Kamendulis LM. Food and Drug Administration (FDA). Mutat Res 2005. Toxicol Appl Pharmacol 1993. LoPachin RM.nih.10(1):78-84. Burgess J. Zhang S.

S. Meyers T. Mutat Res 2005. Benetou V. Acrylamide. Letzel S. Ding X.50(17):4998-5006. Environmental Protection Agency (U. Liu K. Integrated Risk Information System (IRIS). Hemoglobin adducts of ethylene oxide. EPA). Tornqvist M.txt. Cross-sectional study on acrylamide hemoglobin adducts in subpopulations from the European Prospective Investigation into Cancer and Nutrition (EPIC) Study.19(4):527-34. a carcinogen formed in heated foodstuffs.Acrylamide glycidamide by gas chromatography-mass spectrometry. Tareke E. Jin Y. Marko D. Karlsson P. Adv Exp Med Biol 2005. 1994. Drexler H. U. Gray JG. 14 Fourth National Report on Human Exposure to Environmental Chemicals . Automated method for measuring globin adducts of acrylamide and glycidamide at optimized Edman reaction conditions.580(1-2):3-20. propylene oxide. 2/3/09 Vesper HW. Agudo A.gov/iris/subst/0286. Liu Y.56(15):6046-53. Tjaden Z. Drexler H. Ospina M.580(1-2):71-80. Smith A.htm. acrylonitrile and acrylamide-biomarkers in occupational and environmental medicine. Myers GL. et al. J Agric Food Chem 2008. EPA).274(1):59-68. J Agric Food Chem 2002. September. Chae C. Ingham L. Pilot study on the impact of potato chips consumption on biomarkers of acrylamide exposure.134(1-3):65-70. Sun H. Hallmans G. Mutat Res 2005 Feb 7. The carcinogenicity of acrylamide. Licea-Perez H. Slimani N. Angerer J. Schettgen T. Adduction of biomacromolecules with acrylamide (AA) in mice at environmental dose levels studied by accelerator mass spectrometry. Available at URL: http://www. Lee MH. Lee SH. Eriksson S. Han CH. Chemical Summary for Acrylamide. Choi JH. Int J Hyg Environ Health 2003. Washington (DC). Vesper HW. Tjønneland A. Fueller F. A first approach to estimate the internal exposure to acrylamide in smoking and non-smoking adults from Germany. Drexler H. Schettgen T. Toxicological effects of acrylamide on rat testicular gene expression profile.207(6):531-9. U. Reprod Toxicol 2005.163(2):101-8. Environmental Protection Agency (U. Fu D. Weiss T. Puppel N. Ospina M. Xie Q. Toxicol Lett 2002. Yang HJ. Vesper HW.561:89-96. Determination of haemoglobin adducts of acrylamide and glycidamide in smoking and non-smoking persons of the general population. Anal Biochem 1999.gov/chemfact/s_acryla. Angerer J.206(1):9-14. DNA strand breaking capacity of acrylamide and glycidamide in mammalian cells. et al. Office of Pollution Prevention and Toxics. Rapid Commun Mass Spectrom 2006. Rossbach B. Angerer J. Schettgen T.epa.S. Available at URL: http://www. Analysis of acrylamide. Rice JM. Rydberg P. Int J Hyg Environ Health 2004.S. 2/3/09. Broding HC. Meyers T. revised 1/3/06. Kutting B.20(6):959-64. Han DU.S.epa. Toxicol Lett 2006.

stroke.15 (2.068) .300) .187) .63 (2.65 (1.120 (.148-.120 (.066) .540 (.061) < LOD .060 (. acute respiratory illness.180 (.160 (.43 (1.216 (. and exacerbated asthma (U.308 (.320) .53-4.106-.92 (1.5% nicotine by weight (Kozlowski et al.54) size 5999 6819 6320 Total years 99-00 01-02** 03-04 50th .84-3.110 (.790) .230 (.05 ng/mL.770) .057-.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 .310) .66-3.18-3.080 (.70) 2.190-.190-. Children exposed to ETS are at increased risk for sudden infant death syndrome.740-1. and 03-04 are 0.047-.16) .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.164 (.17 (1.44 (2.Cotinine Cotinine CAS No.26-1.050) .059-.62) 2.45) 1.087 (.240 (.660) .220) .110-. Fourth National Report on Human Exposure to Environmental Chemicals 15 .087) < LOD < LOD .630 (.068) .030-. see Data Analysis section) for Survey years 99-00.131 (.030-.44) 2.670) .35 (2.160 (.052 (<LOD-.05) 1.580 (.063) .115-.726) .30) 2.140-.950 (.150) .850 (.110-.180) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.09-2.104-.50-4.96-4.12-4.570 (.48-2.47-3. 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.054 (.015.01 (1.580) .21-1.160) .430-1.32-2.139) * .188) .54 (1.990) .153-.120 (. and more than 50 compounds present in ETS are known or reasonably anticipated to be human carcinogens (NTP.860 (.071) .500 (.570-1.080 (.00) 1.089) Age group 3-11 years 99-00 01-02** 03-04 .00) .310) 90th 1.070-.630 (.062 (.154-.S.175 (. and various other disorders (U.084) .150) .78) 2.234) .120) .111-.33-2.200) 1.95) 1.073) < LOD .85 (1.302) .23-2.260-1.14-1.370-.12) 1. < LOD means less than the limit of detection. 1998).140 (.058 (.052 (<LOD-.110-.220) .410) .94) 1.81-2.20) .57) 2.620 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.88 (. 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. Survey Geometric mean (95% conf.02) 1.520 (.540-.360) .77 (1.20-2.600-1.19) 1. acute respiratory infections.108) * .68 (1.53 (1.163) .900-1.60-2.32) 1.480-1.40) .44) 2.197) .160) .053 (<LOD-..28) .01) 3.030-.060-.20 (.140 (.83-2. 83% of measurements had an LOD of 0.071 (.043-.070) .54 (1.12 (1.120 (.060-.21 (. which may vary for some chemicals by year and by individual sample.110 (.39 (1.09-3.180 (.30) * .50) 3.060 (<LOD-.42-4. and 17% had an LOD of 0.126) .050 (.950-1.050 (<LOD-.167 (.350 (.080) < LOD .090-.14) . population from the National Health and Nutrition Examination Survey.23 (1.32-2.23 (.040 (.910-1.920 (.740-1.505 (.580-1.075 (.09-3.770-1.50-1.220-.050 (<LOD-.030 (.800 (.094) . Cigarettes contain about 1.997-3.710 (.470-.060) .42 (1.090-.88 (1.077) .280 (.050-. The smoke produced by burning tobacco contains at least 250 chemicals that are toxic or carcinogenic.02 (.050) . ear problems.077) .180) .54) 1.730 (.087-.480-.080) < LOD < LOD .48-3.66) 1.625) .55-2.87-3.164 (.060 (.510 (.820) .55 (1.99) 2.621-1.160-.93) .180) . The consequences of smoking and of using smokeless tobacco products are well known and include an increased risk for several types of cancer.44 (1.S.96) 2.070 (<LOD-.124 (.310-1.130 (. DHHS.34 (1.12 (2.310-1. DHHS.040 (.059-.070) 75th .080-.05.77 (2.533-.79) 3.086 (.144 (.428-.120-.210 (.190-.100-.76 (1.047-.15) 2.076-.020-.040 (.110 (.080-.040-.11) .230) .04 (1.120 (.088-.090-.20 (1.506 (.140-. 2006).066-.20) 1.070) . 2004).68) 2.49) 1.180) .960-1.17 (.110) .130) .99) 2.02) 1.63-2.30) 2.28-1.70-2.770) .193) .19-2. Persons exposed to secondhand tobacco smoke (environmental tobacco smoke [ETS]) may have adverse health effects that include lung cancer and coronary heart disease.080-.68) . respectively.050-.62 (2.050 (<LOD-.990 (. producing roughly 1–2 mg of bioavailable nicotine per cigarette (Benowitz and Jacob. cardiovascular disease.110 (.23 (2.38-2.66 (1.75) 1.77 (1.137-.22) 2789 3152 2937 3210 3667 3383 Females Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 * .120-.17) . 2004).89) 1.S.180) .198) * .145) .690 (.060 (<LOD-.22) 2.620-1.163 (.19) . maternal exposure during pregnancy can result in lower birth weight. and 0.930 (.96 (1.142-.50 (1.39) 3.260) 1.400-.015 ng/mL. emphysema.450-.840) 3.630 (.060-.213) .21-1.160 (.040-.110 (.110) .050 (<LOD-.066 (.080-.350-. ** In the 2001-2002 survey period.312) .350-.137 (.14) .201) .49) 1.

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

Respiratory nicotine absorption in non-smoking females during passive smoking. IARC Monogr Eval Carcinog Risks Hum. Schober SE. Benowitz NL. Exposure of the U. U. 1991. population to secondhand smoke: 1988-2002. National Institute for Occupational Safety and Hygiene (NIOSH). Sosnoff CS. Giovino G. 4/13/09 U. Benowitz NL. Cotinine as a biomarker of environmental tobacco smoke exposure. Epidemiol Rev 1996.4:313-316. Curtin LR. Herrera B. Vogler GP. Pharmacol Rev 2005. Benowitz NL. DHHS). Filter ventilation and nicotine content of tobacco in cigarettes from Canada.niehs. 4/13/09 Centers for Disease Control and Prevention (CDC). Giovino GA.280:152-156. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans.S Department of Health and Human Services (U. National Toxicology Program (NTP). U. Centers for Disease Control and Prevention. In Report on Carcinogens. JAMA 1998.surgeongeneral. Environ Health Perspect 2006.57(1):79115.Cotinine and public health officials determine whether people have been exposed to higher levels of ETS than are found in the general population. and the United States. Department of Heath and Human Services. Decrease in the prevalence of environmental tobacco smoke exposure in the home during the 1990s in families with children.cancer. Bernert JT. Modin G. Atlanta (GA): 2005. IARC Monogr Eval Carcinog Risks Hum. Lewis PJ. Hukkanen J.nih.fr/ENG/Monographs/allmonos90. et al. Department of Heath and Human Services. Office on Smoking and Health [online] 2006. population to environmental tobacco smoke: the Third National Health and Nutrition Examination Survey. Clin Pharmacol Ther 1994. Richter PA. Brody DJ. Tob Control 1998. Sweeney CT. Metabolism of nicotine to cotinine studied by a dual stable isotope method. Mowery PD.pdf.cdc.275:1233-1240. Centers for Disease Control and Prevention. Tobacco Smoke and Involuntary Smoking. cigarette smokers: the Third National Health and Nutrition Examination Survey.gov/ntp/roc/eleventh/profiles/ s176toba.fr/ENG/Monographs/ allmonos90. Jacob III P. JAMA 1996.7:369-375. Maurer KR.S. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Coordinating Center for Health Promotion. Nicotine metabolism and intake in black and white smokers.S.php. Caudill SP.S. Pickett MA. Kozlowski LT. Smoking and Tobacco Control Monograph 10 [online].S. Fong I. George CF.gov/tcrb/monographs/10/. Centers for Disease Control. Turner DM. BMJ 1975. National Center for Fourth National Report on Human Exposure to Environmental Chemicals 17 . the United Kingdom.63:139-43. 1988-1991. 4/13/09 Iwase A. Trends in the exposure of nonsmokers in the U. Metabolism and disposition kinetics of nicotine. Summary of Data Reported and Evaluation [online] 1986.gov/eid/rmca/critdocs/ criteriadoc/33.56:483-493.291(3):1196-1203. Strauss WJ.114(6):853-858.S.niosh. 4/13/09 International Agency for Research on Cancer. Tob Control 2006. Ethnic differences in N-glucuronidation of nicotine and cotinine. Kira S.280:135-140. Flegal KM. Coordinating Center for Health Promotion.S. DHHS). National Center for Chronic Disease Prevention and Health Promotion.pdf. 1988-1991. Tobacco Smoke. Jacob P III. Racial/ethnic differences in serum cotinine levels among adult U. 4/13/09 Perez-Stable EJ. et al. International Agency for Research on Cancer. Available at URL: http://www. Warner K. J Pharmacol Exp Ther 1999. Caraballo R.15:302-307. Tobacco related exposures. 2004. Etzel RA. Houseman TH. JAMA 1998. Pirkle JL. 4/13/09 National Cancer Institute (NCI). Pechacek TF. Soliman S. Jarvis MJ.gov/library/ secondhandsmoke/. Available at URL: http://monographs. The Health Consequences of Smoking: The Surgeon General’s Report—Executive Summary. Summary of Data Reported and Evaluation [online] 2004. Current Intelligence Bulletin 54: Environmental tobacco smoke in the workplace. Dollery CT. Available at URL: http:// cancercontrol.iarc. Mehta NY. Health Effects of Exposure to Environmental Tobacco Smoke: The Report of the California Environmental Protection Agency. Schwartz SS. Herrera B. Benowitz NL. 1999. Vol 38. Absorption and metabolism of nicotine from cigarettes. U. Third National Report on Human Exposure to Environmental Chemicals. [online]. 1999-2002. Vol 83. Smoke-free laws and secondhand smoke exposure in US nonsmoking adults.php.S. June.94(2):314-320. available at URL: http://mtn. Benowitz NL. The Health Consequences of Involuntary Exposure to Tobacco Smoke: A Report of the Surgeon General — Executive Summary. Perez-Stable EJ. Bernert JT. Pechacek TF. iarc. References Armitage AK. Biomonitoring data can also help scientists plan and conduct research about exposure to ETS and about its health effects. Pollack HA. Pirkle JL.18:188-204. Int Arch Occup Environ Health 1991. Available at URL: http://ntp.S Department of Health and Human Services (U. Aiba M. Am J Public Health 2004. Jacob P III. Brody DJ. Available at URL: http://monographs. 11th ed. Jacob P.

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

180 (.110 (<LOD-.190) < LOD . DEET is metabolized via hydroxylation and dealkylation pathways and eliminated in the urine within approximately 24 hours (Selim et al.160) < LOD . DEET is not a developmental or reproductive toxicant in animals (U.110-. After absorption.130-.S.110 (<LOD-.120-.100-. 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. One survey detected DEET in 74% of sampled streams in the U.180) < LOD .130) < LOD . About 3-8% of dermally applied DEET is absorbed. 1998). Human health effects from DEET at low environmental doses or at biomonitored levels from low environmental exposures are unknown. (U.180 (.110 (.100-.180 (. 2005).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 . see Data Analysis section) for Survey years 99-00 and 01-02 are 0.140) < LOD .140) < LOD .100 (<LOD-. Fourth National Report on Human Exposure to Environmental Chemicals 19 .N. People in outdoor occupations may apply DEET more frequently or use higher concentration formulations resulting in higher levels of exposure. Additional information is available from U..S..220 (. 2002). DEET is also used in combination with dermal sun screens (U.270) 688 678 518 700 598 956 Limit of detection (LOD.170 (.S.130 (.130 (. 134-62-3 General Information N. 2003).EPA.520) < LOD .100-. 1998).N-Diethyl-meta-toluamide (DEET) CAS No.N-diethyl-meta-toluamide (DEET) is an insect repellent that was first marketed in 1957.170 (.100-.130-.560) < LOD . population from the National Health and Nutrition Examination Survey.110 (. DEET is not genotoxic. Its use is recommended for prevention of several vector-borne diseases.210 (.EPA.100-.110 (.1.140-.S. and they range in concentration from 4% to 100%. Most reports of adverse effects from overexposure to DEET involve skin reactions (Bell et al. General population exposure to DEET occurs from skin application and from inhalation of aerosol formulations.S.140 (.210) 480 580 672 829 825 1126 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . DEET is not registered for use on agricultural commodities.N-Diethyl-meta-toluamide (DEET) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.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 . Survey Geometric mean (95% conf. < LOD means less than the limit of detection. Neurological effects in humans.S.140) < LOD .EPA at: http://www. 2002). and it has not been rated by IARC or NTP with respect to human carcinogenicity.240) < LOD .250) < LOD .. Sudakin and Trevathan.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 . 1995.130-.150) < LOD .110-.epa.N-Diethyl-meta-toluamide (DEET) N. EPA. but higher DEET concentrations and different formulations may result in greater absorption (Sudakin and Trevathan.449 and 0.gov/pesticides/. including seizures and encephalopathy. DEET has low acute toxicity. Urinary N. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD .100-. (Kolpin et al.130) < LOD . Exposure can also occur from consuming food contaminated by DEET on hands or that was sprayed nearby. have been reported as result of self-poisoning by ingestion or excessive dermal application.120-.130 (.110 (.130-. There are over 225 insect repellents brands containing DEET. 2003). DEET can be applied to clothing and the skin to repel biting insects.

490) < LOD .500 (.240) < LOD . Urinary N.440) < LOD .250) < LOD .230-.330 (.230) < LOD ..150) < LOD . In this survey period.350-.93) < LOD .270 (.270-.190 (.330 (. 1992).370) < LOD . 2005). Urinary DEET levels as high as 5. Urinary levels of DEET were characterized only at the 90th and 95th percentiles of the U. DEET was detected in 10% of 60 Latino children in eastern North Carolina farm worker households (Arcury et al.410 (.300 (. the limit of detection was lower than for the NHANES 1999-2000 survey period (CDC.410 (.190-.N-Diethyl-meta-toluamide (DEET) Biomonitoring Information Urinary levels of DEET reflect recent exposure.500) 480 580 672 828 825 1126 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .230-.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 .550) 688 678 518 699 598 956 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.170-.S. population from the National Health and Nutrition Examination Survey.240-.270 (<LOD-.290-.690 µg/L were measured in eight park employees who applied 71% DEET once a day (Smallwood et al.280 (.N.190 (<LOD-.N-Diethyl-meta-toluamide (DEET) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.390-. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.410-.150-.200 (.320) < LOD . Survey Geometric mean (95% conf. representative subsamples from NHANES 2001-2002.270) < LOD .370-.630) < LOD . Finding a measurable amount of DEET in urine does not mean that the level of DEET causes an adverse health effect.350) < LOD .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 .130 (<LOD-.280-1.190 (.640 (..250 (.350) < LOD . Biomonitoring studies on levels of DEET provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of DEET than are found in the general population.S.320 (.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 .480 (. 20 Fourth National Report on Human Exposure to Environmental Chemicals .250-.140-. 2007). interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD .

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

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

Available at URL: http://ec.pdf ..pdf. Biochem Biophys Res Commun 2003.59(9):625-628.780(2):365-370.gov/ntp/htdocs/liason/ LowDosePeerFinalRpt. Available at URL: http://cerhr. 5: 505-523. Hum Ecol Risk Assess 2004. Ecotoxicity and the Environment (CSTEE). National Institute of Environmental Health Sciences. et al. National Toxicology Program Center for the Evaluation of Risks to Human Production (NTP-CERHR). Needham LL. Thomas BF. 4. niehs. Furlong ET. Kroes R. 2007. Munro IC.59(4):403-408.jrc. et al. and other organic wastewater contaminants in U. Brine DR. Han SY.14(2):149-157. Kim YH.137(3):353-362.35(2 Pt 1):238-254.it/DOCUMENTS/ Existing-Chemicals/RISK_ASSESSMENT/SUMMARY/ bisphenolasum325. In vitro and in vivo interactions of bisphenol A and its metabolite..pdf . Haighton LA.68(1):121-146. Sottas CM. Three-generation reproductive toxicity study of dietary bisphenol A in CD Sprague-Dawley rats. Rubin C. Tsugane S. Weight of the evidence evaluation of low-dose reproductive and developmental effects of bisphenol A. Occup Environ Med 2002. Keimowitz AR. 2/4/09 European Commission. hormones. Barr JR.Scientific Committee on Toxicity. Lynch BS.113(4):391-395. Fujii S. May 22. Estimation of intake level of bisphenol A in Japanese pregnant women based on measurement of urinary excretion level of the metabolite. Reidy JA. National Institutes of Health. streams. Zacharewski TR.. Exposure of the U. Barr DB. Bisphenol A prevents the synaptogenic response to testosterone in the brain of adult male rats. Harazono A. Urinary bisphenol A and plasma hormone concentrations in male workers exposed to bisphenol A diglycidyl ether and mixed organic solvents. Caudill SP. Koulova AI. DirectorateGeneral Health and Consumer Protection.J. Ema M. An evaluation of the possible carcinogenicity of bisphenol A to humans. Endocrinology 2004. Joskow R. Watanabe S. Furukawa M. Needham LL. Environ Health Perspect 2008.nih. Kim CS. Urinary concentrations of bisphenol A and 4-nonylphenol in a human reference population. Gender differences in the levels of bisphenol A metabolites in urine.eu/ health/ph_risk/committees/sct/documents/out156_en.36(6):1202-1211. Ispra. Cunha G. Environ Sci Technol 2002. Barton L. NTP-CERHR Panel Report on Reproductive and Developmental Toxicity of Bisphenol A.nih. Measurement of bisphenol A in human urine using liquid chromatography with multi-channel coulometric electrochemical detection. Available at URL: http://cerhr. Chung MK. Marr MC. Department of Health and Human Services. J Chromatogr B Analyt Technol Biomed Life Sci 2002. Ye X. European Commission.S. Estrogenic chemicals in plastic and oral contraceptives disrupt development of the fetal mouse prostate and urethra. with estrogen receptors alpha and beta.gov/chemicals/bisphenol/BPAFinalEPVF112607. Wong LY. Kuklenyik Z. Cha SW. Italy. bisphenol A glucuronide. Inhibition of testicular steroidogenesis by the xenoestrogen bisphenol A is associated with reduced pituitary luteinizing hormone secretion and decreased steroidogenic enzyme gene expression in rat Leydig cells. Reprod Toxicol 2001. et al. Meyer MT. Human Health. Exposure to bisphenol A from bis-glycidyl dimethacrylatebased dental sealants.69(22):2611-2625. 2/4/09 Fujimaki K. NTP-CERHR Panel Report on Reproductive and Developmental Toxicity of Bisphenol A. Kiguchi M. T. National Toxicology Program. MacLusky. 2002.S. NC. Koh WS. Hlywka JJ. Howdeshell KL.145:592-603. Richter CA. Rhomberg et al. Calafat AM. Matthews JB. Research Triangle Park. Ekong J. September. Yang M. Zaugg SD. Brussels. Imai H. Park S.102(19):7014-7019. and Hardy MP. Twomey K. Nippon Eiseigaku Zasshi 2004. Kim JC. Myers CB. Rat two-generation reproductive toxicity study of bisphenol A. and Hajszan. 2/4/09 Ouchi K. Timms BG. Reidy JA. Barber LB. C. Needham LL. Available at URL: http://ntp. vom Saal FS. niehs.niehs.Environmental Phenols References Akingbemi BT. Hughes C. Calafat AM. Han SS. Leranth. Arakawa C. Available at URL: http://ecb. Environ Health Perspect 2005. 2/4/09 National Toxicology Program’s Report of the Endocrine Disruptors Low-Dose Peer Review (NTP).149:988-994. Pharmaceuticals. Szigeti-Buck. Klinefelter GR.nih. Endocrinology 2008. Life Sci 2001. population to bisphenol A and 4-tertiary-octylphenol: 2003-2004. Gray GM. McConnell EE. Calafat AM. August 2001. Evaluation of developmental toxicity in rats exposed to the environmental estrogen bisphenol A during pregnancy. Cohen JT. Bisphenol A. Yoshinaga J. Chem Res Toxicol 2001.pdf.S. Toxicol Sci 2002.10:875-921.116(1):39-44. Pyo MY. Ikka T. Tyl RW. Proc Natl Acad Sci USA 2005. Shin HC.gov/chemicals/bisphenol/bisphenol. Hara K. J Am Dent Assoc 2006. K. Doull J. 32 Fourth National Report on Human Exposure to Environmental Chemicals . Kawamura N.312(2):441-448. 2008. U.4’-Isopropylidenediphenol (Bisphenol-A) Summary Assessment Report. N. 2003. 2/4/09 National Toxicology Program Center for the Evaluation of Risks to Human Production (NTP-CERHR). Thurman EM. Watanabe C. Hanaoka T. 1999-2000: a national reconnaissance. Kolpin DW. Bradley S.pdf. November 26. Regul Toxicol Pharmacol 2002.europa. Joint Research Centre Institute of Health and Consumer Protection. Serizawa S. Belgium.

Yang M. Morgan MK. Chuang JC.44(4):546-51. Colnot T. Kawamoto T. Chang SS. Food Chem Toxicol 2002.Environmental Phenols Volkel W. Kim SY. Wilson NK. Chem Res Toxicol 2002.147(6 Suppl):S56-69. et al. Nagel SC. Low-dose in utero effects of xenoestrogens in mice and their relevance to humans: an analytical review of the literature. Vom Saal FS. III. An extensive new literature concerning low-dose effects of bisphenol A shows the need for a new risk assessment. Metabolism and kinetics of bisphenol A in humans at low doses following oral administration. Endocrine mechanisms mediating effects of bisphenol A at levels of human exposure. Csanady GA.103(1):9-20. Biological monitoring of bisphenol a in a Korean population. Large effects from small exposures. vom Saal FS. Sheldon LS. Hughes C. Endocrinology 2006. bisphenol-A.113(8):926-33. Environ Health Perspect 2005. Environ Res 2007. and nonylphenol at home and daycare. Filser JG. Lee SM. Jang JY. Fourth National Report on Human Exposure to Environmental Chemicals 33 . Arch Environ Contam Toxicol 2003. Welshons WV. Witorsch RJ. An observational study of the potential exposures of preschool children to pentachlorophenol. Lordo RA. Dekant W.15:12811287.40(7):905-12.

Environmental Phenols 4-tert-Octylphenol CAS No.20-2.20) 314 715 1488 03-04 03-04 * * .600) .20-2.10) 1.300-.274-.900 (.60-3. the various alkylphenols have also been used as emulsifiers and modifiers in paints. streams in 30 states (Kolpin et al. altered estrus cycles and reproductive outcomes.30 (.30 (1. industrial cleaners.70 (1.20) size 2517 Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th .900 (.20) 1. and some personal care products. Katsuda et al. and the polyethoxy chain may consist of up to 50 ethoxy units. 1996). which are anionic surfactants used in detergents..5% of 139 U.600) .300 (<LOD-.507) * < LOD . is used to manufacture alkylphenol ethoxylates.00 (. through sewage. and through manufacturing waste streams (Warhurst..3. 140-66-9 General Information 4-tert-Octyphenol. Ying et al. Less frequently. Disposition in humans has not been studied sufficiently. leading to inhalation as another potential exposure route (Rudel et al.S.300 (<LOD-.20-2.600-1.60-3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.40) 1.369 (.700-1.300 (<LOD-. 2006.500-1.268-.20-2.400 (.477) .30 (1.500) .800-1.40) 2.300 (<LOD-.00) 1229 1288 03-04 03-04 03-04 * . 2000.30) 1. have demonstrated estrogenic effects particularly when injected at high doses in animals.30-2. Survey Geometric mean (95% conf. 4-octylphenol monoethoxylate was detected in 43.500) 75th .70 (1.300 (<LOD-. 1995.600) 1.30 (1. During the 1980s and 1990s. Commercial formulations of alkylphenol ethoxylates usually contain a mixture of oligomers and isomers.200-.600) . and was quickly eliminated from the blood (Certa et al.50) .40) 1. 2004). Laws et al. In the 1990s.90) 2.30) 2.90) 2.g.299-.500 (.80 (1.00 (1. several European nations banned the use of alkylphenol ethoxylates in domestic detergents and other uses. 2003. Octylphenols and nonylphenols can also enter the environment directly from manufacturing waste streams.g. Human exposure to alkylphenols and alkylphenol ethoxylates may occur through ingestion of contaminated foods (e.000 tons of alkylphenol ethoxylates were produced annually worldwide.80) 2.500-1.50) 1.60) 1. The alkylphenol ethoxylates enter the environment through human use of products containing them. impaired steroidogenesis.60) .60-3. < LOD means less than the limit of detection. 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. The alkylphenols can bioaccumulate in some fish. did not bioaccumulate.300-..400) 1.10 (.20-2.3-Tetramethylbutyl] phenol) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. 34 Fourth National Report on Human Exposure to Environmental Chemicals .60-3. fish) and drinking water.20 (1. altered neonatal sexual development.400 (. testicular atrophy.50-3.500) . Blake and Boockfor.900 (.. to shorter chain alkylphenol ethoxylates. an alkylphenol. over 500.50) .10-2. In 1999-2000. textiles..00 (.600-1. They are biodegraded to the corresponding alkylphenol (octylphenol or nonylphenol). Indoor and to a lesser extent. Several alkylphenols. and from contact with some personal care products and detergents. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.10) 2. In rats. orally administered 4-tert-octylphenol was well absorbed..40) 2.80 (1. and emulsifiers.389 (.60-3.2. outdoor air may have detectable levels of 4-tert-octylphenol and 4-tert-octylphenol monoethoxylates.50) 1.60) 613 652 1092 Limit of detection (LOD. 2002). which may vary for some chemicals by year and by individual sample.900 (.10 (.30 (1.600-1.357 (.50) 1.S.20-2. and impaired spermatogenesis (e.600-1. These high dose parenteral effects of 4-tert-octylphenol have included altered sex hormone levels and hypothalamicpituitary suppression. Urinary 4-tert-Octylphenol (4-[1.600-1..200-.20) 2.50 (1.10 (1. 2000. Saito et al. population from the National Health and Nutrition Examination Survey.. see Data Analysis section) for Survey year 03-04 is 0.900 (.497) * .50-2.70 (1.60-3.. pesticides.600-1.40 (1.40) * 03-04 03-04 03-04 .80 (1..500) .30) 90th 1.400 (. including 4-tert-octylphenol. Bian et al. and some of their degradation products are toxic to aquatic life.1. 2002). Alkylphenols also have been used as plasticizers and antioxidants in plastics and resins. 1997.70 (1. Nonylphenol ethoxylates are more commonly used than octylphenol ethoxylates. and to alkylphenoxycarboxylates.

59) 1.270 (.640-1. 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.03 (1.73) 2.50 (2.3-Tetramethylbutyl] phenol) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. 2004).470-1.81 (1.349) * < LOD .41) .10-2. 2004.380 (<LOD-.25) 2. Sweeney et al.850 (.08) 1..270-.570) .00) 1.420) .199-.540-1.460 (. nonylphenol.500-1.370 (<LOD-. Kawaguchi et al.53-3.20 (1.00) 2.15) 1.02-4.S.740 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.05-2.29) 2.25-2. representative subsample of NHANES 2003-2004.78) 3.3. 2001).450) 1. Calafat et al.276 (. the urinary concentrations of 4-tert-octyphenol were near or below the detection limit (Inoue et al..890-2.31 (1.78) 1228 1286 03-04 03-04 03-04 * .64 (.630-1.17 (.337-.22) .62 (1.68) 2.610) .14) 314 713 1487 03-04 03-04 * * .11) 2.78 (1. Tyl et al.740 (. Biomonitoring Information Urinary levels of 4-tert-octyphenol reflect recent exposure.. Urinary 4-tert-Octylphenol (4-[1.384) * . Fourth National Report on Human Exposure to Environmental Chemicals 35 .00 (.96-4.320 (<LOD-.270 (. 2005.860 (.60 (1.06 (2.03-6.43-3.00) 2. 2000.1.470-1.71) 2. 4-tert-Octylphenol is not considered directly genotoxic. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. It is unclear if estrogenic or other effects occur in animals through oral dosing.269 (.11) 1. or their corresponding ethoxylates with respect to human carcinogenicity.280-.410 (. In a small number of adult Japanese volunteers. 2003.Environmental Phenols Myllymaki et al.770 (.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 .435 (.300 (<LOD-.43) 1.76 (2.550-1.11-2.43) 1.18-4.31-2.620-1. Yoshida et al.450) ..67-2.170-.59 (1.530) .470) 75th . IARC and NTP have not rated octylphenol.62 (1. Survey Geometric mean (95% conf. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.260 (<LOD-.33 (2.25) 90th 1.54) * 03-04 03-04 03-04 .68-2.40-4.33) 3. Nagao et al. (2008) showed that urinary levels of 4-tertoctyphenol were detectable in slightly greater than half of the participants of the U.910 (.160-.207-.S.62) . at lower or environmentally relevant doses (Blake et al.03 (1.40 (1.. 1999).24) 612 651 1091 < LOD means less than the limit of detection for the urine levels not corrected for creatinine..620) .730-1.85 (1.36-3.65-3. population from the National Health and Nutrition Examination Survey.00 (.560) . 2001.400) . 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.

polybrominated diphenyl ethers. Furlong ET. Seely JC. et al. Environmental fate of alkylphenols and alkylphenol ethoxylates--a review. Karjalainen M. Boockfor FR. Brody JG.121(1):21-33. Nair-Menon JU. Saito Y. 2/4/09 Ying GG.foe. et al. streams. Toxicol Appl Pharmacol 2005. Xu L. Boockfor FR. Reproductive effects in male and female rats from neonatal exposure to p-octylphenol.pdf. Toppari J. hormones. Nakagomi M. Katsuda S. Endocrinology 2000. Sakui N. Cooper RL. et al. Izumi S. Bodman GJ. Katsuda S.28(3):215-226. Taya K. Regul Toxicol Pharmacol 1999. J Chromatogr B Analyt Technol Biomed Life Sci 2004. and testosterone. pesticides. Millette CF.folliclestimulating hormone. Needham LL. Warhurst AM. Effects of 4-tert-octylphenol given in drinking water for 4 months on the male reproductive system of Fischer 344 rats.36(6):1202-1211. and other organic wastewater contaminants in U. Korn LR. Biol Reprod 1997. Kolpin DW. Toxicol Appl Pharmacol 2000. Carey SA. Myers CB. 1999-2000: a national reconnaissance.207(1):59-68. McCoy GL.165(3):217-226. Pharmaceuticals. Horie M. Yoshida M. 2003. Sweeney T. Chen J. Available at URL: http:// www. Brooks AN. Wong LY. Tyl RW. Fedtke N. Ye X. Laws SC. Measurement of 4-nonylphenol and 4-tert-octylphenol in human urine by column-switching liquid chromatography-mass spectrometry. and other endocrine-disrupting compounds in indoor air and dust.71(1-2):112-122. Seto H. An environmental assessment of alkylphenol ethoxylates and alkylphenols. Exposure of the U. Wiegand HJ. bisphenol A and methoxychlor in rats. Reprod Toxicol 2001. Two-generation reproduction study with para-tert-octylphenol in rats. Takai N. Thurman EM. Effects of neonatal exposure to a high-dose p-tertoctylphenol on the male reproductive tract in rats. nonylphenol. Reprod Toxicol 2004. Haavisto TE. Indoor air pollution by alkylphenols in Tokyo.37(20):4543-53. Watanabe G.141(7):2667-2673.57(2):255-266. Taya K. Spengler JD. Ferrell JM. Maekawa A. Ono H. Infantile 4-tert-octylphenol exposure transiently inhibits rat ovarian steroidogenesis and steroidogenic acute regulatory protein (StAR) expression. Estrogenic activity of octylphenol. Calafat AM. Toxicol Lett 2001. Irreversible effects of neonatal exposure to p-tert-octylphenol on the reproductive tract in female rats. Ito R. Williams B. Fail PA.44(8):1355-1361. Wang X. Blake CA. The toxic effects of 4-tert-octylphenol on the reproductive system of male rats. Chronic administration of the environmental pollutant 4-tert-octylphenol to adult male rats interferes with the secretion of luteinizing hormone. Myllymaki SA. Marr MC. Muller AM. Yoshimura Y. alkylphenols. Food Chem Toxicol 2006. Meyer MT. Environ Health Perspect 2008. Brine DR. Anal Chim Acta 486:41-50. Roche JF.S. and sertoli cell number. Yoshida M. 1995. Watanabe G.co. Maternal exposure to octylphenol suppresses ovine fetal follicle-stimulating hormone secretion. Inoue K. Raychoudhury SS. Environ Sci Technol 2003. Onuki A. Maekawa A.Environmental Phenols References Bian Q.uk/resource/reports/ethoxylates_alkylphenols. Qian J. Bolt HM. testis size. Yoshimura S. Blake CA. Toxicol Sci 2000. Arch Toxicol 1996. Camann DE. 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.18(1):43-51. et al. Inoue K. Takenaka A. Reidy JA. Rudel RA.S. Barber LB.14(5):325-332. Nicol L. Nagao T. Kookana R.30(2 Pt 1):81-95. Saito I. Environ Int 2002. Makino T.54(1):154-167. Phthalates. Environ Sci Technol 2002. population to bisphenol A and 4-tertiary-octylphenol: 2003-2004.15(6):683-692. Kawaguchi M.799(1):119-125. prolactin. Zaugg SD. Kawaguchi M. Paranko J. Indoor Air 2004. Song L.116(1):39-44. Okada F. Usumi K. Toxicokinetics of p-tert-octylphenol in male Wistar rats. Certa H. 36 Fourth National Report on Human Exposure to Environmental Chemicals .

toothpastes.. 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. 2007. In 1999-2000. and wound disinfection solutions. and has also been impregnated into some kitchen utensils.Environmental Phenols Triclosan CAS No. triclosan was found in 57. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. acne medications.. Some reports show endocrine effects are observed in amphibians and fish (Foran et al.. IARC and NTP do not have ratings with respect to human carcinogenicity..S.. it is excreted over several days in the feces and urine as primarily as unchanged triclosan (Kanetoshi et al. 3380-34-5 General Information Triclosan is a phenolic diphenyl ether used for over 30 years as a preservative and antiseptic agent... and has not been considered mutagenic or carcinogenic (Bhargava and Leonard. streams sampled in 30 states (Kolpin et al. Matsumura et al. 2006). General population exposure results from dermal and oral use of products containing triclosan. 2004). Mezcua et al. Fourth National Report on Human Exposure to Environmental Chemicals 37 .. In the body it is conjugated to glucuronides and sulfates (Bodey et al.. toys. Veldhoen et al. but not by race/ethnicity and sex. Calafat et al. Moss et al. 2008 has shown higher levels during the third decade of life and among people with the highest household income.. In animal studies.. a process that can result in the formation of small amounts of 2. 2000).. Calafat et al. 1987).. Triclosan is not considered teratogenic at maternally toxic doses. the median urinary triclosan level of 7. 2000. Triclosan has been added to soaps.. In a study of 90 U. deodorants. 2005. 1996. representative subsample of NHANES 2003-2004. 2008). It acts by inhibiting bacterial fatty acid synthesis. Finding measurable amounts of triclosan in the urine does not mean that the levels of triclosan cause an adverse health effect. Human health effects from triclosan at low environmental doses or at biomonitored levels from low environmental exposures are unknown. and medical devices.S. 1988. Triclosan can be absorbed across skin into the blood stream. Lyman and Furia. mouthwashes. young girls. In animal and human studies. Triclosan has a low bioaccumulation potential in fish. 2007. It can be photochemically and biologically degraded. 1969). (Sandborgh-Englund et al. 2007).. it has low acute toxicity.S. Triclosan enters the aquatic environment mainly through residential wastewaters.6% of 139 U. 2007). Biomonitoring Information Urinary triclosan levels reflect recent exposure. 2002).8-dichlorodibenzo-p-dioxin (Aranami et al.2 µg/L was comparable to the median level (8. In a U. 1976.2 µg/L) of children 6-11 years of age who participated in NHANES 2003-2004 (Wolff et al. Triclosan can remain present in the oral saliva for several hours after the use of toothpaste containing triclosan (Gilbert et al. Triclosan formulations may rarely cause skin irritation. There is some concern that widespread use of triclosan and other biocides can alter antibiotic resistance in bacteria (Aiello et al.

6-15.6 (10.45-13.74 (5.8 (21.2) 13.9 (8.20-11.7) 292 (151-432) 132 (78.1 (15.3-15.4’-Trichloro-2’-hydroxyphenyl ether) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.86-12.8) 9.5-341) 245 (163-334) 597 (372-992) 450 (254-750) 461 (383-527) 613 652 1092 Limit of detection (LOD.50) 10.1) 9.7) 123 (36.0-19. Urinary Triclosan (2.6) 39.5) 66.90-10.2 (11.0-213) 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 .93 (7.6) 237 (175-294) 182 (138-217) 384 (294-506) 336 (225-480) 1228 1286 03-04 03-04 03-04 13.9-61.20-10.9) 8.6-65.00 (4.7) 10.5-14.3-31.45 (5.1) 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 9.5 (11.2-58.3 (8.4) 7.3.2) 12.29-12.2 (13.48-10.94 (7.0) 49. Survey Geometric mean (95% conf.60 (6.89-11.40-11.4 (11.0) 9.20 (7.6 (9. interval) 12. population from the National Health and Nutrition Examination Survey.9 (50.Environmental Phenols Urinary Triclosan (2.5-250) 574 (461-716) 380 (258-430) 1229 1288 03-04 03-04 03-04 14.1) 7.9) 32.9) 75th 47.0 (8.9) 7. Survey Geometric mean (95% conf.45-10.0-15.4) 317 (231-433) 144 (96.82 (8.16 (6.8-85. see Data Analysis section) for Survey year 03-04 is 2.5-86.7 (28.2) 9.21 (6.8-60.1 (45.4-163) 304 (134-566) 261 (198-317) 157 (113-380) 655 (310-890) 472 (406-522) 314 715 1488 03-04 03-04 16.6 (12.5) 11.6-14.10) 84.50-10.9 (33.1 (8.32-14.4-19.2 (25.4 (38.4) 357 (225-456) 203 (87.6-20.2 (10.7-318) 224 (186-272) 236 (115-336) 356 (169-580) 385 (308-506) 314 713 1487 03-04 03-04 13.0) 65.6) 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 (36.4) 73.4’-Trichloro-2’-hydroxyphenyl ether) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.4-18.6) 10.80 (5.6-14.7 (9.S.4) 75th 43.00-8.2 (37.38-18.8-63.60 (8.3-35.4 (12.7 (39.0 (11.5) 13.7 (14.9-236) 193 (90.43-13.48 (8.4) 51.72-13.22-10.8) 7.8-127) 37.1) 9.20-13.40-17.6) 31.6) 12.6-37.18 (5.S.1) 13.92-12.11-11.0 (34.0-73.55 (4.2 (27.6-111) 33.3-67.4 (32.1) 9.3) 6.2-14.3 (26.7 (11.0-15.8) 116 (39.0 (26.30-14.1) 9. population from the National Health and Nutrition Examination Survey.1) 50.3) 10. interval) 13.3 (9.4.10-9.8) 14.20 (7.8-112) 30.4) 90th 249 (188-304) 03-04 03-04 03-04 8.70-16.6 (30.4) 25.1) 14.1) 11.54 (8.6) 90th 212 (172-241) 03-04 03-04 03-04 9.2-46.3 (11.5) 20.4.1-39.9 (11.2-58.3) 47.

Randomized trial of a hexachlorophene preparation and P-300 bacteriostatic soaps.4’-trichloro-2’hydroxydiphenyl ether). Mezcua M. Ye X. phthalates.50(1-5):153-156. Adolfsson-Erici M. Larson EL. Wolff MS. Watanabe N. Pinney SM. Ishibashi H. J Toxicol Environ Health A 2006. Environ Sci Technol 2002. Williams PE. Fernandez-Alba AR. Erratum in: Aquat Toxicol 2007. Shiratsuchi H.38(2):64-71. Anal Chim Acta 1004.23(5):579-583.80(3):217-227. Effects of nonylphenol and triclosan on production of plasma vitellogenin and testosterone in male South African clawed frogs (Xenopus laevis). Developmental evaluation of a potential non-steroidal estrogen: triclosan. Bennett ER. Osachoff H. Leonard PA. Am J Infect Control 1996. Mar Environ Res 2000. Zaugg SD. Hernando MD. Toxicology of 2. Fourth National Report on Human Exposure to Environmental Chemicals 39 . Barber LB. Wigmore H. Okui T. Skirrow RC. Wong LY. 4. Sandborgh-Englund G. Aranami K. Consumer antibacterial soaps: effective or just risky? Clin Infect Dis 2007.69(20):1861-1873. Lyman FL. Aguera A. and other organic wastewater contaminants in U. Nagao Y.67(4):532-537. 4’-trichloro-2’-hydroxydiphenyl ether. hormones. Ferrer I. Arch Environ Contam Toxicol 1988.24(3):209-218.8-dibenzodichloro-pdioxin as a photodegradation product of triclosan in water and wastewater samples.524:241-247. Triclosan: applications and safety. Teitelbaum SL. et al. Veldhoen N.. Gomez MJ. Windham G. Benson WH. et al. 1999-2000: a national reconnaissance. Evidence of 2. Levy SB. Howes D. Matsumura N.17(5):637-644. Ebersole R. et al. Calafat AM. Percutaneous penetration and dermal metabolism of triclosan (2. Reidy JA. Environ Health Perspect 2007. Readman JW.S. Gunderson MP.4.28(9):1748-1751. Kaneshima H. Hirano M. Foran CM. Pilot study of urinary biomarkers of phytoestrogens. Meyer MT. Chemosphere 2007. Bhargava HN. Odham G. Urinary concentrations of triclosan in the U. Bodey GP. et al. Williams FM. Needham LL.Environmental Phenols References Aiello AE. J Invest Dermatol 1976. Britton JA. Photolytic degradation of triclosan in freshwater and seawater.38(4):361370. Moss T. Kolpin DW. Food Chem Toxicol 2000.7/2. Pharmaceuticals. Chelimo C.115:116-121. Furlong ET. Ekstrand J.116(3):303-307. Clapson DJ.36(6):1202-1211. Biol Pharm Bull 2005.66:1052-1056.S. Ogawa H. Furia T. streams. Aquat Toxicol 2006. and phenols in girls. The oral retention and antiplaque efficacy of triclosan in human volunteers. Environ Health Perspect 2008. Disposition and excretion of Irgasan DP300 and its chlorinated derivatives in mice. Kanetoshi A. The bactericidal agent triclosan modulates thyroid hormone-associated gene expression and disrupts postembryonic anuran development. Thurman EM. IMS Ind Med Surg 1969. Hong HC. Katsura E. Br J Clin Pharmacol 1987. population: 2003-2004.83(1):84.45 Suppl 2:S137-S147. Pharmacokinetics of triclosan following oral ingestion in humans. Gilbert RJ.

air.54-2. 1976. Survey Geometric mean (95% conf.78) 1.S. Human health effects from PCP at low environmental doses or at biomonitored levels from low environmental exposures are unknown.04) 1.350-2.76) . To-Figueras et al. In the environment. and metabolic acidosis were observed in CAS No.350-1. PCP also may be eliminated in urine as a metabolite of hexachlorobenzene.47-5.50) 1.32 (.S. Effects including hyperthermia.65 (. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.62 (. PCP is eliminated over a few days (Braun et al. PCP is absorbed rapidly and well by all exposure routes.350 (.660 (.00) 1. 40 Fourth National Report on Human Exposure to Environmental Chemicals .770 (.350-2.350 (.350) 90th .80) . so it is relatively non-persistent. PCP use in the U.650 (.350-.5.350-.590-1. 1997).45-2.350 (.350-.350 (.350-..70) 2.67) 1.350-.37 (.09) .33) . and possibly of lindane (IPCS.350-.65 (.350) < LOD .350-.23 (. The parent compound and conjugates.47-3.350 (.350 (.990-2.18 (<LOD-1.350-1.680-1.10) 1.630 (.990 (<LOD-2.350-2.30 (.30) 1.350) < LOD .48-2.350 (.350 (. and dermal contact with PCP-treated products. bactericide.500-2.350) < LOD < LOD 75th .350-.350) < LOD .850-2.350-.390 (.. with repeated or chronic exposure.37) . which may vary for some chemicals by year and by individual sample.350) < LOD .58-2.350-.08-3. water and sediments because of the large amounts that were produced and used historically.10 (.350) < LOD .00) 2.350-.40 (.94 (1. 1979). utility poles and fence posts).350-1. and animals.01 (<LOD-1.48 (.350) < LOD .350-.350 (.350) .510-3.53) 482 577 681 826 831 1125 99-00 01-02 99-00 01-02 * * * * . Kohli et al. 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.350 (.350 (. Workers who manufacture or apply PCP may Urinary Pentachlorophenol Also a Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. After a single dose. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.350 (. herbicide.350-.350) < LOD .350-.350) < LOD . has been restricted.350 (.64) 1. PCP has been detected in soils.350 (. Since 1984.350-..530) 1.350 (.90) 2. algaecide and insecticide. 2002. Acute.890-1. ingestion of contaminated food or water.890 (.73 (1.30 (.10) 1.00 (. along with small amounts of tetrachlorohydroquinone and conjugates.350-1.90 (1.25 and 0. plants.30) 1.76) 1.30 (1.42) 696 680 521 696 603 951 Limit of detection (LOD.350 (. hypertension.70) .94 (1. 1986).91 (1.350 (.350-. PCP cannot be used on wood in residential or agricultural buildings.350 (. General population exposure to PCP may occur by inhalation of contaminated air.510-5.350-.75) 2.350) < LOD .350) < LOD . interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.83 (2.350) < LOD .Fungicides Pentachlorophenol inhale it or absorb it through exposed skin.33-2.350) < LOD .60) 1..350) < LOD . After absorption.350-2.480-2.51) 1. < LOD means less than the limit of detection.350-.53) size 1994 2528 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th .10 (1.350-. the elimination half-life may be a week or more (Uhl et al.350 (.g.350) < LOD .90) 1.350-.98 (1.350) < LOD .960) 1. other polychlorinated benzenes.10 (<LOD-1. PCP is degraded by sunlight and metabolized rapidly by microorganisms.390 (.350 (.350-.980 (.76) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * . Human exposure to PCP has become less common..650) 1.58-2.350-2.60) 1.30) .350-. mollusicide. and it is used primarily as a preservative for wood to be used outdoors (e. PCP is distributed to most tissues and is not extensively metabolized.00) 1.42) 973 1190 1021 1338 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .860-2. 87-86-5 Also a Metabolite of Several Organochlorine Insecticides General Information Pentachlorophenol (PCP) and its sodium salt were once widely used as a fungicide. are eliminated in the urine.350) < LOD .350 (.

320) < LOD .300 (.94 (1.67 (1. Survey Geometric mean (95% conf.67 (1.350) < LOD .320) < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.67 (1.560) < LOD .950-1.cdc.40) 1.73 (1.260 (. environmental levels) and health effects is available from the U.82) 1.00-1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1. The U.310-.40) 1.25 (1.560-.21-2.EPA.700-2.83 (1.06-3.300 (. 2004. and adversely affected thyroid function (U.400 (.08 and 5.370 (.e.52) 1.67-3.S.25 (1..78) 1.16-1.09 (<LOD-2.25-1. In NHANES 2001-2002 subsamples. 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. IARC has determined that pentachlorophenol is possibly carcinogenic to humans.900-1.00) 1.760 (.270-.630 (.310) < LOD .79) 1.S.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 .420) < LOD .84) 1.850 (. 2003).19) 2.990 (.30 (.580-.75 (<LOD-2.Fungicides adults and children severely exposed to PCP through ingestion.780-1.570 (.html.40) 1. 1989).950-1.11) 2. or skin absorption.300 (.320) < LOD < LOD 75th . respectively) (Becker et al. Urinary levels of pentachlorophenol in the general population are far below (hundreds of times lower than) urine levels reported for workplace exposure to PCP or among people living in PCP-treated log homes (Cline et al.35-2.500 (.19) 2. population from the National Health and Nutrition Examination Survey.360-. In a small sample of U.29-3.780) < LOD .950-1.48-2.84 (1.00-1.atsdr. van Raaij et al.78) 1.830) < LOD .26 (1.67-3. 2000).490) < LOD .75) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .650 (. In animals.52 (<LOD-1.19) 2.75) 1.67 (1.250 (.92) 1.560) < LOD .67-2. children in the 1980’s.57 (.35) 1.320 (.84-4.90) 1.25-2.69 (1.40) 1.9 mg/L.34 (. inhalation.30-2.26 (1. Fourth National Report on Human Exposure to Environmental Chemicals 41 .52 (<LOD-1.. 1989). the median and 95th percentile urinary PCP levels were approximately three times lower than comparable values in German adults (2.220-. 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. chronically administered high doses of PCP were hepatotoxic. OSHA has established an occupational standard.510-.650) 90th 1. respectively) (Seifert et al.800-1.470 (. carcinogenic.94 (1. 2003). Pentachlorophenol is not mutagenic or teratogenic. 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.500-1.67 (1.510-.10 (1.910-1.gov/ pesticides/ and from ATSDR at: http://www.99) 482 577 681 825 831 1125 99-00 01-02 99-00 01-02 * * * * .36) .S.55) 973 1190 1021 1337 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .13 (.440 (.94-3.16 (..35-2.18) .650 (.52 (1.55) 1. 1991). 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.gov/ toxpro2.250 (.280) < LOD . EPA has developed standards for PCP in drinking water and the environment.360 (.330-.710-1.610 (.30) 1.500-. and the FDA has established a standard for bottled water.35) 1.290-..25) 1.0 mg/L.51) 1.09-1.18 (1.730) < LOD . Death can result from seizures and cardiovascular collapse.590-1.56) 1.800) < LOD 1.590) < LOD . 1995).380-.epa.920 (.57 (1.240-.. More information about external exposure (i. 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.06 (.21 (.S.82 (1.430-.270-.19 (1..30) 1.25-2.. EPA at: http://www.290) < LOD . Among adults in the NHANES 1999-2000 subsample.95) 3.290-.340-.430) < LOD .06) 1.40) 1.08) 696 680 521 695 603 951 < LOD means less than the limit of detection for the urine levels not corrected for creatinine..S.40-2.6 and 14.10-2.220-.

Seifert B. Barrot C. 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. Seifert B. drinking water and indoor air. Blau GE. et al.54(3):203-208. 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. r e g u l a t i o n s . Cline RE. Baker S. Needham LL. Chenoweth MB. Pesticide residues in urine of adults living in the United States: reference range concentrations. Pesticide residues in food-2002-Joint FAO/WHO meeting on pesticide residues.S. Biomonitoring data can also help scientists plan and conduct research about PCP exposure and health effects. The metabolism/ pharmacokinetics of pentachlorophenol in man and a comparison with the rat and monkey. Arch Environ Contam Toxicol 1989. et al. van den Berg KJ. Safe A. Rodamilans M.71:99108. The metabolism of higher chlorinated benzene isomers. 4/21/09 Kohli J.10:552-65. Shealy DB. Effects of hexachlorobenzene and its metabolites pentachlorophenol and tetrachlorohydroquinone on serum thyroid hormone levels in rats. 2002. Needham LL. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children.18:475-481. Helm D. Seiwert M. hair. Bragt PC.105(1):78-83.S.4:289296. Arch Environ Contam Toxicol 1989. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Becker K. Environ Res 1995. Bailey SL. Lindane. PCP: Human Risk Characterization [online]. References Becker K. Schlatter C. Seiwert M. Braun WH. Metabolism of hexachlorobenzene in humans: association between serum levels and urinary metabolites in a highly exposed population. Dev Toxicol Environ Sci 1979. EPA). U. house dust. 4/21/09 van Raaij JA. Engel R. Can J Biochem 1976. htm. J Expo Anal Environ Epidemiol 2000. Smith SJ. Pharmacokinetics of pentachlorophenol in man.Fungicides Finding a measurable amount of PCP in urine does not mean that the level of PCP causes an adverse health effect. 206:15-24. Hill RH Jr.58:182-186. Notten WR. Int J Hyg Environ Health 2003.org/documents/jmpr/jmpmono/2002pr08. Holler JS. Pentachlorophenol measurements in body fluids of people in log homes and workplaces. To-Figueras J. Schulz C. Schulz C. Otero R. Gregg M. Hill RH Jr. Hill RH. Santiago-Silva M. Schmid P. 42 Fourth National Report on Human Exposure to Environmental Chemicals . Jones D. Toxicology 1991: 67(1):107-16. The German Environmental Survey 1990/1992 (GerES II): reference concentrations of selected environmental pollutants in blood. Krause C. Head SL. Sala M. Available at URL: h t t p : / / w w w. International Programme on Chemical Safety (IPCS). et al. 11/30/2004. Environmental Protection Agency (U. Fast DM.inchem. Arch Toxicol 1986. Environ Health Perspect 1997. available at URL: http://www. Kaus S. Phillips DL. Uhl S.18(4):469-474. urine. To T.

636) * .742) * .624) * .85) 2..470 (<LOD-.836) * .61) 2.790) 2. SOPP is applied topically to the crop and then rinsed off.27 (.498 (. Cnubben et al.780) < LOD . and sanitizers.402-. and it is eliminated rapidly from the body as OPP glucuronide and sulfate conjugates (Bartels et al.20 (.S. it was used in home sanitizers for surfaces. which may vary for some chemicals by year and by individual sample.60-2. In the past. however.EPA. Timchalk et al.370-..00 (1.508 (.30 (1.930 (.860) * 99-00 01-02 99-00 01-02 99-00 01-02 .50 (1.34) 1.840-1.500-2.710-2.20) < LOD 2.90) . 2006). but OPP and SOPP are still used on pears and citrus (U.02) 1.80) 1.00 (1.EPA.20-2.00 (1.23) 695 680 520 695 603 953 Limit of detection (LOD.820 (. and as a wood preservative.00-2.91) 973 1190 1018 1339 99-00 01-02 99-00 01-02 99-00 01-02 .890 (. Both have been used in agriculture to control fungal and bacterial growth on stored crops.632) Selected percentiles ( 95% confidence interval) Sample 95th 2.60 (1. General population exposure can occur via dermal.40-2.50-4.860 (.90) 2.50) < LOD .10 (1. Human health effects from OPP at low environmental doses or at biomonitored levels from low environmental exposures are unknown.30) 1. 1998). on ornamental plants and turfs.800-3.490 (<LOD-.50-3.450 (<LOD-.600-1.490 (<LOD-.600-1.640) < LOD .20 (1.88) 1.S.490 (<LOD-.389-. 2002.03) 1. 90-43-7 General Information Ortho-phenylphenol (OPP. Most agricultural food applications have been revoked.50) < LOD .00) .880-2.390-.20) < LOD 1. < LOD means less than the limit of detection.10) 2.3..600) < LOD 75th .570-1.40-5. whereas SOPP is not volatile and is more water soluble.14 (<LOD-3. 2006).770 (.600-1.600) < LOD .17 (. 1998.50 (1.23) 480 577 681 827 830 1125 99-00 01-02 99-00 01-02 .10) .570 (.600) < LOD 1.520 (.Fungicides ortho-Phenylphenol CAS No.493 (.10) 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 .28 (.10 (1.40-5.570 (.60 (1.350-1.30-2.690-1.60 (1.540-2. fungicides.20) 2.466 (. OPP is volatile.90) .570-.760-2. small amounts of OPP have been measured in human adipose tissue (Onstot and Stanley.10-1.10) 1. OPP is efficiently absorbed from the gastrointestinal tract and through the skin. OPP is considered to be moderately toxic after acute oral doses in animal studies.670) 2. or oral routes from residential use and by ingesting treated food or food that was in contact with treated surfaces or equipment.450 (<LOD-.600) < LOD . Workers who manufacture.890) 1.50) 1.710) 3.349-.30-7.00 (1.10) . EPA.630) < LOD . in paints.696) * . or 2-phenylphenol) and its water-soluble salt. interval) .00) < LOD . Fourth National Report on Human Exposure to Environmental Chemicals 43 .09) 2.07 (. Available evidence suggests that OPP does not accumulate in the body.50) .80-3.30) < LOD 90th 1.610-1.80 (2. Estimated human intakes have been below recommended intake limits (U.50-2.750-2.740 (.19 (. or apply these chemicals may be more highly exposed than the general population.645) * . 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.497 (.830 (.30) < LOD 1.450 (<LOD-.76) 1. sodium ortho-phenylphenate (SOPP).580-1.621) * .10-2.420 (<LOD-.389-.30) < LOD .90) 1. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.3 and 0. and it has limited water solubility.496 (.10) . such as fruits and vegetables.570-2. formulate.28-3.S.590-2.40 (.638) * .490 (<LOD-.50) < LOD .550-1.00) .22 (. Both chemicals degrade within hours to weeks in the environment (U.40-7.364-.22) 2.S. leaving the chemical residue OPP.410-. OPP is still used as a disinfectant fungicide for industrial applications.33 (.20 (1.490 (<LOD-.552 (. 1989). 2006).370-. Survey Geometric mean (95% conf.770 (.92 (.850 (. inhalational. 2006).690) < LOD .20-3.386-. OPP was detected in 40 of 60 different canned beers at concentrations in the low parts per billion (Coelhan et al.370-. population from the National Health and Nutrition Examination Survey.890 (.480-1. are antimicrobial agents used as bacteriostats.90 (1.50 (1.433-.950) < LOD .560-8.509 (.80) 1.970 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.60-3.90 (1.610 (.567 (.

02 (.650-1.750 (. population from the National Health and Nutrition Examination Survey.666) * .24-2. 2000. 2005).810-1. Nakagawa et al. 44 Fourth National Report on Human Exposure to Environmental Chemicals .89 (1.53) 1.04-4.43) 3. leading to production of two metabolites. 2005.27) < LOD . less likely. Brusick.610) < LOD 1.64 (2. U. 2005).980 (.770-2.32) 3...560) < LOD 75th .11 (.21) 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.38) 1.353-. or.780 (..620-1. 1997. and it has classified OPP as not classifiable with respect to human carcinogenicity.473) * .460-.670 (. 1986).74 (1.33) size 1991 2528 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th .360 (<LOD-. Additional information is available from U.320 (<LOD-.38) 973 1190 1018 1338 99-00 01-02 99-00 01-02 99-00 01-02 . U.21-2.4) 3.29) 1.270-.940-2.860 (. 1999.96) 1.508) * .17 (.05-2.88-4.Fungicides anemia.31) < LOD .EPA at: http:// www.910-1.329-..484) * . or developmental toxicity was observed (Bomhard et al.EPA 2006).550 (.514 (..910 (.444 (.43-2.38) 2.750-2.580-1.880-1.62) .750 (.620-1.28 (2.96 (1.01) 1.910 (<LOD-1.500) < LOD . 2002.EPA 2006). Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.480-.06-4.656) * .61 (1.0) 1. 1984.440 (. ortho-phenylhydroquinone and ortho-phenylbenzoquinone.28 (<LOD-4. Bomhard et al. Urinary ortho-Phenylphenol (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. interval) .08) 1.00 (1.40-13.380 (.453 (.590) * . CDC.61 (2.93) 1.248-.52 (.385 (.S.08-2.690 (.47) .11-1.550-.291-.00 (.09-3.17) 2.84 (1. by possible genotoxic mechanisms (Hagiwara et al.75 (1.96 (1.44 (1. but no neurologic. Zhao et al. 2002.382 (. Finding a measurable amount of OPP in urine does not mean that the level of OPP causes an adverse health effect.800-1.410 (<LOD-..93) .580) < LOD .496 (.560-2.81) 1.455-.59) .570) < LOD 1.900-1. 1998.86 (1.93 (1. Murata et al.07) 2..311-.860 (.670) < LOD .32) 1.51-3. Biomonitoring Information Urinary OPP levels reflect recent exposure. Smith et al.640-1.900) < LOD .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. population in the subsamples from NHANES 1999-2000 and 2001-2002 (CDC. 2002).970) 1.09-6.361-. OPP or SOPP produced carcinomas of the bladder only after phase II detoxification pathways were saturated.343 (.33-2.gov/pesticides/.568) * .550) < LOD .43-2. 1999.43 (1.61 (.91) 695 680 520 694 603 953 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.670 (.09 (1..12-2.69 (1.470 (<LOD-.38-3. 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.33) .78 (2. Volunteers exposed to 0.17) * 99-00 01-02 99-00 01-02 99-00 01-02 . IARC has classified SOPP as a possible human carcinogen.58) 2.403-.791) * .S.410 (<LOD-.59) 1.420 (<LOD-. Pathak and Roy. Kwok et al.780-14.600-1.11 (.21 (.301-.558) Selected percentiles ( 95% confidence interval) Sample 95th 2. Ito et al.17 (.. Dermally applied OPP was not carcinogenic in a 2-year experimental study in animals (NTP.06-5.S.75 (1.20) < LOD 3.840 (.93) . In high dose animal studies.950) < LOD . reproductive.470) < LOD .46) < LOD 1.11) 4.13) 1. 1993.S.26) 1.S. 1984.29) 1.08-1.980 (<LOD-1.990) < LOD .91 (1.06 (1.97 (2.11) < LOD 90th 1.24-2. 1992.510-.30) 480 577 681 826 830 1125 99-00 01-02 99-00 01-02 . These metabolites may induce carcinogenicity via nongenotoxic regenerative hyperplasia of the bladder (Appel.25-6.epa..12) < LOD 1.810) < LOD .510 (<LOD-. OPP was not found to be mutagenic.18) 2. Detectable levels were seen in over half the U.420 (<LOD-. Survey Geometric mean (95% conf.96-4.

Available at URL: http://ntp. Regul Toxicol Pharmacol 2002. Toxicol Appl Pharmacol 1998. J Agric Food Chem 2006. Gierthy J. Hagiwara A. 4/9/09. 1989. O-phenylphenol and its sodium and potassium salts: a toxicological assessment. Reregistration Eligibility Decision (RED) for 2-phenylphenol and salts (Orthophenylphenol or OPP). Cano M. Meuling WJ. Bartels MJ. Roy D. Cnubben NH. Bartels MJ. Glas K. Mutat Res 1993. Coelhan M. Centers for Disease Control and Prevention (CDC). Long-term toxicity and carcinogenicity study of sodium o-phenylphenate in B6C3F1 mice. J Agric Food Chem 2002. Tayama S. Vogel JS. Fukushima S. Zhao S. Detection and characterization of DNA adducts formed from metabolites of the fungicide ortho-phenylphenol. Richter M. Narang A. Analysis of genotoxicity and the carcinogenic mode of action for ortho-phenylphenol. Stanley JS. Buchholz BA. Atlanta (GA). Hum Exp Toxicol 1998. Shirai T. Christenson WR. Environmental Protection Agency (U.28(6):579594. Nakagawa Y.703(12):97-104. National Toxicology Program (NTP).pdf.S. Mendrala AL. Determination and levels of the biocide ortho-phenylphenol in canned beers from different countries. Bartels MJ. Determination of orthophenylphenol in human urine by gas chromatography-mass spectrometry. rat and man. Moore GA. Arch Toxicol 2000. Drugs. Arnold LL. Herbold BA.17(8):411-417. Office of Toxic Substances. Elliott GR. The pharmacokinetics and metabolism of 14C/13C-labeled ortho-phenylphenol formation following dermal application to human volunteers. Crit Rev Toxicol 2002. In vivo genotoxicity of sodium orthophenylphenol: phenylbenzoquinone is one of the DNA-binding metabolite(s) of sodium ortho-phenylphenol. Brusick D. Dose-dependent binding of ortho-phenylphenol to protein but not DNA in the urinary bladder of male F344 rats. 2006. Imaida K. Brendler-Schwaab SY. Hagiwara A. Kawanishi S.Fungicides References Appel KE.nih. et al. Christenson WR. July 28. Pathak DN. Sangha GK.. Hirose M. Moriya K. 90-43-7) in Swiss CD-1 mice (dermal studies). Comparative in vitro-in vivo percutaneous penetration of the fungicide ortho-phenylphenol. Brzak KA. food additives and natural products as promoters in rat urinary bladder carcinogenesis. Inoue S. U.EPA). Murata M. EPA 739 R-06004.epa.32(6):551-625.50(11):3351-3358.gov/oppsrrd1/REDs/ phenylphenol_red.pdf. J Chromatogr B Biomed Sci Appl 1997. Biochem Pharmacol 1992. Eastmond DA. Shibata M. Leser KH. Xenobiotica 1998. van de Sandt JJ. EPA).S. Ito N. McNett DA. Ito N. Freyberger A. Bormett GA. Identification of SARA compounds in adipose tissue. Environ Mol Mutagen 2005. Urinary physiologic and chemical metabolic effects on the urothelial cytotoxicity and potential DNA adducts of o-phenylphenol in male rats. Moldeus P. Fourth National Report on Human Exposure to Environmental Chemicals 45 . Timchalk C. Food Chem Toxicol 1984.gov/ntp/htdocs/LT_ rpts/tr301. Hakkert BC. 4/13/09 Onstot JD. St John MK. Sangha G.S. Carcinogenesis 1999. Bartels MJ. Oxidative damage to cellular and isolated DNA by metabolites of a fungicide orthophenylphenol. Environmental Protection Agency (U.286(2):309-319. Fukushima S.22(10):809-814. Bromig KH. Kwok ES. et al.niehs. Available at URL: http://www.45(5):460-481. 2005.54(16):5731-5735.20(5):851-857. Bomhard EM. Relationship between metabolism and cytotoxicity of ortho-phenylphenol in isolated rat hepatocytes.74(2):61-71. Eadon G. EPA-560/5-89-003. Turteltaub KW. NTP Technical report on the toxicology and carcinogenesis studies of ortho-phenylphenol (CAS No. Timchalk C. Third National Report on Human Exposure to Environmental Chemicals.43(7):14311437.159(1):18-24. Selim S. IARC Sci Publ 1984.(56):399-407.35(2 Pt 1):198-208. Toxicol Appl Pharmacol 1999.150(2):402-413. The carcinogenicity of the biocide ortho-phenylphenol.S. March 1986. Roberts AL. Comparative metabolism of orthophenylphenol in mouse. Smith RA. U.

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

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

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

Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa.248(2-3):123-133. Ward EM. J Expo Anal Environ Epidemiol 2005. Volume 65. Coleman S.39(17):6561-6574. Environmental Protection Agency (U. J Expo Sci Environ Epidemiol 2007. Tinwell H.pdf. et al. 5/30/06.S. Lefevre PA.108(12):1151-1157. Hum Exp Toxicol 1996. Environ Health Perspect 2003. Casida JE. pages 3682-3690. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. Hladik ML. Environ Health Perspect 2000. Larsen GL. Sci Total Environ 2000.cce. Hsiao JJ. Report of the Food Quality Protection Act (FQPA) Tolerance Reassessment Progress and Risk Management Decision (TRED) for Acetochlor. Centers for Disease Control and Prevention (CDC).17(6):559-566. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. Environmental Protection Agency (U. Furlong ET.15(9):702-735. imidazolinone. acetochlor. EPA 738-R-00-009. Barr JR. U.html.37(4):10881093. Alavanja MC. Sci Total Environ 2000. and other herbicides in rivers. sulfonamide.248(2-3):115-122.S. Federal Register: January 24. Bravo R. Olsson AO. Feng PCC. Barr DB.S. Rose RL. Third National Report on Human Exposure to Environmental Chemicals. Davison KL. Jefferies PR. Available at URL: http://www. Occurrence of sulfonylurea. Comparative metabolism and elimination of acetanilide compounds by rat. Xenobiotica 1994. Acetochlor (Harness) Pesticide Petition Filing 1/00. Reynolds SJ. EPA). EPA).cornell. Thurman EM.Herbicides References Ashby J. Deddens JA. Chem Res Toxicol 1998. Finding minimal herbicide concentrations in ground water? Try looking for their degradates. reservoirs and ground water in the Midwestern United States.gov/oppsrrd1/reregistration/REDs/acetochlor_tred. Dialkylquinonimines validated as in vivo metabolites of alachlor. Andrews HF. Wratten SJ.111(5):749-756. Roberts AL.EPA): http://pmep. 5/30/06 U. and metolachlor herbicides in rats. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. Battaglin WA. Wilson AG.S. Comparative metabolism of chloroacetamide herbicides and selected metabolites in human and rat liver microsomes. Kier L. Barr DB.edu/profiles/herbgrowthreg/24-d-butylate/acetochlor/acetochlor_pet_100. epa. Atlanta (GA). Quistad GB. Kolpin DW. Burkhardt MR.S. Camann DE. Available at URL(non U. 1998. Identification of human urinary metabolites of acetochlor in exposed herbicide applicators by high performance liquid chromatography-tandem mass spectrometry. et al. Hodgson E. Whyatt RM. 2005. Hines CJ.11(4):353359. March 2006.24(10):1003-1012. Fourth National Report on Human Exposure to Environmental Chemicals 49 . Barr DB. Green T. Kinney PL. Heederik D. Linderman R. Peter CJ. Sanderson WT. J Agri Food Chem 1989. et al. Hein MJ.15(6):500-508. Number 15. Evaluation of the potential carcinogenicity and genetic toxicity to humans of the herbicide acetochlor. Linhart SM. Environ Sci Technol 2005. Feil VJ. Curwin BD. Striley CA. 2000.

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

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

Casida JE. December 1998. Geneva. Shealy DB. Available at URL: http://www. Mutat Res.htm.43(25):2087-94. California. and metolachlor herbicides in rats. Quistad GB. World Health Organization. Hines CJ. Biological monitoring of commercial pesticide applicators for urine metabolites of the herbicide alachlor.47(6):503-517. 1999. Circular 1291. March 2006. Casida JE. Driskell WJ. Feil VJ. Kolpin DW. Life Sci 1988. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor.39(17):6561-6574.S. sulfonamide. reservoirs and ground water in the Midwestern United States.43(9):2504-2512.S. Available at URL: http://water.Herbicides References Battaglin WA.395(2-3):159-171. Kolpin DW. Henningsen G. Andrews HF. Comparative metabolism and elimination of acetanilide compounds by rat. World Health Organization (WHO). The Quality of Our Nation’s Waters Pesticides in the Nation’s Streams and Ground Water. Sci Total Environ 2000.S. Water-Resources Investigations Report: Distribution of Major Herbicides in Ground Water of the United States Water Resource Investigations Report No. MacKenzie B. Tolos W. 1992-2001. Davison KL. Striley CA. Barr DB. Hum Exp Toxicol. Occurrence of sulfonylurea. imidazolinone. Linhart SM. International Programme on Chemical Safety (IPCS). Casida JE. 2003. Hladik ML. Thelin GP. revised February 15. Biagini RE. WHO/ FAO Data Sheets on Pesticides.pdf. Burkhardt MR. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. and other herbicides in rivers. Sci Total Environ 2000.56(9):883-889. Environmental Protection Agency (U. Furlong ET. Gilliom RJ). Reregistration Eligibility Decision (RED) Alachlor.18(6):363-391. Am Ind Hyg Assoc J 1995.int/water_sanitation_health/dwq/chemicals/en/alachlor. 1996. Hill RH Jr. Kier LD. Hsiao JJ.111(5):749-756.11(4):353359. EPA).37(4):10881093. et al. Geological Survey (USGS). Atlanta (GA). Tessier DM.56(6):853-859. An evaluation of the carcinogenic potential of the herbicide alachlor to man. 98-4245 (by Barbash JE. Third National Report on Human Exposure to Environmental Chemicals. 4/2/09 U. U. Feng PCC. Dialkylquinoneimine metabolites of chloroacetanilide herbicides induce sister chromatid exchanges in cultured human lymphocytes. who. Brown KK. Hines CJ. Peter CJ. J Agri Food Chem 1989.usgs. EPA 738R-98-020. 2007. 86. Hull RD. 1997. Supplemental Technical Information (available on-line only). Ann Occup Hyg 2003. Geological Survey (USGS). Roberts AL. Thurman EM. Sanderson WT. J Ag Food Chem 1995. Martens MA.24(10):1003-1012. Hill AB. Centers for Disease Control and Prevention (CDC). 2/27/09 U. Quistad GB. Finding minimal herbicide concentrations in ground water? Try looking for their degradates. et al. Erratum in: Life Sci 1989. ALACHLOR. Xenobiotica 1994. DNA adduct formation by alachlor metabolites. Thake DC. 1998. Camann DE. Lau H. Barr JR. No.org/documents/pds/pds/pest86_e. Environ Sci Technol 2005. Bull Environ Contam Toxicol 1996. Larsen GL. Kimmel EC. Biagini R.gov/oppsrrd1/ REDs/0063. Quantitative assessment of the mutagenic potential of environmental degradative products of alachlor.epa.248(2-3):123-133. Environ Health Perspect 2003. 2/27/09 Jefferies PR. Wratten SJ. Available at URL: http:// www. Alachlor in Drinking-water. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. Deddens JA. Jefferies PR.248(2-3):115-122.44(18):1325. Background document for development of WHO Guidelines for Drinking-water Quality. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. Wilson AG. 1999. Clark JM. Brown MA. Identification of a major human urinary metabolite of alachlor by LC-MS/MS. Dialkylquinonimines validated as in vivo metabolites of alachlor. Chem Res Toxicol 1998.inchem. 2/27/00 52 Fourth National Report on Human Exposure to Environmental Chemicals .pdf.gov/nawqa/pnsp/pubs/circ1291/ supporting_info.S. Sacramento. Kinney PL. acetochlor. Available at URL: http://www. Whyatt RM. Shoemaker DA. 2005. Heydens WF.php.

* Not calculated: proportion of results below limit of detection was too high to provide a valid result.S. In regions where atrazine is used.EPA. It is also used as a non-selective herbicide. Hayes et al.. More than 70 million pounds have been applied annually in recent years. 2003b). with about 75% of corn cropland receiving treatment.. < LOD means less than the limit of detection. 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. Atrazine mercapturate products accounted for a major proportion of human urinary metabolites (Lucas et al. Applicators of atrazine may be exposed dermally and by inhalation. it is one of the more commonly detected pesticides in surface and ground waters (USGS. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. 1990). 1993. 1982. 2003b). and cyanazine. For the general population.. atrazine is slowly degraded to dealkylated products. population from the National Health and Nutrition Examination Survey.. Bacteria and plants can metabolize atrazine to hydroxyatrazine.791 and 0.3. 2007). Survey Geometric mean (95% conf. 2003a). and then eliminated in the urine over a few days (Bradway et al. Catenacci et al. In soils. metabolized. Urinary Atrazine mercapturate Metabolite of Atrazine Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. atrazine use has progressively been restricted in an effort to reduce surface and ground water contamination.S. propazine. Atrazine has limited water solubility and is not tightly bound to soil. Atrazine is well absorbed orally. Fourth National Report on Human Exposure to Environmental Chemicals 53 . U. Related chlorotriazine herbicides include simazine. but estimates of seasonal intakes from drinking water in a small number of communities have exceeded the recommended limits (U. 1912-24-9 General Information Atrazine is a widely used chlorotriazine herbicide that acts against broadleaf and grassy weeds. 2005. 1993). As a result. resulting in atrazine mercapturate and N-dealkylation products (IPCS.. glutathione conjugation appeared to be the major route of biotransformation. all of which act by inhibiting plant photosynthesis. 2002. Atrazine does not bioaccumulate.and post-emergence to agricultural land for crops such as corn and sorghum.S.S.EPA.EPA. which may vary for some chemicals by year and by individual sample.Herbicides Atrazine CAS No. Atrazine was first registered as an herbicide in 1958. It has little toxicity in birds and moderate toxicity in some fish and aquatic invertebrates. which have half-lives of several months. Atrazine is applied pre. Atrazine may alter the sexual development of frogs at environmental levels (Gammon et al. U. drinking water is an infrequent source of atrazine exposure. Timchalk et al. 1996. The dealkylated chloroatrazine metabolites. In animals and humans. but it is leachable into ground and surface waters..

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

Chen H. Reynolds SJ. Determination of urinary residue levels of the N-dealkyl metabolites of triazine herbicides. Toxicol Sci 2000. Heederik D. 1999) and 83 Minnesota children with multiple urine collections during 1997 (Adgate et al. atrazine was detected in only four children (Arcury et al. et al. Hein MJ. Hines CJ. The mammary tumor response in triazine-treated female rats: a thresholdmediated interaction with strain and species-specific reproductive senescence.109(6):583-590. Extrom PC. Stevens JT. Centers for Disease Control and Prevention (CDC). Pesticide urinary metabolite levels of children in eastern North Carolina farmworker households. Jones AD. Available at URL: http://www. Curwin BD. Mendoza M. et al. Barbieri F. Eldridge JC. Lee M.. Bersani M. urinary concentrations ranged from 5-1756 μg/L (Lucas et al. Pfeifer KF. Moseman RF. Breckenridge CB. No. Fleenor-Heyser DG. Goldman JM. Brown KK. Barr DB. Stoker TE. Cooper RL. Stoker TE. the urinary geometric mean levels for herbicide applicators in Ohio and Wisconsin were about 6 μg/L (Hines et al. World Health Organization. Grzywacz JG. atrazine mercapturate was infrequently detected at the detection limit of < 1 μg/L. Hayes TB.69(2):217-222. 82. Sanderson WT. levels of atrazine mercapturate were generally not detectable (CDC. Pest Manag Sci 2005. Collins A. Short-term effects of chlorotriazines on estrus in female Sprague-Dawley and Fischer 344 rats. Ferrell JM. Ann Occup Hyg 2003. Toxicol Sci 2003. A risk assessment of atrazine use in California: human health and ecological aspects.15(6):500-508. McElroy WK.. Atrazine disrupts the hypothalamic control of pituitary-ovarian function. J Toxicol Environ Health 1994. 2001 [online]. Toxicol Sci 2000. Quandt SA. 2005).58(2):366-376.. Finding measurable amounts of atrazine mercapturate in urine does not mean that the levels of atrazine mercapturate cause an adverse health effect. Lioy PJ. Schmid J. The geometric mean of urinary atrazine mercapturate was 1. Toxicological profile for atrazine. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. Deddens JA.115(8):1254-1260. Wetzel LT. 1996. ATRAZINE. Cottica D. Environ Health Perspect 2007. Barr DB. Determination of atrazine metabolites in human urine: Fourth National Report on Human Exposure to Environmental Chemicals 55 . Perry et al. Hermaphroditic. Stoker TE. International Programme on Chemical Safety (IPCS). Blewett C.30(2):244-247.. 3/11/09 Arcury TA. Through immunoassay atrazine equivalents (detected mostly as atrazine mercapturate). WHO/ FAO Data Sheets on Pesticides. J Expo Anal Environ Epidemiol 2005. Eberly LE. 2005. et al. J Toxicol Environ Health 1994. Maroni M.org/documents/pds/pds/pest82_e. 2003. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.64(9):672-678.. Gillis JH. Short-term effects of chlorotriazines on estrus in female Sprague-Dawley and Fischer 344 rats.. In small studies of Maryland residents in 19951996 (MacIntosh et al. Ferrell JM. Biagini RE.43(2):155-167.53(2):297-307. Stuart AA. Sanborn JR.43(2):155-167. Agency for Toxic Substances and Disease Registry (ATSDR). Eldridge JC. Seiber JN. Third National Report on Human Exposure to Environmental Chemicals.cdc. Lucas AD. 3/11/09 Laws SC. The effects of atrazine on female wistar rats: an evaluation of the protocol for assessing pubertal development and thyroid function. Barr DB. Pubertal development in female Wistar rats following exposure to propazine and atrazine biotransformation by-products. 2001). Geneva. et al.html. Aldous CN. demasculinized frogs after exposure to the herbicide atrazine at low ecologically relevant doses. Noriega N. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample. References Adgate JL. Toxicol Lett 1993. In a study of 60 farm worker children. Saiz SG. 1993). In the NHANES 2001-2002 subsample.atsdr.76(1):190-200. Environ Health Perspect 2001.. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. Atlanta (GA).Herbicides Biomonitoring Information Urinary levels of atrazine mercapturate reflect recent exposure. Cooper RL. Gammon DW.99(8):5476-5480. Wetzel LT. Proc Natl Acad Sci USA 2002.inchem. Shoemaker DA. diamino-S-chlorotriazine and hydroxyatrazine. Bradway DE. 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. Biological monitoring of human exposure to atrazine.htm. Vonk A. et al. Clayton CA.47(6):503-517. 2000). J Agric Food Chem 1982. Ferioli A. 2005). Tyrey L. Cooper RL. Carr WC Jr. Freeman NC. Available at URL: http:// www. In a small number of field workers. Catenacci G. Steroids 1999. 2007).61(4):331-355. Laws SC. Goodrow MH.gov/toxprofiles/tp153.2 μg/L in 15 farmers studied several days after spraying the pesticide (Curwin et al. et al. Gillis JH. Striley CA. Simpkins JW. Tapia J.

Geological Survey (USGS). Laws SC. Office of Prevention.php. Supplemental Technical Information (available on-line only). Environmental Protection Agency (U.6(1):107-116. Interim Reregistration Eligibility Decision For Atrazine. Available at URL: http://www. Available at URL: http://water.pdf. Case No. Fenton SE. The Quality of Our Nation’s Waters. Wood C. 0062. J Expo Anal Environ Epidemiol 1999. van den Berg M. Delzell E.61(1):27-40. Rayner JL. Osborne DW. Toxicology 1990. Exposure parameters necessary for delayed puberty and mammary gland development in LongEvans rats exposed in utero to atrazine.gov/nawqa/pnsp/pubs/ circ1291/supporting_info. Singzoni B. Kastl PE. Wetzel L.S. Chem Res Toxicol 1993. Sanderson JT. Guidici DL. Urinary biomarkers of atrazine exposure among farm pesticide applicators. Timchalk C.182(1):44-54. Toxicol Appl Pharmacol 2004. Cooper RL. MacIntosh DL. Christiani D. The effect of atrazine on puberty in male Wistar rats: an evaluation in the protocol for the assessment of pubertal development and thyroid function.58(1):50-59. U.S. Needham LL.S. Washington (DC). Dagenhart D. Induction and inhibition of aromatase (CYP19) activity by various classes of pesticides in H295R human adrenocortical carcinoma cells. EPA).epa. Stoker TE. 2007. Environmental Protection Agency (U.67(2):198-206. 2003b. Cooper RL. J Toxicol Environ Health A 1999. Langvardt PW. 3/11/09 U. Pesticides and Toxic Substances. Lansbergen GW.usgs. May 2003a. EPA Office of Pesticide Programs. Ann Epidemiol 2000. 4/2/09 56 Fourth National Report on Human Exposure to Environmental Chemicals .S. Stoker TE.gov/scipoly/sap/meetings/2003/june/ finaljune2002telconfreport.pdf. The effects of atrazine metabolites on puberty and thyroid function in the male Wistar rat. Toxicol Appl Pharmacol 2002. Toxicol Sci 2000.Herbicides development of a biomarker of exposure. Ryan PB. Pesticides in the Nation’s Streams and Ground Water. Dryzga MD. Tortorelli J. Stevens JT. Determination of the effect of tridiphane on the pharmacokinetics of [14C]-atrazine following oral administration to male Fischer 344 rats. Available at URL: http://www. A longitudinal investigation of selected pesticide metabolites in urine.195(1):23-34. Hammerstrom KA. Crit Rev Toxicol 1997. A risk characterization for atrazine: oncogenicity profile. Perry M. revised February 15.56(2):69-109.S. Boerma J. 1992-2001. Circular 1291. Toxicol Sci 2002. Environmental Fate and Effects Division.10(7):479. A review of epidemiologic studies of triazine herbicides and cancer. Guidici DL. Sathiakumar N. 6/1/09 U.epa. White paper on potential developmental effects of atrazine on amphibians.gov/oppsrrd1/REDs/ atrazine_ired. Breckenridge CB.9(5):494-501.27(6):599612. EPA). Laws SC. March 2006.

and delayed Urinary 2.350) < LOD < LOD < LOD .320) 90th .610-. in 2001 (U.16) < LOD .310) < LOD .250 (<LOD-.4-D were used in the U. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. by direct contact with agricultural and residential areas after applications. It is poorly bound in soils. it acts as a plant growth hormone. It was first registered with U. 2.890 (. population from the National Health and Nutrition Examination Survey. 2007).32 (1. agricultural. Kohli et al.4-Dichlorophenoxyacetic acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. and mecoprop).310 (. hypotension.48) < LOD 1.550-1.890) < LOD .210 (<LOD-.4-D or exposed for prolonged periods. 2.230-.30 (<LOD-2. abdominal pain.2. and by consuming food or drinking water contaminated with 2. with a half-life of several days to several weeks.910) 1.490 (.27 (1. General population exposure to 2.66) < LOD 1.730 (.13) < LOD .20 (<LOD-1.560-.740 (.960-1.S.51 (1. but at higher levels they are herbicidal. It is not well absorbed through the skin. headache.540-.670-1.S.S..80) 1.27 (.400) < LOD .260 (<LOD-. It is rarely detected in ground waters (USGS.930-1.24 (.37) size 1977 2413 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD 75th < LOD . 2.930 (.03) 695 659 520 668 589 892 Limit of detection (LOD.690 (.05-2.410) < LOD . Once absorbed.4-D is eliminated mostly unchanged in the urine with an elimination half-life ranging from 10 to 33 hours (Arnold et al.910) < LOD .440-1. 2005).330 (. and it is often mixed with other chlorophenoxy acid herbicides (such as dicamba.370-.EPA in 1948.680-1.660) 1.02-1.4-D) controls broadleaf weeds in residential.910) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .760 (.10) < LOD 1.EPA. Sauerhoff et al. nausea.690 (. 4-D.4-D has low acute toxicity.10 (<LOD-1.08) < LOD . although dermal exposure may be significant for herbicide manufacturing plant workers exposed to high concentrations of 2.21) 1.60) 1. 1974. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 1.250 (<LOD-. 2004). which may vary for some chemicals by year and by individual sample. MCPA.22) < LOD . As much as 62 million pounds of 2.70) 1.Herbicides 2.4-D can be applied either as an aqueous salt or as oil-soluble esters.49) 477 546 677 797 823 1070 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD .4-dichlorophenoxyacetic acid (2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.55 (1. 94-75-7 General Information Widely used throughout the United States. Survey Geometric mean (95% conf. these herbicides can enhance plant growth.420) < LOD .952 and 0.4-D have been below recommended intake limits (U. dizziness. the chlorophenoxy herbicide 2.560-1.210-. Human health effects from 2.S.690 (.. myotonia. At low levels.22) 962 1135 1015 1278 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .230 (<LOD-. 1989.490) < LOD < LOD < LOD .40) 1. Recent estimates of chronic intakes of 2. Fourth National Report on Human Exposure to Environmental Chemicals 57 . Intentional overdoses and unintentional high dose exposures to chlorophenoxy acid herbicides have resulted in weakness.S.07 (.4-D is rapidly absorbed via oral and inhalation routes.00-2.610 (. < LOD means less than the limit of detection.4-D may occur during residential applications.. Acid and salt forms are much less toxic to fish and aquatic invertebrates than the ester forms.420-.690-1.10 (<LOD-1.27-2. renal and hepatic injury.4-D at low environmental doses or at biomonitored levels from low environmental exposures are unknown.20 (. 1977).43) 1. Similar to other chlorophenoxy herbicides.EPA.810-1. 2. and aquatic environments.4-Dichlorophenoxyacetic Acid CAS No.

4-D reflect recent exposure. 1995.S. Kutz et al.. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.780-1.EPA 2005).610-. IPCS..340-. 2005.820-1. 2003.680) < LOD ..410) < LOD 1. IPCS.4-D was not found to be genotoxic or carcinogenic in animal studies (Garabrant and Philbert. 2005). 2. 2002.4-D levels were detectable in less than a quarter of the individuals studied. 1989). 2000).990-1.660 (.440 (. CDC. and of adults and children (Baker et al. 1985.. Acute high doses administered to laboratory animals produced ataxia. 2. other exposures. developmental.790) 1.620-.740 (.890) < LOD 1.670 (.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 . urinary 2.780) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD . and evidence of histological injury to the kidneys.29) 477 546 677 796 823 1070 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD .35) < LOD . such as soft tissue sarcoma and non-Hodgkin’s lymphoma.39) < LOD 1. 2006.520-.S.24) 1. IARC considers the chlorophenoxyacetic acids group of chemicals as possibly carcinogenic to humans.780) .380 (<LOD-.4-D production plant workers and a few forestry workers spraying 2.890-1.EPA at: http://www.S.640 (.410 (<LOD-..270-. liver.17 (.570) < LOD .3.350 (<LOD-.27-1.19) .550-.S. eyes. Additional information is available from U. population from the National Health and Nutrition Examination Survey.4-D are eye irritants. It is unclear whether these associations are related to the chlorophenoxy herbicides.780 (.7.08 (. with the exposure to chlorophenoxy herbicides as defoliants or contaminated herbicides. IOM.8-tetrachlorodibenzo-pdioxin) (Garabrant and Philbert. Hill et al.390) < LOD < LOD < LOD .32 (<LOD-2. Post-application levels in farmers and home gardeners were dependent on Urinary 2. 2005). 2. The acid and salt forms of 2.14 (. 2005.810-1.490 (.660) < LOD .810-1.41 (1.270 (<LOD-. U.Herbicides neuropathy (Bradberry et al.920) < LOD 1. The 95th percentiles of the NHANES 1999-2000 and 2001-2002 subsamples were roughly similar to the 95th percentile values reported in a nonrandom subsample from NHANES III (1988-1994) (CDC. Frank et al. myotonia.790) < LOD .330-.56) . U.05) . adrenals and gonads (NTP. Pearce and McLean. 2005). In previous samples of the U.16) 1. thyroid. U. 2002.S.470) < LOD . interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 1.08 (.. 1996.gov/pesticides/. population (Hill et al.380 (<LOD-.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. Biomonitoring Information Urinary levels of 2.340 (.4-D had urinary levels several hundred to several thousand times higher than the 95th percentiles of the NHANES subsamples (CDC.700 (. 1996...380-. in small samples of children (Hill et al.670 (. 1995).S. 1994). Epidemiological studies have reported associations of several types of cancer. 2005. Average post-application urinary levels of 2. Knopp et al.480 (. or teratogenic effects in chronic rodent studies (Charles et al.380) < LOD . 2004). 2005.590 (<LOD-1.13 (. 58 Fourth National Report on Human Exposure to Environmental Chemicals .40) 695 659 520 667 589 892 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.590 (<LOD-1. or to contaminants in the herbicide formulations (specifically 2. Survey Geometric mean (95% conf. 1980.S.670 (<LOD-1.26) 962 1135 1015 1277 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD . 1992).410) < LOD < LOD < LOD .580-.EPA.. U.73) . 2005).560-.epa.930-1. 1996..EPA.13 (. 2001.08 (.560-. IPCS.4-Dichlorophenoxyacetic acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.980) < LOD 1.410) 90th .610-.4-D does not have significant reproductive.850) < LOD .EPA. Kolmodin-Hedman and Erne.720 (.

15(6):500-508. Solomon KR. Cook BT.51(3):152-159. The pharmacokinetics of chlorinated phenoxy acid herbicides: a literature. Kutz FW. Cole DC.4-D) epidemiology and toxicology. Heederik D. Hanley TR Jr. Gupta BN.php?record_id=10603. Washington (DC): National Academies Press. Hill RH Jr.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. Forestry workers involved in aerial application of 2. Available at URL: http://ntp. Occup Environ Med 1994. Ripley BD. Carter-Pokras OD. Holler JS. Harris SA. Tandon JS. Frank R. Campbell RA. Chapman P.4-D and 2. Garabrant DH. Dichlorophenoxyacetic acid.nap.4-D).37(2):277-291. Bus JS. Mandel et al. Centers for Disease Control and Prevention (CDC). Biomonitoring for farm families in the farm family exposure study.4:427-435. Needham LL. Reynolds SJ. Exposure of homeowners and bystanders to 2.71(2):99-108. Brody D.4-dichlorophenoxyacetic acid in the chemical industry: results of a five year biological monitoring study. Biomonitoring of herbicides in Ontario farm applicators. Developmental toxicity studies in rats and rabbits on 2. Barr DB. Harris et al. Hein MJ. Sanderson WT.4-Dichlorophenoxyacetic Acid). TOX-63: TOXICITY REPORT CURVES.4:97-100. To T.4-D. Acquavella JF. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. Honeycutt R. Hill RH Jr. 2005. Available at URL: http:// www. 3/17/09 Institute of Medicine (IOM). Tables. 2005. Review of 2. Available at URL: http:// www.. Scand J Work Environ Health 2005.4-D): exposure and urinary excretion. Veterans and Agent Orange: update 2002..4-D in urine does not mean that the level of the 2. Arch Environ Contam Toxicol 1989. Arch Environ Contam Toxicol 1985. Crit Rev Toxicol 2002.31(2):121-125. Sircar KP.4-dichlorophenoxyacetic acid and its forms.10(6 Pt 2):789-798. Absorption and excretion of 2. 914. et al. Gregg M.. Dhar MM.gov/index. Quantification of selected pesticide metabolites in human urine using isotope dilution high-performance liquid chromatography/ tandem mass spectrometry. Khanna RN.4. Arch Toxicol Suppl 1980.edu/catalog. J Toxicol Environ Health 1992. Updated March 7. Barr DB. 3/17/09 Knopp D. Environ Res 1995.4-. general population.4-dichlorophenoxyacetic acid (2. Needham LL. Baker S. References Arbuckle TE. Selected pesticide residues and metabolites in urine from a survey of the U. Wilson RD.org/documents/jmpr/jmpmono/v96pr04. van Ravenzwaay B. Finding a measurable amount of 2.nih. the number of acres to which it was applied (Curwin et al. In farm families. National Toxicology Program (NTP). geometric mean urinary levels of 2. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children. Philbert MA.4-dichlorophenoxyacetic acid in man.4-D will result in an adverse health effect. TOX-63 Peroxisone Project (2. Atlanta (GA).27(1):23-38. Kohli JD. Alexander BH. Vet Hum Toxicol 1989.Herbicides the time since application. International Programme on Chemical Safety-INCHEM (IPCS). Xenobiotica 1974. Pesticide residues in urine of adults living in the United States: reference range concentrations. Bailey SL. Committee to Review the Health Effects in Vietnam Veterans of Exposure to Herbicides (Fourth Biennial Update. Beeson MD. Baker SE. 2005). Survival and Growth Curves from NTP Toxicity Studies. Mandel JS.htm.4:318-321.32(4):233-257. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.31 Suppl 1:98-104. Beasley VR.S. Driskell WJ.4 dichlorophenoxyacetic acid (2. 2005 Charles JM.4-D were highest in the farmers who applied the 2. other family members had levels ranging only slightly higher than the 95th percentile levels in NHANES 1999-2000 and 2001-2002 subsamples (CDC.60(1):121-131. Head SL. 2006. Third National Report on Human Exposure to Environmental Chemicals.5-T).niehs. 2. Toxicol Sci 2001. J Expo Anal Environ Epidemiol 2005 Nov. Fast DM. Scand J Work Environ Health 2005. Curwin BD. Ritter L.inchem. Sirons G J. Arnold EK.31 Suppl 1:90-97. Shealy DB. Stephenson GR. Erne K. Pesticides residues in food: 1996 evaluations Part II Toxicology. Estimation of occupational exposure to phenoxy acids (2. Board on Health Promotion and Disease Prevention. and the use of protective clothing or equipment (Arbuckle et al.. the amount of pesticide applied. Smith SJ. J Expo Anal Environ Epidemiol 2000. Assessment of exposure to 2. Murphy RS.4-dichlorophenoxyacetic acid (2. 2003. et al.4-D than levels found in the general population. Biomonitoring studies of 2. J Environ Sci Health B 1992. cfm?objectid=06FF8DA6-E5A1-90CD-3F26562CEC5CDDE5. Baker BA. et al. Kolmodin-Hedman B. 3/17/09 Fourth National Report on Human Exposure to Environmental Chemicals 59 . 2005).18(4):469-474. 1992).

4/2/09 U.EPA.htm. 2. Pesticides in the Nation’s Streams and Ground Water. Geological Survey (USGS). Pesticide industry sales and usage . Supplemental Technical Information (available on-line only). Blau GE. S.EPA). 60 Fourth National Report on Human Exposure to Environmental Chemicals .EPA). Office of Prevention Pesticides and Toxic Substances.usgs.gov/oppsrrd1/ REDs/factsheets/24d_fs. gov/oppbead1/pestsales/01pestsales/market_estimates2001. Toxicology 1977.S.S.2000 and 2001 market estimates.4-D) following oral administration to man.epa. 3/17/09. Gehring PJ. Available at URL: http://water.S. 3/17/09 U.php.S.Herbicides Sauerhoff MW. Environmental Protection Agency (U.gov/nawqa/pnsp/pubs/ circ1291/supporting_info. The fate of 2. The Quality of Our Nation’s Waters. revised February 15. March 2006. EPA 738 F-05-002.epa. June 2005.4-D RED Facts. Environmental Protection Agency (U.S. Available at URL: http://www.8:3-1U. Braun WH.pdf. Circular 1291.4-dichlorophenoxyacetic acid (2. May. Available at URL: http://www. Washington (DC): U. 2007. 1992-2001. 2004.

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

220) < LOD 1192 1346 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < 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 .240) 679 701 957 Limit of detection (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. Survey Geometric mean (95% conf.200 (<LOD-.440 (<LOD-.S.670 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Survey Geometric mean (95% conf. Urinary Metolachlor mercapturate (creatinine corrected) Metabolite of Metolachlor Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.Herbicides Urinary Metolachlor mercapturate Metabolite of Metolachlor Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. 62 Fourth National Report on Human Exposure to Environmental Chemicals .S. population from the National Health and Nutrition Examination Survey. < 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 . see Data Analysis section) for Survey year 01-02 is 0.200 (<LOD-.500) < LOD 1192 1345 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . population from the National Health and Nutrition Examination Survey.740) 679 700 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.

Supplemental Technical Information (available on-line only). Kinney PL. Hodgson E. EPA). Curwin BD. Gilliom RJ). Burkhardt MR. Background document for development of WHO Guidelines for Drinking-water Quality. Peter CJ. Casida JE. R.24(10):1003-1012. 3/26/09 U. 4/2/09 U.108(12):1151-1157.15(6):500-508.usgs.248(2-3):115-122. Hsiao JJ. Sci Total Environ 2000. imidazolinone. EPA 738R-95-006. reservoirs and ground water in the Midwestern United States. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models.epa. Circular 1291.pdf 3/30/09 Hines CJ. acetochlor. 2005. Sacramento. 2007. Available at URL: http://www. Kolpin DW.ESTfeature_gilliom. Jefferies PR. Furlong ET. Kolpin DW. Environ Health Perspect 2003. Gillion. Xenobiotica 1994. Geological Survey (USGS). March 2006.248(2-3):123-133. Andrews HF. Geological Survey (USGS). Chem Res Toxicol 1998. et al.int/water_sanitation_health/dwq/chemicals/ metolachlor. 1992-2001. Ward EM. Thelin GP. Larsen GL. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor.gov/nawqa/pnsp/pubs/files/051507. Thurman EM. 3/27/09 Fourth National Report on Human Exposure to Environmental Chemicals 63 . World Health Organization (WHO). Coleman S. Brown KK. Deddens JA. Rose RL.11(4):353359. Davison KL. Comparative metabolism and elimination of acetanilide compounds by rat. Feng PCC. Reynolds SJ. Barr DB. Environmental Protection Agency (U. Alavanja MC. Reregistration Eligibility Decision (RED) Metolachlor. 2003. Wratten SJ.41:3409-3414. Roberts AL. J Expo Anal Environ Epidemiol 2005. Barr DB. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. et al. revised February 15. Hladik ML.usgs.S.S. Available at URL: http://water. The Quality of Our Nation’s Waters Pesticides in the Nation’s Streams and Ground Water. Pesticides in U. Centers for Disease Control and Prevention (CDC). Available at URL: http://www.37(4):10881093.pdf. 6/1/09 Whyatt RM. Available at URL: http://water. Ann Occup Hyg 2003. Finding minimal herbicide concentrations in ground water? Try looking for their degradates. Sanderson WT.pdf. Quistad GB.html. and other herbicides in rivers. Barr JR. Occurrence of sulfonylurea. Atlanta (GA). streams and groundwater. Third National Report on Human Exposure to Environmental Chemicals.47(6):503-517.S. 1998. sulfonamide.39(17):6561-6574. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns.S.Herbicides References Battaglin WA.111(5):749-756. usgs. Available at URL: http://water.who. Dialkylquinonimines validated as in vivo metabolites of alachlor. Heederik D. Environ Sci Technol 2007. Comparative metabolism of chloroacetamide herbicides and selected metabolites in human and rat liver microsomes. April 1995. Camann DE. Shoemaker DA.php. Environ Sci Technol 2005. 1999. Linhart SM. Hein MJ. Sci Total Environ 2000.gov/nawqa/ pnsp/pubs/wrir984245/text. Water-Resources Investigations Report: Distribution of Major Herbicides in Ground Water of the United States Water Resource Investigations Report No. 98-4245 (by Barbash JE. and metolachlor herbicides in rats. J Agri Food Chem 1989. Biagini RE. U. California. Feil VJ. Striley CA.S.gov/nawqa/pnsp/pubs/circ1291/ supporting_info. Metolachlor in Drinkingwater. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. Linderman R.gov/oppsrrd1/ REDs/0001. Environ Health Perspect 2000.

The half-life of 2.. these herbicides can enhance plant growth. headache.4. myotonia. and concern about contamination with 2..5-T was once applied as either an aqueous salt or as an oil-soluble ester.7. with the exposure to chlorophenoxy herbicides as defoliants Urinary 2.. ranging from several weeks to many months.. 1989.. population from the National Health and Nutrition Examination Survey.4.4.3. Chlorophenoxy herbicides act as plant growth hormones.5-T (Holson et al. < LOD means less than the limit of detection. 2. and delayed neuropathy (Bradberry et al.1. 1992.g.4.5-trichlorophenol and other degradates. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1814 2538 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 430 580 618 831 766 1127 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 891 1192 923 1346 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 652 679 483 701 531 957 Limit of detection (LOD.4. Ester forms of 2. the general population is unlikely to be exposed to it. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.4.4. Omer. 1974).5-T degrades to 2.S.5-Trichlorophenoxyacetic acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.4. which may vary for some chemicals by year and by individual sample.5-Trichlorophenoxyacetic Acid CAS No. hypotension. nausea.4.5-T has been rarely detected in ground waters (USGS.4.5-T) is a chlorophenoxy acid herbicide that is no longer registered for use in the United States. 2007). 1992).2 and 0. Mohammad and St. 2004). Epidemiological studies have reported associations of several types of cancer. but higher levels are herbicidal.5-T in soil varies with conditions.5-Trichlorophenoxyacetic acid (2.5-T use as a herbicide in 1985.. Human health effects from 2.4.5-T.5-T and 2. 1986.4. see Data Analysis section) for Survey years 99-00 and 01-02 are 1. 2.4. Once absorbed into the body. Nelson et al. dizziness.4. 2. 93-76-5 General Information 2.5-T at low environmental doses or at biomonitored levels from low environmental exposures are unknown. such as soft tissue sarcoma and non-Hodgkin’s lymphoma.8-tetrachlorodibenzo-p-dioxin (TCDD) led to the discontinuation of 2. Agent Orange).5-T is eliminated mostly unchanged in the urine. At low levels. it is not well absorbed through the skin. 2. renal and hepatic injury. Kohli et al. abdominal pain. Given the commercial unavailability of 2. Survey Geometric mean (95% conf.5T is rapidly absorbed via oral and inhalation routes.4-D were used as defoliants in the Vietnam War (e. Intentional overdoses and unintentional high dose occupational exposures to chlorophenoxy acid herbicides have resulted in weakness. with an elimination half-life of approximately 19 hours (Arnold et al. 64 Fourth National Report on Human Exposure to Environmental Chemicals . Teratogenic and developmental effects have been reported in studies of multiple rodent strains treated with high doses of technical grade 2.Herbicides 2.4. Although 2.4.

5-T reflect recent exposure.4.S. Fourth National Report on Human Exposure to Environmental Chemicals 65 . Biomonitoring studies on 2. 2005.EPA at: http://www. Additional information is available from U.5-T measured after a day of exposure in a few asymptomatic herbicide applicators were 35.epa. In the NHANES 1999-2000 and 2001-2002 subsamples (CDC.4.5-T itself is not mutagenic. other exposures. Pearce and McLean.Herbicides or contaminated herbicides.4. 2004).5-T were generally below the limit of detection.5-T also were below the limit of detection (Kutz et al.S. IARC considers the chlorophenoxyacetic acids group of chemicals as possibly carcinogenic to humans. * 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 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.8-tetrachlorodibenzop-dioxin) (Garabrant and Philbert. population from the National Health and Nutrition Examination Survey.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. or to contaminants in the herbicide formulations (specifically 2. 1992).5-T does not mean that the level will result in an adverse health effect.3. 2002. IPCS. Finding a measurable amount of 2.4.7. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.S. U. urinary levels of 2. Urinary 2.EPA.4.000 times higher than the detection limit for the NHANES 2001-2002 data (Kolmodin-Hedman and Erne. Biomonitoring Information Urinary levels of 2. 2005). 1996.gov/pesticides/. Survey Geometric mean (95% conf.4. IOM.4.5-T than levels found in the general population. 1980). similar to results of NHANES II (19761980). 2003.4. 2. in which urinary levels of 2. It is unclear whether these associations are related to the chlorophenoxy herbicides. Mean urinary levels of 2.5-Trichlorophenoxyacetic acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U..4.

5-T in four-way outcross mice. Philbert MA.8(5):551-60.4-D/2.edu/catalog.EPA. Holson JF. Third National Report on Human Exposure to Environmental Chemicals. Wolff GL. 2. Available at URL: http://www. 2005. 3/17/09 Kohli JD. Estimation of occupational exposure to phenoxy acids (2.4. Fundam Appl Toxicol 1992. International Programme on Chemical Safety-INCHEM (IPCS). I. Gaines TB.htm. Beasley VR. Office of Prevention Pesticides and Toxic Substances. Multireplicated dose-response studies in four inbred strains and one outbred stock of mice.37(2):277-91. Developmental toxicity of 2.4. general population. Bradberry SM.5-T). Erne K. Nelson CJ.4-dichlorophenoxyacetic acid (2.4. Atlanta (GA).php?record_id=10603. J Toxicol Environ Health 1992. Available at URL: http:// www. Mohammad FK. Murphy RS. Centers for Disease Control and Prevention (CDC).4-D and 2. Selected pesticide residues and metabolites in urine from a survey of the U.19(2):286-297. Khanna RN. 3/17/09 Institute of Medicine (IOM). et al. Board on Health Promotion and Disease Prevention. 2004.2000 and 2001 market estimates. Agricultural exposures and non-Hodgkin’s lymphoma. Scand J Work Environ Health 2005. Nelson CJ.23(2):65-73. Washington (DC): National Academies Press. II.inchem. Vet Hum Toxicol 1989. LaBorde JB. Sircar KP.epa.4.4-. Brody D.4. discussion 5-7. Holson JF.5-T). McCallum WF. Pearce N. Veterans and Agent Orange: update 2002.4. May. Pesticide industry sales and usage . Cook BT. Arch Int Pharmacodyn Ther 1974.4-D) epidemiology and toxicology. Kolmodin-Hedman B. Behavioral and developmental effects in rats following in utero exposure to 2. Tandon JS. Neurobehav Toxicol Teratol 1986.4:318-21. 210:250-255. S. Review of 2. Washington (DC): U.4.Herbicides References Arnold EK. 2003.31 Suppl 1:1825. Arch Toxicol Suppl 1980. Pesticides residues in food: 1996 evaluations Part II Toxicology.pdf.32(4):233-257. Carter-Pokras OD.5-T). Environmental Protection Agency (U. Dhar MM.nap.5-t mixture. Kutz FW. The pharmacokinetics of chlorinated phenoxy acid herbicides: a literature.S. Crit Rev Toxicol 2002. Proudfoot AT.19(2):298-306. gov/oppbead1/pestsales/01pestsales/market_estimates2001. St Omer VE. Sheehan DM. Available at URL: http:// www.S.5-trichlorophenoxyacetic acid (2. et al.31(2):121-125. Gaylor DW. U.5-trichlorophenoxy acetic acid in man. Developmental toxicity of 2.5-trichlorophenoxyacetic acid (2. Gupta BN. Multireplicated dose-response studies with technical and analytical grades of 2.EPA). 914. Committee to Review the Health Effects in Vietnam Veterans of Exposure to Herbicides (Fourth Biennial Update. Dichlorophenoxyacetic acid. McLean D. Poisoning due to chlorophenoxy herbicides. LaBorde JB. Absorption and excretion of 2. Gaines TB. Toxicol Rev 2004. Fundam Appl Toxicol 1992. Vale JA. Garabrant DH.org/documents/jmpr/jmpmono/v96pr04.S. 3/17/09 66 Fourth National Report on Human Exposure to Environmental Chemicals .4.

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

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

which may vary for some chemicals by year and by individual sample.e. and seizures. 2005). 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).atsdr.. the offspring had altered CNS neurotransmitter levels (Sanchez-Ramos et al. Kanthasamy et al. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 2275 1946 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 03-04 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 756 588 1519 1358 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1057 946 1218 1000 01-02 03-04 01-02 03-04 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 559 456 512 485 1045 881 < LOD means less than the limit of detection for the lipid adjusted serum level. serum aldrin levels were below the limit of detection. When dieldrin was fed to pregnant rodents. 2000). 1989). Studies done in vitro showed that dieldrin binds to estrogen receptors (Soto et al.. dieldrin at higher doses caused irritability. 2000). 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. seizures (Smith. similar to results in a subsample of NHANES II (19761980) (Stehr-Green.. In samples obtained between 1973 and 1991 from Norwegian women. vomiting. and the FDA monitors foods for pesticide residues. 78 Fourth National Report on Human Exposure to Environmental Chemicals . Biomonitoring Information In the NHANES 2001-2002 and 2003-2004 subsamples..gov/toxpro2. In a study of pesticide applicators with occupational exposure to aldrin. tremors. 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.S. EPA has established environmental standards for aldrin and dieldrin. 2004). population from the National Health and Nutrition Examination Survey. Epidemiologic and animal studies have not conclusively associated dieldrin exposure with risk for developing Parkinson’s disease (Corrigan et al. The median level in pooled samples from New Zealand adults obtained in 1996-1997 was generally similar to the 90th percentile for adults in this Report (Bates et al. IARC has determined that aldrin and dieldrin are not classifiable with regard to human carcinogenicity.. Li et al.. both aldrin and dieldrin caused liver enlargement and liver tumors.. OSHA has established workplace exposure standards for aldrin and dieldrin. 1998).. 2005. nausea. in which only 10.S. 2000. Information about external exposure (i. 1998) and behavioral changes (Carlson and Rosellini. When fed to experimental animals.html. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Levels of aldrin also were not detectable in 1996-1997 pooled samples from New Zealand adults (Bates et al. 1995).6% of the subsample had dieldrin levels above the limit of detection (Stehr-Green 1989). The U.Organochlorine Pesticides twitching.. 1987). and occasionally. but no estrogenic effect was noted in a study that used cultured cells (Tully et al.. environmental levels) and health effects is available from ATSDR at: http://www. 2004). the median serum dieldrin level was generally similar to the 90th percentile for females in this Report (Ward et al. 1991). Survey Geometric mean (95% conf..cdc.

0-21.00 (8. 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 9.056-.3 (18.8) < LOD 8.1) 20.062-.4) 19.50 (8.4) 20.8-17.7 (<LOD-15.130) .0 (11.242) .190) .109 (.062 (.170) .147) 1007 954 1152 998 01-02 03-04 01-02 03-04 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .6 (15.090-.090 (.1-19.1 (13.138 (.113 (.1) 13.4) 1007 954 1152 998 01-02 03-04 01-02 03-04 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 8.0) 21.110 (.5) 15.077-.075) < LOD .9 (13.1) 15.160 (.8) 14.090-.0 (10.6-24.2) 11.180) .0 (10.101) .3 (13.5 (<LOD-11.30 (8.064) 90th .120 (.140-.30 (8.80-10.149) .093) .077 (. Fourth National Report on Human Exposure to Environmental Chemicals 79 . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.049-.6-24.160 (.150 (.7) 15.112-.1-16.110-.S.10 (<LOD-16.3 (18.4) < LOD < LOD 16.7 (14.1-18.110 (.8 (18.5) 21.140 (.80 (<LOD-10.5-15.8 (11.80-9.130 (.60-10.100-.098 (.5 and 7.080-.096-.090-.2) Sample size 2159 1952 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD 10.070) .110) .055 (.00-14.0) 19.2) 14.130) .058) < LOD .089 (.180) .7) 716 587 1443 1365 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD 9.1) < LOD 9. which may vary for some chemicals by year and by individual sample.8-17. Survey years 01-02 03-04 Geometric mean (95% conf.070-.0) < LOD 9.9-22.130-.063-.100) .150 (. population from the National Health and Nutrition Examination Survey.109-.080) .3-21.5-17.40-10.108-.069) < LOD < LOD .070 (<LOD-.6-33.S. which may vary for some chemicals by year and by individual sample.7 (15.110 (.138) .109-.130) .5 (16.177) Sample size 2159 1952 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD .103 (.124) .1) 15. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.139 (. see Data Analysis section) for survey years 01-02 and 03-04 are 10.0-25. population from the National Health and Nutrition Examination Survey.5-17.117) < LOD .4 (12. < LOD means less than the limit of detection.8-25.053 (<LOD-.084-.2-15.4) 95th 20.5) 19.064 (.190) .4 (12.100-.6) 16.120 (. Serum Dieldrin (whole weight) Also a Metabolite of Aldrin Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U.120 (.048 (<LOD-.130-.054-.116) .147 (.9-23.90) 90th 15.6) 19.4) 21.102 (.7-19.3 (14.8.3 (19.8 (9.8-24.6) 9.100 (.120) .1 (18.6 (14.160) .9 (14. interval) Selected percentiles ( 95% confidence interval) Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * * 50th < LOD < LOD 75th < LOD .4-17.073-.158) .2) 12.4) 539 456 484 487 980 885 Limits of detection (LOD.9 (12.054-.062 (.140) .9 (13.100-.090 (<LOD-.6 (15.054-.060) .9-38.4-18.8-19.059 (.7-22.202) 539 456 484 487 980 885 < LOD means less than the limit of detection for the lipid adjusted serum level.8) 15.0 (15.1) 10.4) 14.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.110) .100) .1) 14.130-.9 (12.080 (.112) 95th .103 (.139 (.2) 15.120-.50) 15.088-.1-24.083-.182) 716 587 1443 1365 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD . Survey years 01-02 03-04 Geometric mean (95% conf.086-.70 (7.40-9.

Sanchez-Ramos J.91(1):122-126. Dieldrin-induced neurotoxicity: relevance to Parkinson’s disease pathogenesis. Buckland SJ. The E-SCREEN assay as a tool to identify estrogens: an update on estrogenic environmental pollutants. bioaccumulation.org/documents/ehc/ ehc/ehc91.cdc. Li AA. Environ Health Perspect 1995. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Grandjean P.103(Suppl 7):113-122. either singly or in combination.66(4):229-234. Part A 2000. 731-915. Food and Drug Administration (FDA). New York. Ginsburg KS. 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. Serrano FO. J Occup Environ Med 2005. August 2008. 4/21/09 Jorgenson JL. September 2002. J Toxicol Environ Health 1989. Available at URL: http://www. Soto AM.html.gov/toxprofiles/ tp1. Patterson DG Jr. Sodium and GABA-activated channels as the targets of pyrethroids and cyclodienes. Garrett N. Frey JM. Daniel SE. 2007 [online]. Jorgensen T. Toxicity of dieldrin for dopaminergic neurons in mesencephalic cultures.27:405-421. plasma dieldrin. 2 Classes of Pesticides. Revised Feb.352:1816-1820. Lancet 1998.htm. Shore RF. Environmental Health Criteria 91. Teta MJ.54:1431-1443. David VL. Environ Health Perspect 2001. Psychopharmacology (Berl) 1987. United States Geological Survey (USGS). Cox. Available at URL: http://www. Neurotoxicol 2005. 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. Mumtaz MM. Exp Neurol 1998. Chemosphere 2004. Fernandez MG. Wienburg CL.64-65 Spec. Chung KL. 1991. Stehr-Green. Mann D. Demographic and seasonal influences on human serum pesticide residue levels. Tully DB. Effect of occupational exposure to aldrin on urinary D-glucaric acid.html. Rosellini RA. Edwards JW. Aldrin and dieldrin: A review of research on their production environmental deposition and fate. Hartvig HB.gov/~dms/ pesrpts. Carlson JN. International Programme on Chemical Safety (IPCS). Mink PJ. Roy ML. Corrigan FM. and lymphocyte sister chromatid exchange. Finley B. et al. are nonestrogenic in transfected HeLa cells. Evaluation of epidemiologic and animal data associating pesticides with Parkinson’s disease. Vol. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population.59:229-234.Organochlorine Pesticides in the NHANES 2001-2002 and 2003-2004 subsamples (Edwards and Priestly 1994). pp. Organochlorine insecticides in substantia nigra in Parkinson’s disease.47:1059-1087.9:1357-1367. Patterson DG Jr. Brock JW. Sonnenschein C. Ellis H. Academic Press. Organochlorine exposure and risk of breast cancer. Handbook of Pesticide Toxicology.gov/ circ/2005/1291/. Pesticides in the Nation’s Stream and Ground Water. J Toxicol Environ Health. Exposure to low doses of the environmental chemical dieldrin causes behavioral deficits in animals prevented from coping with stress. Song S. Six high-priority organochlorine pesticides.109(Supp1):113-139. Facca A. Inc. Chlorinated Hydrocarbon Insecticides. Needham LL. et al. PA. 80 Fourth National Report on Human Exposure to Environmental Chemicals . Chapin RE. Cancer Epidemiol Biomarkers Prev 2000.fda. Schulte P. Smith AG. 1992-2001. Kanthasamy AG. Anantharam V. 1989. VT. Basit A. Jr. Turner W. Andersen A.inchem. toxicology. Kitzazwa M. References Agency for Toxic Substances and Disease Registry (ATSDR). 6/1/09 Ward EM. Kanthasamy A. Aldrin and Dieldrin [online]. Eds. 4/21/09 Hoyer AP. Available at URL: http://pubs. Int Arch Occup Environ Health 1994.cfsan. In Hayes WJ.26:701-719.150:263-271. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. 15.atsdr. McIntosh LJ. Reprod Toxicol 2000. Olea N. Narahashi T. Jr and Laws ER. 4/21/09 Bates MN. and epidemiology in the United States.14:95-102. Toxicological profile for aldrin/dieldrin [online]. Available at URL: http://www. Serum organochlorine levels and breast cancer: a nested case-control study of Norwegian women. Toxicol Lett 1992. Grajewski B. Priestly BG. No:429-436.usgs.

0 (20.4 (<LOD-12. Chlordane is not currently produced or used in the U. and dairy products are the usual sources of exposure to these chemicals in the general population.30-11.3-49.2-26.1) 90th 34..5-43. which results in exposure to the fetus and nursing infant Serum Oxychlordane (lipid adjusted) Metabolite of Chlordane Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U.3-32.9) 31.8.7 (34.2-49.0-12.4 (35.2) 46.3 (25. from the early 1950’s until the mid-1980’s.3 (<LOD-19.9) 17.4) 37.2-28.3) 18.0) 75th 20.37 (8.9 (11.7 (32.1) 22.2 (10. interval) Selected percentiles ( 95% confidence interval) Sample 95th 44.36-11.Organochlorine Pesticides Chlordane CAS No.8-33.7) 31. buildings.0) 31. 57-74-9 Heptachlor CAS No.5) 37.2 (28.5) 628 557 462 350 501 493 559 1031 898 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.1 (11.1-25.8-42.82-11.1) 30.0-61.9) 23.6-24.1 (20.0-13.0-18.8-20.5 (33.7 (<LOD-13.8) 18.8 (18.9 (26.1 (15.3 (26.6 (9.7-56.6) 20.6) 8.9) 10. in addition to trace amounts of numerous other related compounds (ATSDR.1-50.3) 10.8) 53.3) 10.1-65.2 (36.4 (31. the technical grade product of each chemical contains 10%-20% of the other chemical.2-56.10-11. As a result of the manufacturing process.5-65.0 (32.8) 44.4) 29.5-44.6) 39.4-51.0) 41. 01-02.8) 52.20 (<LOD-11. 1994.5-42. Heptachlor and chlordane and their metabolites bioaccumulate in fatty animal tissues.9 (18.2-21. 2007).7) 42.1-19. foods high in fat such as meat.1-51.8 (42.3) 18.2) 33.0 (16. Until 1988.0-33.9) 37.2) < LOD 11. and 7.4) 18.6 (16.9 (17.90 (8.7 (17.8-32.1-25.2) 22.4) < LOD 11.5-38.2 (41.4 (30.1 (<LOD-12.8 (17. see Data Analysis section) for Survey years 99-00.3 (21.6-12.3) 37.20-11.8 (40.7-39.7) 19.6-18.0-67.1) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * 12.9 (29.3 (20. 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.6) < LOD 11.7 (<LOD-32.10 (8. and in soil.1) 16. 1994).7) 19.4) < LOD < LOD < LOD 23.3-43.0 (26.7 (43.2 (37.3-24.5.9 (31.3) 41.S.9) 23.8) 663 752 595 998 1497 1383 20 years and older Gender Males 99-00 01-02 03-04 * 11.1) * 11.9 (15.6) 9.8-61.5 (41.7 (34.8) 52.5-47.5) < LOD < LOD 9.3 (28.S.S. Fourth National Report on Human Exposure to Environmental Chemicals 81 .89-10.2) 37. Heptachlor was used as a soil and seed treatment and for termite control in and around buildings until 1988. heptachlor use has been limited to treatment of fire ants near power transformers.4) 39.9-42.4 (22.8) 27.8) size 1661 2249 1978 Total years 99-00 01-02 03-04 50th < LOD 11.6-53.8 (10.1) 30. and 03-04 are 14.9-21.5-41.5-13.1) < LOD < LOD < LOD < LOD < LOD 8.3-45.6) 9.2 (39.5) 10.10-18.6) 36.5) 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 * * * * 11.1 (40. < LOD means less than the limit of detection.3 (11.9) 11.74 (<LOD-10.1 (44.8-23.5 (<LOD-12.20-10.8-33.8 (17.2) * 12.6-24. 2007). fish.9-38.5 (31. respectively.2-49.9) 47.5) 56.7-12.1) * 11.0-25.9-40.9 (15.3 (27. 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.6) 23. which may vary for some chemicals by year and by individual sample.0 (<LOD-12.9 (21.0) 27.9-21.9) 13.0 (37.1 (<LOD-12.5-40.3 (9.1 (16. Technical grade chlordane had contained 7% trans-nonachlor.2) 34.2) 36. 10.6 (25. 76-44-8 General Information Chlordane and heptachlor are structurally related organochlorine pesticides and were used in the U.4-40.9) 36.70 (<LOD-10.6) 48. Consequently.7) 35. Survey Geometric mean (95% conf.6 (43.4) 22.0) 21.5.5) 21.63 (8.7-70.4-14.9 (11.9) 11. Both of these chemicals and their metabolites can cross the placenta and are excreted into breast milk.6-45. lawns.2) < LOD 11.5) 9.3-45.7) 9.6) 49. population from the National Health and Nutrition Examination Survey.5) < LOD < LOD < LOD < LOD 13.8-73.2 (9.5) 44.7 (10.5) 38.4 (10.8-43.6) 11.7-14.0) 37.4 (30.7-25.7 (42.5-32.9 (26.8-31.7 (19.9) 39.1-15.7) 28. Since 1992.1 (<LOD-12.4) 12.5 (34.1 (17. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.6 (9.69-10.5 (8.8 (10.4-45.6) 48.2 (21.9 (36.1 (27.1 (25.0) 20. chlordane was used to kill termites and other insects on agricultural crops.4-21.

280-.080 (.220-.370 (.065-. 1986).250-.066-.100 (<LOD-.160) . No clear evidence of excessive cancer rates was demonstrated in human epidemiologic studies (ATSDR. In laboratory animal studies.253-.057) * .119 (.280 (.057-.300) .270 (. Elimination of all these chemicals from the body occurs over months to years.270 (.165-. OSHA has established occupational exposure criteria.070 (<LOD-. Survey Geometric mean (95% conf.240-.320 (.230-.133) 90th .350) .310-.300) .126) . 82 Fourth National Report on Human Exposure to Environmental Chemicals .260 (.130-.079) .286 (.062) < LOD .269 (.230) .203-.231) .120-.360) . and NIOSH and ACGIH have recommended workplace exposure levels for each pesticide.180) .216-. The major metabolite of heptachlor is heptachlor epoxide. which may vary for some chemicals by year and by individual sample.440) .060 (<LOD-.270 (.260 (.120-. and breast milk is a major excretion route in lactating women.079) < LOD < LOD < LOD .280 (. population from the National Health and Nutrition Examination Survey.330 (.075 (.286 (.290 (.128 (. Le Marchand et al.300 (.083) .104-..290-. 1991.400) .280-. 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. 1996.287) .077) .082 (.063 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th . high doses of either chlordane or heptachlor block inhibitory neurotransmitters and result in central nervous system toxicity.071 (. Subtle neurodevelopmental effects have been observed rodents after prenatal exposure to heptachlor (IPCS. 2007.160 (.373) .230-.080) .106-.280) .049 (<LOD-. 2006).207 (. Smith.140 (.090) .130) .087-.070 (<LOD-.302) . 2007).130-.246-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.210 (. EPA has established environmental criteria for chlordane and heptachlor. Human health effects from either chlordane or heptachlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown.290) .560) .310) .225 (.150 (..063) .090-.310 (.140) .290) .120-.242-.073) < LOD < LOD < LOD < LOD .245-.300) . 1986).199-. Chronic feeding studies with either chlordane or heptachlor have demonstrated reduced fertility. The U. chronic doses of heptachlor have produced liver enlargement and injury. Shindell and Ulrich.070-.290-.350 (.068-.070-.061-.180) .190-.400) .130 (.340) . neonatal mortality.048-.S.258-.077) .058-.320 (.170) .220 (. 2002. Chlordane and heptachlor are absorbed after oral.115-.110-.112 (.320) .130-.320) .410) .068) . Epidemiologic studies have not demonstrated teratogenic or developmental effects (Baker et al.380) . and inhalation exposure.210 (.053-.091) .180-.148) .300-. Takahashi et al.140 (.370 (.230 (.350 (.069 (<LOD-.063 (.200-..070) .180-.170) .080) .310) .450) .370 (.150) .080 (.068) 75th .070 (<LOD-.271 (.130) .430) .340) .130 (.074-. dermal.050 (<LOD-.200-.230 (.108-.260 (.066 (<LOD-.070) < LOD < LOD < LOD < LOD < LOD .189 (.063-.058 (.070 (. FDA established allowable residues of chlordane.067 (. 1981).115 (.250 (.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 * * * * .150 (. Rogan.066-.140-.S.070-.070 (<LOD-.220-. Acute.320 (.058-. 1977b.140 (.104) .146) .213) * .130 (. 1991).149 (.168-. characterized by seizures and paralysis. heptachlor.430) .200-.170) .062) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * . and the U.450) .170) . both chlordane and heptachlor induced hepatic cytochrome P450 enzymes and increased the incidence of liver tumors (NTP.510) .320 (.227) < LOD . to heptachlor. 2001.160) .300) .120 (.223) .100-.189-.063 (.170) .148-.260-.160) .280-.090) .S.207) .240-.073 (.083 (.258 (.150-.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. and heptachlor epoxide in foods and bottled water.055-.. and alterations in immune function of offspring. which is also persistent in the body (ATSDR. IARC considers chlordane and heptachlor as possibly carcinogenic to humans.077) .066 (.240) .100 (.210-.204 (.064) < LOD .136) .076) < LOD . IARC.056 (.290-.190-.320) 663 752 595 998 1497 1383 20 years and older Gender Males 99-00 01-02 03-04 * . 1977a.110 (<LOD-.310) .291) size 1661 2249 1978 Total years 99-00 01-02 03-04 50th < LOD .200 (.130-.100-.063) * .315 (.092) .053-.230-.057 (.140-.170-.348) .050-.077) .126 (.150 (.063 (. Chlordane is metabolized primarily to oxychlordane and to a lesser extent.080) .Organochlorine Pesticides (Dallaire et al.047 (<LOD-.190-.146) < LOD < LOD .250 (.140 (.240 (.130-.208 (.

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

3-18.4 (11.6 (12.8) 13.40) 15.8.5 (18. 84 Fourth National Report on Human Exposure to Environmental Chemicals .9) * * * Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 8.6 (16.1-15.4 (15.90 (<LOD-9.7 (13.8) 19.1-16.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 (13.4 (<LOD-54.3) 18.8 (18.0) size 1589 2259 1963 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th 90th 15.1 (16.6 (14.3) 27.0) 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. 10.8) 19.6) 14.6) 13.7 (16.8) 16.5 (<LOD-21.0-54.0-19. population from the National Health and Nutrition Examination Survey. 01-02.0 (15.S.8) 14.3 (<LOD-25.5 (10.2) 20.4 (11. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.7-18.4) 18.1 (19. respectively.6. which may vary for some chemicals by year and by individual sample.7-25.0-16.9-23.1-29.6) < LOD < LOD < LOD 27.9 (15.8 (18.2-16.8) 15.8-24.5 (<LOD-32.8-24.6) 22.1-38.0-17.6-21.6 (16.8-24.3) 10. see Data Analysis section) for Survey years 99-00.9-16.5) 598 553 460 336 503 490 539 1041 888 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.6-17.2-27.9) 15.5 (11. and 03-04 are 14.3) 18.7-19.1) 20. interval) Selected percentiles ( 95% confidence interval) Sample 95th 24.4) 21.1) 23.2-27.3) 22.2 (18.6 (8. Survey Geometric mean (95% conf.2 (<LOD-16.50) < LOD < LOD < LOD 17.0 (11.2) 26.8-46.3) 16.7 (10.9-29.2 (<LOD-62.8 (13.5 (11.9 (12. and 7.20 (<LOD-9.5) 760 1047 956 829 1212 1007 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 7.3 (13.6 (11.9-29.10-13.2) 13.2) 15.9-25.2 (<LOD-25.0) 13.1) 13. < LOD means less than the limit of detection.5.8-23.3) 18.8) 13.8) 21.3) 23.8 (15.4 (<LOD-19.8 (<LOD-23.6 (<LOD-27.8) 20.6 (13.5) 19.5) < LOD 14.8) 14.2-17.0-17.

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

0 (62.4 (67.0 (60.5-95.1) 78.0) 33.8 (26.7-160) 86.3-32.0-23.8-90. see Data Analysis section) for Survey years 99-00.7 (11.5) 14.7) 78.4-67.6-82.5) 35.0) 49.8-110) 59.5 (15.3-86.7 (59.7-34.7 (16.0 (19.0-68.0 (42.7) 56.5.6-19.9 (51.0) 18.2) < LOD 10.1-16.1) 31.8 (12.1-28.6 (50.8-90. and 03-04 are 14.6) 13.5) 26.6 (56.8 (28.9) 51.8 (71.6) 54.3 (58.5) 30.4-62.5-17.7-35.3) 19.9-22.7-38.8-19.2 (59.5) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * 20.7-113) 68.8-19.6-22.8 (49.1-51.6-88.5) 78.0) 75th 31.1) 17. Survey Geometric mean (95% conf.5 (15.2-37.6) 60.3) size 1933 2286 1955 Total years 99-00 01-02 03-04 50th 17.1-18.1 (48. and 7.9-69.2-17.9) 922 1062 955 1011 1224 1000 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 * 11.2-21.9 (36.9 (28.2 (60.7 (74.8-67.2) 17.7-18.4-23.0-59. interval) 18.1) 17.7 (28.7 (30.8 (<LOD-20.8 (30. which may vary for some chemicals by year and by individual sample.9) 14.9 (16.6) 10.8.5) 36.9 (51.9-65.4 (28.2-16.6 (32.0-20. 01-02.5 (45.7) 28.9-65.2 (26.4) 16.5) 14. 10.3 (45.7 (13.1) 62.70 (<LOD-12.10 (<LOD-11.3 (16.1-34.2 (19.2) 19.0) 13.4-22. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.1 (17.8 (16.0 (13. 86 Fourth National Report on Human Exposure to Environmental Chemicals .8-21.9) 51.5) 48.6 (56.5-111) 68.3) 18.0 (42.8 (42.9 (29.6) 34.7) 73.3-39.8) 47.0-93.0-38.1) 30.8 (28.9-89.3-50.2 (36.4) 20.7-21.5) 77.4-35.8 (28.7-17.9 (15.1 (10.9-35.8 (19.8-79.5-87.0 (13.1) 17.5-69.1) 18.8-41.9 (19.8 (26.9 (<LOD-14.7-20.6-54.9) < LOD < LOD < LOD 20.9-64.3-21.7 (35.4) 59.4) 19.4 (16.2) 59.3 (14.2) 34.1-126) 67.0-22.7-32.9-40.3) 15.9-20.9) 14.7-23.7) 17.5-20.2 (25.2 (15.4-36.6-66.1) 14.6 (57.4 (30. population from the National Health and Nutrition Examination Survey.3 (14.0-143) 112 (68.7 (59.2-88.8) 80.5 (13.3 (49.4) 48.3-30.5) 19.4-52.3) 32.9 (15.6) 82.0) 664 758 589 1269 1528 1366 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 17.4) 107 (84.6) 56.0 (48.5-19.8 (17.S.6-20.2-18.9-58.0 (16.2 (64.5-36.1 (41.2) 20.2 (27.0) 19.0) 40.0-123) 74.7) 52.3) 30.0-113) 68.8 (26.1-55.1) 17.1-20.5) 9.8) 19.3) 32.6) 56. < LOD means less than the limit of detection.5) 90th 55.0-37.4 (11.0 (14.7-29.6) 84.4-18.7-77.1) 32.7-22.8-16.86-13.0-24.3-74.2-18.0) < LOD < LOD 8.0 (16.9-45.3) 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.3) 16.9 (66.7) 59.1) 78.3) 25.1 (22.5 (44.3 (17.8 (13.8 (45.3) 36.8 (11.1-16.0 (29.2 (14.1) 16.5) 22.6 (12.2) 39.7) 14.5.1 (47.3) 30.4 (12.2-23.1) 18.7 (18.8) 51.8 (15.9-36.6 (52.3) 18.8 (13.6 (15.1) 17.6 (16.8-77.4 (45.0 (15.0-23.8-129) 74.3-58.7) 35.1 (65.1) 17.5 (25.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) 20.1-34.8-16.1-22.0-93.7) 15.2 (7.7) 78.0 (15.6 (<LOD-14.3-57.6) 25.0) Selected percentiles ( 95% confidence interval) Sample 95th 79. respectively.1) 17.3 (56.4) 55.2) 30.2 (14.9 (47.

096-.080) .124) .420 (.324 (.240) .130) .060-.395-.367) .097) .109 (.047-.120) .110 (.079-.458 (.220 (.087 (.190-.135 (.090) .092 (.111-.183 (.930) .237) .098 (.120) .068-.110 (.460-.490-.109 (.220 (.112 (.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.310 (.327 (.130) .130) .230 (.069-.130) .122) .141) .490 (.250) .110 (.470 (.099-.079-.220 (.186 (.069) .126) .470-.272-.220) .390 (.110-.108) 75th .104 (.220 (.310-.430-.390 (.417 (.285-.237) .120 (.091) .085-.160 (.300-.092 (.380 (.078-.070 (.288-.414 (.116-.090 (.120-.141) .430-.400) .360-.125 (.461 (.130) .089 (.093-.565) .130 (.680 (.080 (.520 (.202 (.099-.120 (.085-.105 (.580 (.343 (.460) .301-.100-.081-.084-.640 (.180-.490) .390 (.410-1.400-.098 (.090-.100 (.103 (.440) .573 (.510 (.108 (.119) Selected percentiles ( 95% confidence interval) Sample 95th .250) .590 (.161-.110) .100-.210 (.210) . Fourth National Report on Human Exposure to Environmental Chemicals 87 .110 (.520) .093-.684) .288 (.161) .830) .190-.131) .397-.242) .280) .371) .081 (.260) .405) .800) .390) .054-.140) .680) .260) .112 (.080-.100-.119) < LOD < LOD < LOD .090-.130) .558) size 1933 2286 1955 Total years 99-00 01-02 03-04 50th .098) .120) .106 (.096-.120 (.240-. Survey Geometric mean (95% conf.690) .370 (.630) .090-.510-.055 (<LOD-.409-.120-.098-.600) .211) 90th .113) < LOD .100) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * .128 (.430-.450) .210) .220 (.395) .470 (.134) .355 (.232) .180-.122) .20) .090-.127) < LOD < LOD .760 (.S.470-.250) .186-.117) .220 (.190-.440-.104-.160-.100-.116) .120-.400 (.150) .106 (.320-.590) .110 (.234) .286-.103 (.093) .300) . population from the National Health and Nutrition Examination Survey.240) .400-.210) .470 (.279-.190-.091-.550 (.497-.500) .350-.080-.190-.840) .210 (.113) .480) .390-.630) .320-.210 (.330 (.350 (.100 (.129) .340) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.565) 922 1062 955 1011 1224 1000 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 * .310-.205 (.580 (.270-.600 (.071 (<LOD-.108) . which may vary for some chemicals by year and by individual sample.400 (.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 .078 (.180-.130 (.114) .410-.061-.240) .116 (.060 (<LOD-.130) .094 (.310-.062 (.158-.370 (. interval) .540) .090 (<LOD-.095-.630) .191 (.420) .220 (.090-.310-.150) .090-.210-.390) .830) .173-.490 (.340-.460) .290-.111 (.190-.594) .210-.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.340-.330-.390 (.220 (.041 (<LOD-.580 (.559) .080-.690) .096) .651) .590 (.960) .520 (.125) .310) .170 (.082) .177-.093-.317 (.330-.360-.110 (.106 (.240 (.120) .145-.080-.171-.060) .085-.

atsdr. Willman E. Temporal trends of organochlorine concentrations in umbilical cord blood of newborns from the lower north shore of the St. Drews K. Jaraczewska K. Dendle WH. Tartter P. Saidein D. maternal serum and milk from Wielkopolska region. 2006. Evaluation of human exposure to the heptachlor epoxide contamination of milk in Hawaii. Environ Health Perspect 2002. Trends in birth defects for a Hawaiian population exposed to heptachlor and for the United States.110(8):835-838. Arch Environ Health. et al.html. Vol. Determinants of serum polychlorinated biphenyls and organochlorine pesticides measured in women from the child health and development study cohort. International Agency for Research on Cancer (IARC) .cdc. 6/1/09 National Toxicology Program (NTP). Chlordane and heptachlor [online]. Wohlleb JC.9:1-109. International Agency for Research on Cancer (IARC). 9/25/07 International Programme in Chemical Safety (IPCS).org/ documents/cicads/cicads/cicad70. Concise International Chemical Assessment Document 70 Heptachlor [online].gov/toxprofiles/tp31. Bjerselius R. 731-915. Kolonel LN. Hansen JC.gov/ntp/ htdocs/LT_rpts/tr009. Chlorinated Hydrocarbon Insecticides. Darnerud PO.41:145–148. Bull Environ Contam Toxicol 1981:27:506-511. Pollutants in breast milk. Glynn AW. 4/21/09 Baker DB. Chashchin V.84:151-161. Available at URL: http://www. Stehr-Green P. Available at URL: http://ntp. Keller JA. Available at URL: http://www.niehs. et al. Senie R. Wong L. Granath F.cdc. Available at URL: http://ntp. 6/1/09 Rogan WJ. Berkowitz GS. Jr and Laws ER. KalubaSkotarczak A. Organochlorine exposures and breast cancer risk in New York City women. Ayotte P. Charles MJ.html. Sci Total Environ 2004.heptachlor. 2 Classes of Pesticides. 4/21/09 Agency for Toxic Substances and Disease Registry (ATSDR). 4/21/09 Dallaire F.330:55-70. Odland JO. 1991 pp. Hertz-Picciotto I. Gilman A.htm. Takahashi W. Smith AG. Shindell S and Ulrich S. Loo S. Poland.150:981-990.nih.111:349355. National Toxicology Program (NTP). 1986. Aune M.pdf.niehs. Canada).372:20-31. Natl Cancer Inst Carcinog Tech Rep Ser 1977b. A Report to the Hawaii Heptachlor Research and Education Foundation. Toxicological profile for heptachlor and heptachlor epoxide [online]. Environ Res 2000. Laliberte C. organochlorine pesticides and polybrominated diphenyl ethers in human umbilical cord serum. Jr. Vol.org/site/foundation/ research/projects2. Covaci A. 79. Mortality of workers employed in the manufacture of chlordane: an update. Toxicological profile for chlordane [online]. 88 Fourth National Report on Human Exposure to Environmental Chemicals . Circumpolar maternal blood contaminant survey. Bleiweiss IJ. Lawrence River (Quebec. In Hayes WJ.htm. 1993. Atuma S. Barker J. et al. 2001. Organochlorines in Swedish women: determinants of serum concentrations. Natl Cancer Inst Carcinog Tech Rep Ser 1977a. Handbook of Pesticide Toxicology.html. Dewailly E.28:497501.8:1-123. Baker DB. An evaluation of serum pesticide residue levels and liver function in persons exposed to dairy products contaminated with heptachlor. Bioassay of chlordane for possible carcinogenicity. New York. Siegel BZ. Available at URL: http://www.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Muckle G.atsdr. Organochloride pesticide residues in human milk in Hawaii.110:617-624. Available at URL: http://www. Environ Health Perspect 2003. JAMA 1988. Inc. Van Oostdam JC. 1979-1980.Summaries & Evaluations. Academic Press. gov/toxprofiles/tp12. Distribution of polychlorinated biphenyls. 1963-1967. J Occup Med 1986. Voorspoels S. Arch Pediatr Adolesc Med 1996.inchem.nih. Wolff MS. Sci Tot Environ 2006. Eds. Lulek J. Hawaii Med J 1991.50(3):108-118.pdf. Dewailly E.259(3):374-377. 1994-1997 organochlorine compounds. LeMarchand L. Royce W.gov/ntp/ htdocs/LT_rpts/tr008.inchem. et al. Environ Health Perspect 2002. August 2007.org/documents/iarc/ vol79/79-12. May 1994. Bioassay of heptachlor for possible carcinogenicity. Takei G. 4/21/09 James RA. Head SL. Brower S. Available at URL: http://www. Estimation of Human Exposure to Heptachlor Epoxide and Related Pesticides in Hawaii.

1 (<LOD-39.1-71. DDT is converted in the environment to other more stable chemical forms. after World War II until 1972.9) < LOD < LOD 9.2 (<LOD-40.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. 2008.1) 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 12.7 (15.0) 26.7-16.8.0) 20.0-15.8-39.7) 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 10.2 (11.S. p.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.8) 36.8) 15.3 (<LOD-21.7) 12.9) 29. interval) Selected percentiles ( 95% confidence interval) Sample 95th 28. or dermal exposure.9 (21. DDT usually refers to the technical product.1 (33. which may vary for some chemicals by year and by individual sample.5 (15.2) 155 (59.Organochlorine Pesticides Dichlorodiphenyltrichloroethane (DDT) CAS No.9 (<LOD-20.0 (18.3) 21. population.0-53. It was produced and used in the U. o. DDT and DDE can cross the placenta. DDT and DDE are distributed to all body tissues with the highest concentrations found in adipose tissues (ATSDR.1’-(2.0-27. and water. sediments.9-28.2-65.6 (25.9 (10.00 (<LOD-10.2) < LOD < LOD 9. Only a small proportion of DDT is metabolized and excreted (Smith.9) 14. see Data Analysis section) for Survey years 99-00. Survey Geometric mean (95% conf.9-34. Smith.0) 19.9) 17.7) < LOD 18.3) 21.90 (<LOD-12. DDT can be absorbed after ingestion.5-36. and 03-04 are 20.5 (14. DDT is converted to DDE and several other metabolites.p’-DDT (15%-21%).4 (23. and dairy products.1) 31. 01-02. inhalation.1’-dichloro-(2.6 (22. population from the National Health and Nutrition Examination Survey.3 (27. 1991).0-155) 83.8) 30. Gunderson. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. depending on conditions. The biodegradation half-life of DDT in soil varies from 2 to 15 years.6) 635 566 461 356 514 490 564 1061 890 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.2) 30. and 7.5-54.0-37.5) size 1679 2305 1965 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * * 11.10-13.1 (23. Food imported from countries that still use DDT may contain the chemical or its residues.7 (19. as well as in plant and animal tissues. In the body. Fourth National Report on Human Exposure to Environmental Chemicals 89 . including 1.6 (31. These chemicals are highly persistent in soil. respectively.p’-DDD (4% or less).S.8-17.0 (10. fish.3 (<LOD-31. which is a mixture containing p.3) 22.2-dichloroethenylidene)-bis[4-chlorobenzene] (DDE) and 1.5) < LOD < LOD 9. In the general U. 17.0-35.3-590) 293 (104-541) 48.0 (18. 2002.5) 23.5) 25.5 (23.8-23.7. air. continues to be the primary source of DDT exposure.0 (21.2-95.p’-DDT (65%-80%).50-11. resulting in fetal exposure.9 (10.6 (9.8-26. 1991).4.3-236) 24. 50-29-3 General Information Dichlorodiphenyltrichloroethane (DDT) has been used widely as a broad spectrum insecticide in agriculture and for control of vector-borne diseases.3) 28.1-27. particularly meat. although DDT and DDE intakes have decreased over time (FDA. food.2-bis(p-chlorophenyl) ethane (DDD). It is still used in some countries. when virtually all use of it was banned.10 (<LOD-12. Both Serum p. 1988).6 (<LOD-25. particularly for endemic vector and malaria control.S.0) 40.70 (8.4) < LOD < LOD < LOD 61. DDT was used at one time as a treatment for head and body lice.9 (10.4) < LOD 17.3-16.5 (23. < LOD means less than the limit of detection.6-33.

400) .063 (<LOD-.054-.p’-DDE can produce anti-androgenic effects (Gray et al.078-.200 (..230) .313 (.160-. Snedeker. 2001).167) size 1679 2305 1965 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * * .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 . accidental exposures.230) .071 (.130 (<LOD-. It is difficult to attribute outcomes in human studies solely to DDT because of potential co-exposure to other persistent organohalogen chemicals (e.. 1995. Calle et al. and seizures. and duration of lactation. lung cancer.150) .128 (.150-.220) . 2002.570-4. 2002.p’-DDD and p..143) < LOD < LOD .061) < LOD < LOD < LOD . Studies of DDT exposure and pancreatic cancer. reproductive organ abnormalities. resulting in exposure to nursing infants (Rogan..180) .084 (.220) .00 (. both DDT and DDE may induce specific cytochrome P450 isozymes (Nims et al..106-.130-. 2004. 2006). DDT may bind to estrogen receptors (Chen et al.330-4. 1956). 2001)..180 (.180) .180-.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 .080-. In laboratory animals.140-.530) . 2006).095) < LOD .01) . 2006. polychlorinated biphenyls...290) .26) 1. Gray et al.065-.106) < LOD < LOD . 2006.34) .130 (<LOD-.150 (<LOD-.087 (. Animal studies reported reduced fertility. and o. Longnecker et al.098-. dioxins and furans).086 (.190-1.069) .048 (<LOD-.120 (<LOD-.146 (.146 (. 1998). 90 Fourth National Report on Human Exposure to Environmental Chemicals . A workplace standard for DDT has been established by Serum p. which may vary for some chemicals by year and by individual sample.064 (. Jusko et al.078 (. Hayes et al.079) < LOD < LOD .627) .00) . Jusko et al.180 (.075) 1.250 (.071-.170 (.170) .106) .189-.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.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 . Mariussen and Fonnum. 2001). Survey Geometric mean (95% conf.S.142 (. Several reviews of cancer epidemiologic studies have concluded that a link between DDT and breast cancer is inconclusive (Beard.114-. although the risk for preterm delivery may be related to maternal DDE levels (Longnecker et al. 2002. 2000. premature delivery. population from the National Health and Nutrition Examination Survey.g.240) . 2001). 2002.190 (.190 (. 2006).203) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Human health effects from DDT at low environmental doses or at biomonitored levels from low environmental exposures are unknown.260) .240 (.343) < LOD ..170-. interval) Selected percentiles ( 95% confidence interval) Sample 95th .62 (.150-.132-. other organochlorines. 1997).. 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. overt signs of acute human toxicity include vomiting.250-1. Beard. In high dose. have not been consistently demonstrated (Beard.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. 2006.051 (<LOD-. Epidemiologic studies of children with environmental exposure to DDT and DDE have not demonstrated neurologic or developmental abnormalities (Gladen et al.530 (.150 (<LOD-.130 (<LOD-.074-.420) ..400 (. Reproductive effects in humans affecting birth weight.201 (.120-.108 (.059-. and altered behavior after neonatal exposure (Eriksson and Talts.Organochlorine Pesticides chemicals are excreted in breast milk.068-. tremor.140) . 1996). Gladen and Rogan. and leukemia have also been inconclusive (ADSDR..105-.112 (. fertility.

Stehr-Green. population declined by about fivefold to tenfold. Declining DDE levels over time have also been observed in the German population.e. In general.. Median DDE levels among a population-based sample of Swedish women in 19961997 were similar to females in the NHANES 1999-2000 subsample (Glynn et al.. respectively. More information about external exposure (i. Heudorf et al. 2002. Biomonitoring Information DDE persists in the body longer than DDT.. Survey Geometric mean (95% conf. 8. the lipid-adjusted geometric mean levels of DDT and DDE were each fivefold to tenfold higher than the 95th percentile and geometric mean levels. Fourth National Report on Human Exposure to Environmental Chemicals 91 . and 03-04 are 18. 1998..Organochlorine Pesticides OSHA and a guidance established by ACGIH.html.S. environmental levels) and health effects is available from the U. 2005). mean DDE levels were about fivefold higher among women of southern Spain exposed by virtue of Serum p. 2004).7-119) 113 (100-140) 93.6.cdc. Smith. NTP considers DDT as being reasonably anticipated to be a human carcinogen. Link et al.6 (81. see Data Analysis section) for Survey years 99-00. and the most recent median levels for German adults and children are similar to levels in this Report (Becker et al.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. 2004). compared to levels observed in this Report (Anderson et al. IARC classifies DDT (p.7-129) 297 (256-344) 338 (303-376) 268 (217-332) 108 (97.3.8.atsdr.. 1991). and 7. mean serum levels of DDT and DDE in the U. levels of DDT and DDE increase as a person ages as a result of cumulative exposure (ATSDR. EPA at: http://www.epa. for males and females in the NHANES 19992000 subsample (Pavuk et al. so serum DDE levels may be an indicator of historic exposure and may be higher than DDT levels in the same person.gov/ pestcides/ and from ATSDR at: http://www. 1989).gov/ toxpro2. 01-02.0-114) 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.. 2003.S.S. population from the National Health and Nutrition Examination Survey. respectively.. Since the 1970’s. 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. interval) 260 (226-298) Selected percentiles ( 95% confidence interval) Sample 95th 1830 (1410-2300) 2320 (1830-2780) 1860 (1400-2380) size 1964 2298 1956 Total years 99-00 01-02 03-04 50th 226 (184-278) 251 (228-278) 203 (163-275) 75th 537 (476-631) 598 (521-699) 509 (376-655) 90th 1150 (976-1350) 1410 (1210-1500) 1170 (836-1570) 295 (267-327) 238 (195-292) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 118 (102-135) 124 (106-146) 105 (84. In a population-based sample of men and women from eastern Slovakia. Compared to females in the NHANES 1999-2000 subsample. 2003). 2002..p’-DDT) as a possible human carcinogen.

600) .26-2.25-14.4-19.45 (1. 1989).15-4.32 (1.38 (1.00 (.07 (5. Consumers of Great Lakes sport fish had mean serum DDE levels that were only slightly higher than nonconsumers.93 (7.25) 8.71) 32.27) 3.04 (6.26 (1.55-9.24 (1.7) 16.36-2.58) 1.5) 22.90) 22.963-1.Organochlorine Pesticides nearby agriculture (Botella et al.75) 6.40-4.52 (3.81) 11.3) 937 1069 955 1027 1229 1001 Females 99-00 01-02 03-04 Race/ethnicity Mexican Americans 99-00 01-02 03-04 3. Serum p.6) 13.25 (1.13 (1. Survey Geometric mean (95% conf.75 (8.4) 14.35) 1.9-17.57-3.51-8.39) 1.85-10..40-4.34) 6.796 (.37-16.76-3.51) 3.80) 3.75 (4.36-11.30-1.03-4.69 (.71 (5.25-16.59 (4.32-1.61-2.77 (1.51-15.516 (.02 (2.80) 1.53) 7.81-5.51 (1.1 (9.70-3.6 (17.14) 2.32) 1.85 (1.22 (7.7-20.500-.60-13..22-1.00-1.6 (7.56-6.430-.18-1.71) 12. In a subsample of NHANES II (19761980) participants.40-8.92 (3.39-1.01-15.59) 3.3) 13.37-4.46 (1.02-8.19) 4.30 (1.69) 4.27-1.520 (.611-1.49 (1.51-49.8 (13.8) 15.6) 12.91 (6..99) 1.24) 1.14-1.2 (6.72) 1.3-43.29 (1.76 (2.07) 1.87-16.994-2.5) 5.6) 9.635) 1.01-11.1) 40.870 (.68-4.63 (1.7) 9.7) 13.5) 7.385-.96) 1..5) 16.34-3.9) 5.12 (6.0) 2.11 (2.0) 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 .96) . considerably higher than levels in this Report (Smith.78 (4. 2004).6 (8. 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.88 (2.01) 1.43-4.32 (1.9 (15.65 (1.01) 1.57-13.p’-DDE in serum does not mean that the level of the chemical causes an adverse health effect.69 (2.10-5.88-35.49 (6. interval) 1.9) 7.52 (1.2 (19.p’-DDT.03-1.36) 3. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.13-2.02) 1.50-17.26) 3.58) 75th 3.8 (9.66-2.3 (9.47 (1.92 (3.91) 3.61 (1.59) 6.80 (2.81-18.58) 1.2 (9.39-2. population from the National Health and Nutrition Examination Survey.91-2.71 (6.3 (8. which is similar to the overall geometric mean of 260 ng/g lipid in the NHANES 1999-2000 subsample (Bloom et al.6) 9. In the NHANES 1999-2000.p’-DDT were below the limits of detection.7 (8.66-4.84 (3.81 (7.97 (3.8 (13.623 (.63 (6.0 (9.68) 2.5) 10.18) 1.83 (1.09-1.57-2.10-1.1) 12.70) 1. or p.76) 1.01-1.79) 4.37-10.419-.66) 3.49 (1.32-1.85-4.7-19.92) 1.31 (1.46 (1.43-4.48-4.51) 1.63-15.21) 90th 7.11-1.57 (1.53 (2. 309 versus 268 ng/g lipid.8 (14.81 (1.49) 8.30-1.34-11.2-32.63 (1.28) 1.4) 9.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.59 (1.3) 10.57 (1.p’-DDT (Stehr-Green.4 (8.25 (.41 (1.01-11.2 (9.488-.680-1.730) .13) 4.32-9.12-1.4) 13.64) 3.52-6.p’-DDT.9-38.82) 1.561 (.79) Selected percentiles ( 95% confidence interval) Sample 95th 11.646) .65) 1.16 (2.57) 2.68 (2.31-2.01-1.726) . 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.66-17.00) 7.69 (1.14-9.26-10.53-15.79) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 .87 (5.06) 1.46-2. less than one percent had detectable serum levels of o.490 ng/L) were found many years ago in a study of pesticide workers in Argentina (Radomski et al.14) 2.23 (7.57 (3.50 (2. 2001-2002 and 2003-2004 subsamples.56-3.6) 9.6) 11.34) 2.75) 1.2) 26.31-12.05) 1.16-1.8-90.17 (3.82 (1.59 (1. serum levels of o.62-6. High mean levels of whole blood DDT (about 3.90-8.66) 4.69) 8.43 (5.7-48.19-14.34 (7.8) 686 758 588 1278 1540 1368 20 years and older Gender Males 99-00 01-02 03-04 1.S.20 (.07) 1.10) 2.43-8.40 (3.38 (1.590 (.36-1.56-2.53) 1. 1971).820-1.3) 16.9 (26.1) 7.97-4.37-1. o. Finding a measurable amount of p.55 (2.05 (3.22) .21) 3.30 (1.00 (6.860 ng/L) and DDE (about 14.18-3.41-12.75) 2.6) 9. 1991).04-1.456 (.56) 2.72) 1.48 (6. 2005).39 (3.36 (3.18-4.77 (1.890-1.91-3.534-.76) 1. 2004).54-7.6) 8.4 (12.557) 1.37 (1.12 (.18 (6.0 (12.965-1.25) 1.01-5.45 (1.47) 3.6 (9.0) size 1964 2298 1956 Total years 99-00 01-02 03-04 50th 1.2) 19.1 (8.10) .14 (1.54 (1.18-1.33-1.66) 1.64-2.44) 1.24-17. Workers involved in production or application of DDT developed neurologic abnormalities associated with blood levels around 100-300 mg/L.66) 1.80) 1.17-3.06) 3.84-3.54) 8.

and 03-04 are 20. Fourth National Report on Human Exposure to Environmental Chemicals 93 .S. 01-02. 17. respectively. population from the National Health and Nutrition Examination Survey. Survey Geometric mean (95% conf.8. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. see Data Analysis section) for Survey years 99-00. < LOD means less than the limit of detection.4. which may vary for some chemicals by year and by individual sample.Organochlorine Pesticides Serum o. and 7.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. 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.7.

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

Katz SH. Transcriptional activation of the human estrogen receptor by DDT isomers and metabolites in yeast and MCF-7 cells. Rogan WJ.111:349355.fda. Notides AC. Wolf CJ. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Biochem Pharmacol 1997.206:485-491. Davis MD. Am J Public Health 1995. April 1982 to 1984. Organochlorines in Swedish women: determinants of serum concentrations. Bjerselius R.54:1431-1443. Cerrillo I. Bull Environ Contam Toxicol 2004. Kashyap R. Savitz DA. Gunderson EL. Baker RJ. Profiles of ortho-polychlorinated biphenyl congeners. Hediger ML.cdc. Sci Tot Environ 2006. Olea N. Environ Res 2005.atsdr. Environ Health Perspect 2003. DDE. FDA total diet study. Drexler H. Association between maternal serum concentration of the DDT metabolite DDE and preterm and small-for-gestational-age babies at birth.106(5):279-289. Klebanoff MA. Fourth National Report on Human Exposure to Environmental Chemicals 95 .html. Gray KA.96:34-40. Heudorf U. Gray LE Jr. DDT and human health. Toxicological profile for DDT.2-bi(p-chlorophenyl)ethylene and risk of cryptorchidism. Environ Res 2004. Bhatnagar VK. Angerer J.71(6):1200-1209. Needham LL. Chen CW. Atuma S.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Talts U. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population.355:7889. et al. Gladen BC. HCH. Zhou H. et al. Paepke O. et al. Zhou H. a biostable metabolite of dichloro(diphenyl)trichloroethane (DDT). Link B. Thun MJ. and DDD [online]. Botella B. Jr. Current internal exposure to pesticides in children and adolescents in Germany: blood plasma levels of pentachlorophenol (PCP). Available at URL: http://www. Effects of environmental antiandrogens on reproductive development in experimental animals. Swanson MK. Burse VW. Garrett N. September 2002. Neonatal exposure to neurotoxic pesticides increases adult susceptibility: a review of current findings. Maternal serum level of 1. Hum Reprod Updat 2001.58:1185-1201. Needham LL. Food and Drug Administration (FDA). and Mirex among male Lake Ontario sportfish consumers: the New York State Angler cohort study. Brock JW. CA Cancer J Clin 2002. August 2008. dietary intakes of pesticides.cfsan. Gabrio T. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. DDE and shortened duration of lactation in a northern Mexican town. Piechotowski I.html. Eriksson P.1-dichloro2. Ellis H. Klebanoff MA. Vorojeikina DP. Rivas A. Lancet 2001. Jusko TA. selected elements. Available at URL: http://www. Ostby J. Am J Epidemiol 2002.53(8):1161-1172. et al. and dichloro(diphenyl)ethylene (DDE). et al. The Great Lakes Consortium. Olson J. The effect of known repeated oral doses of chlorophenothane (DDT) in man. Longnecker MP. Hanrahan L. and other chemicals. Granath F. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. Brock JW. Needham LL. Patterson DG Jr. et al. Biomonitoring of persistent organochlorine pesticides. et al. Crespo J. Frumkin H. Moysich KB. Parks L. Environ Health Perspect 1998. Beard J. Jr. Lepom P. JAMA 1956. Seiwert M.358:110-114. hypospadias. and HCB residues in human blood in Ahmedabad. Koepsell TD. and polythelia among male offspring. J Assoc Off Anal Chem 1988. Buckland SJ. Exposure of women to organochlorine pesticides in Southern Spain. Lambright C. Darnerud PO.205:297-308. Epidemiology 2006. Kulkarni PK. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Levels of DDT.85:504508. Becker K. Willman EJ. Prenatal DDT exposure in relation to anthropometric and pubertal measures in adolescent males. Int J Hyg Environ Health 2003. Hurd C. Glynn AW. dichlorodiphenyldichloroethylene. Organochlorines and breast cancer risk. Schulz C. Cueto C. India. 4/21/09 Anderson HA. Charles MJ. Longnecker MP. et al. Chemosphere 2004.. Environ Health Perspect 2004. et al. Bloom MS. Furr J. Arnold SF. Klebanoff MA. Bates MN. Hayes WJ. Kaus S. lindane (g-HCH). hexachlorobenzene. Int J Hyg Environ Health 2002. Henley SJ.72:261265. Chemosphere 2005.17(6):692-700. Olson JR. 4/21/09 Gladen BC. Vena JE. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. Neurotoxicol 2000.112(17):1761-1767. Barr DB. Falk C. Aune M. Durham WF. Krause C.52:301-309.gov/~dms/ pesrpts. Herrman T. Maternal DDT exposures in relation to fetal and 5-year growth.97(2):178192.155(4):313-322. Zaidi SS.162:890-897. Zoellner I. Saiyed HN.21(1-2)37-48.7(3):248-264.gov/ toxprofiles/tp35. Greenfield TA. Calle EE. Olea-Serrano MF.

Chovancova J. Lynch CF. J Toxicol Environ Health Part A 1998. 2 Classes of Pesticides. Nims R. and DDD in male rat liver and cultured rat hepatocytes. Lubet R. Thomas PE.20(2):186-193. Neurochemical targets and behavioral effects of organohalogen compounds: an update.36:253-589. Toxicol Appl Pharmacol 1971.53:455-477. Rey AA. Smith AG. Pollutants in breast milk. Crit Rev Toxicol 2006.27:405-421. Chlorinated Hydrocarbon Insecticides. Rogan WJ. Comparative pharmacodynamics of CYP2B induction by DDT. Environmental exposure to PCBs and cancer incidence in eastern Slovakia. J Toxicol Environ Health 1989. New York.Organochlorine Pesticides Mariussen E. Arch Pediatr Adolesc Med 1996. Chemosphere 2004. Blood levels of organochlorine pesticides in Argentina: occupationally and nonoccupationally exposed adults. In Hayes WJ. Petrik J. Radomski JL.54:1509-520. Astolfi E.109:35-47. children and newborn infants. Snedeker SM. Demographic and seasonal influences on human serum pesticide residue levels. Schecter A. Academic Press. DDE. Jones CR. Eds. Jr and Laws ER. 731-915. Cerhan JR. Vol. Fonnum F.150:981-990. Jr. Handbook of Pesticide Toxicology. 96 Fourth National Report on Human Exposure to Environmental Chemicals . Environ Health Perspect 2001. Pesticides and breast cancer risk: a review of DDT. Stehr-Green. DDE. PA. et al. Reddy AB. et al. Fox S. Pavuk M. and dieldrin. Deichmann WB. Inc. 1991 pp.

endrin has been detected with declining frequency in U.40) < LOD 547 433 487 446 1000 831 Limit of detection (LOD. 1979.50) < LOD 5... rodenticide and avicide. endrin is converted rapidly to its major metabolite.10 (<LOD-5. interval) Selected percentiles ( 95% confidence interval) Sample 95th 5. Endrin does not accumulate in body tissues (IPCS. unless the dose is high and the exposure is very recent. EPA. manufactured.S. General population exposure can occur after ingestion of endrin residues on food items imported from countries where endrin is still used. Endrin has been detected in soils. anti-12hydroxyendrin. 1992). All uses of the pesticide in the U.50) < LOD < LOD < LOD 5.70) < LOD < LOD < LOD 730 539 1457 1286 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 5. or from contact with contaminated soils and sediments in areas where endrin was applied.60 (5. Serum Endrin (lipid adjusted) Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U. fatty infiltration. Survey Geometric mean (95% conf. have been cancelled by the U. endrin blocks inhibitory neurotransmitters in the central nervous system resulting in excitation and seizures (Narahashi et al. An epidemic of acute endrin poisoning.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 5.20 (<LOD-5.10 (<LOD-5.40 (<LOD-6. In the body. Skeletal abnormalities and cleft palate in the offspring were associated with endrin when it was fed to pregnant laboratory rodents (Chernoff et al. endrin can persist for years. which may vary for some chemicals by year and by individual sample. is no longer manufactured in the U. inhalation or dermal exposure routes. a stereoisomer of dieldrin. Further conversion occurs to 12-ketoendrin and various conjugated metabolites which are excreted in urine and feces. 1996. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 1991).30 (<LOD-6.8. 72-20-8 General Information Endrin. < LOD means less than the limit of detection. Ketoendrin is a major photodegradation product (IPCS. IPCS. endrin usually is not detected in serum of exposed individuals.Organochlorine Pesticides Endrin CAS No. or discarded. largely the result of historical agricultural application or run off from contaminated soils (ATSDR. 1991). Endrin was not widely used as a termiticide. and inflammation (Smith. 1992. Depending on soil conditions. 1992). 1987). Endrin is absorbed rapidly after ingestion.. Kavlock et al. Smith. Because it is metabolized so rapidly.S.S. High doses produced renal tubular necrosis and diffuse kidney degeneration in animals. unlike aldrin and dieldrin. population from the National Health and Nutrition Examination Survey. Endrin was used as an insecticide. At high doses. and occasionally at low levels in sediment and surface waters. 2008). characterized by generalized seizures in previously healthy persons occurred in Pakistan when sugar contaminated with endrin was ingested (Rowley et al.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. Hepatic effects of endrin exposure have included necrosis. see Data Analysis section) for Survey years 01-02 and 03-04 are 5..09 and 7. Over time. Human health effects from endrin at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 1992).40-5.S.30) < LOD 5. total diet surveys (FDA. Fourth National Report on Human Exposure to Environmental Chemicals 97 .S. 1981).20 (<LOD-5.

EPA has established environmental standards for endrin. environmental levels) and health effects of endrin is available from ATSDR at: http://www.gov/toxpro2. Biomonitoring Information In the NHANES 2001-2002 and 2003-2004 subsamples.020 (<LOD-. interval) Selected percentiles ( 95% confidence interval) Sample 95th . Finding a measurable amount of endrin in serum does not mean that the level of endrin causes an adverse health effect. This finding is consistent with other general population studies (Bates et al. which may vary for some chemicals by year and by individual sample. Information about external exposure (i. 2000).020 (<LOD-.020 (<LOD-.atsdr.. 2004). * Not calculated: proportion of results below limit of detection was too high to provide a valid result.S. with the highest value 6.020 (.020-. IARC has determined that endrin is not classifiable with regard to human carcinogenicity.Organochlorine Pesticides The U. Ward et al.020 (<LOD-..e. Survey Geometric mean (95% conf. Biomonitoring studies on levels of endrin provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of endrin than are found in the general population. serum levels of endrin were below the limit of detection.020 (<LOD-.020) < LOD 547 433 487 446 1000 831 < LOD means less than the limit of detection for the lipid adjusted serum level.cdc. population from the National Health and Nutrition Examination Survey..html.020) < LOD < LOD < LOD .020) < LOD size 2187 1825 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 03-04 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .020) < LOD < LOD < LOD 1022 885 1165 940 01-02 03-04 01-02 03-04 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .24 ng/g of serum) (Botella et al. Workplace exposure standards for endrin have been established by OSHA. 2004.020) < LOD .020) < LOD < LOD < LOD 730 539 1457 1286 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .020 (<LOD-.S. and the FDA monitors foods for pesticide residues.24 ng/mL (about 6. Serum Endrin (whole weight) Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U. In a small study of Spanish women hospitalized for elective surgery.. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. endrin was detected in 9% of serum samples. 98 Fourth National Report on Human Exposure to Environmental Chemicals .020) < LOD .

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

S. The general population may be exposed to HCB through diet.9 (14. The FDA dietary surveys have shown that over time.1-16.6) < LOD < LOD 25.4. or game taken from areas with HCB contamination.5-18.6-32.1 (14.2-31.9) < LOD < LOD 16. breast milk is an additional route of elimination in nursing women. 1988).4.6) 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. Gunderson.0.9-17.6) < LOD < LOD 26. respectively. 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.8 (15.6-TCP) (To-Figueras et al..9 (25.3-22.9 (25.4.7) < LOD < LOD 24.3) < LOD < LOD 29..5-15. water.2 (14.8 (26.6 (23.4) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * 13.4 (18. and 7. Survey Geometric mean (95% conf.4-15.. Workers in chemical manufacturing industries may be exposed to HCB via inhalation or dermal pathways. 1997).7 (15.3 (14.6 (24. HCB may be created as either a byproduct or an impurity in the manufacturing process for certain chemicals and pesticides.9) < LOD < LOD 28.0) * * 15.7-30.7 (19.6) < LOD < LOD 26. wildfowl. see Data Analysis section) for Survey years 99-00.5-trichlorophenol (2.8-15.S.4) < LOD < LOD 18.4) < LOD < LOD 33.6-19.5-TCP) and 2.4) < LOD < LOD 19.7-22.7 (15.8) 583 554 460 350 511 488 636 1052 888 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.9 (23.0-19. < LOD means less than the limit of detection.S.5-14.6-33.5-33.9-24.9-30.2) < LOD < LOD 13.7 (27.0 (14. 118-74-1 General Information Hexachlorobenzene (HCB) was used from the 1930’s to the 1970’s in the U.S. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Urinary metabolites include pentachlorophenol (PCP).9) < LOD < LOD 20. 2008.7-15.9-32.7-21.6-26.7-16.2) < LOD < LOD 29.1) * * 15.1) < LOD < LOD 15.0 (18.3) * * 15. Therefore. HCB is well absorbed after oral administration.3 (16. and foods with a high fat content.8) size 1702 2277 1961 Total years 99-00 01-02 03-04 50th < LOD < LOD 14.6-trichlorophenol (2.4. HCB has been detected in fewer foods since the 1980s (FDA.2 (13.7-16.1 (17.4) < LOD < LOD 14. and accumulates in fatty tissues where it persists for years.6) < LOD < LOD 24. and has been detected in soil. 2.9) < LOD < LOD 20. particularly by consuming fish.1-20.4 (22.4-16. EPA cancelled its use in 1984.9-20. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD 28. It is a persistent chemical and bioaccumulates in both aquatic and terrestrial food chains (ATSDR.4) < LOD < LOD 22.8 (22.4 (11.6-44.0 (25.2-15.5 (13.0) < LOD < LOD 15.5-15. Although it is not manufactured as an end-product in the U.1 (13.0) < LOD < LOD 24. and 03-04 are 118. Hexachlorobenzene has entered the environment as a result of industrial activities and pesticide applications. distributes widely throughout the body.2-15.8.4.5) < LOD < LOD 18.9-15.5 (13.7) * * 14.3) 24. primarily as a fungicide and seed treatment until the U.6) < LOD < LOD 14.7) < LOD < LOD 75th < LOD < LOD 90th * * 15.3-26.1 (14. and elimination occurs by renal and fecal routes.9) < LOD < LOD 15.3 (20.7) 807 1058 957 895 1219 1004 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * 16.3 (22. 2005).0-25.2 (14.3 (22.2 (17.0-16.7-29. 1976).8) < LOD < LOD 27. 100 Fourth National Report on Human Exposure to Environmental Chemicals .0) < LOD < LOD 15. air.3-20.5 (14. and sediment (Barber et al.2 (24.9) < LOD < LOD 19. HCB is slowly metabolized. 01-02.9) 19. 2002).Organochlorine Pesticides Hexachlorobenzene CAS No.3 (12. which may vary for some chemicals by year and by individual sample. these metabolites can also be produced after exposure to other chlorinated compounds (Kohli et al.3) < LOD < LOD 20.0-28.0 (18..6 (21.4 (18. population from the National Health and Nutrition Examination Survey.7-26.4) < LOD < LOD 23.5-14. 31.

With chronic exposure.140 (.064 (.182 (.212) size 1702 2277 1961 Total years 99-00 01-02 03-04 50th < LOD < LOD .072-.095 (.077-.121 (.081-.152) < LOD < LOD . This condition. 1982.078 (.102 (.203) < LOD < LOD . as well as hypertrichosis.095-.099) < LOD < LOD .114-. HCB interferes with normal heme synthesis.e.143-.120 (.090 (..102) < LOD < LOD .Organochlorine Pesticides chemical.107) < LOD < LOD .157 (.086) < LOD < LOD .062-.109) * * .097) .135-. environmental levels) and health effects is available from the U.123 (.159-. and many died before 2 years of age (Peters et al..094 (.127-. Biomonitoring Information Serum concentrations reflect the body burden of HCB. The U.085) * * . * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 2002).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 * * .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. reproductive and developmental toxicities.090 (.069) < LOD < LOD . arthritis.073-.225 (.191 (.167) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * .092 (.167 (.123 (.097) < LOD < LOD .092 (.088-.157-.094) < LOD < LOD .118) < LOD < LOD . EPA at: http://www.082-.092-.089-.178-.126) .176-.atsdr.088-.115 (.141) < LOD < LOD .104 (.113-. ACGIH has developed workplace exposure limits for HCB.125 (.147 (.090 (.S.129) < LOD < LOD .155) < LOD < LOD .173) < LOD < LOD .196) < LOD < LOD . which may vary for some chemicals by year and by individual sample.html. EPA has established a drinking water standard. immunologic abnormalities.163 (.107-. which is manifested by increased deltaaminolevulinic acid synthase activity and decreased uroporphyrinogen decarboxylase activity. IARC classifies hexachlorobenzene as possibly carcinogenic to humans.145-.090-.cdc. In humans.081 (.145-.258) < LOD < LOD .176) < LOD < LOD .100) < LOD < LOD .174-.130) < LOD < LOD . thyromegaly.099) < LOD < LOD .226) 807 1058 957 895 1219 1004 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * .114-.S.088-. and NTP classifies hexachlorobenzene as reasonably anticipated to be a human carcinogen.086-.087 (. 1960). 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.099) < LOD < LOD .091-.123 (.gov/pesticides/ and from ATSDR at: http://www.169-. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD .111-.148-.156 (.147-.085-. and weakness. Fourth National Report on Human Exposure to Environmental Chemicals 101 .S.065 (. anorexia.118-.086-.097 (.163) < LOD < LOD .171 (.083) < LOD < LOD . More information about external exposure (i.060-.092 (. and the FDA has established a bottled water standard for HCB. 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.190 (.089-. Infants were exposed transplacentally and through breast milk.095) < LOD < LOD 75th < LOD < LOD 90th * * .160 (.069) * * . very high.118-. Chronic feeding studies in animals have demonstrated kidney injury. Human health effects from HCB at low environmental doses or at biomonitored levels from low environmental exposures are unknown. population from the National Health and Nutrition Examination Survey.079 (.163-. Survey Geometric mean (95% conf.gov/toxpro2.122) < LOD < LOD . a consequence of these heme abnormalities is a condition known as acquired porphyria cutanea tarda.098 (.179 (.203) < LOD < LOD .epa.095 (.095) * * .175) < LOD < LOD .186 (. Schmid. acute doses produce central nervous system depression and seizures. and liver and thyroid cancers (ATSDR.132) < LOD < LOD .111) < LOD < LOD .

In a representative sample of the 1998 German adult population. Toxicological profile for hexachlorobenzene update [online]. Lawrence River (Quebec.fda.. Holland NT. Kaus S. Muckle G. Link B. Can J Biochem 1976. Int J Hyg Environ Health 2002. Lecha M. Urinary porphyrin excretion in a human population highly exposed to hexachlorobenzene. Food and Drug Administration (FDA). Lackmann. 2002).349:144.gov/ toxprofiles/tp90.. Ayotte P. 1986. Over the past two decades. Hexachlorobenzene content in human whole blood and adipose tissue: experiences in environmental specimen banking. Kohli J. declines in background HCB levels ranging from around 50%90% have been documented in studies using cord blood (Dallaire et al. Dogramaci I. only 4. Zoellner I. Available at URL: http://www. Dallaire F. Schwartz JM. Chemosphere 2005. Bryan GT. J Exp Sci Environ Epidemiol 2007. Arch Neurol 1982. Canada). The metabolism of higher chlorinated benzene isomers. and the geometric mean concentration of HCB in whole blood was 0. References Agency for Toxic Substances and Disease Registry (ATSDR). lower than the limit of detection (on a lipid adjusted basis) in NHANES 1999-2000 and 20012002. however.. Seiwert M. In Spain. Finding a measurable amount of hexachlorobenzene in serum does not mean that the level of the hexachlorobenzene causes an adverse health effect.. Bjerselius R. than the limits of detection (on a whole weight basis) in NHANES 19992000 and 2001-2002 (Herrero et al. 102 Fourth National Report on Human Exposure to Environmental Chemicals . 4/21/09 Glynn AW. 2002.44 mg/L. Herrero C. Available at URL: http://www. Link et al.9% of participants had quantifiable levels (Stehr-Green.html. 1999).cfsan. 2005). Eskenazi B. 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. Factors predicting organochlorine pesticide levels in pregnant Latina women living in a United States agricultural area. Biol Neonate 2002. Agerelated increases of HCB in body fat and serum have been consistently noted in general population studies (Becker et al. IARC Sci Publ 1986. et al. Temporal trends of organochlorine concentrations in umbilical cord blood of newborns from the lower north shore of the St.77:173182. Barr DB. Dewailly E. Sweetman AJ. 2002) and among children (Link et al. 2002.. 2005)..111:349355.71(6):1200-1209. Sci Tot Environ 2005. Santiago-Silva M. van Wijk D. Krause C.atsdr. Biomonitoring of persistent organochlorine pesticides. Laliberte C. Safe A. Reference values updated. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. et al. 2002. 2003). Kemper FH. Muller C. trends and processes. but approximately five times higher than the overall geometric mean level in 2003-2004 (Becker et al. Paepke O. Hexachlorobenzene in the global environment: emissions. Peters HA. Lepom P. selected elements. Darnerud PO. Atuma S. Fenster L. Gunderson EL. 2002. Herrman T..81(2):82-85. 1989). Gabrio T.. September 2002. Residency near industrial or agricultural areas has been associated with higher serum HCB levels (Barber et al..39(12):744-749. et al. Sala M. Environ Health Perspect 2003.205:297-308.gov/~dms/ pesrpts. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. factory workers chronically exposed to HCB and residents near the factory had serum HCB levels that were 150 to 50 times higher. Lackmann GM. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. Jones D. Bradman et al. In the 1976-1980 NHANES subsample. more HCB levels were quantified. Otero R. Glynn et al. Gocmen A. As a result of the lower limit of detection in NHANES 2003-2004. Arch Dermatol 1999. HCB detection in serum also was proportional to age. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Lackman.17:388–399.110(8):835-838. levels.54(3):203-208. Cripps DJ. Bertram HP. Aune M. 4/21/09 Barber JL. Granath F. respectively. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. 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. 2006).58:1185-1201.. 2005. FDA total diet study. Epidemiology of hexachlorobenzene-induced porphyria in Turkey: clinical and laboratory follow-up after 25 years. Polychlorinated biphenyls and hexachlorobenzene in full-term neonates. Environ Health Perspect 2002. but overall.html. dietary intakes of pesticides. April 1982 to 1984.cdc. et al. August 2008. Ozalla D. Organochlorines in Swedish women: determinants of serum concentrations. distribution. Schulz C. and other chemicals.Organochlorine Pesticides in the NHANES 1999-2000 and 2001-2002 subsamples. Bradman A. J Assoc Off Anal Chem 1988. Piechotowski I. Becker K.135(4):400404. HCB levels were directly related to age.. Jones KC. Bertram et al.

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

4) 27.0-111) 70.0-21.76.60-13.3-56.9 (62.0) 8.2) 13.7 (30.9-81. formerly referred to as benzene hexachloride.S.8) 12.61-12. EPA cancelled agricultural uses of lindane (ATSDR.66-12.70 (8.04-10.3 (62.2-87. 104 Fourth National Report on Human Exposure to Environmental Chemicals .7 (25.2-20.6-62.0 (37.5) 67.6) 35.4) < LOD < LOD < LOD 46.1) 12. It is no longer produced or sold in the U.0 (19.7) 10.7) 27.80 (<LOD-14.9-178) 48.7) 18.3 (13.7-69.6) 47. 2005).0 (14.7 (53.2) 36.09) < LOD Gender Males 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD 14.4) 11.7-26.6 (33.7) < LOD < LOD < LOD < LOD < LOD < LOD 37. and sediment as a result of historic production and use.5 (11.6-20.9 (30.6) 36.4-111) 84.1-15.0 (35.70-19.6-89.90) 7. Survey years 99-00 01-02** 03-04 Geometric mean (95% conf.1 (27.7) 23.2-46.8) * * * * * * 15. and delta.9 (11.S.6) 653 758 589 1240 1533 1370 20 years and older 10.0 (<LOD-12.1 (30.1) 12. environmental levels declined.2-17. The other isomers can be formed during the synthesis of lindane. commonly known as lindane.7) 73.3) 14.6 (40.7 (35.1 (21.9-21. respectively.36.9) 81.4) 10.5) 22.5 (37.4-73.7) 97.9) 45. 608-73-1 beta-Hexachlorocyclohexane CAS No.30-11.2-67.50) 8.6-14. and have been used either as fungicides or to synthesize other chemicals.Organochlorine Pesticides Hexachlorocyclohexane CAS No.6 (10.6 (16.4) 51.2 (29. 319-85-7 gamma-Hexachlorocyclohexane CAS No. 2005).4 (8.3) 37.87 (9.0 (33. Technical grade HCH is a mixture of all four isomers.5) 40. HCH does not bioaccumulate to an appreciable extent in plants (ATSDR.5) 90th 42.2-42.4 (11. which may vary for some chemicals by year and by individual sample.2-22.8-16.7) 32.6) 16.1-16. see Data Analysis section) for survey years 99-00.90-8.8 (17.2 (48.0) 71.1) 31. beta.1 (11.8) 27.1-32. can be used as an insecticide and has been used to kill soil-dwelling and plant-eating insects.5528.0-34. However.7 (13. interval) 9.5) 11.0) 7.4) 901 1067 952 992 1224 1007 Females 11.8 (9.1 (18.20-16.9 (40.6-42.8 (10. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.46-11.4 (52.9-14.3 (26. particularly alpha and gamma have been detected widely in air.5-29.6-135) 69. and 7.89 (<LOD-9.4) < LOD 9.8 (23.6 (22.0-20.5) 29.4) 44. including alpha.7-96.7-69.7-166) 70.5) 16.6) 18.8 (21.8 (33.8) 52.5 (24. HCH isomers are lipophilic.9-51.0) 17.8 (32. 58-89-9 General Information Hexachlorocyclohexane (HCH).7-20.8 (64.68 (<LOD-10.0-23.4-50.3-85. In 2006.9 (26. so they can accumulate in fatty tissues of animals.1-37.S.8-199) 134 (85. < LOD means less than the limit of detection.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 21.9-24.1 (12. exists in several isomeric forms.6-37.90-8.2) 62.80 (6. the U.5 (8.1) 71.43 (<LOD-9. **In survey period 2001-2002.3 (42.7 (62.3-38.2 (9.5 (43.5) 632 563 460 403 513 487 702 1051 887 Non-Hispanic blacks Non-Hispanic whites Limits of detection (LOD.2-52.2 (50.1-27.1) 13.1 (9.2-98. HCH isomers. 6.45) < LOD Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 99-00 01-02** 03-04 16.3) 51.8. Lindane (1%) lotion and shampoo are available by prescription for singleuse application to treat human scabies and head lice. 01-02.70 (6. Lindane has a half-life of about two weeks in soils and water.3 (42.1 (16.3) 25.0) 41.7-96. gamma.6) 50.4 (16.56-12.1-32.9) 15.3) 34.7 (<LOD-16.70-12.6 (17.2 (31.8-68.9 (32. containing about 64% alpha and 10%-15% gamma isomers.9-56.5 (14.2) 142 (99.8-54.0-70.8) 39.2) 9.8) < LOD 10.4-45. and 03-04 are 9.1-36.8) 7.2 (18.7) 56.4) 21.5 (16. soil.4 (12.0) 35.5) 14.7) 10. As pesticide applications of HCH were increasingly restricted or eliminated.8-19. See the section “What’s New” at the beginning of this Report for details.9 (50.9) 17.1 (9.6-47.6-18.7 (29.4 (50.2 (34. population from the National Health and Nutrition Examination Survey. water.8) 95th 68.9) Selected percentiles ( 95% confidence interval) Total * * 50th < LOD < LOD < LOD 75th 19.5-123) 49.2-55.8-87.0 (8.1-49.9 (9. each result has been multiplied by 1. 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.0-70. The gamma isomer.

380 (.100-.. U.058) < LOD Gender Males 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD .120 (.319) .118-.130) .390-.510) .320 (.480) .096) .450-.066) Selected percentiles ( 95% confidence interval) Total * * 50th < LOD < LOD < LOD 75th .521 (.340-. ingestion.065 (.210 (.S. 1996.240 (.460) . hepatic enzyme induction. Acute high dose toxicity in rodents affects the central nervous system producing decreased activity.270 (. HCH crosses the placenta and is also excreted in breast milk (Radomski et al.410 (.250 (.814) .442 (.070-.200-.400) .047-.310 (. each result has been multiplied by 1.587) 653 758 589 1240 1533 1370 20 years and older .310) .140) . Pesticide applicators or agricultural workers could be exposed to HCH by inhalation and dermal pathways.150) .062 (.120-.070 (.281 (.089) . interval) .S.290) .150 (.410) .410-. OSHA and ACGIH have established workplace standards and guidelines.700) .050 (<LOD-.139 (.216 (.290 (.080 (.470 (.080-.310) . and nephropathy developed (IPCS. EPA has established a drinking water standard.067) .100 (. The U.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.5528.110) .450 (.460 (.081-.330-. tremors.140 (.480 (.214) .080) .048 (<LOD-..118 (.090 (.050 (. population from the National Health and Nutrition Examination Survey.280-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.056-. Rogan.170-.110) .167 (.260) .100-.910 (.150) .057-.501) . After dermal application of lindane 1% lotion. The beta isomer accumulates in fatty tissues and is metabolized more slowly. ataxia.220-.050 (<LOD-.100) .370-.160) .290 (.412 (.120) .297-.077) < LOD .480 (. Survey years 99-00 01-02** 03-04 Geometric mean (95% conf.360 (.600) .092 (.190) .068-.130 (.069) . **In survey period 2001-2002. respectively.250-.050 (. or dermal exposure.050-. resulting in a half-life of about seven years.221-.260-.260) .220-.254) 95th .077) < LOD .560 (.124-.125) < LOD < LOD < LOD .560) .308-.056-.119) .080) * * * * * * .083 (.234 (.059-.065 (. Human health effects from HCH isomers at low environmental doses or at biomonitored levels from low environmental exposures are unknown. Distribution is mainly to fatty tissues.620) .200-.330 (. which may vary for some chemicals by year and by individual sample.089-.120) .470) .110) .690) .173-.37) 1.050-.103 (.01 (.400) . probably by blocking inhibitory neurotransmitters in the central nervous system.040-. Saxena et al.290) . HCH isomers are metabolized to chlorophenol metabolites that are excreted in the urine (Angerer et al.840) .120-.410) .070-.050-. 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.083) .060) .050-.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 .120 (.290 (.170-.067 (. 1986)..32) .300-.240-..140) . Fourth National Report on Human Exposure to Environmental Chemicals 105 .190) .220) .S.350 (.200 (.250-.190-. 1977).191-.062 (.250 (.073-.222 (.070) .Organochlorine Pesticides exposure to HCH is through the diet.160-.580 (.580-1. and FDA has established a bottled water standard and food residue tolerances for lindane.450) .146-.103) 90th . 1971.661) 901 1067 952 992 1224 1007 Females .051 (<LOD-.103-. See the section “What’s New” at the beginning of this Report for details. paresthesias.150-. enlarged livers.210) .160 (.078 (.680) .051-.372 (.057) < LOD Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 99-00 01-02** 03-04 .190-1. 1981).305) .244-. and seizures.360) .294-.382-.287 (.110-. and memory loss (Nigam et al.091) .180-. from 6% of samples in 1982-1984 to 2% in 1994 (FDA. Workers who directly handled HCH have complained of headache. 2008.404) ..120 (.086) < LOD < LOD < LOD < LOD < LOD < LOD .350) .080-.360-.057 (<LOD-.331 (.070-.420-. for lindane.080-.058 (<LOD-.050) .191-.130-.250) .080 (.140) .175 (.340) . HCH isomers are absorbed after inhalation.098 (.090 (.210-. When animals were chronically fed lindane at high doses.174) .131-.230-. Gunderson 1988).220 (. the serum half-life was about 20 hours among children (Ginsburg et al.057-.120-.210 (.100 (. 2002).064) .070 (.072 (.710) .620-1.570 (.144 (.100-. FDA pesticide monitoring program has shown a temporal decline in the detection of lindane.250 (. 1983). Acute high doses of lindane after ingestion or excessive skin application of the 1% lotion have produced seizures in humans.05) .100) .390 (.280-.064 (.090-.090 (.

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

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

html. Astolfi E. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Majumder SK. Organochlorines in Swedish women: determinants of serum concentrations. Bates MN. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. Wood PH. Placental transfer of pesticides in humans. Reisch JS. Brinton LA. Serum concentrations of organochlorine compounds and endometrial cancer risk (United States). Toxicological profile for hexachlorocyclohexanes update [online]. Deichmann WB. dietary intakes of pesticides. Lepom P.html.96:34-4Food and Drug Administration (FDA). et al. Zoellner I. HCH. Bai KM. Piechotowski I. available at URL: http://www. Falk C. Angerer J. Krause C. children and newborn infants. 108 Fourth National Report on Human Exposure to Environmental Chemicals . Environ Health Perspect 1998. Needham LL. Nigam SK. Seiwert M.htm. Bhargava AK.atsdr. Cancer Causes and Control 1998. et al. et al. J Assoc Off Anal Chem 1988.cdc. Krishna Murti CR. et al. et al.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR).71(6):1200-1209. Rev Environ Contam Toxicol 1991. April 1982 to 1984. Exposure of women to organochlorine pesticides in Southern Spain. Brock JW. Int Arch Occup Environ Health 1986. Raju GS.48:127-134. Buckland SJ. and HCB residues in human blood in Ahmedabad. gov/toxprofiles/tp43. Link B. Biomonitoring of persistent organochlorine pesticides. Organochlorine pesticides and polychlorinated biphenyls in human adipose tissue.91:998-1000. FDA total diet study. Darnerud PO. 4/21/09 Anderson HA. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods.120:1-82. Arch Toxicol 1981.205:297-308. Botella B. Rey AA. Available at URL: http://www. Schulz C. Patterson DG Jr. Kulkarni PK.150:981-990. Sturgeon SR. August 2005. Available at URL: http://www. Karnik AB. Gabrio T.54:1431-1443. org/documents/jmpr/jmpmono/2002pr08. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. Herrman T. Potischman N. Levels of DDT. Siddiqui MKJ. Kashyap R. Int Arch Occup Environ Health 1983.cfsan. Garrett N. Stehr-Green. Visweswariah K. Kaus S. Olea-Serrano MF. Bottimore DP. The Great Lakes Consortium.111:349355. and other chemicals. J Pediatr 1977.52(1):59-67. Bull Environ Contam Toxicol 2004.106(5):279-289. International Programme on Chemical Safety (IPCS). Bhatnagar VK. Demographic and seasonal influences on human serum pesticide residue levels. August 2008. Radomski JL. Olea N. Pesticide residues in food-2002-Joint FAO/WHO meeting on pesticide residues.72:261265. Ellis H. India. Occupational exposure to hexachlorocyclohexane. Becker K. Lowry W. Zaidi SS. et al. selected elements.inchem. Saxena MC. Rogan WJ. Aune M. 4/21/09 Kutz FW. Arch Pediatr Adolesc Med 1996. Maass R. Metabolism of gammahexachlorocyclohexane in man. Gunderson EL. Int J Hyg Environ Health 2002. Rivas A. Granath F. Blood levels of organochlorine pesticides in Argentina: occupationally and nonoccupationally exposed adults. Needham LL. VI. 2002. Absorption of lindane (g benzene hexachloride) in infants and children.20(2):186-193. Pollutants in breast milk. Glynn AW. Rothman N. Chemosphere 2005. Bjerselius R. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. Toxicol Appl Pharmacol 1971. Environ Health Perspect 2003. Kutty D. Saiyed HN. 4/21/09 Ginsburg CM. Heinrich R. Chemosphere 2004. Crespo J.58:1185-1201.27:405-421. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Needham LL. Hanrahan L.gov/~dms/pesrpts. Lindane. J Toxicol Environ Health 1989. PA. Atuma S.fda. Olson J. Environ Res 2004. Paepke O. et al.57(4):315-320.9(4):417-424. Serum hexachlorocyclohexane residues in workers engaged at a HCH manufacturing plant. Burse VW. Cerrillo I.

6 (<LOD-23.10 (<LOD-15.Organochlorine Pesticides Mirex CAS No. Mirex contamination of Lake Ontario and adjacent waterways has been well documented (ATSDR.6 (<LOD-31. where it has a half-life of 12 years. 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. mirex was detected in human adipose samples. Survey Geometric mean (95% conf.S. 10. 2385-85-5 General Information Mirex has not been produced or used in the U. where it was applied directly to soil and by aerial spraying. Ingested mirex that is not absorbed is eliminated in the feces within about 48 hours.S. Some states and the U.0 (<LOD-108) < LOD < LOD 50. especially those from persons living in the southeastern U.6) < LOD < LOD < LOD < LOD 71.6) size 1853 2257 1951 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th 15. see Data Analysis section) for Survey years 99-00.1 (13. or pesticide application.8 (12.3) < LOD < LOD < LOD < LOD < LOD < LOD < LOD 15. Mirex has been detected in air.2 (7.0 (12.5. animals. sediments.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. disposal. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.0 (14.7) 8.5 (<LOD-115) 153 (30.2-230) 13.S. 1985.8) < LOD 15.10-37. Mirex is not metabolized in the body.4) < LOD 15.S.5-82.1) 659 728 592 1194 1529 1359 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 16.5 (9.5-291) 11.3) 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. Formerly. soil. after which it is widely distributed in the body and stored in fat. and foods.70 (<LOD-15.2) 51.1 (8. water. In studies conducted in the 1970’s and 1980’s. Human health effects from mirex at low environmental doses or at biomonitored levels from low environmental Serum Mirex (lipid adjusted) Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U.1 (<LOD-65.. Mirex binds strongly to soil.5-425) 40. Mirex is absorbed through the skin and from the gastrointestinal tract.8 (<LOD-73.40 (<LOD-13.70-40. Mirex can cross the placenta and be excreted in breast milk. aquatic organisms. since 1977. < LOD means less than the limit of detection. population from the National Health and Nutrition Examination Survey. its major uses were as a flame retardant additive and as a pesticide to kill fire ants and yellow jackets in the southeastern U. respectively. EPA have issued public health advisories or warnings that fish from contaminated lakes and rivers may contain mirex.1 (<LOD-104) < LOD < LOD < LOD < LOD 39.6 (<LOD-108) 9.3-225) 15. 1991).7 (<LOD-47..7 (12.4-230) 18. resulting in exposure to newborns and nursing infants.4 (8.8.90-29.6.S.6) 9. which may vary for some chemicals by year and by individual sample.7) < LOD 66. it is a highly persistent chemical in the environment. Occupational exposure is limited to workers at sites where mirex contamination is present.3 (15. 1995).70-24.0-374) 11. 01-02. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 57.6-305) 15.5 (<LOD-42. and 7.4) 617 548 459 398 500 484 688 1049 884 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. and 03-04 are 14. Fourth National Report on Human Exposure to Environmental Chemicals 109 . (Kutz et al.4) < LOD 63.3 (15.

450) 1.110 (<LOD-.170) size 1853 2257 1951 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .054 (<LOD-. and NTP classifies mirex as reasonably anticipated to be a human carcinogen.92) .. 1995.170-3. The geometric mean mirex levels of the Inuit mothers were 8.080-1.080-1. population from the National Health and Nutrition Examination Survey.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.430 (.470) . 110 Fourth National Report on Human Exposure to Environmental Chemicals .370 (.37) .220) . Finding a measurable amount of mirex in serum does not mean that the level of mirex causes an adverse health Serum Mirex (whole weight) Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U.170) < LOD .08 (.090 (<LOD-.7 ng/g of lipid. 7. 2001-2002.062-. which may vary for some chemicals by year and by individual sample.450 (.8. Laboratory animals fed high doses developed liver enlargement and liver tumors.470 (.atsdr. as well as in a subsample of NHANES II (1976-1980) participants.S. Survey Geometric mean (95% conf.055-. serum mirex levels were generally below the limits of detection (Stehr-Green.470) .256 (.106 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Smith.79) .S. and 4.cdc. 2005).73) .090 (<LOD-.064 (<LOD-.077 (<LOD-.102) < LOD < LOD < LOD < LOD .112 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD .html..100 (<LOD-.090-1.140 (<LOD-.510) < LOD < LOD .100 (<LOD-.268) < LOD . Inuit mothers from three Arctic areas had geometric mean serum mirex levels that were threefold to sevenfold higher than nonInuit mother from other Arctic regions.Organochlorine Pesticides exposures are unknown.090-1.02) .41) . 1991). In samples obtained between 1994 and 1997. EPA has established environmental standards for mirex.410 (.79) .gov/toxpro2.240) < LOD < LOD < LOD < LOD < LOD < LOD < LOD . reproductive toxicity included decreased fertility and testicular damage.e.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 .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 . Biomonitoring Information In the NHANES 1999-2000. environmental levels) and health effects is available from the ATSDR at: http://www. 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.310 (. In addition.635) < LOD . and the FDA monitors foods for pesticide residue and has established an action level for mirex in fish tissue.106) < LOD .053-.079 (<LOD-.. More information about external exposure (i. 2004).070-1. The U.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 .093 (.690) . developmental abnormalities including cataracts and edema in the offspring have been reported (ATSDR. 1989).090-1.090 (<LOD-.089-.220 (<LOD-.052-. and 2003-2004 subsamples. IARC classifies mirex as possibly carcinogenic to humans. 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.108 (.059 (<LOD-.610) < LOD < LOD < LOD < LOD .

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

0 (5.5-TCP) and 2.0) 2.4.9 and 0.0 (4.4.6-TCP in any of the samples (U. 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. 1999).0 (3.0) 14.9 (<LOD-121) 9.3.40-11.57 (<LOD-15.6-TCP were used as intermediates in the production of certain pesticides.0) < LOD 21.00 (2.0) 2.42 (<LOD-8.30-11.80 (2. 88-06-2 Metabolites of Organochlorine Pesticides and Other Environmental Chemicals General Information The chlorophenols.80-41.00 (3.60 (4. usually at herbicide production or waste incineration facilities.0) 2. and sediments. surface water. 2.4.30) < LOD 4.S.4.0) 5. Exposure to trichlorophenols also may result from metabolism of lindane.40 (2.40 (1. but they may be produced as by-products during manufacturing of other chlorinated aromatic compounds.42 (<LOD-12. General population exposure may occur by ingesting contaminated food or water and by inhaling contaminated air. are metabolites of several organochlorine chemicals.6-Trichlorophenol CAS No.40-18.60) < LOD 8.72) < LOD 1.50 (. 2006). population from the National Health and Nutrition Examination Survey.20-36.40 (2.8) 21.71 (<LOD-8.0) 2.0 (3.S.40 (1. hexachlorobenzene.0) < LOD 11.5-Trichlorophenol Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.0) < LOD 5.940-3.980-3.5TCP and 2.20) < LOD 90th 5.8-tetrachlorodibenzo-p-dioxin occurs during the synthesis of 2.20) < LOD 5.30-27.50-16.40) < LOD 1. including hexachlorobenzene and hexachlorocyclohexanes.60-8. EPA.7. Formation of 2.40) < LOD 4.0) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 1.50 (2.0) < LOD 973 1178 1021 1319 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .60 (2.0) 2.4. recent sampling of U.71 (<LOD-8.30-3.900-2.50-25. 112 Fourth National Report on Human Exposure to Environmental Chemicals .60 (.19 (<LOD-6.0) < LOD 11.980-3.50) < LOD 1.6-TCP).30-27. Occupational exposures.40) < LOD 6. 1999).03) 9.0) < LOD 5.Organochlorine Pesticides 2. Both chemicals have been detected in air. 2.20 (4. Survey Geometric mean (95% conf.5-trichlorophenol (2.27) 696 661 521 696 603 939 Limit of detection (LOD.27) 482 570 681 815 831 1112 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD 1. Such workers would probably Urinary 2. 2.4. 1976). Trichlorophenols have been detected in fish taken from waters near waste water treatment and industrial discharges (ATSDR.20-71.4.90-33.7) 24. Environmental sources of these compounds include industrial discharges or run off from pesticide facilities or disposal sites. however.6-TCP was also used as a wood preservative and may still be used in production of some fungicides (ATSDR.40 (2.30) < LOD < LOD < LOD < LOD < LOD 1.50 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.5-trichlorophenol. interval) Selected percentiles ( 95% confidence interval) Sample 95th 16.0 (4.80 (1.63) 18. may occur by inhalation or dermal routes.4.0 (4.00-3.60-18.S. and polychlorinated benzenes (Kohil et al.50-63.27) 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 1.4.00-3.30-44.4. other organochlorines.0) 2. Historically. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. Trichlorophenols are no longer manufactured commercially.9.30-40.80) < LOD 1. which may vary for some chemicals by year and by individual sample.30 (.00-8.40 (2.920-3. soils.5-Trichlorophenol CAS No.30-27. < LOD means less than the limit of detection.0) < LOD 5. public drinking water systems did not detect 2.31 (<LOD-9.40 (..0 (8.4.20) < LOD 1.950 (<LOD-1.4.6-trichlorophenol (2. 95-95-4 2.40 (.10-3.

which includes trichlorophenols.e.00) < LOD 4. environmental levels) and health effects is available from ATSDR at: http://www.5) < LOD 12.6-TCP.Organochlorine Pesticides be exposed to mixtures of chlorophenols.6) 4.24) < LOD 6. IARC considers the experimental evidence for animal carcinogenicity inadequate for 2.5-TCP and limited for 2.4 (6.74) 11.53-3.24 (3. Human health effects from 2.33) < LOD < LOD < LOD < LOD < LOD 2.4.24) < LOD 1. 2003.9) 12.6-TCP as reasonably anticipated to be a human carcinogen. IARC classifies combined exposures to polychlorophenols.60-3.1 (<LOD-58.13-13.3 (5.24-11. 1989).3 mg/L reported in German adults aged 18-69 years (Becker et al. interval) Selected percentiles ( 95% confidence interval) Sample 95th 11.37-11.19-12.6-TCP were developmental or reproductive toxicants in animals (ATSDR 1999).3) < LOD 973 1178 1021 1318 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * . 2003).4.11) 482 570 681 814 831 1112 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD 1.75 (<LOD-6.32) < LOD 4.4.90 (4. 1989).95 (3.78) < LOD 1.6) 4.8) 4.02-3. population from the National Health and Nutrition Examination Survey..2) 2. In the same 2-6 year old children. Urinary 2. but almost twenty times higher than 95th percentile values reported in German adults aged 18-69 years (Becker et al.920-2.80 (1.50) < LOD 2.79-4.64 (4.980 (<LOD-1. the 95th percentile urinary 2.5-TCP nor 2.4.57 (3. However. Radon et al.9 (5.05-8.15) < LOD 2. Survey Geometric mean (95% conf.24) < LOD 5.68 (<LOD-8.820-2.. The 95th percentiles for 2.4. as being possibly carcinogenic to humans. 1995) and up to 19 times higher than the 95th percentile value of 1.atsdr.02) < LOD 7.17) 9.6-TCP had increased rates of hepatic tumors.86 (3.27-17..16 (.0 mg/L.62-20.67 (1.37) 16.4.5-Trichlorophenol (creatinine corrected) Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.00-19.43) < LOD 12.5) 11. animals showed hepatocellular abnormalities.cdc.1) 2.78 (3. Neither 2. the 95th percentile urinary 2.00-29.. Biomonitoring Information In the NHANES 1999-2000 and 2001-2002 subsamples.53-3.05-17.68-4.82 (<LOD-32.31) < LOD 2. NTP classifies 2.6-TCP at low environmental doses or at biomonitored levels from low environmental exposures are unknown. and lymphomas.16) < LOD 90th 5. Among 6-11 year old children in NHANES 1999-2000..67 (1.3 mg/L in a nonrandom subsample from NHANES III (Hill et al. More information about external exposure (i.44 (1. in addition to dioxins.html.36 (1. 7.57 (<LOD-7. 2003).46 (1.4.4) < LOD 3.5-TCP or 2.83-12.75 (3.88-16.81 (<LOD-9..2 (2.11) size 1994 2496 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD 75th 2.8) < LOD 9.gov/toxpro2..5-TCP.7 (4.69 (2. recent small studies have not demonstrated increased exposure to trichlorophenols in workers who dredged contaminated soils or incinerated waste materials (Agramunt et al. furans. Fourth National Report on Human Exposure to Environmental Chemicals 113 .8 (5. At lower doses.4.28-25. Laboratory animals chronically fed high doses of 2.44 (.57 (<LOD-7.2) < LOD 5. 2004). urinary 2.43 (2.6-TCP levels at the 95th percentile were up to eight times higher than 3.4) < LOD 3.78-19. was similar to the corresponding percentile for 6-11 year olds in NHANES 1999-2000 (Hill et al.37) 696 661 521 695 603 939 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.6-TCP level was approximately eight times higher than the corresponding percentile in a small group of 2-6 year old children living near an herbicide manufacturing facility: 33 versus 4 mg/L (Hill et al.4. 1995) were similar.4.19-4.S. and other chlorinated compounds.2) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 2.5-TCP among adults in this Report and in a nonrandom subsample from NHANES III (Hill et al.73 (<LOD-8.69-18..6) 4.55 (4.20-6.47-8..49 (1. leukemias.0) 7.4.4. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.93-11.4) 5.29 (1.4.

0) 14.5 mg/g creatinine) were similar to the limit of detection for 2.6-19.7 mg/L.4-17. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.60) 6.0) 14.0) 11.4.48-26.1-25.40) 2.4.0 (9.10-3.52-3. population from the National Health and Nutrition Examination Survey. Mean values of 2.30-11.0 (14.Organochlorine Pesticides A small study of adults who ate Great Lakes sport fish reported a mean urine 2. < LOD means less than the limit of detection.51-12.6-TCP were monitored in a group of hazardous waste incinerator workers from 19992002.40-14. respectively.0-43.0) 17.90 (4.00-4.70-3.89 (3.0 (4.2 (14.84) 2.69 (3.24 (2.6TCP causes an adverse health effect..0) 7.S.0 (15.2) 25.18-3. 1991).4.8 (9.40-7.0-38.5-TCP or 2.98-7.0) 10.36 (1.2-0.4 (17.0 (16. 0. Urinary 2. Sawmill workers exposed to chlorophenol wood preservatives had urinary 2.4.6-TCP exposure and health effects.14 (2.0) 11.08 (2.5-TCP and to the median 2.75 (8.5-TCP and 2.40) 4.40) 3.3 (11. In harbor workers exposed to chlorophenol-contaminated river silt.63) 90th 15.49 (6.47 (3.6-22.68 (<LOD-2.30-2.23) 2.8) 32. for males in NHANES 19992002 (Agramunt et al.0 (7.1 (8.70-6.3) 20.8-15.18) Selected percentiles ( 95% confidence interval) Sample 95th 25.6 (11.80-7.79 (5.45-9.60 (3.0) 6.95) 3. Biomonitoring data will also help scientists plan and conduct research about 2.00 (4.20) 4.4.3) 23. was about six times lower than the median urinary levels for males in this Report (Radon et al.72-10.46-3.10) 2.6-Trichlorophenol Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.67) 4.5-TCP or 2.4.4.5-46.78 (2.4.1) 16.5-TCP or 2.70) 1.0) 19.6TCP values.30) 4.0-50.36-5.90-8.10) 6.20-3.09-7.70) 5.20-6.25-11.7-3.31 (3.70 (2.6-17.4 (10.0) 10.10 (5.8-13.10-3.56 (3.0 and 1.0 (6.0-37.60 (3. Survey Geometric mean (95% conf. which may vary for some chemicals by year and by individual sample.10-2.02) 2.40 (2. 2003).0) 9.0) 9.0 (8.80-25..30-2.32-4.4.20-23.80) 1.52 (2.0) 12.7) 21.70 (2.80-6. see Data Analysis section) for Survey years 99-00 and 01-02 are 1.4.6-TCP than are found in the general population.40) 2.76) 3.4.9) size 1989 2503 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th 2.91-4.0 (6.28) 24.0) 17.0 (12.0 (8.4 (8.54) 6.00-21.95 (4. 114 Fourth National Report on Human Exposure to Environmental Chemicals .80 (2.59-6.45) < LOD 11.1 (10.7-16.60-3.99) 6.0-41.74 (2.0 (11.85) * 3.6) 970 1178 1019 1325 99-00 01-02 99-00 01-02 99-00 01-02 2.20 (3.40 (2.9 (13.4.26 (2.00 (2.95-6.53) 2.50 (2.0) 15.. Finding a measurable amount of 2.70) 5.6-TCP in urine does not mean that the level of 2.57 (<LOD-2.5-TCP (0.3-17.7 (9.32) * 3.5-TCP or 2.40-4.23-2.6 (12.8) 18.0) 7.5-TCP and 2.0 (20.6 mg/g creatinine) and 2.90) 2.06) * 2.73-9.60) < LOD 5.67-12.0-38.0) 19.4.0) 13.4.4.80-20.98-11.45 (2.65) 15.0) 13.6-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.58 (1.7 (13.90 (3.0) 13.80 (3.7) * 99-00 01-02 99-00 01-02 99-00 01-02 4.28) * 2.6-TCP (0.65 (5.4 (9.60-21.44) 75th 4.80 (2.7) 33.23) 3.78 (2.01-6.3-26.0-54.60 (2.0 (14. Urinary 2. similar to the limit of detection for this Report (Anderson et al.31) * 2.45 (5.50-5.4.3 (11.0-68.20 (3.04) 2.2) 481 574 678 820 830 1109 99-00 01-02 99-00 01-02 2. 1998).07 (<LOD-3.12) 2.4.09) 15.5-TCP level of 0.6-TCP provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of 2.0 (13.4.30-33.87-14.74-3.55-3.66 (8.89-6.0 (6.85 (2.9) 694 677 519 696 602 931 Limit of detection (LOD.70) 3.53) 4.9 (11.6-TCP level.0-44.60-37.40-2.0-18.4.6) 21.40-2. interval) 2.2) 12.33-4.6) 26.0 (20.36 mg/g creatinine.3) 37.8-24.70-6.40-32.32) 3.00 (1.3.0 (15. 2004).59) 4.0 (14.4.9) 13. the median urinary 2. Biomonitoring studies on levels of 2.35-3.58-3..0) 13.92 (2.

41-6.Organochlorine Pesticides Urinary 2.81) 2.70-9.17) 2.6 (5.27-9.0 (6.6 (10.41 (3.25 (3.17) 13.44 (3.3 (9.32-19.6 (9.46-14.6 (12.50-8.51) 18.26 (6.82 (3.33) * 2.38 (2.65) 18.83-5.58 (4.5-28.54 (2.22 (3.29 (6.9) 8.82-2.83-6. Fourth National Report on Human Exposure to Environmental Chemicals 115 .77-4.8) 11.00 (3.0 (9.88) 1.94-13.52 (5.33 (7.9) 19.23 (1.5) 11.83 (3.8) 12.30-2.53-11.9-64.3-23.05 (3.76-8.29-4.5) 12.59 (2.65-2.87-7.02 (1.16-10.42) 2.89-2.88 (2.5 (8.22-2.47-5.23) 4.1 (8. Survey Geometric mean (95% conf.20-2.53) 4.62-15.11) 10.90) 2.63-13.49) 4.79-17.15 (6.52) 2.77) 2.14-13.8 (7.56 (7.43 (2.65) 2.73-22.4) 9.7) 6.68) 2.4 (12.40 (7.87) 2.04-16.5) 9.15 (1. population from the National Health and Nutrition Examination Survey.6 (9.02) 3.88-7.87-6.52) 2.24 (1.72-16.22 (<LOD-2.83-6.91-2.06) 11.88) * 2.68) 2.04-2.8) 21.53 (3.18-4.75) 75th 4.8) 19.90 (1.2 (8.89) 10.2 (12.71 (3.9 (9.87) * 2.5) 11.26) * 99-00 01-02 99-00 01-02 99-00 01-02 4.76) 1.7) 25.35 (3.1) 11.9) 7.3) 8.S.0 (11.6) 8.2 (7.72) 32.88) 5.22-9.76) 2.43 (<LOD-2.87 (3.1) 14.10-9.0) 10.38) 22.6) 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 2.7 (14.9-34.21-11.48-2.7-36.4) 8.6-Trichlorophenol (creatinine corrected) Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.18-2.60 (4.81) Selected percentiles ( 95% confidence interval) Sample 95th 21. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.25-15.98) 10.52 (3.78) 2.63) 4.92) 4.14-2.63 (<LOD-2.38 (4.66-4.26-13.40 (2.08-2.13 (1.6-31.63-15.5 (7.56-5.1 (13.2) 19.22 (1.5) 8.9 (9.73) 5.91 (7.60-2.82) 2.88) 4.00 (2.78 (2.4 (11.10) 4.00) 4.4) 4.63 (2.67-17.63) * 4.28-4.2 (13.9) 481 574 678 819 830 1109 99-00 01-02 99-00 01-02 2.5 (10.01 (3.55-2.10 (6.65-21.32 (2.33 (1.00) 4.51-21.6) 13.25 (3.43-7.4.0) 8.25-2.88) 4.06) 4.6) 12.13-6.96) < LOD 4.99-2.95-2.6 (22.25-17.50 (2.29-4.8 (8.76) 4.17-4.6) 970 1178 1019 1324 99-00 01-02 99-00 01-02 99-00 01-02 2.1) 694 677 519 695 602 931 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.38-5.09-3.6 (6.56) < LOD 11.49-3.9-32.91 (3.9) 8.05 (6.3-37. interval) 2.9-29.06-2.1-21.53) * 2.33-2.19-5.81-9.82 (8.1-32.98 (1.51 (2.78) 90th 12.42 (2.

Hill RH Jr.gov/safewater/ccl/pdfs/reg_determine2/report_ ccl2-reg2_ucmr1_occurrencereport. Poschadel B. Jones D.146:83-91. Smith SJ. To T.54(3):203-208.gov/toxprofiles/tp107. Jarvisalo J. Safe A.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Pesticide residues in urine of adults living in the United States: reference range concentrations.atsdr. Baker S. Baur X. Falk C. Domingo A. Gregg M.S. Arch Environ Contam Toxicol 1989. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children. Fast DM. Can J Biochem 1976. Environ Health Perspect 1998.63:57-62. Domingo JL. Hanrahan L. Heinrich-Ramm R. et al.106(5):279-289. Aitio A. Kaus S. Chlorophenol exposure in harbor workers exposed to river silt aerosols. Luotamo M.18(4):469-474. S. Anderson HA. html. Pekari K. Becker K. Corbella J. 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]. Seifert B.epa. Toxicological profile for chlorophenols [online]. Environ Res 1995. Schulz C. Needham LL. Int J Hyg Environ Health 2003. 206:15-24. Olson J.EPA). Int Arch Occup Environ Health 1991. Urinary excretion of chlorinated phenols in saw-mill workers. Am J Ind Med 2004. Head SL. 4/21/09 Agramunt MC. Available at URL: http://www. Bailey SL. Toxicol Lett 2003. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. Needham LL. Monitoring internal exposure to metals and organic substances in workers at a hazardous waste incinerator after 3 years of operation. et al.cdc. Wegner R. Shealy DB. The metabolism of higher chlorinated benzene isomers. December 2006 Draft.45:440-445.71:99108. Hill RH Jr. U. Available at URL: http://www. 5/19/09 116 Fourth National Report on Human Exposure to Environmental Chemicals . Lindroos L. Burse VW. Seiwert M. Szadkowski D. et al. The Great Lakes Consortium. July 1999. Holler JS. Radon K. Environmental Protection Agency (U. Kohli J.pdf.

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

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

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

30-4. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.970-2.05-7.70) < LOD < LOD 75th 3.2) 14.80) 3.63) 1.52) 6.21 (.599-1.S.11 (.80) .0) 11.27-3.90-5.56 (6.35-11.0) 11.80-22.86 (1.954 (.0) 15.2 (14.1) 10.10) < LOD .33 (5.40-5.74 (8.20 (2.60 (5.2 (9. < LOD means less than the limit of detection.66) * * 1.61 (3.54 (3.9) 14.14) * * .08 (<LOD-2.46) 10.717-1.2 (14.60) < LOD < LOD 4.53) 4.82-12.530 (<LOD-2.2 (7.32) 1.70-14.80) 2.40-11.0-27.2 (7.70-19.5-17.0) 12.82) 10.0 (9.00-19.90-4.33-18.5) 15.10 (.80) 11.58 (5.79 (5.51) 2.80) 2.2 (11.9) 8.96-3.07-10.94) 3.10-7.93-24.0 (9.47) * * 1.9-18.00 (5.5-16.290 (<LOD-1.27-15.758-1.0 (7.71-9.61) 4.0 (6.2-20. 01-02.620-1.80 (4.30 (2.97) 8.39 (3.71 (2.4 (7.56 (4.2) 16.28) 1.50-5.579-1.43-12.50-36.8) 19. 120 Fourth National Report on Human Exposure to Environmental Chemicals .290 (<LOD-.04) < LOD 1.32 (.2) 672 678 473 509 696 578 595 948 752 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.20 (.0) 5.52) * * 1.58) Selected percentiles ( 95% confidence interval) Total * * 50th 1. 0.0 (6.7) 11.73) * * .47) 5.42) .0 (5.50 (2.15-12.3) 17.0) 10.8 (9. and 0.80) 2.955 (.13-2.91) 4.0) 5.0) 10.16 (2.00-27.600 (<LOD-1.7 (14.70-23.0) 11.40-1.3-15.58 (3.00-7.98-12.00-12.6) 18.12) 4.12-19.56-13.70-11.8) 11.34-3.757-2.44-3.37 (3.490-2. and 03-04 are 0.70) < LOD < LOD 1.00-27.840-1.90) 2. population from the National Health and Nutrition Examination Survey.30 (4.8-32.67) 3.94) * * .1) 13.38-5.10) < LOD < LOD 4.8) 7.5 (8.13 (2.80) .60-11. which may vary for some chemicals by year and by individual sample.20-7.8 (14.2.0) 20.4 (9.0) 9.1-17.36-4.30 (2.00-12.1) 95th 13.1 (10.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.03 (.0 (12.02-5.99 (5.8 (8.10 (2.48-7.74 (8. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.623-1.16) 4.85 (3. respectively.0 (8.02) 4.6) 7.2.60-25.0) 10.1.740-2.0) 10.750-1.81) 11.35-12.0 (8.0) 6.0-28.4) 20.40-19.50) 2.95) 5.1-23.22 (.98-5.55-6.70 (2.5) 20.0) 6.2) 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 1.1 (9.39 (8.0 (7.42-3.890 (<LOD-2.81) 1.70 (4.860-2.52-11.20 (.26-8.0 (4.4 (9.810-1.0 (8.34-7.93 (4.60) .0) 7.2) 16.8) 7.83 (5.50 (.40 (.70) .35-16.00) 3.56 (1.4 (7.68-7.80-24.40-14.13 (2.29) * * 1.00 (4.72) 5.97) 90th 7.20 (.80 (2.830 (<LOD-3.7 (12.4) 17.2 (7.20-4.26-6.58 (2.2) 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 1.17-3.55-8.10 (2.670-1.10 (.44 (2.30-6.01) * * 1.08-15.79-7.50 (4.20-30.86-15. see Data Analysis section) for Survey years 99-00.9 (8.2 (9.26 (5. interval) 1.20 (.40-16.5 (11.0 (7.981 (.0) 6.8 (12.700-1.0) 5.23-5.57-7.90 (1.00 (1.0 (7.81) 11.15) 14.9) 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 1.3) 14.45 (2.00) 3.0) 10.780) < LOD 3.08-2.60 (1.19) 9.76 (2.89) 9.0) 11.90) 3.4) 18.21) 9.44-38.80) 4.80-4.60-18.3) 16.

09) 2.54-11.34) < LOD < LOD .53) 9.7) 18.2 (8.75) 14.66-34.64-5.80 (6.4) 4.84) 7.510-1.75-7.6) 8.88) 2.62) .6 (9.87 (3.34) * * .61-13.45-11.0) 6.61 (1.60) * * .66 (5.44 (2.47 (3.34 (6.53 (6.37) 9.37-3.5) 7.996 (.46) 2.3) 5.5-13.32-12.47 (3.773-1.7 (8.56) .43 (.932 (.83) 8.40) < LOD < LOD 75th 2.8) 12.85) 2.36) * * 1.820 (.6) 9.890 (<LOD-1.02 (7.9) 12.5) 7.87-5.02-2.7) 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 .608-1.2) 9.566-1.47) * * .46-5.67) 4.72) 11.0) 7.855 (.98) .95 (3.92-2.41-12.5-32.5) 11.61-29.560-1.9 (9.2 (6.7) 672 678 472 509 695 577 595 948 751 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.38) .35) < LOD < LOD 3.5) 8.94 (2.540-1.7 (9.74) 4.93-9.1-15.41) Selected percentiles ( 95% confidence interval) Total * * 50th .6) 11.90-8.9) 11.41) .09 (.1 (6.26) * * .75) 2.29 (2.620-1.66-15.05) .30) 2.5-20.87 (1.56) 4.56) 7.98-5.25) < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.89-3.67) 1.1 (9.960 (<LOD-2.38 (1.88 (5.04 (1.0 (8.1) 4.574-1.81 (1.27) < LOD 2.430-1.40-28. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.80) 9.76-4.06-2.57 (6.94-23.870-2.28-9.28 (5.45-5.95) 2.04-6.4 (4.98 (3.01-2.31 (3. interval) .14 (3.94-9.85 (6.18 (.10-13.500-1.37 (5.57-10.52) 4.9 (5.00-19.62-5.00 (4.76) < LOD .69-10.47) 2.1) 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 1.05 (1.39 (2.750 (<LOD-1.84 (5.81-5.890 (<LOD-1.35 (1.40-3.5-16.440 (<LOD-2.73 (1.3) 15.03-6.66 (2.8) 7.40 (3.570-1.6 (10.88-10.924 (.82-6.8) 8.47 (1.82-14.2) 7.9 (9.818 (.633-1.71-2.2) 5.533-1.54-2.69) 2.98) .40) 4.56-13.54-15.88-15.02 (2.54) .58) * * 1.53-11.68) < LOD < LOD 3.43) 2.1 (11.7) 5.10 (3.03) 2.57 (4.1 (8.25) 6.00-17.75 (7.94-22.98) 9.650-1.23 (4.03 (7.790 (.03) 2.3) 12.19 (4.4) 4.30 (1.45-5.92-5. population from the National Health and Nutrition Examination Survey.29) * * .42) 12.55-20.51-5.37 (4.75 (3. Fourth National Report on Human Exposure to Environmental Chemicals 121 .50) 7.93-5.900 (.8) 6.90-5.28 (4.3) 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 1.830-1.2) 95th 12.710 (<LOD-1.1 (7.82-14.79-9.31-14.94 (4.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Diethylphosphate (DEP) (creatinine corrected) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.80 (2.34 (6.78 (2.61 (1.1) 4.69 (4.40-12.57) 4.79-3.40-5.40-14.4) 13.4 (9.00) 8.80 (7.13) 4.83 (7.03 (2.74) 90th 7.28 (2.60-9.00-13.960 (.07 (.05 (.71) 10.98-22.2) 8.2) 13.93) 9.23) 4.S.02-14.94-10.20-8.549-1.3) 16.00 (4.883 (.1 (10.43 (3.77 (6.780 (<LOD-1.15-10.11-6.28) 10.7 (10.920 (.5) 12.54-4.09-11.60) 2.9-28.8 (10.2) 5.6) 13.66 (1.42 (3.37-5.69) 4.8) 16.24-3.5 (4.67-19.9) 16.860 (.21-23.89) * * 1.2 (10.7) 12.68-4.82-26.

8-20.0) 18.35 (6.92-17.74) * * * * * 1.6) 14.2 (9.670 (<LOD-1.2 (7.64) 10.0) 11.910 (<LOD-2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.80-3.47-6.80) .30) 8.20 (<LOD-2.0) 9.42 (1.S.6) 14.90-15.8-20.10-15.9-14.0 (5.670 (<LOD-1.670 (<LOD-1.78) 5.90) 8.0) 23.0 (9.20) 3.88) 10.3 (9.89) 2.40) < LOD < LOD 75th 2.1-23.4 (14.9) 10.40 (2.92) 9.0) 12.46-28.7-19.6-19.06 (2.00) 8.790 (<LOD-1.51) < LOD 1.3) 20.4-17.39-13.00) < LOD .4 (10.6) 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 (10.10-4.8) 9.90 (2.90 (1.24-5.0 (10.89 (2.8) 8.27 (7.5) 21.50) 3.95-9.9 (12. which may vary for some chemicals by year and by individual sample.70-9.0) 14.9-15.49-4.30) < LOD < LOD .0 (14.50) 5.70) 2.0 (13.8-21.20-4.41) 3.58.10 (<LOD-1.0 (15.0) 13.34 (6.04 (3.0) 13.80-21.88) 3.00) 3.95 (5.650-1.3) 22.3 (7.61-32.10) 6.35-3.0) 19.0) 12.8 (12.75 (2.0-24.0-33.5) 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 * * * * * * .60 (2.12 (4.18) * * * * * * * * 1.77-14.99 (3.1) 11.67-10.70-9.80-12. 122 Fourth National Report on Human Exposure to Environmental Chemicals .6-41.22 (6.0-29.27) .70-5.18 (3.6 (10.00-16.80) .96) 90th 7.34-5.90-15.10-10.8) Sample size 1949 2519 1965 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.27) 9.70 (1.90 (5.24 (2.86-10.37 (3.75 (3.00) 3.29-4.740 (<LOD-1.77-3.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.58 (1.90) 4.7 (10.50-4.4) 11.0-24. < LOD means less than the limit of detection. respectively.3 (11.580-2.39 (5.46-4.66-13.67) 3.0) 14.15-6.82) 8.80-4.5 (8.7) 14.0) 12.97-4.970 (<LOD-2.0) 6.22-12.31-7.90 (6.9) 9. and 03-04 are 0.70 (8.14 (6.7) 22.81-6.00-9.90-31.17 (7.80 (5.22 (6.80-8.60 (6.5. and 0.4) 672 678 498 509 695 579 595 948 757 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.7-21.00-4. population from the National Health and Nutrition Examination Survey.9 (7.84-4.60) < LOD < LOD 2.59-3.27 (3.7) 16.3) 8.95 (2.6 (10.80 (2.30) 3.52 (6.27) 4.25 (2.00-18.11-6. see Data Analysis section) for Survey years 99-00.5 (8.8 (12.20-18.0 (9.50-5.90 (6.9-17.61 (3.3 (12.7) 10.3 (6.53 (3.67) 4.6) 11.73) 7.15-2.7) 15.50) .5.30) 3.680 (<LOD-1. 0.3 (9.80-14.00 (.90 (2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.35) 4.34-3.16-1.60 (5.0) 7.9) 16.72) 2.34-10.31-12.63-14.96) 3.1 (10.9) 95th 14.3) 14.80) 5.37) 2.30) < LOD < LOD 4.5-26.41-5.0 (8.90 (6.28 (7.20-8.0) 11.80 (2.10 (.70-8.4) 7.40 (2.01 (2.20) 3.6) 18.45 (3.31) 1.670 (<LOD-1.3) 10. 01-02.62-17.0) 9.00-18.00) 7.7 (11.66) 4.8-17.0-19.2) 14.5 (9.1 (10.80-6.29) < LOD < LOD < LOD < LOD 3.4 (10.98-9. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th .00-4.90 (2.90 (6.20) .22) 8.33-11.90-9.0 (7.

79-9. Fourth National Report on Human Exposure to Environmental Chemicals 123 .99 (4.00) 8.33-10.55) 16.6 (12.67 (1.93 (<LOD-2.530-1.850 (<LOD-1.6 (13.27-13.4) 16.77 (2.6) 95th 16.0 (8.63 (6.63 (2.0) 14.16-14.45) 6.4) 15.620 (<LOD-.29 (5.39-17.8) 11.3-34.96-10.89 (3.59-3.38 (1.14 (2.51-10.27) < LOD .940) < LOD < LOD 1.20-3.5 (11.48 (2.33) 3.5 (15.9) 19.00 (7.3) 9.51-7.54 (7.12) < LOD < LOD 4.2) 12.5) 10.55) .6) 13.5) 22.19) 3.5 (9.4) 7.3) 8.5-17.94-14.03 (2.5) 13.920 (<LOD-1.00 (5.85-8.21-21.8) 16.38-13.4) 6.00 (<LOD-1.9-25.4-18.34) < LOD < LOD < LOD < LOD 3.760 (<LOD-1.8 (8.36 (2.890-2.950) .00) 2.1) 10.28-12.06 (<LOD-1.74-4.64-11.06) .2) 12.6) 14.S.4-15.973 (.01-5.00 (3.07-3.83 (6.94 (5.29 (2.54-5.42) 7.12 (7.6-19.45) 3.11 (5.92 (5.7) 15.32-8.78) 4.05-3.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.2 (9.04) 9.96-11.77 (2.30) 2.75-3.0-21.11-3.80) 3.3-21.41 (7.78 (4.6) 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 * * * * * * .0 (10.9 (9.7 (8.70-2.27) 1.89) 5.75-3.00 (2.32) 2.89-13.30) 8.54) 9.97-4.89-10.9 (9.5) 8.3-17.07) 2.93 (6.91) 3.1 (13.38) 1.42-19.89-3.1 (8.55 (2.8) 14.780-1.0-19.0 (13.6 (11.43 (2.8 (10.7 (10.77) 3.68-4.2) 15.6 (10. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.00 (<LOD-1.5 (8.28 (1.91-9.16 (3.68-19.78-10.61 (2.34-18.93-10.47-9.7-19.590 (<LOD-.3-17.9-17.68-10.71 (1.29) 3.09-11.15) < LOD < LOD 75th 2.5 (10.86 (3.30-5.88-7.81 (7.0 (11.68) .87 (3.2-30.58 (4.78 (6. population from the National Health and Nutrition Examination Survey.86-3.95 (2.3-15.2) 10.25 (4.29-2.6) 6.71) < LOD < LOD 2.72-4.27) 5.6) 12.85-17.92) 3.03) 3.3) 6.86) 9.7) 14.38 (.02-4.7) 9.50-17.69-11.30) 7.42) 8.2) 672 678 497 509 694 578 595 948 756 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.9 (9.910 (<LOD-1.7 (11.72) 4.93 (2.89 (2.2) 16.6 (11.50 (6.4) 9.73 (5.07) 2.2) 8.37-5.4-16.27) * * * * * * * * 1.7-23.83 (7.6) Sample size 1949 2518 1962 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.4) 7.95) 90th 8.99) 2.28) 6.1 (19.4-16.67 (7.52-3.97) < LOD .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 * * * .23-3.95) 3.18) 2.3) 12.70-35.79-6.82-11.2) 19.6) 7.6 (13.74-19.7 (10.89-3.7) 14.88 (1.7) 12.4) 7.37) 3.2 (9. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th .9) 16.82-8.3 (7.1) 13.38 (2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.53-8.2-15.21) * * * * * 1.44-6.25-9.07 (5.690 (.2) 12.1) 20.810 (<LOD-1.4 (11.03 (6.09-11.15 (1.

710 (.592-.83) .97 (2.50 (1.467 (.960-1.592) * 50th .810) .710 (.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 * .336-.80 (1.950) 90th 1.75 (2.910-1.30-3.260 (<LOD-.90) 3.30) 4.63 (1.S.10-1.740 (.380-.30 (1.96-5.20-3.550 (.570 (<LOD-.76-6.33-2.58 (1.80) 3.70 (1.94) .50 (1.95) 2.930) < LOD .50-2.592) * .75-2.680-1.60) 3.510 (.455 (.01) .584) .73 (2.390-.80) 3.670) .10) 3.160 (<LOD-.80) 2.79) .453 (.970) 1.78) 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 * .11-3.46 (2.27 (3.280-.749 (.990-1.36-4.20 (2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.597) * .95-5.74-5.00-4.83 (2.980) 1.570-1.30) 1.20) 3.59-6.790 (.90-4.90) 2.41 (2.30) 2.910 (.760 (.30) 4.77-2.69-4.00 (1. 124 Fourth National Report on Human Exposure to Environmental Chemicals .29-2.930-1.00) 1.350-.20 (1.17) 1.20-2.23-3. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.880 (.91) 2.61 (1.930) 1.201-.16-3.860) < LOD < LOD .73-5.449 (.240 (<LOD-. see Data Analysis section) for Survey years 99-00.585) * * .68-5.50-2.83) 2.690-.94 (3.40 (1.83 (2.20) 1.22-3.31) 95th 2.42-2.600 (<LOD-.20 (1.15) 2.400) .60 (2.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.54-2.22 (1.550 (.390-.720-1.350-.13) .618) * .50 (1.960) .83) 1.15) 2.960) 1.47 (1.510 (<LOD-.70-2.50 (1.05-3.16) 1.380) .34) 2.35) 1. interval) Selected percentiles ( 95% confidence interval) Total * .353-.740-1.22-8. and 0.459 (.19-1. < LOD means less than the limit of detection.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 * .01-1.13) 2.780 (.30 (.89) 1.46) 1.26) .440-.70 (1.549 (.32 (1.86) 3.57 (2.80) 5.340-.98) .73 (1.37-2.38) 1.70 (1.780 (.00-2.00) 2. 0.930 (.780) .657) * * .45 (2.680-1.89) .46 (1.03) 1.09 (.49) 2.710) .840 (.830 (.89) 672 678 478 509 695 553 595 948 745 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.700) . which may vary for some chemicals by year and by individual sample.460-.18 (.425 (.587) * * .690-1.80 (2.54 (2.27 (2.20-2.20) 2.740 (.17-4. 01-02.22-2.303-.210 (<LOD-.88) 1.30 (.90) 2.40 (1.50 (1.580-1.620-1.46-3.570 (.750) 1.45-4.48 (2.20-1.382-.98-3.29) 1.850) < LOD .25-1.820 (.457 (.31) 2.940) < LOD .730) .77 (1.20) 1.45 (1.94 (2.490 (<LOD-.48 (1.800 (.2.41-5.16) 2.450 (<LOD-.54) .380-.17) 1.500 (<LOD-.09.880) < LOD 75th .570) * .90 (1.949) .32-1.343 (.50) 1.540 (.59-2.26 (2.759) * .70-7.98 (2.65 (2.32) 3.78) .60-4.960) .45 (1.750-1.39) 2.910) 1. and 03-04 are 0.47) 2.87-3.720-1.20) 2.49) .01-3.11-3.20 (1.590-.690) .720 (.820 (.34) 2.600-1.31-3.970) .600-.89-6.08 (2.10-1.60) 2.30 (.04) 1.76 (1.650-.1.55 (3.05-2.80) 2. respectively.14-1.30-1.570 (<LOD-.10) 1.30-3.14 (1.10) 1.96-3.22-3.74) 3.398-.580-.880) < LOD .560-.570 (.740-.388-.20) 3.10) 1.21) 3.04) .18 (1.505 (. population from the National Health and Nutrition Examination Survey.700) .79) .359-.690 (.80) 3.95 (2.31-3.08 (2.86 (1.960 (.64 (1.57 (1.

64 (2.95) 1.250 (<LOD-.300-.500-.750 (.00-1.06) 4.790 (.88 (1.77-4.560-.22) 1.55-3.320-.310 (<LOD-.870) .403) .08-3.820) .22) 4.03-2.57-2.280 (<LOD-.460-1.270-.11) 1.50) 1.39 (1.62 (2.06-2.11-2.08 (2.04) 95th 2.72 (2.590) * 50th .72-4.580 (.42-8.660-. Fourth National Report on Human Exposure to Environmental Chemicals 125 .760) .67-3.38 (2.510 (.550-.13 (1.630) * .23) 2.640 (.320-.739) * .76) 1.453 (.305 (.08) 2.580) .33) .830) 90th 1.58-6.32 (.77-3.29-4.470 (<LOD-.30-2.520-.75 (2.690) < LOD < LOD .552 (.23 (.50 (1.180 (<LOD-.480) .58) 3.08-3.07) 1.250 (<LOD-.02-6.550-.47 (1.53) .670 (.550-1.720 (.09) .38 (1.10) 2.11 (.740) < LOD 1.05-2.840) 1.89-3.447 (.448 (.08-3.79) 1.550) .234 (.20) 1.90) 2.42-6.16-2.880) 1.790) .710 (.08-3.350) .43) 2.67 (1.700 (.70 (3.16) 1.377-.530 (.590 (.597) * .368) * .23) 2.41 (.285-.04-1.67 (1.400-1. interval) Selected percentiles ( 95% confidence interval) Total * .08-2.49-4.34 (1.485) * * .980-1.510 (.700 (.380-.25-3.32) 5.08) 1.92-8.710 (.17-2.60 (2.840) 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.14 (2.00-3.740) .97) 1.580-.94) .23) 1.300 (<LOD-.510-.44) 2.515) * * .32) 1.S.92) 3.64 (2.760) < LOD 75th .393 (.22) .07 (.390-1.688) * .62 (1.43) 1.70 (2.73 (2.870 (.253-.372 (.800-1.60 (1.57 (1.318-.52 (1.72) 1.43) 2.66) .08-2.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Diethylthiophosphate (DETP) (creatinine corrected) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.900) 1.22 (2.710 (.58 (1.47-4.380) .28 (1.32-1.88) .38-3.78) 3.645) .20-2.75 (1.67) 1.370-.33 (1.348-.22-2.97) 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.49 (1.136-.509 (.43 (1.591 (.61) 2.940-1.82) 2.75) 6.335-.742) * * .520 (.950-2.800) < LOD .470) .75-3.73-3.19 (1.471-.57-4.66 (2.310-.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 * .39) 2.440-1.680 (.08 (.270-.720-1.460 (.36) 3.24) 4.18-2.02-3.820) 1.97 (1.60) .45 (2.17) 2.390) .91 (1.47 (1.16-1.98) 952 1187 906 997 1331 997 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * .20-7.79 (1.84-6.31-1.97 (1.97) 2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.490 (.61 (3.700 (.99) 1.850) 1.61-3.04-5.42 (.71 (1.92 (1.32) 2.02-3.71) .380-1.42) .400) .08-2.57 (3.05-4.460) .990-1.330 (<LOD-.05 (1.00 (3.730) .55 (1.330-.444-.910) < LOD .45 (1.412-.84 (2.535 (.750 (.72 (1.07) 1.270 (<LOD-.69 (1.920) .80) 2.640 (.05) 1.930-1.72) 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 * .17) 2.540-.30) 3.230 (<LOD-.61-3.71) 2.65) 2.87 (2.07) 5.07-3.05) < LOD .310 (<LOD-.52) 3.03-1.830 (.22-3.77 (3.98) 1.82 (2.640 (.560 (.63 (1.44-2.07-2.89 (1.69 (3.22-3.67) .560-.99) 2.23) 3. population from the National Health and Nutrition Examination Survey.81) 2.07) 1.480-1.590-1.840) .60) 1.

10 (7.91 (4.13 (1.05) * 2.0) 6.0) 28.9 (19.44) Selected percentiles ( 95% confidence interval) Total * 2.25-3.0 (6.57-2.20-4.99 (2.0 (38.06) * 2.0 (21.8) 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 1.61-2.70 (.52 (4. 126 Fourth National Report on Human Exposure to Environmental Chemicals .30) 4.8 (26.1-47.81-2.80) 1.7-41.5-40.530-4.0-49.20 (2.04) 3.50-7.12) 1. which may vary for some chemicals by year and by individual sample.46 (.0-31.6-54.5-27.46-2.3) 26.4 (15.41 (1.04 (<LOD-2.0-69.9) 17.2-27.5) 69.0) 3.40-4.1-40.1) 38.0) 16.0 (40.0 (17.83-2.71-2.7-22.0-58.74-2.58) 16.3) 28.49-2.0-43.0) 4.0-58.0-47.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.45) 2.21 (1.96) 5.2-33.2-47.23-2.0 (20.50-20. respectively.0) 13.0 (38.29-4.41) 1. and 0.42) 1.6-45.0) 19. < LOD means less than the limit of detection.93-3.5-45.8) 41.80) < LOD 1.8-21.2 (19.0-52.53) * 2.94 (1.86-3.0-230) 35.59 (1.30) 11.70) 1.14) 5.0) 16.0-39.0 (37.64-8.0) 30.18) 6.2) 31.18) 14. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.0) 18.66-5.1 (22.19-2.50 (2.7 (12.83 (3.4 (19.79 (1. 0.20) 1.04-8.0) 31.0 (33.06 (1.8) 39.41) 5.23-2.79-2.54 (1.3 (12.05-3.81-3.69) 2.0-110) 34.79 (2.88) 3.63-6.30 (.77 (1.600-2.09 (4.0) 20.1-20.11 (4.3 (12.8 (22.61 (1. and 03-04 are 0.0 (25.70-17.50-2.90) 11. population from the National Health and Nutrition Examination Survey.19) 2.40-16.0-39.92-5.80-2.1 (26.0-53.78 (1.13 (1.1) 95th 48.58-2.53) 1.83-2.1-46.2-39.53) 40.0) 28.0-53.8) 32.0 (26.0 (7.16) 2.33 (5.2-62.0 (38.5 (24.70 (1. 01-02.35-6.6 (15.0-62.41) 1.86 (1.0 (20.0-29.0-110) 42.10 (1.S.0-41.830-4.0 (19.83 (1.1 (10.1 (25.0 (38.02 (2.7) 20.41-4.21 (3.0) Sample size 1948 2518 1965 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 2.97) 6.0 (38.0-92.9 (10.72 (1.9-51.67 (1.40) 50th 2.11) 2.9 (27.36-2.23) 9.3) 38.90 (1.71) 5.6 (9.9 (19.76 (2.1 (11.0) 3.0) 42.2-27.88) 1.90 (1.0) 45.610 (<LOD-1.3 (14.3) 33.4 (10.10) 39.0-41.90-8.0) 3.6) 52.92) * 2.10-13.8 (12.29) 2.0) 8.7) 47.48-2.10 (1.8 (12.5.85 (1.87-7.80) 90th 38.3 (23.0) 15.0) 3.31-6.46-6.50-17.05) 1.29-9.8) 671 678 498 509 695 579 595 947 757 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.16) * 1.1) 140 (46.0) 33.2-80.0 (13.18) 20.7 (28.70 (7.80) .10-4.00 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.1) 38.12 (3. interval) 1.44) 3.70) 5.59 (1.660-2.76 (2.0) 4.2-26.85) * 2.70) 1.0 (38.0 (8.5-74.65 (4.0) 4.3) 31.2 (12.4) 19.0 (11.18.78) 9.1-19.44) 2.40) < LOD 2.0) 17.4.54 (3.21 (4.80-18.6-22.6 (26.98) * 2.6 (11.10) .48-2.0) 471 575 310 664 822 717 813 1121 938 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 2.10 (1.13) 12.10 (1.50-5.30-14.57-2.470 (<LOD-1.690-3.9) 48.8) 62.44-7.0 (8.00-24.5) 30.48) 5.27-6.75-14.17-2.82 (1.0) 5.70-6.4-76.60) < LOD 1.0 (38.0) 32.0-41.4) 38.3 (10.00 (.8-24.07-5.26 (.95 (5.7 (12.0 (24.70 (1.1-25.1 (25.0) 15.26) 75th 11. see Data Analysis section) for Survey years 99-00.0 (32.9) 18.71 (4.0-260) 34.3 (24.6-27.5-20.4-22.9 (23.2) 16.53 (1.77) 38.98 (1.0) 17.1) 18.60 (2.0 (8.64-3.0-62.0-50.32 (2.0) 20.9-21.830-3.9) 38.45) 2.43-7.40) < LOD 1.

7) 61.3-27.22-3.02 (.9 (13.71 (1.46-6.7-19.40-7.80-8.9) 24.870-3.1 (33.0 (23.8) 15.38-1.45-1.27) 50th 2.2 (22.14-8.91 (6.60) 4. interval) 1.88 (4.888-1.2) 471 575 310 664 821 715 813 1121 937 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.3 (10.7-47.94) 1.52 (1.2-47.28 (1.02) * 1.3) 28.4 (21.06-1.7-37.5-36.7 (18.70-4.66 (1.95 (2.0-40.16-2.00) 6.1) 52.5 (15.5 (34.4-39.61-22.7-43.7 (24.62 (2.4 (12.2) 36.9 (7.4 (25.71-2.08 (1.51) .4-71.1) 25.870-3.07-2.7 (18.0 (23.32 (3.64 (1.9-95.11-2.1 (34.9) 24.8) 23.2) 13.27-3.2 (9.4-34.0-71.46-22.30) 28.6-49.32-3.899-2.8) 32.48) 1.3 (9.0 (32.3-42.7-38.28) 1.6) 11.9) 12.870-3.07) 9.75 (1.5 (13.19 (1.6-38.57 (6.3) 13.57) 4.38) 5.7-109) 22.12 (1.40 (5.2) 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.68) 47.7) 15.1 (50.20-5.91-2.1) 15.33) < LOD 1.33) 1.58-17.37 (1.1) 13.1-63.3 (8.0) 30.69-5.9) 3.5 (41.1-22.82) 1.40 (2.2) 4.0-118) 29. population from the National Health and Nutrition Examination Survey.03-2.97 (1.23-1.43) * 2.4) 12.9) 54.8-34.83) .06) 1.69-18.7 (10.6) 3.3-22.2 (15.6-51.6) 112 (40.5-97.86) * 3.S.19) 5.4 (9.5) 70.3 (20.2) 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 (25.7-20.8 (7.03) 1.24 (1.94) 19.7) 30.88 (4.59-2.55 (2.90 (.09 (5.33) 2.47 (3.52-4.35) 1.0) 13.9-37.59-2.36-13.3 (10.94-20.59-15.54-2.4-67.58-2.0 (19.0) 25.80 (1.6) 3.00) 1.82 (2.54-15.02) 1.83 (.29-5.2 (8.16 (1.680-4.95) 90th 32.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Dimethylthiophosphate (DMTP) (creatinine corrected) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.9 (19.79-17.75 (1.0) 3.66) 8.62) 4.8) 3.9 (10.46-5.68 (1.19-14.36) 10.8-37.9 (39.6) 19.40-4.43-2.56) 1.1) 27.19) 5.27) 10.07-2.31) 2.17) 2.4 (19.7) 66.0 (39.8-45.67-3.23) < LOD 2.5 (15.39 (1.6) 23.14 (.2-38.3-19.61 (1.12) 3.93) 5.08) 1.0) 48.21 (4.75) * 1.9) 3.1-60. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.890-4.2-34.4 (11.22-2.00 (4.22 (.1) 13.6-32.860 (<LOD-1.0 (17.11) < LOD 1.26-2.37-2.79 (2.18) 3.5 (17.5-190) 30.95-16.1 (12.1) 36.9-36.75-6.0 (14. Fourth National Report on Human Exposure to Environmental Chemicals 127 .17-3.2 (21.18-1.43-12.1) 25.27 (6.0-70.88 (1.4) 12.0 (6.38-5.6 (7.00-16.46) 1.4 (25.0) 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 1.88 (1.930 (<LOD-1.6 (24.2) 13.19-6.4) 3.7) 26.26-4.6 (11.50 (2.1) 17.8-43.41 (2.96) 2.72) 2.1 (39.71) 8.36 (4.51) < LOD 1.0) 47.5 (6.0 (25.44) 9.5) 27.7) 23.2 (16.670-1.70 (1.7) 34.8-26.2) 41.7) 95th 51.16 (1.01 (.67 (1.6 (27.76-2.9-18.5 (8.67 (1.47-17.6) 7.18) * 2.8) 11.2-28.63-5.35) .96-16.9-41.7 (11.61-2.48 (4.750 (<LOD-1.16 (1.0) 10.38 (3.34) * 1.9-52.47 (1.99-4.20) Selected percentiles ( 95% confidence interval) Total * 1.15 (.8) 31.4 (5.67-16.45 (1.56 (2.5-43.9 (26.50-5.86) * 2.06) 1.35 (2.2-70.1) 27.23) 37.4-21.2) 33.22 (2.06) 75th 9.33-5.25-3.4) 14.95-16.60 (.84-13.53) 1.66 (1.

280) < LOD < LOD < LOD < LOD . see Data Analysis section) for Survey years 99-00.12 (.860-1.870 (.370-.730-.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 * * * * * * * * * .160-.900 (.117 (.120-.30) .05.230-.36) .310-.310) < LOD < LOD < LOD < LOD .660 (.090 (<LOD-.150 (<LOD-.190 (.650 (.860) .190 (.320 (.090 (<LOD-.42) .171) * * .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.1.560 (.190 (.130) .760) < LOD .610-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.600 (.58) .680-1.650) .870 (.830 (.870 (.350) < LOD < LOD < LOD < LOD . population from the National Health and Nutrition Examination Survey.440-1.1.380-.690-1.10 (.10) .090 (<LOD-.30) .310 (.870 (.090 (<LOD-.220 (<LOD-.140) .290) < LOD < LOD < LOD < LOD .350) .540) .300-1.700-1.820 (.610-.870 (.450 (.160) .160) . 0. and 0. and 03-04 are 0.540) 672 678 498 509 694 579 595 947 757 Non-Hispanic blacks .03) .140-.080 (<LOD-.380-.30) .680) . interval) Selected percentiles ( 95% confidence interval) Total * * * 50th 75th .270 (.370-.110-.290 (<LOD-.100 (.084-.090 (<LOD-.410) < LOD < LOD < LOD < LOD .130 (.430-.620 (.850 (.720 (.720-1.330-.390) < LOD < LOD . which may vary for some chemicals by year and by individual sample.40) .390 (.650-1.700) 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 .550) .300-.720) .990 (.230) . < LOD means less than the limit of detection.180) .700-1.380-.650) .490 (.650-1.S.540 (<LOD-.700-1.140-.410-.290) < LOD < LOD < LOD < LOD 90th .780) < LOD 1.470 (.570) .930 (.080 (<LOD-.430 (.700-1.130-.610 (.120-.630 (.830 (.20) .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 * * * * * * .640) .630 (.050-.32) .870) < LOD . 01-02.090 (<LOD-.42) .130-.830) < LOD .360-.990) .310 (.140-.560 (.15) .450 (.990) .13) .200) < LOD < LOD .450 (.770) < LOD 95th .470-1.460 (.840) .420-.400-.640) .940 (. 128 Fourth National Report on Human Exposure to Environmental Chemicals .310) < LOD < LOD < LOD < LOD .850) < LOD .360-.099-.130-.460-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.510-1.530-.680-1.00) .260 (.770 (.210 (.170-.10) .10) .820 (.60) 1.240 (<LOD-.680 (.740) < LOD .210 (.220 (.410-1.150) .162) * * * * * .830) .120 (<LOD-.130) .640-1.640 (.850 (.730) .610 (. respectively.320-.290) < LOD < LOD < LOD < LOD Non-Hispanic whites Limit of detection (LOD.540) .840) .410-.

340-.730) .260-.360) < LOD < LOD < LOD < LOD .110) .500) .760) .730) .140-.170 (.700-1.550 (.330 (.540) .700 (.640-1. Fourth National Report on Human Exposure to Environmental Chemicals 129 .320 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.550 (.230-.990) .S.700) .070 (<LOD-. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th 75th .280) < LOD < LOD < LOD < LOD .750) < LOD 95th .380-.210 (.110) .060-.870) .140-.260) .66) 1.300-.090 (.150-.19 (.190 (.240-.410 (.300 (.057-.110) .58) 1.390-.29 (.730) .460 (.570-.03 (.600-1.01 (.940) .540 (.470 (<LOD-.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 * * * * * * .310) < LOD < LOD < LOD < LOD .880-1.380 (.720 (.02-1.580 (.850 (.560 (.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 .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 * * * * * * * * * .570 (. population from the National Health and Nutrition Examination Survey.670 (.43) .740 (.370 (<LOD-.660-1.86) .410) < LOD < LOD .180-.380-.250-.67) .540 (.500 (<LOD-.78) .090 (<LOD-.670-1.080 (<LOD-.140-.290) < LOD < LOD < LOD < LOD 90th .580) .220) < LOD < LOD < LOD < LOD .12) < LOD .960) .860-2.890 (.380-.300-.520) 672 678 497 509 693 578 595 947 756 Non-Hispanic blacks .86) .580 (.650) < LOD .940) .390-.360-.970) .410-.170) < LOD < LOD .20) 1.490-1.190 (.00) < LOD .410-.800-1.161) * * .520-.270 (.120) .860 (.200 (.700 (.510-.120) .140-.310) < LOD < LOD < LOD < LOD Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.200 (.14) 1.070 (<LOD-.780 (.450) .500-1.450 (.230) < LOD < LOD < LOD < LOD .230 (<LOD-.140) .24 (.720 (.03 (.100 (<LOD-.100-.710-1.110) .670 (.410) .380-1.03 (.070 (<LOD-.610-1.084-.360-.62) 1.170 (.740) < LOD 1.360 (.860 (.140-.09) .050 (<LOD-.070 (<LOD-.330 (.650-1.330-.580-1.190-.440 (.60) .03) .410 (.440-1.02) .570-1.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.36 (1.580) < LOD .330-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.220 (.730 (.400) .780) < LOD 1.990) .110-.116 (.080 (.111) * * * * * .810 (.080) .880 (.330-.38) 1.600) .270) < LOD < LOD < LOD < LOD .400 (<LOD-.24) .

0) 3.40 (1.30 (1.350-.39) .0 (17.62) 471 575 306 664 821 699 814 1122 925 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * .770) 2.28-9.83-3. and 03-04 are 0. see Data Analysis section) for Survey years 99-00.590 (.20-4.42) .74 (3.00) .0 (17.510-.10 (3.88-3.05 (2.46 (1.0) 5.0) 5.750-1.97) 20.10 (3.40-20.40) 1.6) 672 678 498 509 695 552 595 947 752 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.0 (5.840-3.53 (2.83) 2.70-7.67) .1.00 (.30 (.35) 11. which may vary for some chemicals by year and by individual sample.40-7.42) 2.890 (.59-5.0 (5.0 (5.99) 19.90-28.20-17.11) .18) 1.0-40.35-10.0 (4.40) 2.48 (2.1.00 (1.05 (3.0 (17.65) 1.86) 4.400-1.96 (1.28) .39 (2.14-5.0) 2.15) 19.90-20.20) < LOD < LOD < LOD < LOD < LOD 1.85-3.99) 11.50) 2.29-10.32-9.S.40-8.30 (1.770 (<LOD-1.94-3.63) 32.87) 12.50) .07 (1.0 (5.00-17.13 (3.750-2.0-39.21) 3.99 (1.07 (3.90-9.720) 2.68) 2.76 (1.20 (1.0-38.90 (2.26 (2.10-3.600 (.0 (4.63 (3.67 (1.00-17. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th 2.425-1.60) .47 (3.0 (17.36-3.12) * * * * * * * * .0) 2.480-.900 (.07) 1.0 (17.70-17.90-37. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.07-3.640 (.880) 5.960 (.0 (16.31-10.960 (<LOD-1.0) 2.370-.80 (4.870) < LOD < LOD .0) 5.0) 2.0) 2.0-38.260-.0) 2.10-3.690 (.840 (.11 (1.82-4.67 (2.00) 1.730 (.0-38.0 (6.11) 13.910) 2.190-1.740 (.43-4.0 (5.170-1.32 (1.30-3.610) < LOD < LOD < LOD < LOD < LOD 2.37) .850) 16.3) 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 * * * * * * * * * .08.23-6.90 (1.360-1.20 (1.52 (1.16) 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 .48) 13.94 (1.07-3.40 (1.0 (13.38-3.0-44. 0.0) 7.94-8.380-.640 (. respectively.830 (.0) 4.0 (3.350-.90) .51-8.97) 20.70) 2.07 (3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.14) .800-4.80) < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 4.691 (.00) .66) 4.62-8.49) 17.0) 5.800) 90th 13.6) 5. 130 Fourth National Report on Human Exposure to Environmental Chemicals . 01-02. < LOD means less than the limit of detection.70-3.840 (<LOD-1.30) .30 (2.83-3. and 0.800) 17.610 (.210-1.330 (<LOD-1.45 (2.15) 14.51 (2.52 (1.0 (7.0) 4.90) .12-1.53-7.0) 4.30 (1.55-4.110 (<LOD-.53) 20.20-4.49 (1.35) 5.31) .74) 5. population from the National Health and Nutrition Examination Survey.30) 95th 19.250 (<LOD-.580 (.33 (4.0) 4.05-3.30-6.60) 1.36-3.01) 5.30-7.28) 1.61 (1.14) 2.03 (.49 (1.55-8.70-50.620-1.080-1.21-3.70-30.10-9.87) 5.52) 5.40-4.24-7.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) 2.0-40.10 (.90) .

310-.630-1.650 (.690-5. Fourth National Report on Human Exposure to Environmental Chemicals 131 .48 (4.38 (2.50 (2.47) .5) 2.240-.71 (2.260-.81-17.7) 4.01 (1.340 (.85-3.47-10.7) 3.57 (.02 (.700) 6.790) 11.02 (1.50) .370-1.12-4.88 (.S.98 (4.0) 4.270 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.580-1.320-1.88-3.9) 6.2 (8.4-34.3) 2.360 (.5 (11.64) 30.190-1.5) 7.37) 4.05) .890 (.430 (<LOD-.82-11.15) 9.65 (2.51-4.07-21.33 (1.600 (<LOD-1.840-3.86) .8) 4.52 (.620-3.960 (.07 (2.24) 3.67 (2.7 (6.9) 5.540 (.5-40.250 (<LOD-.500 (.97) .2-38.32-6.14-6.84) 9.49-2.25-9.67) 1.79 (.8) 7.80 (.85 (1.11-5.69) 2.940-4.40) 1.930) .560 (.970-3.6) 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 * * * * * * * * * .8) 7.670 (.18) 95th 21.96) 2.580 (.47-10.390-.00-19.66-47.474-1.10 (2.75) 5.06 (.56 (1.650) 90th 10.60) < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 4.4) 2.80) 3.8-33.59 (1.91-4.730-3. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.830-3.860-2.74 (2.8) 2.820) .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.35 (.580) 1.56) .12 (4.96-25.08) .29-4.40-12.57-40.69-7.41 (4.55) 21.55 (3.260-.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 .18) 1.03) 2.62-17.580) 16.29 (4.03) 16.40-2.10-3.60 (1.30 (4.340-.590) 2.73 (4.790 (.91) 2.86 (3.43) .96-8.40 (.660) < LOD < LOD .53) 27.1) 2.748 (.57) 1.5 (9.820 (.830 (.7) 5.1) 471 575 306 664 820 697 814 1122 924 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * .470 (.150 (<LOD-.55) 21.9 (11.00) .3) 3.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.53) .31) .800-2.09-3.92 (2.430) 1.23-7.50) 11.45 (1.10) 2.7) 6.31-18.17) 5.71 (.22-27.04 (1.22) 2.270-.57) 8.33 (3.31-7.770) .04-16.27 (2.4 (4.51-44.02-4.33-3.8) 1.5 (8.8 (20.18) * * * * * * * * .13 (2.5) 2.17 (1.32) 9.47) 5.11) .33-4.56) 2. population from the National Health and Nutrition Examination Survey.83-11.44-11.780-4.370) < LOD < LOD < LOD < LOD < LOD 1.740-1.67-6.1 (5.850-3.02) .450 (.28-6.340-.50 (4.44) .25-38.31) . interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th 1.90-6.0 (4.48-7.1 (7.14 (1.540-1.64-4.48-42.88) 17.710 (<LOD-1.330-1.340-.83 (4.7 (12.370 (.88 (2.39) 20.21-3.77 (.8) 2.36 (.89 (2.33-5.67) 2.700) < LOD < LOD < LOD < LOD < LOD 1.0 (9.62 (1.41) 18.25 (1.

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Visuthismajarn P. Environ Health Perspect 2005. Bull Environ Contam Toxicol 1994. Berry H. Am J Ind Med 1987. and spatial learning in monkeys and rats. Arch Environ Health 1975. Samuels S.58(11):702710. J Toxicol Environ Health A 2005. Pedersen L. Biological monitoring of organophosphate pesticides in preschool children in an agricultural community in Thailand. Ruberu DK.20(2):115-22. Monitoring of urinary alkyl phosphates in pestcontrol operators exposed to various organophosphorus insecticides. Keefe TJ. Washington (DC): U. Bravo R. et al. Rohlman D. Phillips J. The presence of dialkylphosphates in fresh fruit juices: implication for organophosphorus pesticide exposure and risk assessments. Levy LS. Hore P. Muniz J. Thompson ML. 1993 [online]. Occup Environ Med 1995. Stark A.44(4):352-357. Lewis JA. gov/oppbead1/pestsales/01pestsales/market_estimates2001. 2004. discrimination.epa. Frasca G. Scand J Work Environ Health 1998. Twenty-four-hour urinary excretion of ten pesticide metabolites in healthy adults in two different areas of Italy (Florence and Ragusa). Chronic neurological sequelae to organophosphate pesticide poisoning. Sci Total Environ 2004. Russo J. McConnell R.S. Rosenstock L. A behavioral evaluation of pest control workers with short-term. Lambert WE. Smit LA. Buchanan D.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Krieger RI. Int J Occup Environ Health 2006. Stokes L. Gladstone EA.edu/ openbook. Lancet. Effects of occupational exposure to organophosphate pesticides on nerve and neuromuscular function. Schenker M. Spurgeon A. Myers JE. Ames RG. Kidd M. Malathion deposition. 1/12/09 Peiris-John RJ. Chrislip D. Salvini S.pdf.43(1):38-45. Aprea C.345(8958):11351139. Chronic central nervous system effects of acute organophosphate pesticide intoxication. et al. Steenland K. Petchuay C.114(5):691-696. Narang A. Robson MG. National Research Council (NRC). Rodnitzky RL.332(1-3):71-80. Pilkington A. Pesticide industry sales and usage . Arch Environ Contam Toxicol 2000.338(8761):223-227.24(1):18-29. et al. O’Malley M. Available at URL: http://www. Saieva C. Seiber J. Available at URL: http://books.S. metabolite clearance. Scherer J. Neurotoxicol Teratol 1998. McCauley L.php?record_id=2126&page=1. London L. Caltabiano LM. Eskenazi B. Environ Health Perspect 2006.2000 and 2001 market estimates.84(5):731-736. Hansen S. Environmental Protection Agency (U. Vitayavirasak B.30(2):98-103. J Occup Environ Med 2002. et al. Wickremasinghe AR. Heaton RK. Neurotoxicology 2005.12(2):153-172. Weisskopf C. May. Takamiya K. Neuropsychological effects of long-term exposure to organophosphates in sheep dip. vibration sense and tremor among South African farm workers. Jamal GA. Gillham R. S.113(4):504-508. Santana J. Masala G. Tumino R.38(4):546-563. Lasarev M. and cholinesterase status of date dusters and harvesters in California. EPA. Occup Environ Med 2001. Dinoff TM. Occupational exposure to organophosphate pesticides: a neurobehavioral study.26(2):199-209. National Academy of Sciences. 4/7/09 Young JG. low-level exposure to the organophosphate diazinon. Organophosphate pesticide exposure and neurobehavioral performance in agricultural and non-agricultural Hispanic workers. Jenkins B. Beach J. Savage EP. 1991. Association between in utero organophosphate pesticide exposure and abnormal reflexes in neonates. Fourth National Report on Human Exposure to Environmental Chemicals 133 . Stephens R. Weerasekera G. Nell V. Rothlein J. Lasarev M.52(2):190-195.12(2):134-141. Effects of chronic. Claypoole K. Muniz J. Calvert IA. Mounce LM. Rothlein J. EPA). U. low-level organophosphate exposure on delayed recall. Johnson C. Keifer M.52(10):648-653. Washington (DC). Terry AV Jr. Burcar PJ. Lu C. et al. 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. Arch Environ Health 1988. Chronic neurological sequelae of acute organophosphate pesticide poisoning. Barr DB. The Pesticide Health Effects Study Group. Daniell WE. Irish RM. van der Hoek W.68(3):209-227 Maizlish N. Marshall E. Effects of long-term organophosphate exposures on neurological symptoms. Prendergast MA. Variation in organophosphate pesticide metabolites in urine of children living in agricultural communities. Pesticides in the Diets of Infants and Children.nap. Am J Public Health 1994. Lancet 1995. Buccafusco JJ. Bradman A. Office of Prevention Pesticides and Toxic Substances. Neurotoxicity among pesticide applicators exposed to organophosphates.

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 . These metabolites differ from the dialkyl phosphate metabolites because each specific metabolite derives from one or only a few parent insecticides.5. see the section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites. parathion and methyl parathion are metabolized to para-nitrophenol.” Organophosphorus insecticide (CAS number) Chlorpyrifos (2921-88-2) Chlorpyrifos-methyl (5598-13-0) Coumaphos (56-72-4) Diazinon (333-41-5) Malathion (121-75-5) Ethyl parathion (56-38-2) Methyl parathion (298-00-0) Pirimiphos-methyl (29232-93-7) Primary urinary metabolite (CAS number) 3.Organophosphorus Insecticides: Specific Metabolites Organophosphorus Insecticides: Specific Metabolites General Information The specific metabolites of the organophosphorus insecticides discussed in this section are those that are often measured in biomonitoring studies. For example. For general information about the organophosphorus class of insecticides. The table below shows the parent organophosphorus insecticides and their metabolites measured in this Report. In addition to reflecting exposure to the parent insecticide. the level may reflect exposure to the environmental degradation products of these pesticides. malathion is metabolized to malathion dicarboxylic acid.

78 (7.32) 2.14) Selected percentiles ( 95% confidence interval) Sample 95th 10. dermal. For instance.28-3.00) 3. The general population may be exposed to chlorpyrifos via oral.95) 7.89 (2.55-5.61-7.70-11.and post-construction structural applications for termite control were to be phased out by 2005 (U.0 (7.60 (5.Organophosphorus Insecticides: Specific Metabolites Chlorpyrifos CAS No.91) 16.2 (10.40 (5. interval) 1.20-11.10) 6.9 (7.66-4.83) 1.9) 697 660 521 701 602 947 Limit of detection (LOD.26) 7.0-28.13-3.80 (1.0) 10.74-9.47-11.87-6.97) 2.36 (4.50-4.95 (4.39) 4.51-2.4) 481 573 681 823 832 1113 99-00 01-02 99-00 01-02 1.71 (6.20) 10.30) 4.50-8.70 (1.34) 1.70-17.5-24.63 (8.50 (2.4-15. 1999.30-11.09 (2.10 (1.45 (1.0) 11.39-2.32-1.80-8.9-18.37 (4.52-2.67 (1.20-2.S.92 (1.96) 3.000 pounds are used per year.61) 75th 3..EPA.0) 6.02 (1.10 (4.29) 90th 7.20 (2.S.03) 1.70-15.16) 2.5 (8.8) 9.77-6.44-2.2) 972 1183 1022 1326 99-00 01-02 99-00 01-02 99-00 01-02 1.76 (1.0 (13.04-10.60 (2.50-2. 2002).90-7.88 (1.46-2.99-4.10) 2.40) 9.0) 14.76 (1.30-5.0) 12.50 (1.5.68-2. 2007).38 (3.68 (7.71 (1.50-14.3 (8.0 (7.90) 7.57 (2.71 (2.60 (4.43-2.0) 7.0) 12.80) 4.91 (1.60-2.90) 3. Chlorpyrifos is Urinary 3. chlorpyrifos was no longer registered for indoor residential uses in the United States. USGS.37 (1.67 (2.40 (5.9 (9.30 (4.97-7.7) 9.40 (6. and sprayed to kill mosquitoes.43-2.35) 1.13 (1.47) 1.50 (2.90-2. Approximately 80.0) 8.44 (3.7-23.50 (1.90 (3.0) 10. and is infrequently detected in ground water (IPCS.0 (10.30-9.94 (4.37) 5.20-3.77-15.40) 2. and on plants for days to several weeks.9) 11.3 (11. 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. 2921-88-2 Chlorpyrifos-methyl CAS No.80) 1. Survey Geometric mean (95% conf.09 (3.S. Chlorpyrifos-methyl is an organophosphorus insecticide also used in agriculture and not registered for residential use.79-2.10 (3.40-26.80 (7. chlorpyrifos and TCPy were detected in all indoor air and dust samples (Morgan et al.47-9.31-2.70-16.89-2.72) 2.51 (1.47-13.0) 15.28) 2.97) 4.40-10.20-14.20-16.80) 2.7) 13.22 (1.00-8.6-Trichloro-2-pyridinol Metabolite of Chlorpyrifos and Chlorpyrifos-methyl Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. Chlorpyrifos is not well absorbed through the skin but dermal exposure can be significant when other routes of exposure are low.50-2.81-2.31-2.62-2.24-3.97) 2.63 (1. Chlorpyrifos is degraded in agricultural soils with a half-life of several months.10 (5.3) 8.03) 99-00 01-02 99-00 01-02 99-00 01-02 2.40-13. Chlorpyrifos is a broad spectrum organophosphorus insecticide that has been widely used to control insects on food crops such as corn.72-4.01) 1. pre.98-15.6) 7.21) 3.80-10.02) 1.0) 12.30-1.90-8.1) 5. applied to structures to kill termites. 2005).05-5.50 (2.59) 2.61 (1.19 (1. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.63 (2.05) 1.0) 18. After 2001.30-12.0 (7.30 (2. 2002).40-2.02 (7.19-3.27 (7.04-10.30) 5.20-4.70) 1.53 (1.90 (2.97) 7.0) 10.90 (6.47 (4. Estimated intakes from diet and water have not exceeded recommended intake limits.8) 10.20) 2.0) 8.7) 8.0 (9.70-5.24-1.90 (1.30-2.4 (9.67 (2. Chlorpyrifos is very toxic to fish and aquatic invertebrates and shows modest degrees of bioconcentration.15 (1. Exposure can also result from contact with contaminated surfaces.90-4.22) 2. and inhalation routes.59-2.10-17. staying bound to soil particles.20) 4.50-4. air.77) 1.52-12. Approximately 21-24 million pounds per year were used domestically from 1987-1998.60) 5.74 (1.66-15.77 (1.4 and 0. in 142 urban homes and preschools in North Carolina. population from the National Health and Nutrition Examination Survey. but can be detected in streams receiving runoff from application sites.0) 12. and dust.5.4.3) size 1994 2509 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th 1.50-5.5) 7.00-24.86) 4.00) 1.29-1. It has low leachability.00) 2.60-3.4 (8.30) 4.44-5. It also has been applied directly on animals to kill mites.35) 2.0) 9.25) 1. Inhalational and dermal routes of exposure are important in pesticide formulators and applicators.9 (10.EPA.17 (1.6-trichloro-2-pyridinol (TCPy) is a metabolite of chlorpyrifos and chlorpyrifos-methyl.20) 2.3 (10.4 (10. Fourth National Report on Human Exposure to Environmental Chemicals 135 .84) 1.30 (2.1-16.8-15. 5598-13-0 General Information The chemical 3.60-3.51) 1.25) 3.20 (4.0 (7.0) 12.70 (1.60-4.64) 3.0 (7.90 (1.80) 12.

35) 1.65-15.76 (3..44 (5.2) 6..98 (7.92-2.Organophosphorus Insecticides: Specific Metabolites rapidly absorbed following ingestion.88-8.85 (3.30-4. cholinergic effects.0) 12.6-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. Survey Geometric mean (95% conf.1 (10.57-2. ubiquitous lowlevel environmental exposures in humans would not be expected to result in inhibition of cholinesterase activity. Once absorbed.31) 1.06 (1.62-7.EPA. paralysis.5) 5. 2002).00 (7.56) 5.25-12. 2006b). Ricceri et al.92 (1.14-8. Chlorpyrifos is eliminated from the body primarily in the urine with a half-life of approximately 27 hours (Nolan et al.06-4.52 (5.59) 3.55 (4.2 (7.33-7.91-13.33 (.94-14.05-4.05) 3.62) 90th 5.85) 1.88 (1. TCPy is more persistent in the environment than chlorpyrifos itself (U. and producing acute symptoms such as nausea.83-2.69 (1.22-6.19) 6.7) 7.01) 1.22 (6. Urinary 3.42-2.60-3..S.93 (4.23-1.11-9.58 (4.43 (4.33 (1.87-3.56) 2.35) 2.58 (1.1 (7.42 (6.91) 1. population from the National Health and Nutrition Examination Survey.90-9.31-4.57) 2. chronic exposure to chlorpyrifos may be associated with slight alterations in some components of neurophysiologic testing (Steenland et al. weakness.84-6.20 (2..58) 1.47 (1. and other metabolites.00-8.82 (3.3) 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 1.33 (5. interval) 1.28) 2.3) 8.20-1.0) 6.02 (5.24-4.05-8.88-10.55 (1.57-2.45 (1.26-14.05-3.56 (1.73 (1.49-2. 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.0) 16.24-24.44 (1.07) 1.23) 14.32) 1. 1984). and behavior may occur at systemically nontoxic doses or at doses of chlorpyrifos that do not result in cholinergic signs (Aldridge et al.11 (2.33) 2.58) 5.63 (5.09-2.91-4.72) 2.57) 9. Chlorpyrifos and chlorpyrifos-methyl both demonstrate moderate acute toxicity in animal studies.01) 3.44-6. Human health effects from chlorpyrifos or chlorpyrifosmethyl at low environmental doses or at biomonitored levels from low environmental exposures are unknown.99-8.92) 3. 2005.37 (1. Slotkin et al.6) 10.0) 481 573 681 822 832 1113 99-00 01-02 99-00 01-02 1.6) 9.3 (7.48 (2.19-1.81) 2. Metabolic hydrolysis leads to the formation of TCPy.50 (4.09-1. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”).47 (5. phosphorothioates such as chlorpyrifos are metabolically activated to the “oxon” form which has greater toxicity than the parent insecticide.30-1.85) 4.74) 1.71) 3.83) 1.19) 3.24) 75th 2.66) 1.72) 1.80) 3.64 (1.06 (5.0) 10. 2005.97 (2.27-1.80-4.940-1.49 (1.03) 1.68) 6.09 (1.88-8.01) 99-00 01-02 99-00 01-02 99-00 01-02 3.09-3.93 (2.46 (1.5.91 (3.11) 7..S. 2006.9 (12.29 (3.01) 3.44 (1.38) 3. Thus.89) 4.85) Selected percentiles ( 95% confidence interval) Sample 95th 8. 2000).63 (4.80-6.53-5. Howard et al.68) 1.62) 1.95 (3.22 (4. Recent in vitro and in vivo animal studies suggest that effects on neuronal morphogenesis.12-1.86 (3.14) 1. Betancourt et al.1-21.53 (2.5 (6.72-2.66 (1.34-1.12-3.36) 1.82) 8.83-11.78 (1.54) 5.24-1.59-2.31-1.28) 2.71 (1.81 (3.44 (6.70-4.64-7.58 (1.41 (1.8) 972 1183 1022 1325 99-00 01-02 99-00 01-02 99-00 01-02 1.56 (4.77) 1.86 (1.75) 6.1-38.3) 9.49-2.49-2.55) 1.93) 2.08) 6. 2006. In pesticide applicators.12) 1.93 (1.24 (1.00) 1.48 (1. neurotransmission..19-2. Overt cholinergic toxicity from chlorpyrifos has been described following suicidal ingestion and unintentional high level occupational exposure.85-4.88 (1.00-13.86 (1.80-11.39 (4.05-1.45-1.97-3.25-1.95 (1.65-11.16 (4.25-11. 2006a.16) 6.47 (1. The metabolite TCPy does not inhibit acetylcholinesterase enzymes.82 (2.39-1.82-4.85 (2.3) 8.22) 1. 2005.91) 10.91) 1.4) 4.02) 7.97) 3.76 (2. These organophosphorus insecticides share a mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system. Roy et al.51 (1. vomiting. In addition to being a metabolite of chlorpyrifos and chlorpyrifos-methyl in the body..21-1. Based on animal data and human cholinesterase monitoring during occupational exposure.63-2.44 (5. resulting in excess acetylcholine at nerve terminals.47-2.60 (1.75 (1. the detection of TCPy in a person’s urine may reflect exposure to the environmental degradates.64-2.97 (3.54 (2.35-1.17-4.96) 3.94-12.88) 6.8) 9.07) 5.91 (4..21-6.7) 697 660 521 700 602 947 136 Fourth National Report on Human Exposure to Environmental Chemicals .91) 2.88-9.66-11.42 (5.98 (6.56-2.27-7.99) 1.43-10. TCPy can also occur in the environment from the breakdown of the parent compounds.46 (2.79-13.39) 6. and seizures.17-4.97) 3.58-5.15 (4.11 (2..93) 5.24) 5.24-5.40) 1.39 (2.

urinary TCPy levels in children were reported not to have increased (Hore et al. Perera et al. EPA at: http://www. CDC. Haidar S.Reference values of urinary 3. 2005).S. Environ Health Perspect 2001. 1999). 1995) and were similar to levels reported in studies of healthy adults in Germany (Koch et al.109(6):583-590. 2001). Whyatt et al. urinary TCPy levels averaged about sixfold higher than those in the NHANES 1999-2000 subsample (Mandel et al. Betta A. Estimation of dose or intake based on the urinary excretion of TCPy indicates that environmental doses are generally below recommended limits (Hore et al.S. 2005). Koch et al.. 2000). Fourth National Report on Human Exposure to Environmental Chemicals 137 ..atsdr. 2002)..gov/pesticides/. the geometric mean urinary TCPy levels were similar in parents and children. Following crack-and-crevice application of chlorpyrifos in their homes. Additional information about external exposure (i. Environ Health Perspect 2005.. 2005). 2001) than the corresponding values reported for the group aged 6-11 years from the NHANES 1999-2000 subsample (CDC. Slotkin TA. suggesting changing low-level exposure and variance in collection timing with respect to exposure (Meeker et al. Barisano A.epa. Clayton CA. Finding a measurable amount of TCPy in urine does not mean that the level will result in an adverse health effect. 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.Organophosphorus Insecticides: Specific Metabolites 2004.. In Iowa farm families using several different pesticides. 76% had detectable levels of TCPy and levels were similar to those reported for NHANES 1999-2000 (Eskenazi et al.5. et al. 2005). Burns CJ.EPA. Lotti A. 2001) and Italy (Aprea et al. Measurements of urinary TCPy in single spot urine collections show variability over time in environmentally exposed individuals and are poorly correlated between collections. 2004). subsamples of NHANES 1999-2000 and 2001-2002 (CDC. Betancourt AM.S. Giordani B. the weighted population mean of TCPy measurements was approximately three times higher (Adgate. Other small studies of environmentally-exposed persons have shown a high frequency of detecting low levels of TCPy.92(2):500-506.113(8):1027-1031.S. 2004). 2005). References Adgate JL.. Chlorpyrifos exposure and biological monitoring among manufacturing workers. population (CDC.63(3):218220. Eberly LE. 2006). Urinary levels of TCPy have been found to be hundredsfold higher for chlorpyrifos manufacturing workers (Burns et al. In a probability-based sample of 102 Minnesota children aged 3-13 years. MacIntosh et al. J AOAC Int 1999. Replacing conventional diets with organic diets in 23 children led to about a fourfold decrease in urinary levels of chlorpyrifos. median urinary levels on the conventional diet were several fold higher than those in the NHANES 1999-2000 subsample (Lu et al. 1992.. Burgess SC. Levels of TCPy in the U. 2005.82(2):305-312. Toxicol Sci 2006.. 2005.. Garabrant D.. Effect of developmental exposure to chlorpyrifos on the expression of neurotrophin growth factors and cell-specific markers in neonatal rat brain. Occup Environ Med 2006. Lioy PJ.6-trichloro-2-pyridinol in the Italian population—validation of analytical method and preliminary results (multicentric study). Meyer A. 2005) appear roughly similar to values reported for a nonrandom subsample of NHANES III (1988-1994) participants (Hill et al. Berent S. Chlorpyrifos levels in house dust and hand rinses did not correlate with levels of TCPy in urine (Lioy et al.. (1999) reported mean urinary TCPy levels in a sample of Maryland adults that were about three times higher than adults in the U. 2003.. representative subsample of NHANES 19992000 (CDC. Carr RL. but levels were roughly four to six times higher than the geometric means in the U.. 2007). Barr DB.. Some reproductive and teratogenic effects in animal testing were only observed at high doses of chlorpyrifos that caused overt maternal toxicity. U. Seidler FJ. et al. environmental levels) and health effects is available from ATSDR at: http://www.gov/toxpro2. Freeman NC. et al. Of 482 pregnant women living in an agricultural community.e. Biomonitoring Information Urinary TCPy levels reflect recent exposure. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample. Albers JW. In Minnesota and South Carolina farmers who used chlorpyrifos. Chlorpyrifos is not considered to be mutagenic or carcinogenic (NTP.S. Curwin et al. Catenacci G.html and from U. Aldridge JE. Alterations in central nervous system serotonergic and dopaminergic synaptic activity in adulthood after prenatal or neonatal chlorpyrifos exposure..cdc. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.. Aprea C. 2006) and episodically many times higher for pesticide applicators than median levels from NHANES 1999-2000 (CDC. 2005. Magnaghi S. but not chlorpyrifos. 2005).

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Quantitative morphological assessment reveals neuronal and glial deficits in hippocampus after a brief subtoxic exposure to chlorpyrifos in neonatal rats. Baker BA. Ryde IT. Gurunathan S. Barr DB. Executive summary of safety and toxicity information. MacIntosh DL. Jewell NP. gov/ntpweb/index. Hines CJ. Hore P.15(4):297-309. Barr D.51(1):53-65.207(2):112-124. Urinary pesticide concentrations among children. et al. Third National Report on Human Exposure to Environmental Chemicals. Temporal variability of urinary levels of nonpersistent insecticides in adult men. Ricceri L. Bravo R. Ann Occup Hyg 2007.6-trichloro-2-pyridinol. Tsai WY. Howard AS. et al.113(2):211-219. Environ Health Perspect 2006a. chlorpyrifos. 4/7/09 Koch HM.9(5):494-501. Brain Res Dev Brain Res 2005.org/documents/jmpr/jmpmono/ v99pr03. mothers and fathers living in farm and non-farm households in Iowa. 1992. Chuang JC. Slotkin TA. J Expo Anal Environ Epidemiol 1999. Shealy DB. Toepel K.S. Pellizzari E.31 Suppl 1:98-104. Ryan PB. EPA). Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. Slotkin TA. Bravo R.nih.73:8-15. A longitudinal investigation of selected pesticide metabolites in urine. Environ Health Perspect 2003. Bennett DH. Hammerstrom KA. et al. Adgate JL.15(3):271-281. Environ Health Perspect 2006b. Environmental Protection Agency (U. Needham LL. Environ Res 1995. 2005. Wartenberg D. February 5. Morgan MK. Ozkaynak H. Fenske RA. Freshour NL. International Programme on Chemical Safety-INCHEM (IPCS). Robson M. et al.cfm?objectid=6F5E95EB-F1F6-975E7C20F4211536F46F. Scand J Work Environ Health 2005. Capone F.niehs. Freeman N. Available at URL: http://ntp.inchem. Kromhout H. Int J Hyg Environ Health 2001. Kinney P. Heederik D. Lein PJ.114(2):260-263. Saunders JH.5. Toxicol Appl Pharmacol 1984. Fortuna S. Levin ED. J Expo Anal Environ Epidemiol 2005. Jones PA. Slotkin TA. Toxicol Appl Pharmacol 2005.108(4):293-300. Irish R. Chlorpyrifos: pharmacokinetics in human volunteers. Striley C. Zhang J. Sharma V.S. et al. Pesticide residues in urine of adults living in the United States: reference range concentrations. Atlanta (GA). Sheldon LS. Hein MJ. Nolan RJ. Hill RH Jr. Environ Health Perspect 2004. Bucelli R. Biological monitoring of exposure of the general population to the organophosphorus pesticides chlorpyrifos and chlorpyrifos-methyl by determination of their specific metabolite 3. Environ Health Perspect 2006. Rick DL. Venerosi A. et al. Howell RJ. U. Levin ED. House dust levels of selected insecticides and a herbicide measured by the EL and LWW samplers and comparisons to hand rinses and urine metabolites. Comparative developmental neurotoxicity of organophosphate insecticides: effects on brain development are separable from systemic toxicity. Environmental Health Criteria 198. Developmental neurotoxicity of organophosphorous pesticides: fetal and neonatal exposure to chlorpyrifos alters sex specific behaviors at adulthood in mice.204(2-3):175-180. Meeker JD. Seidler FJ. Baker S.6-trichloro 2-pyridinol in their everyday environments. J Expo Anal Environ Epidemiol 2000. Robertson GL. Mandel JS. 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. Cometa MF. et al. Barr DB.Organophosphorus Insecticides: Specific Metabolites Centers for Disease Control and Prevention (CDC). Yang D.155(1):71-80.71:99108. Harley K. Edwards RD. Lorenzini P. J Expo Anal Environ Epidemiol 2005. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population. Acquavella JF. Roy TS. Angerer J. Environ Health Perspect 2000. Chlorpyrifos exerts opposing effects on axonal and dendritic growth in primary neuronal cultures. Available at URL: http://www. Bailey SL. 2921-882. Eskenazi B. Lioy PJ. Hardt J. Gregg M. Honeycutt R. Seidler FJ. Head SL. Freeman N. Steenland K. et al. Exposures of preschool children to chlorpyrifos and its degradation product 3.112(10):1116-1124. Toxicol Sci 2006.114(10):1542-1546. Sanderson WT. Alexander BH. Dick RB.

Available at URL: http://pubs.usgs. Fourth National Report on Human Exposure to Environmental Chemicals 139 . Kinney PL. et al. Available at URL: http://www. Geological Survey (USGS). Andrews HF.pdf. 1/14/09 U. 6/1/09 Whyatt RM. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns.gov/ oppsrrd1/REDs/chlorpyrifos_ired. Environ Health Perspect 2003. February 2002.Organophosphorus Insecticides: Specific Metabolites 01-007.gov/circ/2005/1291/. revised February 15. The Quality of Our Nation’s Waters. Camann DE. Pesticides in the Nation’s Streams and Ground Water. 2007 [online]. 1992-2001. Barr JR.epa.S. March 2006.111(5):749-56. Barr DB.

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

Organophosphorus Insecticides: Specific Metabolites Urinary 3-Chloro-7-hydroxy-4-methyl-2H-chromen-2-one/ol Metabolite of Coumaphos Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.2.200 (<LOD-.S.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 . 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 . which may vary for some chemicals by year and by individual sample.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 .270) < LOD 659 701 920 Limit of detection (LOD. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.380 (<LOD-. Survey Geometric mean (95% conf. population from the National Health and Nutrition Examination Survey.560) < LOD 659 700 920 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 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 . population from the National Health and Nutrition Examination Survey. Urinary 3-Chloro-7-hydroxy-4-methyl-2H-chromen-2-one/ol (creatinine corrected) Metabolite of Coumaphos Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.S.200 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Survey Geometric mean (95% conf. Fourth National Report on Human Exposure to Environmental Chemicals 141 . < LOD means less than the limit of detection. see Data Analysis section) for Survey year 01-02 is 0.

S. Third National Report on Human Exposure to Environmental Chemicals. September 2000.376(6):808-815. 1/14/09 142 Fourth National Report on Human Exposure to Environmental Chemicals .Organophosphorus Insecticides: Specific Metabolites References Astroff AB. Comparative organophosphate-induced effects observed in adult and neonatal Sprague-Dawley rats during the conduct of multigeneration toxicity studies. Eigenberg DA. Atlanta (GA). Centers for Disease Control and Prevention (CDC). Reregistration eligibility decision (RED) addendum and FPQA tolerance reassessment progress report: Coumaphos. Barr DB. Olsson AO. Anal Bioanal Chem 2003.S. Nguyen JV.12(6):619-645. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine. Environmental Protection Agency (U. Freshwater KJ. Reprod Toxicol 1998.gov/oppsrrd1/ REDs/0018tred.pdf. Sadowski MA.epa. EPA). Available at URL: http://www. 2005. EPA 738-R-00-010. U.

2004). 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. fruits. 1998.S. since 2004. seed and foliar applications are planned to be phased out (U. < LOD means less than the limit of detection. in the past. but these uses have been phased out. in some pest strips. Prior to 2000. It is toxic to birds. 1998). diazinon was widely used in residential and garden application. Experimental diazinon exposure in people has demonstrated its rapid elimination into urine. 333-41-5 General Information The chemical 2-isopropyl-4-methyl-6-hydroxypyrimidine is a metabolite of diazinon. 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.49 (<LOD-2. and other metabolites. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”). phosphorothioates such as diazinon are metabolically activated to the “oxon” form which has greater toxicity. population from the National Health and Nutrition Examination Survey. USGS. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. but is rapidly absorbed orally (IPCS. 2007). an organophosphorus insecticide that is used to control insects on nuts. about 13 million pounds of diazinon were used annually on agricultural sites in the United States. Metabolic hydrolysis leads to the formation of 2-isopropyl4-methyl-6-hydroxypyrimidine. Diazinon is biologically and chemically degraded in soils with a half-life of about a few weeks.S. and particularly when it was ingested in granular form.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 1.7.2 and 0. which may vary for some chemicals by year and by individual sample. diazinon produced wild bird kills before use restrictions were in place. Survey Geometric mean (95% conf.EPA. Most granular formulations. Estimated intakes from diet and water do not exceed recommended intake limits (U. diazinon cannot be sold for residential use. Fourth National Report on Human Exposure to Environmental Chemicals 143 . Before these restrictions.Organophosphorus Insecticides: Specific Metabolites Diazinon CAS No. and forage crops.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. Diazinon is not well-absorbed through the skin.45 (<LOD-3. 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. Once absorbed. vegetable. Inhalational and dermal routes of exposure can be significant for pesticide applicators. It is also used for cattle ear tag applications to control flies and ticks and. see Data Analysis section) for Survey years 99-00 and 01-02 are 7.EPA. It has been infrequently detected in general groundwater sampling but has been detected in streams receiving runoff from application sites (IPCS.S. 2004). aerial.

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

Toepel K. Oloffs PC. Study for Future Families Research Group. Environmental Protection Agency (U.44(11):2243-2250. EPA 738-R-04-006. Cocker J.50(5):505-515. Atlanta (GA). Barr DB. Fenske RA. Effect of sublethal levels of diazinon: histopathology of liver.htm.. May 2004. Ann Occup Hyg 2006. Kruse RL. Drug Chem Toxicol 1986. Oloffs PC. Needham LL. urinary 2-isopropyl-4-methyl-6-hydroxypyrimidine levels were below the limit of detection (Bouchard et al. Geological Survey (USGS). In 54 Canadian greenhouse workers. Beeson MD. In 23 children. 2006). Redmon JB. Interim reregistration eligibility decision (IRED. Bouchard M.epa. 2007 [online]. The Quality of Our Nation’s Waters. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. In a small number of men visiting fertility clinics in Missouri and Minnesota.usgs. Liu F. Dumas P. revised February 15. Environ Health Perspect 2006. Drobnis EZ. References Anthony J. Centers for Disease Control and Prevention (CDC). 2005. Semen quality in relation to biomarkers of pesticide exposure.111(12):1478-1484. 4/7/09 Lu C. International Programme on Chemical Safety-INCHEM (IPCS). Banister E. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.134(1-3):105-113. Pesticides in the Nation’s Streams and Ground Water.376(6):808-815. Third National Report on Human Exposure to Environmental Chemicals. Exposure to the organophosphate diazinon: data from a human volunteer study with oral and dermal doses. Rajendra W.gov/ oppsrrd1/REDs/diazinon_ired. Garfitt SJ.37(4):501-507.gov/circ/2005/1291/. Quantification of selected pesticide metabolites in human urine using isotope dilution high-performance liquid chromatography/ tandem mass spectrometry. 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.9(2):117-131. Driskell WJ. Bravo R. Effects of chronic intake of diazinon on blood and brain monoamines and amino acids.org/documents/ehc/ehc/ehc198. J Expo Anal Environ Epidemiol 2000. Available at URL: http://www. urinary 2-isopropyl-4-methyl-6hydroxypyrimidine was detected in less than 14% of multiple samples collected during varied diets (Lu et al. Diazinon. Olsson AO. Sadowski MA. EPA). Environmental Health Criteria 198. Irish R.inchem. Barr DB. Bull Environ Contam Toxicol 1986. Biochem Pharmacol 1992.S. Mason HJ. Carrier G. 1998. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine. Seifert J. Baker SE. Alteration of mice L-tryptophan metabolism by the organophosphorous acid triester diazinon.S.10(6 Pt 2):789-798. Toxicol Lett 2002. Barr DB. 6/1/09 Fourth National Report on Human Exposure to Environmental Chemicals 145 . Brunet RC. Swan et al. 2006). Swan SH. Barr DB. Noisel N. Nguyen JV. 1/14/09 U. 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.S.114(2):260-263.pdf. Environ Health Perspect 2003. U. (2003) found that 2-isopropyl4-methyl-6-hydroxypyrimidine was detectable in 96% and 58% of the subjects. Biological monitoring of exposure to organophosphorus insecticides in a group of horticultural greenhouse workers. 1992-2001.. Jones K. et al.Organophosphorus Insecticides: Specific Metabolites 2005). Available at URL: http://pubs. Pewnim T. Diazinon. Available at URL: http://www. Anal Bioanal Chem 2003. Banister EW. March 2006.

It has a short halflife in soils and water and is not considered persistent in the environment. Pesticide applicators and agricultural workers can have higher exposures via dermal. resulting in excess acetylcholine at nerve terminals.S. Human health effects from malathion at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 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. 2006). or oral routes (U. inhalational. In addition to being a metabolite of malathion. malathion and other organophosphorus insecticides share a common mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system. and other metabolites. ornamental trees. It is moderately to highly toxic to fish. phosphorothioates such as malathion are metabolically activated to the “oxon” forms which have greater toxicity than the parent insecticide.EPA. Survey Geometric mean (95% conf.EPA. Once they are absorbed. the detection of malathion dicarboxylic acid in a person’s urine may also reflect exposure to the environmental degradate. When malathion is used on food or feed crops. shrubs. 2000).S. malathion has low acute toxicity. malathion dicarboxylic acid.S. It is highly toxic to aquatic invertebrates and rare fish kills have been reported from wide area applications onto surface waters and runoff into waters. Malathion is slowly absorbed through the skin. and producing acute symptoms such as nausea. < LOD means less than the limit of detection. 2006). population from the National Health and Nutrition Examination Survey.Organophosphorus Insecticides: Specific Metabolites Malathion CAS No. About 31-35% of oral doses of malathion are excreted in the urine as malathion monocarboxylic acid (Krieger and Dinoff. vomiting. 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. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.. Most of the estimated 15 million pounds used annually are applied to cotton (U. cholinergic effects. which may vary for some chemicals by year and by individual sample. and in government programs such as the USDA’s Boll Weevil Eradication Program. Malathion is rapidly eliminated from the body within 12-24 hours (Bouchard et al. gardens. Malathion is infrequently detected in groundwater sampling (USGS. and seizures. Metabolism of malathion leads to the formation of malathion monocarboxylic acid. 2007). weakness. as well as lawns. malathion dicarboxylic acid can also occur in the environment from the breakdown of the parent compound. in fruit fly control. but is more rapidly and efficiently absorbed via ingestion. paralysis. At high doses.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. usually only a small fraction of the crop is treated. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”). It is registered for use in public health mosquito control. depending on the species. 121-75-5 General Information Malathion dicarboxylic acid is a metabolite of malathion.80 (<LOD-5. 146 Fourth National Report on Human Exposure to Environmental Chemicals .64.5%) to kill body lice. Thus. Malathion is also used medically in lotion form (0. see Data Analysis section) for Survey year 99-00 is 2. and plants. Compared with other organophosphorus insecticides. Limited general population exposure occurs through the diet. which is an organophosphorus insecticide that is used on a wide variety of agricultural crops. Estimated intakes for the general population have not exceeded recommended intake limits. 2003).

. 1993.EPA. Thomas et al.. Biomonitoring studies of malathion dicarboxylic acid provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of malathion than are found in the general population. 2001. 2005). 2002.74 (<LOD-5. 1990).. Human studies of single oral doses between 0. Additional information about external exposure (i.5 and 5. IARC considers malathion not classifiable as a human carcinogen. Toxicity from unprotected bystander exposure during applications is rare (U. 30% had detectable levels of malathion dicarboxylic acid at a detection limit about tenfold lower than the detection limit in the NHANES 1999-2000 analyses (Eskenazi et al. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.EPA. Fourth National Report on Human Exposure to Environmental Chemicals 147 . Giri et al..cdc. Pluth et al.html and from U. 2005.S.. 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. 2000). 1987. 2006). Malathion dicarboxylic acid was infrequently detected in multiple samples from 80 Maryland residents in 1995-96 (MacIntosh et al.. Of 382 pregnant women living in an agricultural community. 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. CDC. 2006).atsdr. 2006). 2005). but isomalathion. Replacing conventional diets with organic diets in 23 children led to a tenfold decrease in urinary levels of malathion dicarboxylic acid. 1999. 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. population from the National Health and Nutrition Examination Survey.. 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. 2004). Malathion does not appear to produce human reproductive or teratogenic effects at environmental levels of exposure (Grether et al. Malathion itself has not been considered genotoxic (U. Lu et al.. representative subsample from NHANES 19992000 (Adgate.. 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. and it is not considered an animal teratogen or a reproductive toxicant.epa. 2003). Flessel et al. Biomonitoring Information Levels of urinary malathion dicarboxylic acid reflect recent exposure.S. a malaoxon metabolite and a technical grade impurity tested positive in some chromosomal tests (Blasiak et al. Survey Geometric mean (95% conf.. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.gov/pesticides/. Finding a measurable amount of malathion dicarboxylic acid in urine does not mean that the level will result in an adverse health effect.Organophosphorus Insecticides: Specific Metabolites direct ingestion of agricultural strength solutions.. environmental levels) and health effects is available from ATSDR at: http://www. but cholinesterase activity was not affected.50) < LOD < LOD 453 660 807 99-00 99-00 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 937 983 99-00 99-00 99-00 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 680 498 580 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.gov/toxpro2.e.S. 1996. median urinary levels on the conventional diet were similar to the detection limit in the NHANES 1999-2000 subsample (CDC.S. 1999). EPA at: http://www. some of the postshift urine levels in duster-applicators were thousandsfold higher than the detection limits in the NHANES 1999-2000 subsample.0 mg/kg/day have shown no acetylcholinesterase inhibition or other short term effects (IPCS.S.

2005. Centers for Disease Control and Prevention (CDC). Fenske RA. Clayton CA. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population. Ryan PB. Quintana PJ. Mutat Res 2002. Am J Epidemiol 1990. Barr DB. Hooper K. Bradman A. March 2006. Irish R. Jewell NP. Cancer Res 1996.S. Brunet RC. Barr DB. Giri A.38(4):546-553. A toxicokinetic model of malathion and its metabolites as a tool to assess human exposure and risk through measurements of urinary biomarkers. Malathion (addendum).56(10):2393-2399.445(2):275-283. Reregistration eligibility decision (RED) Malathion. 2007 [online]. EPA). Trzeciak A.gov/circ/2005/1291/. Blasiak J. Available at URL: http://www. 4/7/09 Kissel JC.S.74(2):following table of contents. Third National Report on Human Exposure to Environmental Chemicals. Grether JK. Nicklas JA. Reproductive outcome in women exposed to malathion. Bravo R. Curl CL. Available at URL: http://pubs. Environmental Protection Agency (U. In vitro studies on the genotoxicity of the organophosphorus insecticide malathion and its two analogues. Increased frequency of specific genomic deletions resulting from in vitro malathion exposure. Freeman NC.S. Pluth JM. Krieger RI. MacIntosh DL.Organophosphorus Insecticides: Specific Metabolites References Adgate JL. Sharma GD. International Programme on Chemical Safety-INCHEM (IPCS).114(2):260-263. Genetic toxicity of malathion: a review. Griffith W. Albertini RJ. Environ Health Perspect 2004. O’Neill JP. Toepel K. Harley K. Environ Health Perspect 2006. htm. Gosselin NH. Neutra R. Lioy PJ. Toxicol Sci 2003 May. Barr DB. Barr DB.132(4):794-795. Available at URL: http://www. Malathion deposition. Erratum in: Toxicol Sci 2003 Aug. J Expo Anal Environ Epidemiol 2005. Kedan G. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. 6/1/09 148 Fourth National Report on Human Exposure to Environmental Chemicals . revised February 15. Bouchard M. Dumoulin MJ. EPA 738-R06-030. Petitti D. Kizer KW: Exposure to aerial malathion application and the occurrence of congenital anomalies and low birthweight.112(10):1116-1124. Swan SH. Dinoff TM.15(2):164-171.77:1009-1010. Jaloszynski P.gov/oppsrrd1/REDs/ malathion_red. Thomas D. A longitudinal investigation of selected pesticide metabolites in urine. 6/1/09 U. Carrier G. Comparison of organophosphorus pesticide metabolite levels in single and multiple daily urine samples collected from preschool children in Washington State. Szyfter K. Arch Environ Contam Toxicol 2000. Mutat Res 1999. Hertz-Picciotto I. The Quality of Our Nation’s Waters. et al. and cholinesterase status of date dusters and harvesters in California.org/documents/jmpr/jmpmono/v2003pr06. Samuel O.22(1):7-17. et al. metabolite clearance. J Expo Anal Environ Epidemiol 1999. Am J Public Health 1987. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample. Pesticides in the Nation’s Streams and Ground Water. Rappaport E.epa. July 2006. Geological Survey (USGS). et al.109(6):583-590. Needham LL. Eskenazi B. Environ Mol Mutagen 1993. U.pdf. Genotoxic effects of malathion: an organophosphorus insecticide using three mammalian bioassays in vivo.usgs. Atlanta (GA).514(1-2):223231. Hammerstrom KA.73(1):182-94. Lu C. Environ Health Perspect 2001. Weltzien E. Eberly LE. Harris JA. Flessel P. Goldhaber M. Pesticides residues in food: 2003 FAO/WHO Meeting on Pesticide Residues.inchem. 1992-2001. Prasad SB.9(5):494-501. Lu C. Giri S.

91-3.21 (2.12) < LOD < LOD 1.0) 3. on cereal grains.850) < LOD .32 (1.8 and 0.74) 5. first registered in 1948.70) 2. methyl parathion was rapidly absorbed after ingestion.48) 90th 2.37-4.37-2.09-1.37-4.0) 3.10) 4.71) 971 1164 1018 1313 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD . Methyl Parathion.60-5.47) 2.30-3.70-3. interval) Selected percentiles ( 95% confidence interval) Sample 95th 5.790 (<LOD-.28 (1. but by 2003.24) 479 565 680 813 830 1099 99-00 01-02 99-00 01-02 * * * * < LOD . O-ethyl-O-(4-nitrophenyl) phenylphosphonothioate. Once absorbed.910) < LOD < LOD . < LOD means less than the limit of detection.69) 4.16) < LOD 1.32-1.90-9. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Urinary para-Nitrophenol Metabolite of Ethyl Parathion.80 (1.67 (1. which may vary for some chemicals by year and by individual sample. 2002. and Nitrobenzene Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.32-1. It had been applied to cotton.910) < LOD < LOD < LOD 1.50 (1.940 (<LOD-2.30 (2. and eliminated rapidly from the body after absorption (Kramer et al.11) 2.0) 3. phosphorothioates such as methyl and ethyl parathion are metabolically activated to the “oxon” forms which have greater toxicity than the parent insecticides.0 (3.18-3.70-3.10 (3.70 (2.02-6.50 (1.990-1.60) 1.0) 3.45 (1.46 (3.70) 2.70 (3. binds tightly to soils resulting in low leachability.26 (1.300-. 2003).90-11.50-14.50 (2.700 (<LOD-.67) < LOD 1.S. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.00) 3.27) 2.40 (1.22-3.37) 2.69 (2.92-2.EPA.45) 5.Organophosphorus Insecticides: Specific Metabolites Methyl Parathion CAS No. Ethyl and methyl parathion are infrequently detected in groundwater sampling (USGS.11-4.72 (3.32-3.60-36.50) 2.10 (<LOD-6.61) < LOD 1.40-3. Estimated intakes from diet and drinking water have been below recommended limits. more slowly absorbed through the skin.20-5. Methyl parathion is not registered for residential use in the United States. all registered uses were voluntarily cancelled (U..30-16. pulmonary.10) 22. Both are toxic to birds.36-1.0) 3. Many previous registered agricultural uses of methyl parathion have been cancelled (U.57) 1.62 (1.71 (2.40) 2.00 (2.S.02) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD . In the 1990s.20 (2.28 (1.50) 3.40) 4.50 (1.79) 4. ethyl parathion.40-4.70 (<LOD-3.10-1.58) 3.30 (1.33 (1.19 (.298-00-0 Ethyl Parathion CAS No.50 (2.770 (.05) 4. and aquatic invertebrates.15-3.90 (1.34 (3.10 (3.00 (2. population from the National Health and Nutrition Examination Survey.60 (4. 1977).70-6.730 (<LOD-. Increased risk of exposure via dermal.1. and of the chemical nitrobenzene.50 (1.70) 2. Metabolism of ethyl or methyl parathion leads to the formation of paranitrophenol.20 (<LOD-2. 2000).40-4.60-19.21-1. Morgan et al. fish. 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 1.71 (3. 2007). Methyl parathion use is highly restricted.33) 2. 56-38-2 General Information Para-nitrophenol is a metabolite of the insecticides methyl parathion.0) 2.57-4. Survey Geometric mean (95% conf.20) 5.80) 2.910) < LOD .860 (<LOD-1.28-4. Fourth National Report on Human Exposure to Environmental Chemicals 149 ..50) 1. with limited applications in agriculture.85 (2.92) 5.70 (2.40) 1.EPA.80 (2..50) 3.44) 2.30-5.13-1. and oral routes can occur in pesticide and agricultural workers (Muttray et al.60-24.01-4. peak domestic use was as high as 5-6 million pounds per year.66 (2.0) 4.10-11.41-4. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.S.70 (2.89 (2.80 (2. was once a restricted-use insecticide with limited applications on certain agricultural crops.61) < LOD 1.49 (1. and has a short half-life in soils and on plants.01) 4. Given its limited use.70-6. and to a lesser extent. the potential for human exposure to either ethyl or methyl parathion through the diet or drinking water is low.50-9.01) 695 660 518 679 603 941 Limit of detection (LOD. Ethyl parathion.70-6. In animal studies. Methyl parathion has low water solubility.

2003.48-4.20) . Urinary para-Nitrophenol (creatinine corrected) Metabolite of Ethyl Parathion. resulting in excess acetylcholine at nerve terminals.70) 3. Survey Geometric mean (95% conf.31) < LOD .37-1.88 (1.33) 479 565 680 812 830 1099 99-00 01-02 99-00 01-02 * * * * < LOD .43) 4.4 (3.44-3. WHO.. 150 Fourth National Report on Human Exposure to Environmental Chemicals .20 (3.60 (1. methyl parathion.atsdr..29 (2.29) 2.61) 4.20) 3.72-2.82) < LOD . retinal atrophy and sciatic nerve degeneration have also been observed (IPCS.26) 17.79) 1.10) 90th 2.04) 1.11-4.33-3.91) 1. paralysis.38-3. gov/toxpro2.93 (2.04 (2.71) 1.800-1.97 (2.84) 3.730-1.2) 2.67 (3.15-10. weakness.89 (2. Additional information about external exposure (i. In large doses.790-1.640) < LOD < LOD 1.830-1. the detection of para-nitrophenol in a person’s urine may also reflect exposure to the environmental degradate.e. Zurich et al.67-2.00 (1.07 (1.17-4. accidental exposure. cholinergic effects. Lores et al.55 (<LOD-3.78-2.39 (1. teratogenic.59 (1.39) 1.9) 1.30) 3.930 (.1) 2..78 (2.440 (<LOD-.430 (.78-2.970 (.94-47.57-7.930 (. Slotkin et al.01 (2.310-. 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.25 (2. and other organophosphorus insecticides share a common mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system.09) 2. and unintentional acute or chronic high-level occupational exposure (Hill et al..80 (1. U.79 (1.35-3.91 (1.03) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .950) < LOD .44-3.08) < LOD .33-3.94-4. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Methyl Parathion.83 (1. Overt cholinergic toxicity and death from methyl and ethyl parathion have been described following suicidal ingestion.S.500) < LOD < LOD .05) 4.cdc. interval) Selected percentiles ( 95% confidence interval) Sample 95th 4.980 (.S.680 (<LOD-1.. 1991).00) 2.30-1.57-2. gov/pesticides/.720-1.epa. Karanth and Pope et al.13-12.92 (2. In addition to being a metabolite of methyl and ethyl parathion. 1995.23) 1.35-3.01 (.370 (<LOD-. population from the National Health and Nutrition Examination Survey..60) 2.89 (2.90 (1.. IARC does not consider ethyl parathion and methyl parathion classifiable as human carcinogens.60-2.96 (1. vomiting. and producing acute symptoms such as nausea.790-.690-1.96 (1.10 (1.21-21.88) 1. para-nitrophenol can also occur in the environment from the breakdown of the parent these organophosphorus pesticides and from nitrobenzene. paranitrophenol.850-1. 2005.98-7.55) 2. 1990. does not inhibit acetylcholinesterase enzymes. 2006.95) 1.08 (1.71 (1. The metabolite.56-2.15) 3.29) 1.530) < LOD < LOD < LOD . and other metabolites.540) < LOD .26 (1.76-14.87 (1.73 (1.940 (<LOD-1.11) 1.7) 3. Jaga and Dharmani.Organophosphorus Insecticides: Specific Metabolites Metabolites”).17) .80 (1. Methyl parathion is not considered genotoxic. EPA at: http://www.77-7.25) 1.23) size 1989 2476 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD 75th . but lists ethyl parathion as a possible human carcinogen. and seizures.82 (2.21) 1.97-10.400 (<LOD-.07) 2.33-6.13) 4.57) 6.00 (1.870) < LOD . 1978.16-4.97 (<LOD-4.720 (<LOD-. environmental levels) and health effects is available from ATSDR at: http://www.01-3.880 (. Human health effects from parathion or ethyl parathion at low environmental doses or at biomonitored levels from low environmental exposures are unknown.3) 2. At high animal doses of methyl parathion.45) 695 660 518 678 603 941 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.86 (2.31-3. or generally to have reproductive toxicity at doses below those causing acetylcholinesterase inhibition in most animal studies (IPCS.2) 2.78) 2.840 (. and Nitrobenzene Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.14-3. Orsorio et al.S. 2004).08-3. 2004).html and from U.06) 971 1164 1018 1312 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .EPA considers methyl parathion unlikely to be carcinogenic to humans. ethyl parathion.41-2..970 (. Parathion and methyl parathion have high acute toxicity in animal testing. 1995). Thus. 2006.

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. Barr DB.56(7):449553. Kramer RE. and levels were similar or slightly lower that those in a small convenience sample of the U. et al. In a study of workers who handle parathion.inchem.htm. Fourth National Report on Human Exposure to Environmental Chemicals 151 . Third National Report on Human Exposure to Environmental Chemicals. et al. Hill et al. Weltzien E. Hryhorczuk DO.. 2005. Gregg M. Giordano G. Barr DB. International Programme on Chemical Safety-INCHEM (IPCS).. 2002).. Griffith W. Kedan G. 2005. 1999). Barr DB. Arch Environ Contam Toxicol 1977. Role of individual susceptibility in risk assessment of pesticides. Bradman A. Alley CC. and many residents were symptomatic (Barr et al. Centers for Disease Control and Prevention (CDC). CDC. Toxicology 2005. DiPietro E. Curl CL. Rockhold RW. Available at URL: http:// www. Finding a measurable amount of para-nitrophenol in urine does not mean that the level will result in an adverse health effect.112(10):1116-1124. Guizzetti M. 4/7/09 Jaga K. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 2003) and in 482 pregnant females from an agricultural region of California (Eskenazi et al. Costa LG. J Expo Anal Environ Epidemiol 2005. 1995).. Baker SE...25(5):599-606. Bradway DE. Hill RH Jr. Cline RE. Environ Health Perspect 2004.15(2):164-171. Lin LI. Harley K. Karanth S. Kissel JC. Morgan DP. Environ Health Perspect 2002. Measurement of p-nitrophenol in the urine of residents whose homes were contaminated with methyl parathion. Occup Environ Med 1999.5 mg (500 µg)/g creatinine for workers at the end of shift. Bailey SL. Pope C.33(5):270-276. Moomey CM. Dharmani C. Ashley DL. et al. Effect of organophosphorus insecticides and their metabolites on astroglial cell proliferation. 2002.9:311-320. Leng G. end-of-shift urinary para-nitrophenol levels ranged from 190 to 410 µg/ gram of creatinine (Leng and Lewalter. 2005). Pesticide workers may have much higher levels following pesticide applications. References Barr DB. Baker S. Hetzler HL. Lores EM. Jewell NP. Shealy DB. Environ Health Perspect 2002. Atlanta (GA).org/documents/jmpr/jmpmono/v95pr14.110 Suppl 6:1085-1091. 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.21(1):5767. McClure PC.215(3):182-190. Wellman SE. Rev Environ Health 2006. Head SL.71:99108. McCann KG. ACGIH recommends a BEI of 0. oral or dermal administration. J Anal Toxicol 1990. et al. Neurotoxicol Teratol 2003. J Biomed Sci 2002. 2005).6(2-3):159-173. Baker RC. Hill RH Jr. Comparison of organophosphorus pesticide metabolite levels in single and multiple daily urine samples collected from preschool children in Washington State. Arch Environ Health 1978. Pesticide residues in urine of adults living in the United States: reference range concentrations. general population (CDC. population (Olsson et al. Turner WE. Eskenazi B. et al. Chicago area methyl parathion response. Methyl parathion: an organophosphate insecticide not quite forgotten. 2002.S.110 Suppl 6:1075-1078. Slach EF. Barr JR.Organophosphorus Insecticides: Specific Metabolites Biomonitoring Information Urinary levels of para-nitrophenol reflect recent exposure. Urinary excretion of paranitrophenol and alkyl phosphates following ingestion of methyl or ethyl parathion by human subjects. Pathak S. Runkle KD. Organophosphorus pesticide poisonings in humans: determination of residues and metabolites in tissues and urine. Needham LL.S.14(4):213-216. a range of values several hundred times higher than levels found in the U. McCann et al. Biomonitoring studies of para-nitrophenol can provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of parathion than are found in the general population. 2005. Clark JM. 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. Moseman RF. Lu C. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population. Environ Res 1995. Lewalter J. Laboratory investigation of a poisoning epidemic in Sierra Leone. Pharmacokinetics of methyl parathion: a comparison following single intravenous.. Age-related effects of chlorpyrifos and parathion on acetylcholine synthesis in rat striatum. Parathion-Methyl (addendum). 1995. Head SL. 2004). Rubin et al.

114(10):1542-1546. Assessment of human exposure and human health effects after indoor application of methyl parathion in Lorain County. Olsson AO.376(6):808-815.110 Suppl 6:1047-1051.S. Osorio AM. Pesticides in the Nation’s Streams and Ground Water. Seidler FJ. 1/12/07 U. 152 Fourth National Report on Human Exposure to Environmental Chemicals . September 2000. Am J Ind Med 1991. March 2006. Levin ED.pdf. External and internal exposure of wine growers spraying methyl parathion. Available at URL: http://www.S. 5/19/09 Zurich MG. Schilter B. Jung D. R. Environmental Protection Agency (U. Environmental Protection Agency (U. Geological Survey (USGS). Available at URL: http://www.epa. Honegger P. Rubin C. Rosenberg J. WHO/SDE/WSH/03. pdf. U.gov/circ/2005/1291/. Facts. Ames RG. Ryde IT.20(4):533-546.int/water_sanitation_health/dwq/chemicals/ methylparathion. EPA). Anal Bioanal Chem 2003.usgs.162(2-3):219-224.E.gov/oppsrrd1/REDs/factsheets/0155fct. 1/14/09 U.S. Barr DB. Environ Health Perspect 2002. Monnet-Tschudi F. Backer G.04/106. The Quality of Our Nation’s Waters. 1992-2001. 1995-1996.who. Esteban E. May 2003. Interim reregistration eligibility decision (IRED) for Methyl Parathion. Hill RH Jr. revised February 15. Involvement of glial cells in the neurotoxicity of parathion and chlorpyrifos.epa. gov/oppsrrd1/REDs/methylparathion_ired. Kieszak S. EPA). 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. Sadowski MA. Available at URL: http://www. Mengle DC. Slotkin TA. Hill G. Letzel S. 2004. Dunlop B. Available at URL: http://pubs. 0153. Costa LG. Tate CA. 6/1/09 World Health Organization (WHO). Methyl parathion in drinking water. Environ Health Perspect 2006. Nguyen JV.pdf.201(2):97-104. Case No. 2007 [online].S. Toxicol Lett 2006. Ohio.Organophosphorus Insecticides: Specific Metabolites Muttray A. Yacovac R. Ethyl parathion. et al.D. EPA-738-FOO-009. Toxicol Appl Pharmacol 2004.S. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine. Investigation of a fatality among parathion applicators in California.

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

410 (<LOD-1.210-.21) < LOD . population from the National Health and Nutrition Examination Survey.670 (<LOD-1.740 (.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 .880) 567 810 1104 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD . Survey Geometric mean (95% conf.820) < LOD < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.780 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th . which may vary for some chemicals by year and by individual sample.700-.850 (. < LOD means less than the limit of detection.2.430 (<LOD-.Organophosphorus Insecticides: Specific Metabolites Urinary 2-(Diethylamino)-6-methylpyrimidin-4-ol/one Metabolite of Pirimiphos-methyl Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.55) .94) .780 (<LOD-1.740-1.S. 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. 154 Fourth National Report on Human Exposure to Environmental Chemicals .17 (.580-1.840 (.840) 669 687 929 Limit of detection (LOD.31) .15) < LOD .S.210 (<LOD-.760 (<LOD-.27) . see Data Analysis section) for Survey year 01-02 is 0.460) 1165 1316 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . population from the National Health and Nutrition Examination Survey.08) 1165 1316 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .610 (<LOD-1.780 (<LOD-1. Survey Geometric mean (95% conf.300-1.07) .210-1.250 (<LOD-.680 (<LOD-.670) 567 810 1104 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD .500 (.770) size 2481 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD . interval) Selected percentiles ( 95% confidence interval) Sample 95th .200-.00) 669 687 929 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.780 (.700-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.950) < LOD < LOD 1.64) .470 (.

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

Soderlund et al. The table shows the urinary pyrethroid metabolites measured in this Report. Pyrethroid pesticides have low volatility. Unmetabolized pyrethroids have been measured in breast milk. but may be poorly transferred across the placenta (ATSDR. and synergists. Soderlund et al.2-Dichlorovinyl)-2.Pyrethroid Pesticides Pyrethroid Pesticides General Information Pyrethroid pesticides are synthetic analogues of pyrethrins.. 1997. and deltamethrin have been used frequently on cotton.S. 2007).S.. After absorption from inhalation or ingestion. Leng et al.2-dimethylcyclopropane carboxylic acid (55701-05-8 ) trans-3-(2. Pyrethroids are not well absorbed through the skin (ATSDR.S. Pyrethroid insecticides are the most common active ingredient in commercially available insect sprays and are also used as structural termiticides. In agriculture. Certain pyrethroid insecticides (such as permethrin. Dermal exposure with the potential for inadvertent ingestion may occur when lotions or shampoos are applied to treat lice or scabies. in some situations replacing the use of DDT. 1999. where these chemicals prolong sodium channel opening when a nerve cell is depolarized (Shafer et al.2-Dichlorovinyl)-2. cypermethrin. and greenhouses. pyrethroid pesticides have less acute toxicity in animals and people.2-dimethylcyclopropane carboxylic acid (55701-03-6) cis-3-(2. 2003.2-dimethylcyclopropane carboxylic acid 3-Phenoxybenzoic acid (3739-38-6) 156 Fourth National Report on Human Exposure to Environmental Chemicals . 2002). so usage is restricted near water (U. Outside the U. solvent oils.EPA. Pyrethroid pesticides are used to control a wide range of insects in public and commercial buildings. Pesticide applicators can be exposed to pyrethroid pesticides via dermal and inhalation routes from powders and liquid formulations. The general population may be exposed to pyrethroid insecticides primarily from the ingestion of food or from residential use. 1992). About two million pounds of permethrin and one million pounds of cypermethrin have been applied annually (U.. followed by conjugation. Compared with other classes of insecticides such as organochlorines. 2002... organophosphorus. agricultural fields. or carbamate pesticides. Human health effects from pyrethroid pesticides at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 2005. 2005). cyfluthrin. 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. and then eliminated over several days in urine and bile (Kuhn et al. 2003. such as piperonyl butoxide. Estimated intakes from diet and drinking water are below recommended limits. Adverse effects from large doses are related to the action of pyrethroids on the nervous system. Pyrethroid pesticides are generally formulated as complex mixtures of different chemical isomers. They are ranked as having moderate acute oral toxicity. Woollen et al. and are rarely detected in ground waters (USGS. 2006b). This class of pesticides has low toxicity in birds and mammals. deltamethrin has been used for indoor protection against mosquitoes that carry malaria. bind to soils. Woollen et al. they are not persistent in the environment due to their rapid degradation within days to several months. warehouses... and sumithrin) are also registered for use in mosquito-control programs in the United States. There are about 30 different pyrethroid pesticides in use.. pyrethroids are rapidly metabolized.2-Dibromovinyl)-2. by either ester hydrolysis or hydroxylation. EPA. They are also applied on livestock to control insects. Generally. 2002). 1992). Permethrin is also used in skin lotions and shampoos as medical treatments for lice and scabies. animal facilities. 2006a. which are natural chemicals found in chrysanthemum flowers. but pyrethroids are highly toxic to fish and some aquatic invertebrates. resmethrin. WHO.

35(2 Pt 1):227-237. Levsen K.50(2):245-255. Go V.gov/pesticides/ and from ATSDR at: http://www. Leng G.108(1):78-85. Shin JH. Moniz AC. Sunami O. 1999.1/15/09 Aziz MH. Kuhn K. Bull Environ Contam Toxicol 1999. 2005). Available from URL: http://www. et al.300(3):161-165.html. Pauluhn J. Human cases of systemic poisoning are rare and usually result from accidental exposure or intentional ingestion of pyrethroid insecticides. Kim et al. and striatal dopamine levels in male and female rats. 2005).. Ranft U. 2000. Zhao RC.gov/toxprofiles/ tp155. Fourth National Report on Human Exposure to Environmental Chemicals 157 . Berger-Preiss E. Ose K.atsdr. and permethrin) in the Hershberger and uterotrophic assays. The pyrethroids in general use are not considered teratogenic or to have significant reproductive toxicity (ATSDR. bioallethrin and deltamethrin. et al. Kim IY. Wang SL. J Reprod Dev 2004.cdc. dopaminergic. Yamada T. 2006. Transient dermal paresthesias have been reported among pesticide applicators after direct contact with certain types of pyrethroid pesticides. 2001. Leng A. Bernardi MM. Lewalter J. Environ Health Perspect 1999. Idel H.. [Effects of fenvalerate on reproductive and endocrine systems of male rats] Zhonghua Nan Ke Xue 2002. Effects of prenatal exposure to deltamethrin on forced swimming behavior.107(3):173-177. epa. and seizures (ATSDR. choreoathetosis. Pyrethroid pesticide-induced alterations in dopamine transporter function. cyfluthrin was the most frequent pyrethroid associated with symptomatic effects (irritant respiratory and dermal effects.23(6):665-673. Seth PK. neurochemical changes in cholinergic. Spinosa HS. Eriksson and Fredriksson. WHO. Toxicological profile for pyrethrins and pyrethroids. Pogo BG. Kim HS.. 2005). Garey J. Concomitant exposure to organophosphorus insecticides may increase pyrethroid toxicity by slowing metabolic clearance of the pyrethroid. McCarthy AR. Idel H... tremor. 2003. McCarthy et al. Toxicokinetics of pyrethroids in humans: consequences for biological monitoring. paresthesias) reported in agricultural workers from 1996 to 2002 (Spencer and O’Malley. 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.27(4):609-614.gov/toxpro2.atsdr.html.205(6):459-472. 2002. Ray et al. Kuhn KH. In developing rodents.. Lee SJ. Leng G. Signs and symptoms of acute pyrethroid poisoning after massive ingestions include agitation. Neurotoxicol Teratol 2005. Cruz-Casallas PE. hypersensitivity. 2002). 1991. Assessing estrogenic activity of pyrethroid insecticides using in vitro combination assays. Kunimatsu et al. 2002).S. Estrogenic and antiprogestagenic activities of pyrethroid insecticides. motor activity. 2003. Neurotoxic effects of two different pyrethroids. Song L. on immature and adult mice: changes in behavioral and muscarinic receptor variables.251(3):855-859. Xenobiotica 1997. Neurosci Lett 2001. In California. Okuno Y. Bernardi MM. Estrogenicity of pyrethroid insecticide metabolites. Abell AD.. Agrawal AK. 2001.Pyrethroid Pesticides and other ion channels may also explain some pyrethroid effects. Soderlund et al. Generally. Lazarini et al. Leng G. J Environ Monit 2006. Go et al. Hu JY. the pyrethroids are not considered genotoxic in in vitro testing or carcinogenic in animal testing (WHO. Hu et al. Toxicol Appl Pharmacol 2006. Human doseexcretion studies with the pyrethroid insecticide cyfluthrin: urinary metabolite profile following inhalation.8(1):18-21. Estrogenic potential of certain pyrethroid compounds in the MCF-7 human breast carcinoma cell line. Additional information about pesticides is available from U. Florio JC. Shukla Y. Neurodevelopmental consequences of gestational exposure (GD14-GD20) to low dose deltamethrin in rats. et al. Lemonica IP. Shaw IC. Yang J. Toxicol Appl Pharmacol 1991. salivation. Elwan MA. References Agency for Toxic Substances and Disease Registry (ATSDR). September 2003.27(12):1273-1283. Varoli FM. Wieseler B. Int J Hyg Environ Health 2002. Indoor pyrethroid exposure in homes with woollen textile floor coverings. IARC considers deltamethrin and permethrin as not classifiable as to their human carcinogenicity. Salzgeber SA.211(3):188-197.. Adhami VM. Thomson BM. Caudle WM. Lack of (anti-) androgenic or estrogenic effects of three pyrethroids (esfenvalerate. Miller GW. fenvalerate.62:101-108. 2005). Guillot TS. Kang IH. Kamita Y. Garey J.. Elwan et al. Lazarini CA. Wolff MS. Kunimatsu T. Behavioral and endocrine changes induced by perinatal fenvalerate exposure in female rats.. Moniz et al. Wolff MS. Garey and Wolff. 2004. 1998. Sugiri D. Regul Toxicol Pharmacol 2002. and catecholaminergic pathways and behavioral changes have been demonstrated at subacute and subchronic doses for some pyrethroid pesticides (Aziz et al. Neurotoxicol Teratol 2001. Richardson JR. 2003. EPA at: http://www. et al.. 2006). Eriksson P. Fredriksson A.8(1):197-202. Chen JH... 2006. 2003. Kim TS. though a few pyrethroid pesticides and some metabolites have shown weak or inconsistent estrogenic effects on standardized assays (ATSDR. Shafer. Biochem Biophys Res Commun 1998. cdc.

2007.gov/oppsrrd1/REDs/cypermethrin_red.10. Environ Health Perspect 2005. 5/26/09 U. Forshaw PJ. 5/26/09 U. Spencer J. J Toxicol Clin Toxicol 2000. and therapy. Available at URL: http://pubs.gov/oppsrrd1/REDs/ factsheets/permethrin_fs.htm. Mullin LS. et al. Toxicology 2002. March 2006. April 2002.186:57-72. pdf. 5/26/09 Woollen BH. Developmental neurotoxicity of pyrethroid insecticides: critical review and future research needs. Laird WJ.epa.S.epa. Sargent D. Lesser JE. sumithrin synthetic pyrethroids for mosquito control. The metabolism of cypermethrin in man: differences in urinary metabolite profiles following oral and dermal administration. Revised February 25. O’Malley M. 2005. Pesticide and Evaluation Scheme. Reregistration Eligibility Decision for Cypermethrin. Meyer DA. U. Available at URL: http://whqlibdoc. World Health Organization (WHO).who. Crofton KM.S.38:95-101. June 2006a. EPA). Permethrin.S.S. EPA).int/hq/2005/WHO_ CDS_WHOPES_GCDPP_2005. June 2006b. synergies.usgs. 1992–2001. Mechanisms of pyrethroid neurotoxicity: implications for cumulative risk assessment.epa. Environmental Protection Agency (U. 5/26/09 U. EPA). 5/26/09 158 Fourth National Report on Human Exposure to Environmental Chemicals .gov/ circ/2005/1291/. Clark JM. Piccirillo VJ. Pesticides in the Nation’s Streams and Ground Water. resmethrin. Shafer TJ. Sheets LP. Available at URL: http://www. Rev Environ Contam Toxicol 2006. Marsh JR. Available at URL: http://www. Permethrin Facts (Reregistration Eligibility Decision Fact Sheet).S.gov/pesticides/ health/mosquitoes/pyrethroids4mosquitoes. Available at URL: http://www. Pyrethroid insecticides: poisoning syndromes. 19962002.pdf.S.S.Pyrethroid Pesticides Ray DE. Environmental Protection Agency (U.171:3-59.22(8):983-991.113(2):123-136. Soderlund DM. Geological Survey (USGS). Safety of pyrethroids for public health use.htm. Xenobiotica 1992. Environmental Protection Agency (U. Pyrethroid illnesses in California.

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

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. < LOD means less than the limit of detection.2. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. population from the National Health and Nutrition Examination Survey. which may vary for some chemicals by year and by individual sample. 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. Survey Geometric mean (95% conf. 160 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.2 and 0.S.

S. * 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 . population from the National Health and Nutrition Examination Survey. 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.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. Survey Geometric mean (95% conf.

Berger-Preiss E. Bernard CE. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. 2005. Krieger RI. Williams RL.77(1):67-72. Heudorf U. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. Int J Hyg Environ Health 2006. Idel H. Olsson AO. Human exposure to indoor residential cyfluthrin residues during a structured activity program. Heudorf U. 162 Fourth National Report on Human Exposure to Environmental Chemicals . Third National Report on Human Exposure to Environmental Chemicals. Environ Health Perspect 2001. Angerer J. Kolossa-Gehring M. Hoppe HW. Spencer J. Sugiri D. O’Malley M.109(3):213-217.13(2):112-119.46(3):281-288. Ranft U. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Centers for Disease Control and Prevention (CDC). Angerer J. Butte W. Int Arch Occup Environ Health 2004. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine. Pyrethroid illnesses in California. Isotope dilution highperformance liquid chromatography-tandem mass spectrometry method for quantifying urinary metabolites of synthetic pyrethroid insecticides. Seiwert M.209(3):221-233. Angerer J. J Expo Anal Environ Epidemiol 2003. Int J Hyg Environ Health 2006. Drexler H. Atlanta (GA). Schulz C. Angerer J.209(3):293-299. Barr DB. Ball M. Int J Hyg Environ Health 2003.206(2):85-92. Rev Environ Contam Toxicol 2006. Heudorf U. Leng G.186:57-72. 19962002. Arch Environ Contam Toxicol 2004. Hadnagy W. Becker K.Pyrethroid Pesticides References Baker SE. et al.

The cis-isomer of permethrin has more potent insecticidal activity than transpermethrin.870) 1.420-.2-dichlorovinyl)-2.880 (.Pyrethroid Pesticides Cyfluthrin the cis-metabolite is found in the urine.202 (. Kuhn et al.580-1.200) .68359-37-5 Cypermethrin Permethrin CAS No.670-1. cis-permethrin.370-.150 (.300-.80) .460-1.28) 671 680 518 701 591 957 Limit of detection (LOD.790-1.21) .220-.500 (.630) .270-.54) .1.15) .380-.08) 947 1193 1004 1346 99-00 01-02 99-00 01-02 99-00 01-02 * * .200-.630) . cis-cypermethrin.640 (.610) . The chemical trans-3(2.600-1.680-3.570 (. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.710) . 1985.270 (.300-.730 (.900 (. which may vary for some chemicals by year and by individual sample. 1999).2-dichlorovinyl)2.2-dimethylcyclopropane carboxylic acid is a metabolite formed from cis-permethrin.200-.220-.510 (.730 (.140 (.580) 1.200) .1 and 0.340) .160 (<LOD-.300 (.460 (.850 (.490-1.2dichlorovinyl)-2. and ciscyfluthrin.110-. < LOD means less than the limit of detection.07 (.600 (.110-.43) .520) .2-dimethylcyclopropane carboxylic acid is a metabolite formed from trans-permethrin.920) 1..2-dichlorovinyl)-2.550) .52645-53-1 General Information Several pyrethroid pesticides are formulated as a mixture of cis.2-Dichlorovinyl)-2.340) .2-dimethylcyclopropane carboxylic acid that is formed in the environment from the degradation of these pesticides (George. but can also reflect exposure to trans-3(2. ciscypermethrin and cis-cyfluthrin. In the body. and trans-cyfluthrin.200) < LOD < LOD < LOD .120-.330 (.13 (.240) .600) . Survey Geometric mean (95% conf.910-5.670 (.790) .2-dimethylcyclopropane carboxylic acid formed in the environment from the degradation of these pesticides (George.110-.300 (.180) .380) .230) .210) .2dimethylcyclopropane carboxylic acid in urine not only reflects the metabolic transformation of any of the three pesticides.250 (.670-1.380-.2-dimethylcyclopropane carboxylic acid Metabolite of cis-Permethrin.270 (.120-.220) .340-.570-. trans-cypermethrin. 52315-07-8 CAS No.77 (.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 .68) .740-1.220-.410) . and cis-Cypermethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.400-.44 (.460-.630-.260 (.180 (.120-.2-dichlorovinyl)- CAS No. The presence of cis-3-(2.470-1.12 (.500 (.08) .120-.770) . 1999).270 (.170 (.310) .140 (<LOD-.and trans-isomers.or trans-3-(2.210-.700) . trans-permethrin.280-.50) .490-.2-dichlorovinyl)-2.960 (.220-. more of the trans-metabolite than Urinary cis-3-(2.890 (.780) .790 (.690) . 1985.350) .262) * * * < LOD < LOD .440 (.770-1.510 (.410) .250-. population from the National Health and Nutrition Examination Survey.380-. but it can also reflect exposure to cis-3-(2.110 (<LOD-.370 (.240) .155-..380 (. Generally.740-2.680 (.280 (. Fourth National Report on Human Exposure to Environmental Chemicals 163 .11) .630 (.890 (.710-1.610) .68) .510 (.740 (.53) .430-.490-.740) 1.790-1.950-2.160 (. Similarly.2-dimethylcyclopropane carboxylic acid in urine not only reflects the metabolic transformation of any of the three pesticides.32) .490-1.330) . interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.S.650-1.670-2.200 (.160 (.680) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .2dichlorovinyl)-2. transcypermethrin and trans-cyfluthrin.24) 1.730 (.530 (.820 (.47 (.470 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.200-. Kuhn et al.68 (.28) 468 580 667 831 816 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .210) 90th . Cyfluthrin.35) . the presence of trans-3-(2.35) 1. Biomonitoring Information Urinary levels of cis. cis-3-(2.

11) 947 1193 1004 1345 99-00 01-02 99-00 01-02 99-00 01-02 * * .390-.250-.400-1.250-.800 (. Lu et al.220 (.440-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 2001) showed urinary levels of cis. 2005).540) . 2001. 2002).67) . 2004). Studies in Germany of 396 children and adolescents (Becker et al.700) .270) .890) .2-dichlorovinyl)-2.250) 90th .750 (.690-1.450 (. 2005).680-1.37) .29 (.260 (.560) 1.120 (.250 (<LOD-.160 (<LOD-.182) * * * < LOD < LOD .180-.. 2006) and 1177 urban adults and children (Heudorf et al.260 (.640 (.430-.220 (.260-.590 (.380 (.150-. representative NHANES 2001-2002 subsample (CDC.300-.340) .11) .300) .920 (. 2006. 2002).33 (.750-1.200 (.2-dimethylcyclopropane carboxylic acid reflect recent exposure to either their parent pyrethroid pesticides or their environmental degradates.550-1.11) 1. 2005).600 (.12-2.11 (.370-. post- Urinary cis-3-(2. 2006.200) .14) 671 680 518 700 591 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.230-.280-.250) .430 (.59) .170 (.80) .540 (.2-dichlorovinyl)-2.370-.640-.450-. In a study of volunteers.340-.220) .150-.2-dichlorovinyl)-2.300 (.900 (.104-.180 (.2dichlorovinyl)-2.2dimethylcyclopropane carboxylic acids at the 95th percentile that were similar or slightly less than the 95th percentiles in the U.12 (.570) .260 (.550 (.2-Dichlorovinyl)-2.290) .230 (.59 (1.380) .320) .03) 1.2-dichlorovinyl)-2.680-1..270 (. median urinary levels of trans-3-(2.550) .270) .360-1.540 (.510-1.130-.420 (.190) ..2-dimethylcyclopropane carboxylic acid did not increase at 24-72 hours after exposure to nearby pest control operations (Leng et al.550-1.24) .500 (.470-1.640-1. 2003). Survey Geometric mean (95% conf.560) .290) ..710-3.03) 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 . Urinary levels of the two chemicals in adults were similar to those in children in these studies (Heudorf et al. and cis-Cypermethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.230-.. the levels at 24-72 hours were slightly less than the 95th percentile in the NHANES 2001-2002 subsample (CDC.700-2. 2005) In a small group of indoor pest-control operators.170) < LOD < LOD < LOD .230-.200-.840 (.11) .380-. Other studies have provided evidence that urinary levels of cis. Cyfluthrin.710 (.810 (.640-1. Estimated daily pyrethroid intakes based on urinary levels in the German children were below the acceptable daily tolerances (Heudorf et al. urinary trans-3-(2..890 (.31) . interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.080-..270-.840 (.250-.880) ..300 (.2-dimethylcyclopropane carboxylic acids in children were related to residential pesticide use and house dust levels (Becker et al.780 (.340) .300) .59) .700) .33) . 2006).390 (.Pyrethroid Pesticides 2.430-1.2-dimethylcyclopropane carboxylic acid levels at the 95th percentile were about one-third of the 95th percentile in the NHANES 20012002 subsample (CDC.450-1. 2003).680 (.240 (<LOD-. though the 95th percentile levels increased several fold after exposure to nearby pest control operations (Leng et al. urinary levels of cis-3-(2. In a study of urban residents in Germany (Berger-Preiss et al.440 (..250) .08) 468 580 667 830 816 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD . In these volunteers. 164 Fourth National Report on Human Exposure to Environmental Chemicals . These studies indicated that intake is mainly from the diet and that dermal absorption contributes little to intake (Heudorf et al.830) .2dichlorovinyl)-2.S.170 (. the levels at 24-72 hours were slightly less than the 95th percentile in the NHANES 2001-2002 subsample (CDC..190 (. In the same residents.260) . the median and 95th percentile of urinary levels of cis-3-(2.and trans-3(2.140-. 2006).S.580-1.780) 1.200-.640) 1.49) .550) .21) .350) .350 (.67 (.320-.2-dimethylcyclopropane carboxylic acid did not increase.440 (.290 (.2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of cis-Permethrin. population from the National Health and Nutrition Examination Survey. 2005).440-.410) .590) .400 (.390-.190) .2dimethylcyclopropane carboxylic acid at the 95th percentile were about half the 95th percentile in the NHANES 20012002 subsample (CDC.530 (. 2004.370-.280 (.290-. Schettgen et al.210-.580) ..520) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .150-.138 (.and trans-3-(2.530 (.

4.2-dichlorovinyl)-2. 2005).23) 2.2-dimethylcyclopropane carboxylic acid in urine does not mean that the level causes an adverse health effect. and trans-Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.840-1.39 (1.97-11.620) < LOD 2.77 (1.500 (.55-4.41-14.07 (1.520) .84 (1.820) .90) 1.700) .77) 1.730) .28 (2.760) .420 (<LOD-.85) 4.49-5. Survey Geometric mean (95% conf.35) 1.20 (.23 (.610) 1.43) 2.26 (.56 (1.810-1.17 (.95) 3.560 (.68) 2.91 (1.08) 1. < LOD means less than the limit of detection.S.01 (1. Urinary trans-3-(2.95) 2.87 (1.58) 961 1184 1015 1341 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .800-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.480-.77) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .68-3.69 (1.54 (1.55-5.470 (.710 (.410 (<LOD-.2-Dichlorovinyl)-2.400-.7) 2.19 (2.55-3.76-4.63) 1.22 (1.59 (1.460-. Fourth National Report on Human Exposure to Environmental Chemicals 165 .66) 478 576 675 826 823 1123 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .48) 4.42 (2.410 (<LOD-.25-3.460-.08-6.60-4.2-dimethylcyclopropane carboxylic acid Metabolite of Cyfluthrin.54) 4. population from the National Health and Nutrition Examination Survey.14-6.and trans-3-(2.500-.560 (.2dichlorovinyl)-2.07-3.750) .60) 1.2-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.11-1. Finding a measurable amount of cis.66) . interval) Selected percentiles ( 95% confidence interval) Sample 95th 3.19 (3.03-1.17-1.68) 1.850-1.63) 1.470 (<LOD-.17 (.20 (.42) 1.580 (.14-2.970 (.28 (1. however.69) 1.19) 1.940 (.10) 2. 2005).25 (1.660) 1.16) 1.or trans-3-(2.440 (<LOD-.77) 2.20 (.860) .39-5.08-4.680-1.01) 4.76-3.560 (.40 (1.Pyrethroid Pesticides application median urinary levels of summed cis.50 (1.11-2. 2003) were similar to the 95th percentiles for adults in the NHANES 2001-2002 subsample (CDC.670) .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 .49-3.5) 2. Biomonitoring studies on urinary levels of cisor trans-3-(2.68) 1. were up to 27 times higher than the 95th percentile for adults in the NHANES 2001-2002 subsample (CDC. which may vary for some chemicals by year and by individual sample.530) .910-1.570) 90th 1.49-3.2-dichlorovinyl)-2.03-1.41 (1.550 (.62 (1.81) 2.68-2.500) .56 (1.56) 2. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.37 (1.89 (2.830-1.910-1.12-6.780 (.09 (.27 (1.490 (<LOD-.520-.2-dimethylcyclopropane carboxylic acid (Hardt and Angerer.64-4.66) 691 680 518 690 595 954 Limit of detection (LOD.410-.56) 2. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.4 and 0.14) 1.94 (1.400 (<LOD-. The maximum post-application urinary levels.670) .920-1.410-. trans-Cypermethrin.490-1.60) .700-1.13) .

820-2.22-1.570-.02-1.65 (2.80) 1.07-3.2-Dichlorovinyl)-2.470 (.780 (<LOD-. trans-Cypermethrin.74) .56-5.760 (.15-3.880 (<LOD-1.660) .07-1.800-1.87) 1.470-.65) 1.42 (.91) 1.770) < LOD 2.16 (1.33-2.12-1.40-2.47 (1.07-2.11) .56 (1.610-.19) .87-8.00-5.37 (1.520 (<LOD-.87 (1.34-4.850) .47-2.35 (1.48 (1.26 (1.31 (.750) .39 (1.780) 90th 1.720-1.670) .880-1.640) .28) 2.88) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 1.55 (2.19 (1.15 (1.00 (1.89) 2.730) .540) .29) 1.15) 3.57) 3.930-1.850-3.11) 478 576 675 825 823 1123 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .570 (.530 (<LOD-.45-2.580 (.87-3.87) 1.47-2.91-11.970 (.42) 1.570 (<LOD-.60) 2.15) 2.60 (1.700 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.68) 3.86 (2.75 (1.70 (.850) 1.720 (<LOD-.61) 1.57 (1.33-1.36) 2.55 (2.36 (1.08 (.67 (2.07) 2.13) .15-3.22) 1.22-2.700-.44) 2.00) 5.27-2.440-.560 (.30-3.Pyrethroid Pesticides Urinary trans-3-(2.31) 1.20-2.27-2.45 (1.19) 961 1184 1015 1340 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .74) 2. and trans-Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.56-2.780) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.35) 1.12 (.480-. Survey Geometric mean (95% conf.00) 1.31 (2.10) size 1976 2524 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD 75th .800-1.13) 1.15-3.00) 1.08 (.39) 1.S.60) 2.98 (1.34-3.41) 1. population from the National Health and Nutrition Examination Survey.740) .11) 691 680 518 689 595 954 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.700 (.64 (1.720-1.81 (2.48-2. 166 Fourth National Report on Human Exposure to Environmental Chemicals .500-.580) .880 (.410-.33 (1.55 (2.3) 2.30-6.07) 2.20 (1.530 (.900 (<LOD-1.2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of Cyfluthrin.91 (1.

Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. Bull Environ Contam Toxicol 1999. Idel H. Schettgen T. Hoppe HW. Angerer J. Angerer J. Berger-Preiss E. Int J Hyg Environ Health 2003. Environ Health Perspect 2006. Pyrethroid exposure of the general population-is this due to diet? Toxicol Lett 2002. Int J Hyg Environ Health 2006. Levsen K. Sugiri D. Heudorf U. A longitudinal approach to assessing urban and suburban children’s exposure to pyrethroid pesticides. Environ Health Perspect 2001. Seiwert M. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides.114(9):14191423. Angerer J. J AOAC 1985. Int Arch Occup Environ Health 2003. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides. Atlanta (GA). Kuhn K. Leng G. Sugiri D. Wieseler B. Fourth National Report on Human Exposure to Environmental Chemicals 167 . Third National Report on Human Exposure to Environmental Chemicals. Int Arch Occup Environ Health 2004.62:101-108. Leng G. Butte W. et al. Drexler H. Angerer J. Hadnagy W. Ranft U. Bartell S. Indoor pyrethroid exposure in homes with woollen textile floor coverings.77(1):67-72. Heudorf U. Angerer J.76(7):492-498. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. Hardt J. Leng G.68(6):1160-1163. Pearson M. Drexler H. Ranft U. Permethrin and its two metabolite residues in seven agricultural crops. Berger-Preiss E.209(3):293-299.Pyrethroid Pesticides References Becker K. Heudorf U. Int J Hyg Environ Health 2002. Bravo R. Toxicokinetics of pyrethroids in humans: consequences for biological monitoring. Idel H.134(1-3):141-145. Lu C. Heudorf U. 2005. Idel H. Schulz C.109(3):213-217. Angerer J.206(2):85-92. Ball M. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine.205(6):459-472. Int J Hyg Environ Health 2006. Kolossa-Gehring M. George DA.209(3):221-233. Barr DB. Centers for Disease Control and Prevention (CDC). Biological monitoring of workers after the application of insecticidal pyrethroids.

2-dimethylcyclopropane carboxylic acid is a metabolite of the pyrethroid insecticide deltamethrin. Finding a measurable amount of cis-3-(2. urinary levels of cis-3-(2.2-dibromovinyl)2.5 μg/L) than the detection limit (0...Pyrethroid Pesticides Deltamethrin CAS No. 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.. 2004).39 µg/L. Deltamethrin can degrade to cis-3(2.2-dibromovinyl)-2. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.2-dibromovinyl)-2. Thus. Urinary levels for adults and children in these studies were similar (Heudorf et al. Studies in Germany of 396 children and adolescents (Becker et al.3-0.. Biomonitoring Information Urinary levels of cis-3-(2. 2006) and 1177 urban adults and children (Heudorf et al. The peak mean levels in these children were more than 800-fold higher than the detection limit in the 2001-2002 NHANES subsample. 2001. Following residential spraying with deltamethrin for malaria protection in Mexico.2-dibromovinyl)-2. 2001) showed that urinary levels of cis-3-(2. In an analysis of 217 urine specimens from a nonrandom sample of United States residents. Outside the U. 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..1 μg/L) for the NHANES 2001-2002 subsample (CDC. mean peak urinary levels of cis-3-(2.2-dibromovinyl)-2.2-dibromovinyl)-2. (2004) reported a geometric mean concentration of cis-3(2.2-dimethylcyclopropane carboxylic acid of 0. 2005).2-dibromovinyl)-2.S. 1990).2-dimethylcyclopropane carboxylic acid were below the limit of detection (CDC.2dimethylcyclopropane carboxylic acid reflect recent exposure to deltamethrin or its environmental degradate. In the NHANES 2001-2002 subsample.2dimethylcyclopropane carboxylic acid formed in the environment. 2005). Baker et al. 52918-63-5 General Information Cis-3-(2. 168 Fourth National Report on Human Exposure to Environmental Chemicals .. in some situations replacing the use of DDT.2-dimethylcyclopropane carboxylic acid at the 95th percentile ranged slightly higher (0.2-dibromovinyl)-2.2-dimethylcyclopropane carboxylic acid in the urine may reflect exposure to deltamethrin or to cis-3-(2.2-dimethylcyclopropane carboxylic acid in urine does not mean that the level will result in an adverse health effect. 2005). deltamethrin has been used against mosquitoes that carry malaria. in detection of cis-3-(2.2-dimethylcyclopropane carboxylic acid in children increased at least 450-fold relative to the non-detectable background levels for several days and mean levels remained slightly above background levels 45 days after the spraying (Ortiz-Perez et al.2-dibromovinyl)-2.2-dimethylcyclopropane carboxylic acid in the environment (IPCS.

population from the National Health and Nutrition Examination Survey.2-dimethylcyclopropane carboxylic acid Metabolite of Deltamethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. which may vary for some chemicals by year and by individual sample. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. < LOD means less than the limit of detection. Survey Geometric mean (95% conf.Pyrethroid Pesticides Urinary cis-3-(2.1 and 0.S.1. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1698 2539 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 415 580 570 831 713 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 818 1193 880 1346 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 578 680 445 701 527 957 Limit of detection (LOD.2-Dibromovinyl)-2. Fourth National Report on Human Exposure to Environmental Chemicals 169 .

* Not calculated: proportion of results below limit of detection was too high to provide a valid result. Survey Geometric mean (95% conf. 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. population from the National Health and Nutrition Examination Survey.S.2-Dibromovinyl)-2.2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of Deltamethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.Pyrethroid Pesticides Urinary cis-3-(2. 170 Fourth National Report on Human Exposure to Environmental Chemicals .

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

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

62) 5.69 (1.960 (.570-1.49-2.330) .610) .352-.53) 1.336 (.560-.38 (2.830) 90th 1.265-.406) .270) .210-.297 (.16-1.760 (.270 (.292 (.51-6.35) 2.38 (2.434) .50 (2.530-.16) 483 580 682 831 833 1128 99-00 01-02 99-00 01-02 .510-.43) 3.36) 1.340) .01 (1.62-6.13) .29-1.33) .510-.390) .25 (2.93 (1. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.230-.35) 1.26-2.420) .340) 75th .25 (2.89-71.32 (1.320) .590 (.78) 1.41) 3.49 (1.360) .75 (1.26) 2.233-.370) .42-2.590-.190-.226-.27-2.369) .700-1.27-2.750) .210-.200-.507 (.288 (. and Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.850) .300) .78) 6.34-6.63-3.670 (.35 (1.49 (1.52-5.55 (1.870 (.35 (2.387) .325 (.46) 2.34) 8.13 (. population from the National Health and Nutrition Examination Survey.246-.32 (2.780) 4.190-.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 .560-1.250 (.240 (.840-1.78 (1.277-.220-.750-1.750) .48-2.S.247-.73) 1.600 (.03 (3.30) 3.300 (.830-2.680 (.273 (.04) .230-.340) 1.41-3.315 (.190-.65 (1.92-3.292-.14-6.260 (.64) 697 680 524 701 603 957 Limit of detection (LOD.45-5.250 (.76 (1.314) .298 (.54) 1.160-.51-3.160-.417 (.16) 974 1193 1024 1346 99-00 01-02 99-00 01-02 99-00 01-02 .355) .32-21.570-.48-2.630) .200-.41-2.290 (.710 (.730 (.28) 1.800) 1.550-.227-.39) 2.1) 3.601) .238-.21 (2.30 (.373) .180-.595) .450 (.45 (2.320) .44) 5.8) 3.250 (.990) . Fourth National Report on Human Exposure to Environmental Chemicals 173 .83-11.260 (.314 (.260-.41 (1.640 (.428-.27-11.384) .65-2. interval) .940) 1.30 (1.560-.276-.470-.72 (1.440) .300 (.260 (.190-.490-.800 (.271-.26) 2.620-1.311 (.250-.230 (.18 (1.345) Selected percentiles ( 95% confidence interval) Sample 95th 4.200-.253-.430-.280 (.320 (.04-5.740 (.266-.23 (2.86 (1.230 (.1.25-1.650 (.700 (.328 (.350-.300 (.12 (.90) 1.295) .79) 3.267 (.520 (.374) 99-00 01-02 99-00 01-02 99-00 01-02 .320) .52-4.Pyrethroid Pesticides Urinary 3-Phenoxybenzoic acid Metabolite of Cypermethrin.81 (1.353 (.35) 2.330) .60) .1) 3.53-3.586) .240 (.810) 1. Deltamethrin.71 (1.05) 1.288-.427) .78) 1.02-6.12) 4.33 (1.33 (2.1) 3.12) .850) .16) 1.62-8.1 and 0.25-7.530-.25-4.362) .230-.05) .56-5.18 (2.320) .69) 3.710 (.430-.49-2.820) .63 (3.820) . Survey Geometric mean (95% conf.46) .34 (2.490) .454 (.364) .740 (.321 (.

35) 1.446) .320) .48) 697 680 524 700 603 957 174 Fourth National Report on Human Exposure to Environmental Chemicals .37 (1.490-.350) .91) .190-.17 (.330) .640 (.02 (2.677) .00) 1.440-.670) 3.41-4.43 (1.05-3.55 (1.290) .49) 3.309) .41) 1.261-.220-.365) 99-00 01-02 99-00 01-02 99-00 01-02 .52) 2.226-.44 (1.75-8.550 (.240-.580) .272 (.590) .230) .84 (1.11 (.329) .230-.550 (.280 (.09-2.250 (.21-4.19) 2.350 (.720) 90th 1.423 (.62) .91) 9.300-.510 (.534) .380 (.323 (.210-.229-.330) 75th .178-.227 (.275 (.02-1.860-1.730-1.173-.91 (2.300-.S.280-.362 (.330 (. Survey Geometric mean (95% conf.240-.81 (1.420-.580 (.278) .190-.210 (.312 (.387) .19 (2.224-.88-5.500) .510 (.760) .440-.272) .264 (.316 (.13 (.380-.92) 483 580 682 830 833 1128 99-00 01-02 99-00 01-02 .35-3.370-.17-1.540 (.67 (1.40 (1.750-1.590) .670) .440-.54 (1.72 (1.530-.280 (.240 (.730) .35) .40) 2.234 (.43-64.37) 1.810) 1.60) 1.240-.400) . and Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.372) .67) 1.270) .25) 2.63-3.04 (3.410-.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 .390-.321-.860 (.270-.630) .590) .240 (.03-1.270 (.67 (1.311 (.32 (2.560 (.07) 2.200-.274-.36 (1.91-4.49 (1.25-5.290) .73) 1.74) 3.225-.740) .55) 3.299-.Pyrethroid Pesticides Urinary 3-Phenoxybenzoic acid (creatinine corrected) Metabolite of Cypermethrin.570) .00) 1.44) 2.250) .450 (.401) .460-.15-2.610 (.261 (.200-.53 (1.49) 1.200-.36-6.160-.510 (.410) .27) 1.230-. interval) .437) .700-1.19) 974 1193 1024 1345 99-00 01-02 99-00 01-02 99-00 01-02 .400-.61-2.480-.550 (.280 (.640 (.246 (.304) Selected percentiles ( 95% confidence interval) Sample 95th 3.16-4.86 (1.19-6.00) 5.190 (.64-5.280) .240 (.216-.60-4.43 (2.210 (.530-.0) 3.238-.200-.590-1.328) .271-.03 (.49-2.335-.09-2.83) 1.290-.309 (.310) .04 (.480 (.35 (1.48 (1.80) 4.460-.270) .860-1.13-1.21 (1.330) . population from the National Health and Nutrition Examination Survey.62) 1.730) .329) .83 (1.930) 1.51-7.720 (.274 (.13-1.09) 3.39) 1.370 (.490 (.43) 1.95) 1.250 (.240 (.270 (.202-.63) 1.240-.22 (1.490 (.150-.280) .10 (2.930) .840-1.09 (.11 (.52 (1.330) 1.06-3.96 (1.650) .400-.253) .378 (.07-5.357) .960-1.90) 3.73-4. Deltamethrin.220 (.94 (1.25-2.

Int J Hyg Environ Health 2006. Becker K. Carranza C. Seiwert M. Barr DB.205(6):459-472. Isotope dilution highperformance liquid chromatography-tandem mass spectrometry method for quantifying urinary metabolites of synthetic pyrethroid insecticides. Environ Health Perspect 2005. Torres-Dosal A. Bravo R. Idel H. Lapinski R.Pyrethroid Pesticides References Baker SE. Deych E. Environ Health Perspect 2006. Lopez-Guzman OD. Hadnagy W. Environ Health Perspect 2003. Int J Hyg Environ Health 2002. Fourth National Report on Human Exposure to Environmental Chemicals 175 . Berkowitz GS. Batres LE. A longitudinal approach to assessing urban and suburban children’s exposure to pyrethroid pesticides. Sugiri D. Int J Hyg Environ Health 2003. Ranft U. Centers for Disease Control and Prevention (CDC). Arch Environ Contam Toxicol 2004. Idel H. 2005.111(1):79-84. et al. Obel J. Godbold J. Environmental health assessment of deltamethrin in a malarious area of Mexico: environmental persistence. Levsen K. Kolossa-Gehring M.113(6):782-786. urban cohort. Berger-Preiss E. Hardt J. Grimaldo M. Third National Report on Human Exposure to Environmental Chemicals. Ranft U. Angerer J. Int Arch Occup Environ Health 2003. and genotoxicity in exposed children.206(2):85-92. Berger-Preiss E. et al. Atlanta (GA). Ortiz-Perez MD. Lu C. Sugiri D.46(3):281-288. Exposure to indoor pesticides during pregnancy in a multiethnic. et al. Barr DB. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Ball M. Leng G.114(9):14191423. Leng G. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation.209(3):221-233. Pearson M. Indoor pyrethroid exposure in homes with woollen textile floor coverings. Biological monitoring of workers after the application of insecticidal pyrethroids. Hoppe HW. Bartell S. toxicokinetics. Angerer J. Olsson AO. Liu Z.76(7):492-498.

200-.130 (.130-.260-.340) .164-.260-.130) .230) . People are exposed to antimony primarily through food and.123 (.110-.350-.130-. 176 Fourth National Report on Human Exposure to Environmental Chemicals .119-.360-.390-.160) .200) .320) 787 683 618 554 667 723 768 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.330) .150-.176 (.150) 90th .135) * .410) .197) .330-.220) 95th .200 (.140) .120) . The absorption.160) .440 (.340 (.154-.300) .250-.120-.110) .120-.090 (.350-.200 (.240 (.200) .250-.390) .570) .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 .390-. Stibine is a metal hydride form of antimony used in the semiconductor industry.400 (.170 (.260 (.310-.169 (.210-.310 (.100 (.280 (.120 (.115-.128 (.114) .250 (.150 (.136-.490 (.290-.126 (.170 (.200) . 01-02.200 (.150-.260 (.280-.100-.099 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.140-.200-.142) * Sample size 2276 2690 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .430 (.140) .400 (.210) .400) .280) .120) .110-.260) .103) .240-.160) .270 (.070 (<LOD-.120) .156-. enamels.126-. see Data Analysis section) for Survey years 99-00.310) .270 (.190 (.260 (.100-.070-.260) .109-.120 (.260) .350-.190 (.330) .160-.230-.390) .190) .130-.160) .122 (.220-.150) .130 (.130-.280) .210) .410-.100 (.390 (.240 (.190-.220-.220 (.132 (.131-.270) . and glass.320-.080-.710) .120-.250) .230 (.240 (.310) .320-.S.290 (.154) .150 (.130 (.220) . population from the National Health and Nutrition Examination Survey.320 (.220-.144) .340 (.280) .160-.070 (<LOD-.04.180 (.170-.130 (.310 (.130-.093 (.230 (.280-. fireworks.098-.470) .160 (.128 (.110-.145 (.230 (.07.300-. 7440-36-0 General Information Antimony is found in ores or other minerals.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 .134-.100) .330 (.350 (.146 (. castings.470) .160-.130 (.120 (.120-.080) .180 (.190) .320) Total .230-.250-.210 (.160 (.230) .220 (.350 (.530) .280-.180 (.142 (.350) .330) .190-.180 (.470 (. 0.120-.490) .207) .Metals Antimony CAS No.350) .095 (.120-.330 (.120-.390) .130 (.310 (.108-.150) . respectively.300-. +3.210) .130) .190-.170-.108 (.117-.140 (.560) .360 (.170-.400-. and 03-04 are 0.088-.190 (.158 (.190-.150-.330 (.160) . which may vary for some chemicals by year and by individual sample.500) .134 (.280-.090-. and +5.157) .190) .200) .440) .110-.180 (.090 (<LOD-.190 (.300 (.090-.130-.180) .420) .170-.125 (. 0.270 (.400 (.600) .400) .170) . Antimony can exist in one of four valences in its various chemical and physical forms: -3.119) .320-.430 (.440) .190-.140 (.180-.250 (.360) .190 (.130-.240-.136) * .350 (.190) . to a lesser extent. solder.161) . distribution.180 (.210) .300 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.110 (.350 (.140 (.090) 75th .210 (.220) .320 (.280 (. often combined with oxygen to form antimony trioxide or with sulfur to form stibnite.112-.160 (.220-. ammunition.180) . Workplace exposures can occur at smelters.220-.137) .180-.290-.150) .360 (.150 (.240) .200-.140 (.080) .120) .160-.320-. and pewter.230) .140) .310 (.200 (.210) . coal-fired plants.120 (.320) . Dermal contact with soil.087-. metal bearings.410) .143 (.370-. Antimony enters the environment from natural sources and from its use in industry.120 (.240 (.230-.117-.270 (.460 (.137) .210-.200 (.154) .079-.220-.250 (.140) .178) .141-.460) .200 (. It is also used in paints. or other substances containing antimony is another means of exposure.180-.430 (.170-. < LOD means less than the limit of detection. and as a fire-retardant in textiles and plastics.350) .300) .04.360) . interval) .460 (.330-.500) .148-. and 0.190) .120-.300) .130 (. 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.150-.350 (.130) < LOD .390-.270) . ceramics.175 (.095-.400) .184) .115) . and refuse incinerators that process or release antimony.280) .350) . and excretion of antimony vary depending on its oxidation state.133) * . sheet and pipe metal.330) . from air and drinking water.230-.390) . water.120-.180-.160) .180-.105 (.300-. Two antimony compounds (sodium stibogluconate and antimony potassium tartrate) have been used as antiparasitic medications.220) .130) .145) Selected percentiles ( 95% confidence interval) 50th .150-.130 (.132 (. storage batteries.080 (<LOD-.230-.140) . It is used in metal alloys.510) .140) .240 (.460 (.270-.310-.200-.370) .250-.280-.

Survey years 99-00 01-02 03-04 Geometric mean (95% conf.298 (.281-.447 (. 1944).069-.171) .333-1.113-.167 (.117-.135) ..143) 90th .192-.256 (.352 (.163 (.098-.338 (.238) .400 (.208-.272) .238 (.250-.162-.209) .074 (.255-.207) .317) .167 (.160 (.170 (. 1958) and occupational exposures (Briegner et al.195-.115 (.315) .318-. and route of exposure (Elinder and Friberg.438) .082 (<LOD-.095-.150-.185 (.119 (.741) .114 (.Metals than for trivalent compounds (Elinder and Friberg.138-.181) .271-.152) .151) .161) .173 (.080 (<LOD-.250-. The toxicity of stibine after acute inhalational exposure is similar to that of arsine.116-.417) .115 (.405) .087) .096-.242-.175 (.300) .310) .300) .265-.257) .248) .099-.280 (.235-..188) .146-.148-.129 (.124 (.076-.385 (.128-.167-.115) .131 (.268) .250) .250 (.192 (.108-.213 (.195-.130 (.196 (.183) .200-.103-.152) .122 (. Inorganic antimony salts irritate the mucous membranes.164) .233-.120 (.286 (.269 (.122 (.143 (.127) .143) .112-..129 (. Human health effects from antimony at low environmental doses or at biomonitored levels from low environmental exposures are unknown.371 (.444) .181) .077) .310 (.164-.278 (. interval) .228-.320-.193) .125 (.727) .115-.373) .239-.173) .121) .082) .149-.126-.320 (.429 (.159-.123 (.267 (.138) * .076-.138-.084) .061-.137 (.203) .129) * .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.30) .100 (. Dysrhythmias and T-wave changes on electrocardiogram have also been noted after both therapeutic (Berman. skin.245) .140) .208 (. population from the National Health and Nutrition Examination Survey.209) .485) .276 (.236 (.238) .308) .095-.143) Selected percentiles ( 95% confidence interval) 50th .135) .113) .430) .140) < LOD .429) .225 (.136) .086) 75th .071-.144-.338) .135) .130) .106-.253-.135 (.130) .209 (.127 (.120 (.108-.126) .129) .220) .124) .112 (.230) 95th .195 (. 1953).178-.250-.147-.176 (.189 (.364 (.471 (.154-.338 (.112 (.333 (.167 (.107-.111 (.176 (.081 (<LOD-.203) .130) .200-.159-.127) .086 (.211) . An elimination half-life of approximately 95 hours has been estimated after occupational exposures (Kentner et al.267) .233 (.317) .192) .320 (.114 (.391) .132) .278) .107-.132 (.500) .118 (.146-.259 (.209-.741 (.471) .125-.480) .318-. abdominal pain.099-.068-.185 (.250 (.241-.217 (.081) .380 (.204-. Acute antimony poisoning may cause a metallic taste.109 (.228 (.263 (.111-.186) .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 .124-.187) .172-.228 (.069-.294) Total .078 (.173 (.181) .194-.119-.248-.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 .153-.115-.146-. 1973).391) .109-.131) .357) .444) .143) .247) .229-.233) .198) .121 (.159-. species.425) .085) . and gastrointestinal symptoms such as vomiting.148) * .068 (.117-.163 (.188-.193 (.226 (.176-.079 (<LOD-. and kidney have been demonstrated in high dose animal studies depending on the dose.126 (. 1962).121 (. Pulmonary edema may occur in severe cases of inhalation exposure (Cordasco et al.227-.102-.417) .313-.108-.182 (.117-.214) .102-.295 (.124-.352) .224 (.199-.280-.133) .139 (.200-.104-.108 (.123) .333-.244-.092-.222 (.080 (.150-.075 (.127) ..114 (.082) .191 (. 1986).098) .127) .300 (.092) .115 (.097-. 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.225) .253 (.106-.075 (.333 (.104-.200) .364 (.134) .149) .343 (.333 (.310) .153 (.131-..185-.178 (.147) .S.206-.261) . 1995).156-.308-. Ming-Hsin et al.103-.139 (.173-.333) 1132 1334 1281 1144 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .241-.145) .255) .333-.164 (.266 (.105-.118 (.109 (.148-. and eyes.267-. diarrhea. Histopathologic inflammatory and degenerative changes in the lung.288 (. resulting in hemolysis with abdominal and back pain (Dernehl et al.161) .421) .320-.263-.265 (.116 (.098-. 1988.179-.414) .107-.156 (.120 (.250-.089) .320) .321) . myocardium.120 (.333-. liver.138 (. 1954). * Not calculated: proportion of results below limit of detection was too high to provide a valid result.119-.135 (. Fourth National Report on Human Exposure to Environmental Chemicals 177 .113-.230-.146) .333) . 1986).277 (.205-.357-. Acute inhalation of antimony has been associated with irritation of the respiratory tract and impaired pulmonary function (Renes.317) . and ulcers (Werrin.

Several investigations of airborne antimony exposures in workers have found urinary levels that are many times higher than those seen in NHANES 1999-2000. Urinary antimony in infancy. Konings J. Bailly R. 20012002. Iavicoli I.. Chia-Yu H. Industrial Medicine and Surgery (Dec. Piatnek DA. Iavicoli et al. and 2003-2004.)1954. Liao Y-H et al. et al. Weltle D. 1991. 1994) have reported values slightly higher than those in this Report. arsenic. Industrial Medicine 1944. respectively. Sabbioni E. 2nd ed. Dezateux et al.51:238-240. Bolten C. Experimental and human studies on antimony metabolism: their relevance for the biological monitoring of workers exposed to inorganic antimony. and future strategies. Mahieu P. Elinder CG.. et al. Liao Y-H. gov/toxpro2. 1998). Sci Total Environ 1994.. clinical efficacy. Roland H. Chest 1973. Paschal et al.76:432436. Rev Infect Dis 1988.16: 33-39. Ludersdorf et al. Kiberd B.64(2):182-185. 1998. Lenert G. Skulsukai G.. Matthews T. Dernehl CU. Van der Venne MT. Biomonitoring of a worker population exposed to low antimony trioxide levels. Cordasco EM. Int Arch Occup Environ Health 1987. Sabbioni E. Yu H-S.10(3):560-586. 1986. 1987).. Human biomonitoring of arsenic and antimony in case of an elevated geogenic exposure. Stead FM. 26-42. Pozzoli L. Kentner M. Shao-Chi C. Industrial antimony poisoning. environmental levels) and health effects is available from ATSDR at: http://www. Element reference values in tissues from inhabitants of the European community. Luedersdorf R. HH.atsdr. and a drinking water standard has been established by the U.521-523.. 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.48:93-97. indium. Dezateux C. Stasney J. Costeloe K. Pulmonary edema of environmental origin. Kuo-Juie Y.html. Ju-Sun P. Pietra R. Information about external exposure (i. External and internal antimony exposure in starter battery production. Mechanism and treatment of cardiac arrhythmias in tartar emetic intoxication. Leinemann M. Stocks J. Buchet JP. Biological assessment of exposure to antimony and lead in the glass-producing industry.cdc. Finding a measurable amount of antimony in urine does not mean that the level of antimony causes an adverse health effect. Cheng-Wei L. Apostoli P. population. even when exposure levels were below workplace air standards (Bailly et al. et al. Carelli G. Mayer P. Br J Ind Med 1991. O’Regan M. 2002. Alimonti A. Biomonitoring Information Levels of urinary antimony reflect recent exposure. Cullen A.158:165-190. Wade A. 1998) or compiled reference ranges (Hamilton et al. and antimony in optoelectronic industry workers. Chemotherapy for leishmaniasis: Biochemical mechanisms. Urinary antimony was not associated with locally elevated soil levels in a study of more than 200 German residents (Gebel et al. J Occup Environ Med 2004.. pp. Chin Med J 1958. 1995. J Trace Elem Med Biol 2002. Pilgrim L. Gallorini M. Dunkelberg. Chen J-R. Environ Health Perspect 1998. Mayne P. Levels of urinary antimony in infants appeared to be similar to those reported by CDC (2005) for young children (Cullen et al. Vouk VB. 2004.59:469-474. Antimony trioxide is rated by IARC as a possible human carcinogen. Hamilton EI. Trace element reference values in tissues from inhabitants of the European community I. Earlier measurements in general populations (Minoia et al. Minoia C.. New York: Elsevier. Schaller KH. EPA. 2005. gallium.106:33-39. Petrucci F.. Nau CA. Yang C-Y. eds. Lauwerys R.67:119-123. which may be due to methodologic. Third National Report on Human Exposure to Environmental Chemicals.e. Stone FD. Centers for Disease Control and Prevention (CDC). Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Caroli S. 1990.S.76(2):103-115. Delves HT. Delves HT. Ming-Hsin H.. Gebel TW. 1997). Fuchs A. Arch Dis Child 1997. References Berman JD. Semisch CW. Suchenwirth R. Kentner et al. Biological monitoring of exposures to aluminum.46:931-936. A study of 46 elements 178 Fourth National Report on Human Exposure to Environmental Chemicals . Atlanta (GA). Friberg L. Antimony in blood and urine of infants... In: Friberg L. Briegner H. Ho C-K. Arsine.Metals to antimony have been established by OSHA and ACGIH. Wu M-T. Review of elements in blood.13:361-362. Handbook on the toxicology of metals. and hydrogen sulfide. stibine. Int Arch Occup Environ Health 1995. Schacke G. J Clin Pathol 1998. Antimony. Nordberg GF. or exposure differences. VI. plasma and urine and a critical evaluation of reference values for the United Kingdom population.

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

8) 34. it is found in over 200 crystalline or mineral forms.8-61.13-8.19-9. and monosodium methyl arsenate were used as pesticides but contemporary uses are restricted. to a lesser extent.50 (8. Water sources contain mostly inorganic arsenate.2 (12.55 (7.2) 15.90 (7.S.80-9.5 (40.4 (26. Arsine (AsH3) is a reactive. 180 Fourth National Report on Human Exposure to Environmental Chemicals .3-19.Metals Arsenic CAS No. arsenocholine. Arsenic and its compounds have had many uses in the past and present as medicines. Arsenic trioxide is approved to treat acute promyelocytic leukemia.70-9. or rarely as elemental metalloids (yellow. black.4 (31.6 (32. grain.5) 41.34-9.5) 95th 65.6 (13. lead hydrogen arsenate.7) 65.7) 90th 37. Arsenic can combine with such non-carbon chemicals as sulfur and oxygen to form arsenides.4 (48.77) 6.90-14.10 (6. population from the National Health and Nutrition Examination Survey.00 (6.4 (24. In nature. trimethylarsine oxide. and foods. CCA-treated wood has been restricted since 2003 and no longer can be used in residential applications such as decks.74. Various arsenic compounds were used in paint pigments and for tanning animal hides.0 (22. 7440-38-2 General Information Arsenic is an element that is widely distributed in the earth’s surface in small amounts. and play sets.12 (6.20 (8.7 (11. Gallium. though in some locations arsenite may be prevalent (WHO.97) 8.5-178) 46.2-20.9 (8.6 (15. such as arsenopyrite (FeAsS) and realgar (As4S4).8-77.90 (5.84) 8.10) 10.8 (48.2-61.6) 11. arsenites. were used as treatments for syphilis. In the last century.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 7.80) 6. 2001).30) 17. Also.9) 68. and produce. cancers. arsenic as elemental metalloids may be used in some ammunition. Before the 20th century.27) 9.4) 40.3-111) 78.1) 7. and gray forms). to a lesser extent.90 (7.1) 1281 1276 03-04 03-04 03-04 9.1-40. semiconductors.9-62.2) 46. and as homicidal poisons. and arsenosugars.6-43.90-8.08 (5.41 (7. Survey years 03-04 Geometric mean (95% conf. retaining walls.5-52.8) 7. +3 and +5).4 (7.29 (8. as alloy in metal bearings. and as a cosmetic to lighten complexion.70) 8.8) 33. The United States no longer produces arsenic from mining but imports about 22. Arsenic can also combine with organic substances in nature to form such organic arsenic compounds as arsenobetaine.34-10.10-7.90) 75th 16.4) 13. arsenic compounds.30 (6.02-8. Various forms of inorganic arsenic can occur in groundwater from natural sources or as a result of soil application or industrial waste. pesticides.0 (11.7-83.6) 618 722 1074 Limit of detection (LOD.1) 15. and.57) Selected percentiles ( 95% confidence interval) 50th 7. General population exposure to inorganic arsenic can occur through consumption of drinking water and.1 (38. a trivalent compound known as white arsenic) is a common natural and commercial form that can be released into the air during volcanic action. copper arsenates. Although it is still widely used in the United States.0 (43. lead. meats.5) 66.7) 24. ocean and fresh waters.12-10.80 (5. interval) 8. and other metals.5 (23.70 (6.1) 290 725 1542 03-04 03-04 9.0 (14.3) 10. mental disorders.2-17.25-9.1-18.9) 21.5-19.90-11. see Data Analysis section) for Survey year 03-04 is 0.9-34.2 (41.0-19.66-8. chromated copper arsenate (CCA) has been used to treat outdoor timbers and pressure-treated woods to prevent wood rot. solders. Arsenic trioxide (As2O3.0-60.5-41.2 (13.8) 7. Arsenic is measurable in most soils. and in lead-acid storage battery grids.6 (9. alloys.2 (51. psoriasis.90) 16. Groundwater Urinary Total Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.5 (34. gaseous hydride manufactured in small quantities for use in the semiconductor industry. aluminum.50-14. Roxarsone and other organic arsenicals are anticoccidial agents added to poultry feed. from coal burning.30 (7.40) 7. referred to as inorganic arsenic compounds.0 (15. 2005).8) 17.4-65.90-7.2-93.8) 29.9-46. particularly arsenic trioxide. sodium arsenite.5 (14. cacodylic acid. mostly for use in wood preservation (ATSDR.6-35. and arsenates (oxidation states of -3.9 (17.000 metric tons annually.4) 60.84) 8.3-15.7-95.00-9.5) 43. and indium arsenides are used in the semiconductor industry.1 (32.90-8.8) 30. the smelting of copper. Since the 1940s.5 (36.6-141) 53.10-10.

2007.9) 13.47 (6.59) Selected percentiles ( 95% confidence interval) 50th 7.3-41.8 (12.9) 618 722 1074 Fourth National Report on Human Exposure to Environmental Chemicals 181 .8-75. Chowdhury et al.8 (21. trimethylarsine oxide (TMAO).12-10. 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.47-6. arsenocholine.g.0-26.40) 8.. Ingestion of arsenosugars in kelp and algae can also lead to the excretion of DMA.8-32.4 (11. mine tailings). 2001). Smoking tobacco is also a source of inorganic arsenic.41) 6.20-9.10-16. TMAO is also formed in the environment from microbiological action and is a metabolite of arsenic in certain mammals. population from the National Health and Nutrition Examination Survey.61 (7.1) 6.4 (12.4 (26. WHO. 2007. 2001.. 2001).7 (25.88 (5. but is poorly absorbed dermally (WHO.0) 33.3-53.9 (45. Smelter workers can have significant inhalational exposures to airborne arsenic trioxide for which air standards have been established.0-38.44-11.76 (6.31 (6. 2001).33-10. 2003.7 (11.04) 7. Tseng. selenium.7-18. gallium arsenide and indium arsenide. EPA.8 (27. and arsenosugars.8 (20.38-10.3-62.8-62..6 (10. After absorption.25 (6.30-9.64 (7.51) 75th 14. Inorganic arsenic is well absorbed from the gastrointestinal tract and absorbed to a lesser degree through inhalation. 2006.3-64. with trivalent inorganic arsenic (arsenite) being more toxic than pentavalent inorganic arsenic (arsenate) (NRC. and folate status (Chen et al. NRC.04 (5.1 (11.2) 90th 30.00 (6. and contact with CCA-preserved wood structures.8 (11.93-8.0) 26. Fish. 1988). Gamble et al.3) 6.1) 24.S.0) 1281 1276 03-04 03-04 03-04 8. 2007. dose level.2 (12.2-15.5) 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 8.5) 17.81-9.0) 12. WHO.2) 15. 2001).58-10.88) 7.28-7. Survey years 03-04 Geometric mean (95% conf. In aquatic sediments.6-17. and some other seafood can contain organic forms of arsenic including arsenobetaine.0-69.2) 40.33 (6.47 (7.66 (7.1) 8. 2001).6) 45.01) 7. 2001).24 (7. dust.0 (17.6 (17. Some studies suggest that variation in the degree of methylation among persons is related to the susceptibility of arsenicinduced disease and may involve consideration of genetic polymorphisms.3 (27.4) 32. Inorganic arsenic and its metabolites have elimination half-lives of approximately 2–4 days (Lauwerys and Hoet.S.06 (4. Direct exposure to DMA and MMA may result from use of the two pesticides. 2001). In aquatic organisms.4) 54.32 (5.9) 53.4 (42.93-9.1) 7. kelp.07-9. These organic forms of arsenic from seafood are absorbed and quickly excreted in the urine (WHO.1) 58.7) 28.6 (35.5-17.11 (5. shellfish. organic arsenic can be converted back to methylated and inorganic arsenic.7) 95th 50. Steinmaus et al. interval) 8.13) 8.25-9.Metals sources of drinking water often have measurable arsenic and several regions of the United States have naturally higher arsenic levels than the U.4-64. as observed in Bangladesh where millions of people have been exposed.S.18 (5.1 (14.50 (6.7 (9. inorganic arsenic is widely distributed within the body.7-17.23-7.7-188) 27. Children may have additional exposures from ingestion of contaminated soils (e.8) 27. 2001. arsenic does not show biomagnification in the food chain (WHO.10-8.1-36. have caused clinical arsenic poisoning.35) 7.9-56.0) 42. Though modest bioconcentration occurs in some aquatic life.66-8.0 (31.2-46.01) 11.0-18. U.0) 14. Inorganic forms of arsenic demonstrate high acute toxicity.7-35. Arsenate is reduced in the body to arsenite (oxidation state +3).. age.75 (5.5) 290 725 1542 03-04 03-04 8.75) 13. arsenocholine is converted to arsenobetaine and also to small amounts of TMAO (Christakopoulos et al.45) 5.99-9. The semiconductor dopants.5-120) 40.5 (9. are used in enclosed ultraclean operations within the semiconductor industry.. though some reduction may occur in the gut prior to absorption.86-17.44) 6.66-8.8) 22. EPA’s maximum contaminant level (Hughes.7-34. Extremely high groundwater arsenic levels. 2006.3) 9.3 (24.96) 12.4 (40. so exposure to the general population is extremely limited.. 2001).4 (24. cacodylic acid and monosodium methyl arsenate. Arsenite is then oxidatively methylated to the monomethylarsonic acid (MMA) and dimethylarsinic acid (DMA) with subsequent excretion primarily in the urine (NRC.

S.50) 1. including drinking water sources with elevated arsenic levels (e...30) 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1.20 (<LOD-1. food residue. Acute unintentional inhalation of arsine gas can produce hemolysis of red blood cells. and diarrhea. apoptosis. Survey years 03-04 Geometric mean (95% conf. U.10 (<LOD-1.80) 1. increased oxidative stress.20 (<LOD-1. arsenic trioxide) includes hemorrhagic gastritis with nausea.. 2006) or when exposure occurs in smokers (Chen et al. and altered gene expression. it may have its own separate toxic action by substituting for phosphate in glycolysis and other pathways. vomiting.Metals +3) shows greater toxicity than arsenite itself (Aposhian et al. Cardiac arrhythmias.10 (<LOD-1.60) 1. and childhood neurodevelopmental effects in observational human studies. Bangladesh. Chronic elevated arsenic intakes have been associated with diabetes. Taiwan. and production of glutathione may be affected as well. drinking water have not been associated with increased cancer rates (Schoen et al. Arsenic has many actions demonstrated in cellular studies..10 (<LOD-1. 2000. 1998. 2001. WHO.S. including inhibition of numerous enzymes. peripheral vascular disease. 2001.10 (<LOD-1. With chronic exposure. and bladder cancer (IARC. Chile). Chronic arsenic exposure in humans is considered to be a cause of skin.g. which may vary for some chemicals by year and by individual sample. Such actions may lead to decreased energy production. Although arsenate is reduced in the body to arsenite.50) 2568 95th 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1. hypertension. 2001). Acutely.. and hyperpigmentation of the skin (NRC.. which can lead to dehydration and shock. cell transformations. Raml et al. arsenite will inhibit cellular pyruvate dehydrogenase by binding to the sulfhydryl groups of dihydrolipoamide.. NRC. Acute toxicity resulting from the ingestion of large amounts of trivalent arsenic (e. and endothelial injury (Kumagai and Sumi.30) 1.50) 621 725 1078 Limit of detection (LOD.60) 1. 2004).50) 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD 1.S. NRC. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Studies of arsenic at levels typical of U. 2001).S. 2007).EPA has established drinking water. and by uncoupling oxidative phosphorylation (NRC.. WHO. substitution in phosphate metabolism. some of these effects may take years to develop. The U.. noncirrhotic portal hypertension. and DNA repair inhibition (Cohen et al. cytotoxicity. leading to a decrease in adenosine triphosphate energy production. renal failure. 2001). gluconeogenesis.. 2001). interference in signal transduction pathways. respectively. Bredfeldt et al. can cause peripheral sensorimotor neuropathies. 2006. see Data Analysis section) for Survey year 03-04 is 1.0. Laboratory studies using inorganic arsenic have shown chromosomal aberrations. lung. and it also will inhibit succinate dehydrogenase. 2004). 2006. 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. hyperkeratosis. and peripheral neuropathy may also occur with large doses or after surviving an acute overdose. Cellular glucose uptake.. 2004. 2007. 2006) and newly discovered thioarsenic metabolites may also be as toxic (Naranmandura et al. < LOD means less than the limit of detection. Chronic human intake of arsenic at less than acutely toxic doses. WHO. 2007. hepatotoxicity. hematocytopenias. 2001). OSHA and ACGIH have established workplace standards and guidelines for arsenic exposure and monitoring.20 (<LOD-1. 2001). 182 Fourth National Report on Human Exposure to Environmental Chemicals . Cohen et al.10 (<LOD-1.. fatty acid oxidation. 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. population from the National Health and Nutrition Examination Survey. WHO. 2006. The organic forms of arsenic occurring in seafood have little known toxicity.g.EPA.20 (<LOD-1. The risk of lung cancer appears more pronounced when large environmental exposures start in childhood (Smith et al. but additional or confirmatory research is needed (Kapaj et al.

cdc. Meza et al. Levels of total urinary arsenic in the U. 2000)..html.50) 1. 2006).S. hand washings from children playing on CCA-treated wood compared to children playing on non-CCA-treated wood playground equipment were slightly to fivefold higher (Kwon et al. population from the National Health and Nutrition Examination Survey. 2001). and the FDA has established a bottled drinking water standard.33 (<LOD-3. 2006. population (Rubin et al. higher mean or median total urinary arsenic levels have been reported among people living in specific western areas of North America (Calderon et al.. 2008.. IARC and NTP recognize inorganic arsenic and arsenic compounds as human carcinogens. In the German Environmental Survey III of 1998. though air levels of arsenic fume and dust are correlated with urinary arsenic levels at higher occupational inhalational exposures (Jakubowski et al. 1998. 2006).19) 3. In a Nevada town where groundwater levels were naturally elevated. WHO. Shalat et al. 2004. 1992... 2003. 2004. 2006). 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..S. Caldwell et al. Caldwell et al. Pellizzari and Clayton 2006). Survey years 03-04 Geometric mean (95% conf.18) 3. arsenic has been fetotoxic and teratogenic. 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. environmental levels) and health effects is available from ATSDR at: http://www. 1999. 2008). 2005) and Urinary Arsenic (V) Acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. Pellizzari and Clayton.41) 3. Consequently.61 (<LOD-3.69 (<LOD-3..95) 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. DMA produced bladder cancer in some chronic rat studies (Cohen et al.33 (<LOD-3. Shalat et al. Josyula 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.. Pellizzari and Clayton. Fourth National Report on Human Exposure to Environmental Chemicals 183 ..00) 1. gov/toxpro2. but generally only at maternally toxic doses (WHO.. median urinary total arsenic levels in 4052 adults varied with seafood intake.89) 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2.18 (<LOD-3.75 (<LOD-2.S. Calderon et al.. Biomonitoring Information Urinary arsenic levels reflect recent exposures and are moderately to highly correlated with arsenic intakes from drinking water and dietary sources (Ahsan et al. 2006..S. urinary arsenic levels have been accepted as a good biomarker of dose (WHO. Valenzuela et al.75 (<LOD-2.Metals compounds. In animal studies.. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.04 (<LOD-3. 2001). the median total urinary arsenic in about 200 people was approximately four times higher than that of the U. Compared with this Report. 2007. and were about two-fold lower than those for the U. Vahter et al. Offergelt et al.. 2000. 2001). Daily variation in creatinine-corrected urinary arsenic is relatively small when intake is constant (Calderon et al. 2006).. 2006. had decreased since the prior 1990– 1992 survey.80 (<LOD-4.70) 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD 2. 2007.... 1986). 2008). 1999. although urinary arsenic levels were not associated with CCA contact (Shalat et al.50) 2568 95th 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2. Additional information about external exposure (i. population in NHANES 2003–2004 (Schulz et al.atsdr. Though CCA-treated wood contains several thousand times more arsenic than untreated wood. 1999).. 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.e..

dermal keratosis. 2008. 2008. and TMAO.55 (1.20 (2.50) .700-1.30 (1. The higher percentiles of total urinary arsenic levels in the U. 2000.6 (25. 1. 1985.S.7 (13.70-21.800 (.68) .5) 292 728 1548 03-04 03-04 1. In most human studies.3-39.30 (2.S.80 (3. see Data Analysis section) for Survey year 03-04 is 0..8-50.00-12..70 (3. < LOD means less than the limit of detection.7 (21..4 (16.. Caldwell et al.10) 8.20-25. After recent seafood ingestion. Caldwell et al. 4. For residents of Inner Mongolia.0 (26.6) 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.S. and peripheral neuropathy) have been associated with urinary levels as low as 50–100 μg/L in chronically exposed populations (ACGIH.2-35. 2005.3 (9. 2000.30) 10.40-6.43-1.S. arsenobetaine. Sun et al. 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. vasospasm.5) 29. Pellizzari and Clayton.3% of a representative sample of the U.00) 3.20-190) 31... 2007).45 (1.1-51.900-1..17-1...40) 5.871-1.7) 13.80 (4. and two methylated metabolic products. when seafood organic arsenic is subtracted).74 (1.800) 1. as evidenced by trace or nondetectable levels of arsenobetaine and arsenocholine in the urine.66 (1. In the late 1980s. population showed a higher contribution of arsenobetaine (Caldwell et al. Caceres et al.28) 1.6. 2007) with higher levels of arsenic in the drinking water. WHO.1) 18.80-5.90-7.8) 35. population (Sun et al.500-1. and TMAO were detected in only 7.4-35. a control population of 696 Tacoma residents had median urinary DMA levels similar to those for NHANES 2003–2004 (Kalman et al. 2000.800-1. geometric mean levels were about 70-fold higher than for the U.83) Selected percentiles ( 95% confidence interval) 50th 1.4) 31.80 (. 2003). arsenocholine.600 (.37 (1. 2006).1-25. median levels of urinary DMA were about 40-fold higher than the adult median reported in NHANES 2003– 2004. arsenite. 184 Fourth National Report on Human Exposure to Environmental Chemicals .62) 2.00-4. 2008)...00-6. Detectable levels of MMA reported in NHANES 2003–2004 were found only at the upper percentiles and.50) 90th 16. 2001). interval) 1.29 (1.6.8 (12. respectively.6-44. Survey years 03-04 Geometric mean (95% conf. Urinary Arsenobetaine Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.. Measurable organic arsenic species in this Report are three biologically generated environmental forms.93) 1. 2005.20-3. 2005. and arsenobetaine being the main contributors to the total urinary arsenic levels (Caldwell et al. Some noncancer effects of arsenic (e.1) 45. population (Ahsan et al. Arsenate. Total arsenic measured in the urine includes all species of inorganic and organic arsenic.00-1..0) 4. 2008).5) 621 725 1078 Limit of detection (LOD. arsenocholine..6 (13.10) 4..70) 6. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Great Lakes region residents had median urinary DMA levels that were slightly less than median levels in NHANES 2003-2004 (Caldwell et al. population from the National Health and Nutrition Examination Survey.g. which may vary for some chemicals by year and by individual sample. 2008). in NHEXAS 1995–1996.6 (11.90-29.9-23.20) 7.0 (27.20 (.8 (17. DMA has been the predominant metabolite composing the majority of measurable inorganic-related arsenic in the urine (i.3) 95th 35.400-.900 (.8-40. 2008).3) 1284 1284 03-04 03-04 03-04 1. and urinary DMA represented about 67% of the total urinary arsenic (Hopenhayn-Rich et al.5 (14.e.S. population in the NHANES 2003–2004 subsample.0-23..31-1.20 (1. Levels of DMA and MMA increase in approximate proportion to the intake of inorganic arsenic.3 (21.40) 75th 5.3) 35. Caldwell et al.50-6.4.80) 1. Also.9) 13. In the residents of a Chilean town who consumed water with high levels of arsenic. and other factors such as nutrition..40-7.50) .7) 15. When seafood intake is avoided.70-21. MMA. DMA and MMA compose most (about 75%) of the total arsenic species measured in urine. DMA and MMA.05) < LOD .11-1.00 (1.70 (5. Blom et al. Tseng et al. arsenobetaine and arsenocholine will greatly increase the level of total urinary arsenic and comprise the highest percentage of the total urinary arsenic level. China.9 (6.700-1.5 (26.800-4.800 (.60) 1.7-22. and duration of exposure are also considered important.4) 23.19 (. Aposhian et al. with DMA.8. Individually measurable species resulting from inorganic arsenic exposure are arsenate.20) 18. and 0. methylation capacity.5) 32.48-2.0) 29.1-94. 1996.20) 3.30) 2.. Valenzuela et al. arsenite. 1990. Chowdhury et al.60-3..20 (4. These associations are stronger at higher urinary levels.Metals other areas of the world (Ahsan et al.9 (7.10 (4.00 (.2 (6. 2001..2-38.

2006. Information about the biological exposure indices is provided here for comparison.901-2.786-1. population for the sum of inorganic related species was 18.79 (1.4-82.36) 2.70) 5.81 (4.6-32. Caldwell et al.43) 75th 5.25-7.65 (1.3 (10.0) 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.78 (3.15-1.91 (4. interval) 1. Survey years 03-04 Geometric mean (95% conf.62-6. 1992.51-2.7) 17.93 (1.1 (26.2 (13.29 (4.32-7.S.833-1. 2008).531 (.. Vahter et al.21) 5.3 (10.05 (. 1998.76-27.877 (.1-36.2 (12.909-1.47 (2. Biomonitoring studies of urinary arsenic can provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of arsenic than are found in the general population.9-18.51) 5.18-1. 2001).5 (18.30-1.7) 30.7) 9.6 (9.37-2.68 (1.3-24.9 (13.43) 14.959-1.6-46.80-153) 17. 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. Finding a measurable amount of arsenic in urine does not mean that the level of arsenic causes an adverse health effect.3) 1284 1284 03-04 03-04 03-04 1.0-36. population from the National Health and Nutrition Examination Survey. WHO..83) 2. 2001).5) 17.67) 1.00 (3.91) 90th 16.6 (6.47 (1.16 (. Sun et al.11 (. Urinary Arsenobetaine (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.2 (4.638) 1.4 (24.4) 13. 1986.5-20.6-29.9 (25. In recent years.25 (.5) 26.54 (1. 2007).19-2.14 (1.4 (11.4) 292 728 1548 03-04 03-04 1.55) 1. these levels were much lower than those found in other studies where environmental exposures were highly elevated (Chowdhury et al..78-5.72) 12.88) 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.10 (.40) 1.938-1. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.5 (18.82) 4..88 (5..00 (1. 2008).39-3.29-14.8) 29..4-21.82) Selected percentiles ( 95% confidence interval) 50th 1.4) 32.3) 95th 29.612-1. The 95th percentile of the U.45) 1. occupational monitoring and research studies have focused on the sum of inorganic-related species (arsenate + arsenite + DMA + MMA) as a measure of inorganic arsenic intake. Offergelt et al.2 (12.28) 1.15-4.80) .1-18. Timber treatment workers had median urinary DMA levels that were about 15-fold higher than the general adult median levels reported in NHANES 2003–2004 (Morton et al.9) 32.73-6.Metals as with DMA.83) 8.13-39.44 (1.53 (. Fourth National Report on Human Exposure to Environmental Chemicals 185 . not to imply a safety level for general population exposure.400-.40 (1.58 (3.61-6.4-28. The American Conference of Governmental Industrial Hygienists (ACGIH) provides an occupational biologic effect index (BEI) for urinary inorganic arsenic plus metabolites equal to 35 μg/L (ACGIH..6) 19.4) 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 * * 1.0 (9. 2003.30) 1.12) < LOD .50-7.1) 26.67) 4.S.9 μg/L. which is below the ACGIH BEI (Caldwell et al..50-15.15-1.05) 1.9) 14.64-29.

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

08 (<LOD-4. * 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. see Data Analysis section) for Survey year 03-04 is 1.80) < LOD 621 725 1078 Limit of detection (LOD.00 (<LOD-3. Survey years 03-04 Geometric mean (95% conf.76) < LOD 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 3.44) 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 < LOD 90th < LOD 95th < LOD Sample size 2568 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1.29) < LOD 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.70) < LOD 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2. population from the National Health and Nutrition Examination Survey.40 (<LOD-1.Metals Urinary Arsenous (III) Acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.00 (<LOD-2.2.S. which may vary for some chemicals by year and by individual sample.00) 1. < LOD means less than the limit of detection. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th < LOD 90th < LOD 95th < LOD Sample size 2568 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1.S. Survey years 03-04 Geometric mean (95% conf.95 (<LOD-2. Urinary Arsenous (III) Acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.20 (<LOD-1. Fourth National Report on Human Exposure to Environmental Chemicals 187 .

73) 6.00 (6.7) 12.65-8.1-22.6) 1284 1284 03-04 03-04 03-04 4. Urinary Dimethylarsinic Acid (creatinine corrected) Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.0) 9.0) 13.92) 3.9) 11.08 (2.00-13.00-12.0 (11.0) 16.90 (3.0 (10.18 (6.00-7.61-16.90) 5.0 (12.3 (8.00) 4.33-4.30) 3.20-4.00-8.00 (5.00) 6.45) 8.00-7.7) 1284 1284 03-04 03-04 03-04 4.0 (9.0-18.14) 3.72 (4.61-11.16-11.81 (5.00 (5.37 (3.0-19.00-4.8) 7.16 (4.00-15.44 (2.6) 292 728 1548 03-04 03-04 3.82-5.00-4.00 (3.00-4.70-12.0 (9.00-3.71 (3.38 (3.95-3.94-3.70-3.9) 5.9) 12.06) 5.48 (2.44) 5.00) 6.84-8.82-9.34) 3.0-12.50 (4.3 (7.71) 3. population from the National Health and Nutrition Examination Survey.0 (8.S.00 (5.52) 3.86-7.65-6.89 (3.00 (6.03 (3.27-5.00-11.95-4.16 (2.00 (4.78 (4.0-16.6-18.0 (10.00) 4.S.24-4.97-3.32 (8.50-15.00 (5.74) 90th 9.90) 2.0-17.45 (8.0-16. Survey years 03-04 Geometric mean (95% conf.12-4.77 (3.60-4.9) 13.0 (9.0) 16.27 (2.42) 3.00) 3.78) 4.7-16.1 (8.69-6.4 (7.7 (10.27-2.00-11.0) 17.00-22.00-4.12 (3.00-5.69-3.46 (4.80-3.8) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites Sample size 2568 03-04 03-04 03-04 3.34 (3.30 (7.39-3.00-4.5) 95th 13.05) 5.00 (7.45) 3.14) Selected percentiles ( 95% confidence interval) 50th 3.00-10.0) 95th 16.74 (2.00) 5.34-4.80) 7.0 (14.7.28) 2.00-4.73 (3.00 (3.0 (10.10) 6.32 (4.5) 12.1-15.80 (4.09 (7.29-4.32-10.17-6.86 (2.31-4.00-15.11 (3.20) 11.85 (3.Metals Urinary Dimethylarsinic Acid Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.0) 292 728 1548 03-04 03-04 4.05) 10.60-7.0 (12.34 (3.00) 75th 6.80-6.4) 621 725 1078 188 Fourth National Report on Human Exposure to Environmental Chemicals .0) 12.71 (4.00) 90th 11.67) 9.00-9.0) 11.70) 5.0) 17.0) 14.00 (3. see Data Analysis section) for Survey year 03-04 is 1.5 (11. population from the National Health and Nutrition Examination Survey.92-12.25 (4.49) 10.00) 12.00) 6.57 (3.00 (3.00) 6.84-18.00-7.00-15.00) 9.59 (6.82) 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 4.49-4.60-3.00 (7. interval) 3.67) 8.00 (6.80-5.00 (3.20-12.00-11.94) 3.55 (2.24) 3.71-4.70-4.86-21.33) 3.0) 9.9 (7.0) 9.0 (10.0 (13.69 (3.0 (13.0-25.13-4.79 (3.0) 10. Survey years 03-04 Geometric mean (95% conf.0-17.37 (2.11) 4.50-5.9 (11.70 (3.0) 13.31) 4.00 (3.00) 3.34-4.88 (4.00-3.48 (3.69 (3.3 (8.57-5.95-6.62) 4.00-7.98) 4.05) 3.2) 10.6 (9.22) 4.91) 75th 5.19) Selected percentiles ( 95% confidence interval) 50th 3.8) 7.60-6.10) 3.15) 4.7) 13.80) 2.95 (4.00) 7.27 (3.0) 621 725 1078 Limit of detection (LOD. interval) 3.0) 11.03-6.0 (8.17-4.1-18.00-12.00 (5.17 (2.

50) 621 725 1077 Limit of detection (LOD.22) 3.20 (1. Survey years 03-04 Geometric mean (95% conf.30-1.00 (2.10 (.80) 1.30 (1.40) 1.00-1.30-1.71-2.54) 90th 2.33 (1.50 (<LOD-1. see Data Analysis section) for Survey year 03-04 is 0.70-2.816 (<LOD-.90 (1.30 (1.75) 621 725 1077 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.9.15-1.853-1.86 (2.Metals Urinary Monomethylarsonic Acid Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.90) 2.70-2.60-2.53 (1.45) 3.90) 1.40-3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.70-3.34) 2.30) 2.53-2.80-2.80) 1.00 (<LOD-1.16 (2.50) 1.40) 2.63 (<LOD-1.20 (1.10) 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.30) 1.40 (1.80-2.10 (1.10-3.80 (1.985) 1.28 (1.88 (1.53) 292 728 1547 03-04 03-04 * * < LOD < LOD 1.77) 1.79) 2.40-3. population from the National Health and Nutrition Examination Survey.60) 1283 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.S.85) 1.80 (1.58) 2. Survey years 03-04 Geometric mean (95% conf.90 (2.40 (2.10-1.84-3.82-2.80) Sample size 2567 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.60) 292 728 1547 03-04 03-04 * * < LOD < LOD 1.88 (1.10 (<LOD-1.36) 1.85) 2.46 (1.80 (1.00-4.82-2.50 (1.30 (1.35-3.31 (1.60) 1.33 (1. population from the National Health and Nutrition Examination Survey.11-1.28 (1.30) 90th 1.50 (2.17) 2.93) .00 (1.50-2.50 (1.900-1.46-2.30) 1.20 (1.07 (1.40-2.00) 2.00) 1.20-1.20-3.86 (2.18-1.00) 1.60 (2.96-2.10 (.80 (2.90) 2.88-2.57) 95th 2. which may vary for some chemicals by year and by individual sample.00-2.10-1.07-3.31-3.43-3.07) 2.81) 1.62) 2.10) 95th 2.23) 1.20 (1.70-2.05-1.80 (1.61-3.00-2.52 (2.37 (1.60) 2. Fourth National Report on Human Exposure to Environmental Chemicals 189 .40) 1.61) 2.73-2.53) 1283 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD 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.30-2. 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 1.40-2.86) 3. < LOD means less than the limit of detection.00) 1.36 (1.20) 2.60 (1.70-2.20 (1.00) 2.70) 2.22 (1.00 (<LOD-1.53) Sample size 2567 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.00-1.30 (2. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th 1.14-1.S.18-1.20 (1.60) 2.86) 2.10 (1.00 (2.

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

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41-3.00) 6.60) 3.78) 1.75) 2.01 (4.50-1.80-7.22-1.50-6.15 (2.50 (4.78-2.65) 3. see Data Analysis section) for Survey years 99-00.19) 2.38) 2.91) 2.24-1.80) 7.47-1.95 (4.70) 5.30) 2.40 (5.56 (1.56 (1.60-2.46-1. fireworks.51 (1.12 (2.27) 2.69 (1. 0.70) 4.59) 3.27 (1.37 (4.15) 5.30 (5.87-14.10) 5.52 (1.28-1. depilatories.50 (5. Barium salts have also been available as rodenticides.8) 9.25 (1.55-7.98) 1.10 (4.63) Total 1.40 (4.73) 3.91 (2.51) 7.43) 6.87-9.76 (3.87 (6.61 (5.93-8.18-1.53) 692 683 618 540 667 723 765 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.61 (2.99-5.86 (4.67) 6.62 (1.15-11. and ceramics.40 (5.20-5.20-1.15-1.86 (4.72) 75th 3.54) 1.40 (1. Certain foods.12.76-3.47-1.50 (1.37) 5.21-2.40) 3.30 (5. such as brazil nuts.48 (6.19-1.20-6.71 (2.87-3.35 (2.70) 7. interval) 1.10) 3.15 (1.12) 7.30-2.50-1.4) 7.39 (1.41) 1.76-2.35 (3.50) 2.70-3.50 (2.71) 2.30) 8.00) 1.64) Sample size 2180 2690 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 2.65-1.00) 1.49 (1.54) 2.09 (1.20-8.72) 4.50 (6. rubber.49-1.05-2. water.53-5.S.8) 5. Urinary Barium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.65) 1.62 (1.70-2.99 (4.40 (1.50) 4.86) 6. Workers employed by industries that make or use barium compounds can be exposed to barium dust.61 (1.43 (5.90) 2.g.65) 1.60) 1. bricks. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.1) 9. respectively.05% of the earth’s crust.50 (4.56) 1.12) 6. barium sulfate and barium carbonate). and 0.70-2.08 (6.60-6.14-6.10-5.43 (1.61 (3.41-1.15-1. and food.68 (1.32) 8.80) 1.20-1. Small amounts of barium can be released into the air during mining and other industrial processes.61 (1.36) 5.64 (1.93 (4.77 (3.21 (1.31.62) 1.80) 6.20 (1.56 (2. such as barium chloride.37-1.90 (4.34 (1. 2001).20-8.00-76.76-7.08-8.46) 1.66) Selected percentiles ( 95% confidence interval) 50th 1.21-8. 7440-39-3 Medically.46) 1.30-2.36 (1.49) 8.25-1.63 (8.4) 6.85) 1.88) 4.50 (1.29) 5.60 (2.45 (1.12.12-1. tiles.42 (1.11-1.60 (1.00-8.43 (1.86-4.10) 1083 1335 1281 1097 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.63 (5.07 (2.04-6.80-3.88) 1.11 (2.47) 4.63 (2.26) 5.80 (1.45) 7.00) 4. barium sulfate is used as a contrast medium for taking radiographs of the gastrointestinal tract.57) 3.50) 2.30 (1.30-3.26) 2.78) 1.30-1.00 (2.82) 1.60-3.65 (5.35 (1.80-2.80 (1.25-11.80 (2.36-1.54-1.82-6.39-1.22-1.70-5.87) 7. glass.00-3.36-1.4) 9.14 (6.12 (2. soluble forms of barium.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 1.56) 4.88 (5.50) 1.61-8.49) 2.59-11.00 (1. and 03-04 are 0.91) 6.51) 2.20-8. Barium compounds are also used commercially in paint.30) 4.20 (4.76) 1.30) 3.11 (3.54 (6.16 (1.17-1.71) 1.82) 2.74-2.64-3.54) 1.44-5.48) 1..04-2.84) 5.60) 1.33 (1.62) 1.85) 1.18) 3.29-5.37-8. 01-02.06-1.74) 3.65-8.40) 7.34) 2. In single dose animal studies.54-1.77) 1.34 (2.50 (1.60-6.70) 1.50-6.73) 1. Barium compounds are used by the oil and gas industries to make drilling muds.95-6.20-1. were relatively well absorbed following inhalation (60-80% of a dose) or ingestion (11-32 % of a dose).54-8.94-6.48) 1.26-1.71) 95th 6.55-3. whereas others are practically insoluble (e.73-5.29-1.78-3.35) 5.38) 8.73 (5.43) 2.40 (5.66 (4. In nature.30 (3.01-7.56 (6.39) 1.90) 4.10 (2.32-1.50 (3.70) 1.9) 5.60-10.74-3.80 (1.20 (3.31 (2.50 (4.38 (1.30) 5.53) 2.77-3.63) 1.40-13.35-1.26-7.63 (1.18 (6.50 (1.50 (1.49) 11.90) 2.85 (2.92) 2.71-9.70) 3.53) 1.81-2.39) 4.09 (2.52 (4. The general population can be exposed to low amounts of barium in air.63) 1.93-2.57 (5.24 (4.28) 90th 5.90 (1.60) 4.44 (1.48-4.80 (5.39 (1.90-9.35-1.86-5.Metals Barium CAS No.73 (6.40 (1.11 (3.57-7.54 (2.70 (1.24-1.51) 1.75-3.10-4.38 (1.16) 5.80-5.70 (5.32-7.27 (1. it combines with other chemicals such as sulfur or carbon and oxygen.30) 5.14-1.8 (6.35-4.21 (1.81-2.30 (2.2) 6.02 (7.90 (6. population from the National Health and Nutrition Examination Survey.88) 7.90-2.30) 5.36 (4.97 (1.22) 6.06-2.65-5.90-13.10 (3.81-3.37) 1.40) 7.49-9.30-5.72) 1.34 (1.31-2.30-1. Ingested soluble barium General Information Elemental barium is a silver-white metal which comprises approximately 0.44-2.96-2.87 (5.49) 4. Some barium salts are freely soluble in water.03 (1.15 (6. Fourth National Report on Human Exposure to Environmental Chemicals 193 .48-4.20-1.90) 1.70-8.80 (2. are high in barium (Genter.87-7.20) 2.70-6.

chemical form.10-1. 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.52) 7.10 (6.40-1.76 (4.58-6.05-1.45-8.29-3.00-1.84-2.29 (3.46-22.76 (2.33) 6.0) 5.38-7.04) 1.31-1.36 (5.59) 2.45-1.48-1.98 (2.77) 1.28) 5..32 (1.34-3.39 (2.89) 90th 4.83) 2.47) 10.30) 2. Wones et al.04 (2.52-4.26-1.24 (5.881 (.76) 2.96-6.02) . 1986).62) 2.58 (2.84 (3.62 (1.26-1.41 (2.60 (2.04) 5.02) 4.23-2.5) 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 1.56) Selected percentiles ( 95% confidence interval) 50th 1. 1984.38 (1.40 (1.25 (1. Following intravenous injection in animals.84-5.00 (3. The health effects of exposure to barium compounds depend on the dose.99 (4.38) 4.51) 4.44 (1.58) 75th 2.70) 1. 1989).S.75-22.55-5.10) 6.2) 6.62 (2.77) 1.72) 4.92) 2.53 (2.90-2. Human health effects from barium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.29-4. about 75 % of a dose of soluble barium was eliminated within 3 days (Reeves.48 (1.30 (1.37) 2.22-1.49-1.777-1.28-1.82) 1.97-3.3 (6.56 (1.31) 5.38) 1.23-5.29-4.02 (3.52-10. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.50) 2.34) 1.00) 4.51 (1.58) 1.51) 6.46) 1.8) 4.38 (4.96) 4. 1994.22-4.64 (1.24-1.72 (2. diarrhea.40 (1.65 (2.703-1.63) 1.75) 2.96 (4.49-1..79-5. a benign condition that may occur among barite ore miners.55 (1.34 (1.38-5. 1985.31-1.24-11.97 (4.91 (3.75) 1.76-3.44-2.37-1.55 (5.27) 692 682 618 540 667 723 765 1132 1074 Non-Hispanic blacks Non-Hispanic whites 194 Fourth National Report on Human Exposure to Environmental Chemicals .85-5.57) 2.70) 10.19-2.73) 2. 1990).33-1.25) 4. in urine.73-2.45 (3.48-3.13-2.86) 5.38 (1.10-2.97) 1.69-9.91-2.10) 3.20) 4.27 (2.47) 4.11-2.24 (3.26-1.39-5.03) 1.69 (5.00 (3.00) 6.41 (1.47 (5.29-7.4) 5.23-1.78 (2.48 (1.67-6.81-7.74 (5.33 (1. Chronic high doses in animals resulted in kidney damage (McCauley et al.27-3.16 (1.77) 1.43-6.80) 3.03) 3.26) 4.33 (5.13-3.47 (2.37 (1.891 (.38 (4.01) 1.55 (4.57 (6.48-5.80-6.41) 5.68 (2.86 (2.16) 11.49 (1.58) 4.53-21.35-1.24-6. hypertension.06) .52) 1.59 (1.37-2.64 (1.34-5.09) 6.54 (2.36-1.31 (4.70) 4.66 (1. 2001).50) 1.68 (3.77-5.02-5.51 (1.56-3.00 (2.39-10.84) 2.56 (1.97 (5. such as those used in medical radiographic procedures.41) 4.33 (1.24-6.28-11.03) 2.20-8. NTP.18 (1.06) 2.88 (2.34-1.26-1. Symptoms following acute high dose include perioral paresthesias.32 (2.77) Total 1.92 (4.55 (1. and route of exposure.89 (2.0) 6.51) 4.18 (1.86-7.01 (5.74) 1.26-4.68 (3.32 (1.71 (5.45 (1.64) 7.25-11.79) 1. Toxicity from soluble barium salts is rare.35-3.36 (1. Urinary Barium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.73-4.50 (4.00 (5.19-1.31-1.963 (. but can occur after intentional or accidental ingestion of barium carbonate in rodenticides (Genter.28-7.47) 1. population from the National Health and Nutrition Examination Survey.91) 2.39) 4.20-2.49-1.76) 1.56) 4.15-4.55) .27-1.62 (4.36 (3.61) 2. weakness.0) 7. Barium blocks cellular efflux of potassium resulting in profound hypokalemia.37 (1.921 (.710-1.57-5.52) 2.39-1.16-1.53) .68) 1.19-1.64) 7.54) 2.47-8.50) 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 1.68-3.72) 6.81-6.76) 2.47) 1.32) 2.60 (5.64 (1.38) 1.754-1. Chronic accumulation of inhaled barium dust in the lung tissue may cause baritosis.28-6.48) 2.76 (3.39 (2.41 (1.64 (1.11) . and cardiac dysrhythmias.00-7.32) 2.39 (3.832-1.42) 1.08-2.20-1.54 (1.75) 1.00) 1.42) 1.44-2.96 (4.35-1.24-3.905 (.51 (3.28 (1.20 (1.4 (5.39 (2.45) 95th 6.55-6. Perry et al.68) 3.01 (4.58 (4.91 (3.60 (1.21 (1.60 (1.80) 4.915 (.87) 1.48 (1.2) 5.96) 7. paralysis.Metals was eliminated primarily in feces and to a lesser extent.51-3.30 (1.52 (3.88 (6.61 (4.36-2.40 (1.96) 4.63-4.00) 4.24) 3.24-1.36 (1. vomiting.33-4.43) 1.46) 3.96) 4.59) 1.59) 1.08-1.880-1..29) 1.74) 1.59-7.12) 2. interval) 1.81-6.68-3.97-4.2 (3.46 (2.57-10.29-1.65 (5.99) 1.39-1.11) .36 (3.42 (4.31 (1. Insoluble barium salts.59 (1.83) 3.29 (1.60 (2.45-6.19-1.60) Sample size 2180 2689 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 2.50) 1.03-1.22-1.27) 7.77) 5.3) 6.22-2.33) 1.49 (1.82) 1.45-1.99 (2.75-3.36-1. Barium is not rated for human carcinogenicity.38-1.14-2.45) 1.03-1.54) 1.75) 2. are not absorbed when administered.46) 2. water solubility.57-7.

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

Beryllium compounds are commercially mined. 0. In studies of laboratory animals. A half-life of 450 Urinary Beryllium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. soil. which may vary for some chemicals by year and by individual sample.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 . 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 . 01-02. or drinking water containing the metal. eating food. < LOD means less than the limit of detection.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. In medicine. nuclear. population from the National Health and Nutrition Examination Survey. near some hazardous waste sites.140 (<LOD-. less than one percent of the inhaled dose was slowly absorbed into the blood and eventually incorporated into the skeleton.130 (<LOD-. inhaled insoluble beryllium sulfate was retained in the lungs and nearby lymph nodes. are mined for commercial recovery of beryllium. beryllium is used in instruments. respectively. Burning coal and oil can produce small amounts of beryllium dust that can be released into the air. Beryllium is also used in the production of sports equipment such as golf clubs and bike frames.13.130 (<LOD-. 196 Fourth National Report on Human Exposure to Environmental Chemicals . and can be found in mineral rocks.13. and refined beryllium is used in mirrors and special metal alloys for the automobile. x-ray machines. Exposure to beryllium occurs mostly in the workplace. computer. and machine-parts industries. and from breathing tobacco smoke. 7440-41-7 General Information Pure beryllium is a hard gray metal. aircraft. and dental bridges.13.160) < 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. Two types of minerals. and 0.S. and volcanic dust. and 03-04 are 0.Metals Beryllium CAS No. see Data Analysis section) for Survey years 99-00. coal. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. the lightest of all metals. electrical. bertrandite and beryl. Low-level beryllium exposure in the general population can occur through breathing air.

EPA. Air levels greater than 100 µg/m3 can result in erythema and edema of the lung mucosa.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 . Human health effects from beryllium at low environmental doses or at biomonitored levels from low environmental exposures are unknown. is a granulomatous interstitial lung disease that is caused by chronic beryllium inhalation and the resultant immunologic response. Maier. IARC has classified beryllium as a human carcinogen. and drinking water and environmental standards have been established by U.346 (<LOD-. including contact dermatitis and subcutaneous nodules. or berylliosis. Fourth National Report on Human Exposure to Environmental Chemicals 197 . Genetic factors modify individual sensitivity to beryllium and susceptibility to developing chronic beryllium disease (McCanlies et al. The effects of occupational exposure to beryllium depend on the concentration of beryllium in the inhaled air and the duration of air exposure.281 (<LOD-. Skin exposure can result in delayed hypersensitivity reactions. 1990). NTP considers beryllium to be a known human carcinogen. 2002). 2003. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. 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 . population from the National Health and Nutrition Examination Survey. Workplace air standards and guidelines for external exposure have been established by OSHA and ACGIH.Metals days has been calculated for beryllium elimination from the human skeleton (IPCS. Chronic beryllium disease. 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.231 (<LOD-. S.S. based upon excess lung and central nervous system cancers in studies of workers.333) < LOD < LOD < LOD < LOD 1227 1334 1281 1238 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . respectively.391) < LOD < LOD < LOD < LOD < LOD < LOD < LOD 884 682 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.. which produces pneumonitis.

20012002. 106. urinary levels for general populations have been either undetectable or had different detection limits than in this Report (KomaromyHiller et al.23:827-839. Paschal DC. 2001).95:89-105.inchem. 3/27/08 Komaromy-Hiller G.12 to 0.15 μg/L in workers exposed at the recommended threshold limit value (Apostoli and Schaller. Trace element reference values in tissues from inhabitants of the European community I.html.. Available at URL: http://www. which approximate this Report’s limit of detection. Kriess K.76(1):53-59. Sabbioni E.htm. (1994) noted that analytical methods used in several general population studies appeared to have limits of detection that were insufficiently low (i. VI. References Apostoli P. Int Arch Occup Environ Health 2001. Sampson EJ.cdc. et al. 198 Fourth National Report on Human Exposure to Environmental Chemicals . Howerton K.atsdr. et al. Jackson RJ.. Levels of beryllium in urine for the U. McCanlies EC. Maier L.157:388-398. Clin Chest Med 2002. blood. Atlanta (GA) 2005. 1990..S. less than 0.Metals (i. In other studies. environmental levels) and health effects is available from ATSDR at: http://www. and the fact that most NHANES participant levels were undetectable. Minoia et al. Paschal et al. 1990. 0. They reported urinary beryllium levels ranging from 0. Weston A. and 2003-2004. Environ Res 1998. population were generally undetectable in NHANES 1999-2000.gov/toxpro2. Gallorini M. it is likely that urinary beryllium levels in the U. Genetic and exposure risks for chronic beryllium disease. Costa R. Urinary beryllium--a suitable tool for assessing occupational and environmental beryllium exposure. Finding a measurable amount of beryllium in urine does not mean that the level of beryllium causes an adverse health effect.S. Minoia C. Sci Total Environ 1990. population are lower than levels in workers.74:162-166. 2000. International Programme on Chemical Safety (IPCS). plasma and urine and a critical evaluation of reference values for the United Kingdom population.e. Morrow JC. patient population and literature reference intervals for urinary trace elements. Andrew M.296(1-2):71-90. Pozzoli L. Element reference values in tissues from inhabitants of the European community. Ash KO. Review of elements in blood. Apostoli and Schaller (2001) stated that detection limits in earlier studies were inadequate to estimate nonoccupational exposures. Ting BG. Am J Epidemiol 2003. Pirkle JL. Sci Total Environ 1994. Clin Chim Acta 2000. Biomonitoring Information Urinary beryllium levels represent recent and accumulated exposure.e. Hamilton EI.S. 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. 1998). Apostoli P. Schaller KH. Beryllium [online]. HLA-DPB1 and chronic beryllium disease: a HuGE review.. Centers for Disease Control and Prevention (CDC). Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.13 μg/L. and the 95th percentile for males in NHANES 2001-2002. and serum of Italian subjects. Environmental Health Criteria. Hamilton et al.. Sabbioni E. Van der Venne MT. A study of 46 elements in urine. Comparison of representative ranges based on U. Pietra R. Given these results. Third National Report on Human Exposure to Environmental Chemicals.1 μg/L).158:165-190.org/documents/ehc/ehc/ ehc106. Trace metals in urine of United States residents: reference range concentrations.

30) 1.300-.40 (1.20) 1.300-.60) 1.400) < LOD .70) 2742 2268 2085 1842 2219 2292 2716 3806 3478 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.300 (.500 (. and 0.40) 1.600-.300-.400 (.452) .50-1. and nonferrous alloys.S.S.300-.362-.00-1.400) .40 (1.700) .60 (1.500-.200-.400 (.10 (1.900-1.40 (1.400 (.70) 3913 4339 4131 4057 4606 4241 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .600) .500) .40 (1.900-1.20) 1.600) .00 (.403) .400-.30-1.400-.500) .300) .300-. Blood Cadmium Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U.800) .50) 1.600 (.500 (.300 (<LOD-.500-.400-.200) .600) 1.400-.382 (.300-.300 (.70) 1.900-1.400) < LOD .600 (.300) .700) .30-1. Important sources of airborne cadmium in the environment are burning fossil fuels such as coal or oil.10 (1.90) 723 898 910 905 1044 856 2135 2231 2081 4207 4772 4525 6-11 years 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .304 (.300) 1.20) .600) 90th 1.900-1.00 (.400) .00 (1.449) Selected percentiles ( 95% confidence interval) 50th .309-.400 (.90) 1.400 (.500-.500) .900-1.376-.283 (.10 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.400) . as zinc sulfide) and to a lesser extent.10 (1.300 (.600) .421 (.300-.500-.400 (.50 (1.00 (. interval) .800-1.00 (.300-.300) .300-.800) 1.20-1.20-1.3.60) Total * .00-1.400 (.313 (. and 03-04 are 0.500-.255) .400) .300 (.500) .300) .20-1.10) 1.60 (1.359-.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 * * * * * * .60 (1.600 (.200 (.70) 1.00-1.300 (.386-.800) .368-.30-1.200 (<LOD-.300) .20) 1.400 (.216-.300) .500-.500-.400-.20) 95th 1.10) 1.20) 1.300-.200 (.403 (.700 (.460) .275-.50 (1. 0.427) * .700) 1.500) .200-.30) 1.700-1.400) < LOD .10) 1.30) .600) .400-. or copper smelters (U.10 (1.600 (.500-.500-.60) 1.300 (<LOD-.600) .400) .900 (.900-1.300-. respectively.700) .424) * .200) .304 (.331) .20) 1.425 (.900 (.412 (.400) .600 (.14.20-1.400) .20) 1.40 (1.10 (1.600) .300-.40-1.600 (.50-1.60 (1.500) . cadmium use has declined in response to environmental concerns (http:// minerals.300-.300-.400) .400-. EPA.20-1. malleable.441) * .50-1.200-.700) .600) .600 (.30-1.00-1.200 (<LOD-.500-.10 (1.300 (<LOD-. Since 2001.500 (.400) .600 (.00-1.40-1.367-.378-. and incineration of municipal waste materials.00 (.80) 1.600 (.500-.420 (. < LOD means less than the limit of detection.10) 1.400 (.700) .470) * .500-.10) 1.40 (1.300) .700) .600 (.500-.395 (.00 (.289-.500 (.400 (.400 (.400 (.300-.333 (.600) .70) 1.300-. Other uses include pigment production.300-.30) 1.50) 1.60) 1.400) .00 (1.300 (.600 (.600-1.400 (.500-.20-1.468 (. coatings and plating.300) 75th .300-.500-.400) .235 (. bluish-white metal that is obtained chiefly as a by-product of processing zinccontaining ores (principally sphalerite.50-1.326 (.500 (.gov/minerals/pubs/commodity/cadmium).80) 1.337) .200 (.300 (<LOD-.40) 1.400-.30 (1.300) . plastic stabilizers.300) .361-.304-.700-1.usgs.00 (.400-. U.10) 1.900-1.600 (.300 (.200-.300 (.300 (.600 (.200-.400-.10) 1.266-.600) .400 (.344) .50 (1.30-1. population from the National Health and Nutrition Examination Survey.800 (. Fourth National Report on Human Exposure to Environmental Chemicals 199 .80 (1.500 (.50) 1.20-1.60-1. 7440-43-9 General Information Cadmium is a soft.600-. which may vary for some chemicals by year and by individual sample.300-.400) .00-1.600 (.393 (.366) * * .500-.300) .00-1.10 (.800-1.400) .300-.300 (.20) .600-.00) .20 (1.300 (. lead. during refining of lead and copper from sulfide ore.300 (.400 (.426-. see Data Analysis section) for Survey years 99-00.300-.300 (.500 (.40 (1.400 (.00-1.20) 1.300-.20) 1.500 (.700-1. The predominant commercial use of cadmium is in battery manufacturing.500-.500 (.500) .3.50 (1.700) .300) .400-.00 (.700) .S.900-1.400 (.400) .400) < LOD < LOD < LOD .300 (.300) .378 (. 01-02.296-.900-1.500-.398) < LOD < LOD < LOD < LOD < LOD < LOD .00 (.70) 1. Cadmium also may be emitted into the air from zinc.300) .60 (1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.513) .00) .800 (.Metals Cadmium CAS No.00 (.20 (.00-1.10) 1.900-1.

843-1.892-1.25) 1. ingestion through food is the largest source of exposure. Cadmium in soil is absorbed by plants..890 (.060-.530 (.200-.700-.202-. Diamond et al.09-1.960 (.589 (.540) .440 (.06-1.229-.980-1.83) 1.43) 1. Inhalation of cigarette smoke is a predominant source of exposure in smokers.157) .336) .820 (.226) Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 * .160) . cadmium accumulates in the liver and kidneys where it is bound to metallothionein.886-1.01-1.940-1.221) .273 (.280 (.817 (.326) .551 (.713) .230) 75th .196-.433-.989-1.20 (1.980-1.551) .299) .530) .12 (.219 (.519) . Renal tubular and glomerular damage.157-.153-.114-.210) .810-1.150) .412) .265 (.393-.194-.077 (.38) .230 (.880) .450 (.234 (. Urinary Cadmium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.963-1.135-.480) . 2003).680 (.257) . **All results are corrected for molybdenum oxide interference in the ICP-MS method.19) 1. rice.232 (.436-.101) .06.222) .36) 1.350 (.892 (.120 (.354) .160) .313) .919) .20 (1.** Survey Geometric mean (95% conf.22 (. Kikuchi et al.57) 1. wheat.476-.28-1.13-1.507) .310 (.327 (.445 (.37) 1121 1335 1277 1136 1355 1266 Females 99-00 01-02 03-04 Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 .220-.07-1.800 (.596) .74) 1.360) . however.187 (.126) .17 (.366) .818 (.430) .855-1..339) .169-.493-.559 (.262) .065-.479) .219 (. and 03-04 are 0.519) .875 (.229) .28) 1.490) 1.289-.257-.191-.320) .179-.714-1.260-.206 (. population from the National Health and Nutrition Examination Survey.206) .17 (.195-.700-.13) .700-.198) . The estimated half-life of cadmium in the kidney is from one to four decades (ATSDR.52 (1.456-.25 (1.210 (.470-.191 (.02-1.193 (.135 (.717-.82) 1.211 (.20 (1.20) 1.15 (.226) .466 (.092 (.199 (. The kidney is a critical target and shows the earliest sign of cadmium toxicity.539) .918-1.12-1.235) . respectively.500) 90th .210 (.820-1.285-.32 (1.15) 1.633-1.170 (.03) . calcium.462 (.208-.447 (.281 (.366-.229) .077 (. zinc.246) .492 (.766 (.550 (.249) .06.219 (.081) . 2003). 200 Fourth National Report on Human Exposure to Environmental Chemicals .633 (.100-.210 (. whose body burdens of cadmium can be approximately twice that of nonsmokers.733) .858 (.183-.Metals 2000).255) .121 (.22 (1..284) .203 (.623) .061-.310) .. drinking water is a source for cadmium intake. 2003.181 (.300) .490) .394-.231) .400-.130 (.741-1.813 (.283 (.265) .806) .390 (.189-.247) . Cadmium absorption may be increased with iron deficiency (Berglund et al.458 (.170-.221 (. Cadmium is absorbed via inhalation and ingestion.253-.136) .500) .38) 1.48 (1.220) .167-.300 (.580) . 2004a.04 (.836-1.329 (.061 (<LOD-. individual values vary and are affected by factors such as dietary intake of essential nutrients (iron.238) .30-1.270 (.227 (. With chronic exposure.200-.241) .870) .980) .192-.72) 1.387) . a factor that may contribute to the higher absorption of cadmium by women (Diamond et al.330-.475 (.498-..223 (.47) 1.455 (.753-.S.148) .178-.128 (.080 (.308) . interval) .686-.210 (.092) .977) .607) . see Data Analysis section) for Survey years 99-00.705-.01) .189-.151-.173) .06) .216 (. 1994).230) .255) .263) .390-.238-.445 (.733-.290-.175 (.520-.15) .210) .366-.204 (.237-.13 (.20-1.141 (.28 (1.748-1. To a lesser extent.239 (.763-.209 (.260-. including many food crops such as cereal grains.272-.277 (.200 (.233) .990) .316 (..232) .087-.01 (.171-. and 0.790 (.17) .260 (.980) .38) . For nonsmokers who are not exposed to cadmium in the workplace.960) 1. and various seeds. About one-third to one half of the total body burden accumulates in the kidney tissues (Nordberg and Nordberg.107-.430-.220) Selected percentiles ( 95% confidence interval) Sample 95th 1.180 (.170-.400-.200 (.201 (.10 (1. potatoes.279 (. an inducible metal binding protein.848 (. The gastrointestinal absorption of dietary cadmium is about 5% in adult men and 10% or higher in women (Diamond et al.240) .04 (. 01-02.193-.730-.390-. 2003).067-.210 (.890-1.972 (.261-.177-.800-.203) .240-.090) .790 (.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 .510) .423-.184-.148-.817 (. Horiguchi et al.112-.510-.220-.255) .110-.090) .243-.362) .202 (.251) .207-.270 (.115-.481) .190-.150-.160-.17 (.640) .322 (. 1999.372) .160 (.233) .452 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.381-.41 (.140 (.351-.426 (.886) .295) .06.078 (.860) 1.165-.191-. 2001).134) .302 (.839 (.261-.545 (.450 (.875) .482) .26) size 2257 2690 2543 Total years 99-00 01-02 03-04 50th .067-.306 (.214-.189) .211-.190-.980 (.220 (.388-.610) .249-.440 (.06-1.192-.190-.34) 1.282 (.51 (1.440-. copper) and protein.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. 0.109 (.109-.24) 1.38) 1.820) 1.175 (.

199 (.560-.398-.190 (.. 1999).687 (.667) .228-.233 (.818) .078 (.828) .614) .221 (.678 (.225) .708-1.202 (.818) .444-.261) .212 (.220 (.168-.177) .470) .137-.449) .278) .917) .226) 75th . 2003.438-.663 (.255-.331 (.440) .690 (.725-1.158-.250) .176 (.716-.387-. 2002.239-.234-.159 (.288-.631) .491-.219 (.767) .288 (.622 (.813-1.171-.147-.143-.161-.210) .204-.166 (.850) . 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.196 (.686 (.650-. **All results are corrected for molybdenum oxide interference in the ICP-MS method.210 (.516-.191) .04) size 2257 2689 2543 Total years 99-00 01-02 03-04 50th .806-1. 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.273 (.154-.08) .206-.225) .263 (.078-.218) .200 (.178) .304) .130-.207-.238) .308 (.440) .05) 1.182) .562-.143) .185) .490 (.13) . 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.551) .795) 1.074-.159 (.067-.101) .718 (.387 (. population from the National Health and Nutrition Examination Survey. 2004).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 .38) .308) .140-.292) .162 (.219) Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 * .830-1.438) 90th .157-.245 (.274) 1.415) .700 (.325 (.856) .232) .077-.941 (.311) . Noonan et al.607) .211 (.148 (.100 (...247-.716) .194-.690-.189-.940 (.170-.104) .792 (.227-.187-.267 (.097) .16) 1.106) .729 (.085 (.591 (.17) .979 (.446) .240) .282 (.484 (.178-.687-.647-.156) .234 (.S.487 (.865 (.197-.388-.235) .168-.147-.533) .431) .267 (.653) .329 (.253) .318 (.541) .084 (.296 (.084-.754) ..316 (.192) .350) . Horiguchi et al. 2004b).531 (.221-.093 (.784) .940-1.674-1.175-.432 (.906) .645-.303) .173 (.293-.481 (.559-.181) .876-1.931 (.696-.190 (. During the 1950’s and 1960’s. a condition known as “itaiitai” (“ouch-ouch”) affected postmenopausal women living in a cadmium-polluted region of Japan. Fourth National Report on Human Exposure to Environmental Chemicals 201 .09 (.537-.418) .873 (..209) Selected percentiles ( 95% confidence interval) Sample 95th .297) .146-.712 (.140-.170 (..208-.377-.779 (.270 (.181 (.126 (.304-. 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.175 (.253 (.191 (.201-.917 (.091) .184-.441-.414 (.826-1.156-.111-.157-.998) .617 (.289) .668-.219 (.123-.16) .950) .404 (.234) .176 (.222-.802 (.280 (.075 (<LOD-.183) .00 (.833-1.136-.02 (.281) .690-.205 (.423-.263-.789 (.199-.500-.518) . Staessen et al.181 (. Jarup et al.769 (.473 (.364) .240) .338 (.300-.919 (.536 (.423 (.113-.143-. 1996.136-.757) .507-.096) .12) 1.. 2002.433-.472) .229) .336-. 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.209) .545) .874-1.289) .247-.135) . 2000.094) . 1999).382-.185 (.719 (.163 (.063-.826-1.678-.107) .382) ..223) .Metals manifested by irreversible proteinuria and progressive reduction in glomerular filtration rate.727-.434 (.783 (.216-.283 (.215 (.131-. two studies in Japan did not find an association between cadmium in urine and renal biomarkers (Ezaki et al.688-.335 (.381-.783) .091 (.391-.538) .07) .340) . 2002.086 (..071 (.929) . 1999).321) .104) .051-.** Survey Geometric mean (95% conf.343-.261-.412 (.414-.168 (.123-.183 (.693 (.691-.985 (.181-. can result from high dose chronic exposure.962) .666-.256-.830) .247-.173-.232) .224 (.07 (.10) 1.479 (. interval) .404) .927-1.08) 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.06 (.187) .210 (. However.150-.182) .208 (.236-.085-.238-.184) . At lower environmental exposures.261 (.884) .856 (.182) .156 (.470) .198) .098) .207) .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 .501 (.083-.175 (.839) .075-.426-.316) .722-.144-.090 (.252 (.850) .909-1.630-.137 (.352) .813-.112) .241) . most often a result of occupational exposure (Roels et al.147 (.184-.091 (.700) .476) .281) .418-.163) .266) .174-..767 (.288) .191-.122 (.242) .421 (.827) .757 (.268 (.00 (.266-.740 (.154 (. Olsson et al.

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

Environ Health Perspect 2002. Ezaki T. 102:10581066. Sasaki S.13(11):1627-1631. Environ Res 2006. and cadmium burden on dietary cadmium absorption in cadmium-exposed female Japanese farmers. ShkiryakNizhnyk AZ. Kaus S. Nomiyama T. Palomar M. et al. Olfactory function in workers exposed to moderate airborne cadmium levels. References Akesson A. Dietary exposure to cadmium at close to the current provisional tolerable weekly intake does not affect renal function among female Japanese farmers. Available at URL: http://www. possibly better than b2microglobulin. Machida M. Furuki K. Schulz C. Mannino DM. Anthropometric. Takebayashi T. Bregante G. et al. Consonni D. Lauwerys R. Nermell B. Toxicol Appl Pharmacol 2004a. Int J Hyg Environ Health 2002. Bo M. et al. Lancet 1988. Comprehensive study of the effects of age. Chiappino G. Seifert B. 4/8/09 Alfven T. Lundh T. Howerton K. Jin T. Urinary cadmium levels predict lower lung function in current and former smokers: data from the Third National Health and Nutrition Examination Survey. Greves HM. Taylor AJ. Neurotoxicology 2003. Tsukahara T. Cadmium and lead in blood in relation to low bone mineral density and tubular proteinuria. Dekio F. 206:15-24. Komaromy-Hiller G. Environ Res 2004.76:186-196. et al.atsdr. Clin Chim Acta 2000. Horiguchi H. Uptake of cadmium in meals from the digestive tract of young non-smoking Japanese female volunteers.1(8587):663-667. Uemura T. Cadmium fume inhalation and emphysema. et al. Ukai H. Fayers PM. Lidfeldt J. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Lancet 1999. Toxicological profile for cadmium update.html. 1999 [online]. Pickering CA. Osteoporosis and renal dysfunction in a general population exposed to cadmium in China. Atlanta (GA).000 women in the Japanese general population: a nationwide large-scale survey. et al. et al. Thorax 2004. Lison D. et al. Ye T. iron deficiency. Kumagai N. Ash KO. Third National Report on Human Exposure to Environmental Chemicals. et al. Vahter M. diabetes mellitus. Berglund M. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population.66(Pt A):2141-2164. Thayer WC. Horiguchi H. Elinder CG. Toffoletto F. environmental. Hellstrom L. Low level exposure to cadmium and early kidney damage: the OSCAR study [published erratum appears in Occup Environ Med 2002. Zhu G. Seiwert M. et al. Furuki K. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. a1-Microglobulin as a promising marker of cadmium-induced tubular dysfunction.24:717-724. population.cdc.110:699-702. Kundiev YT. Fukui Y. Okamoto S. Intestinal absorption of dietary cadmium in women depends on body iron stores and fiber intake. Jones RL.45:43-52. Serra J. 2005. Fernandez MA. Mascagni P.102:83-89. Bernard A.Metals with reference values so they can determine whether people have been exposed to higher levels of cadmium than are found in the general population.148(1-2):11-20. Comparison of representative ranges based on U. Moriguchi J. Becker K. Costa R.296(1-2):71-90. Agency for Toxic Substances and Disease Registry (ATSDR). Buchet JP.46:372-374. Fatal chemical pneumonitis due to cadmium fumes. Nerbrand C. Schulz C. Becker K. J Toxicol Environ Health 2003. Toxicol Lett 2004. Holguin F. Nordberg G. Ikeda Y. Fourth National Report on Human Exposure to Environmental Chemicals 203 . J Occup Health 2003. Tsukahara T. 196:114-123. Wang H. Darbyshire J. Environ Res 2004b. and dietary predictors of elevated blood cadmium levels in Ukranian children: Ukraine ELSPAC group. Lepom P. Moriguchi J. Seiwert M. Oguma E.S. Venables KM. Int Arch Occup Environ Health 2003. Fukui Y.59:497].gov/toxprofiles/tp5.96:353-359. Akesson A.S. No clear-cut evidence for cadmium-induced renal tubular dysfunction among over 10. Environ Health Perspect 1994. patient population and literature reference intervals for urinary trace elements. Miyamoto K. et al. Bellerup P. Jarup L. Chislovska NV. Int J Hyg Environ Health 2003. Sanz P. Krause C. Diamond GL.205:297-308.354:1508– 1513. Davison AG. Savage-Brown A. Mucha A. Renal effects of low-level environmental cadmium exposure: 5-year follow-up of a subcohort from the Cadmibel study. Occup Med 1996. Friedman LS. Carlsson MD. Ezaki T. Kaus S. Lukyanova EM. Pharmacokinetic/ pharmacodynamics (PK/PD) modeling of risks of kidney toxicity from exposure to cadmium: estimates of dietary risks in the U. Centers for Disease Control and Prevention (CDC). Kikuchi Y. Occup Environ Med 2000. Hotz P. Grubb A.95:20–31. Machida M. Gadea E. Persson B. Choudhury H. Sasaki S. Jarup L. Ikeda Y. Environ Health Perspect 2005. Vahter M.57:668-672. Miyamoto K.59:194-8. Stock AL. Alfven T. Tubular and glomerular kidney effects in Swedish women with low environmental cadmium exposure. Oguma E.

Oskarsson A. Tanebe K. Nakagawa H. Available at URL: www. iron status. Stegmayr B.S. Salpietro CD. Honda R. Occup Environ Med 2002. Liu QF. Mutat Res 2003. Relationship between newborn size and mother’s blood cadmium levels. Lundh T.gov/ttn/atw/ hlthef/cadmium. lead. Schultz C.30(5):395-399. et al. Ginucchio G.533(12):107-120.39:2507-2515.3:26-41. Roels H. Zhang YL. created 1992. Kuznetsova T.59(1):22-25. Campagna D.epa. Toyama. Environ Res 2000. New York: Plenum Press. Time trends in burdens of cadmium. Arch Environ Health. et al.110:1185-1190. In: Clarkson TW. Nordberg M. Fan YG.100:330-338. et al. Lijnen P. et al. United States Environmental Protection Agency (U. Honda R.Metals Nishijo M. Jansson J-H. lead. Wang JX. Nakagawa H. Environ Health Perspect 2002. forearm bone density. and former smoking – association of renal effects. Minciullo PL. Nishijo M. Environ Res 2006.209:301305. Nordberg GF. Kathman SJ.110:151-155. dietary intake. Tanebe K. Emelianov D. Renal effects of cadmium exposure in cadmium nonpolluted areas in Japan. et al. Cadmium concentration in maternal and cord blood and infant birth weight: a study on healthy non-smoking women. Environ Health Perspect 2002. 2001. Wennberg M. Usefulness of biomarkers of exposure to inorganic mercury. Cadmium carcinogenesis. Schwenk M.84 (Section A):4455. Revised and new reference values for arsenic. age. Vangronsveld J. 151-168. Saito S. J Cardiovasc Risk 1996. Ren Fail 1999. Noonan CW. and risk of fractures: prospective population study. Staessen JA. Ottosson H. cadmium. Gallmans G. Sarasua SM. et al. Gangemi S. Tawara K. J Environ Sci Health B 2004. Sager PR. Skerfving S. Wilhelm M.353:1140-1144. Kobayashi E. Biological monitoring of toxic metals. Mueller PW. Lybarger JA. Revised 2000 [online]. 4/8/09 Waalkes MP. Nogawa K. Cadmium compounds. Effect of environmental exposure to cadmium on pregnancy outcome and fetal growth: a study on healthy pregnant women in China. Lancet 1999. Zhao YC. Zhu HD. 204 Fourth National Report on Human Exposure to Environmental Chemicals . Bergdahl IA. pp. Lison D. Merlino MV. Roels HA. Kido T. J Perinat Med 2002. Okubo Y. and mercury in blood or urine of children: Basis for validation of human biomonitoring data in environmental medicine. Roels HA.59:394-397. Hazard Summary. Staessen J. Lauwerys R.html. Cadmium in blood and urine – impact of sex. Nakagawa H. Effects of maternal exposure to cadmium on pregnancy outcome and breast milk. Biological monitoring of cadmium. Bensryd I. 2000. Buchet JP. Public health implications of environmental exposure to cadmium and lead: an overview of epidemiological studies in Belgium. Olsson IM. Thijs L. Suwazono Y. Stelitano A. lead. Friberg L. and mercury in the population of northern Sweden. Bruiglia S. Effects of exposure to low levels of environmental cadmium on renal biomarkers. Nordberg GF.21(3-4):251-262. Hoet P. eds. Int J Hyg Environ Health 2006. Japan. Lundh T. Environmental exposure to cadmium. 2004. or cadmium in controlling occupational and environmental risks of nephrotoxicity. EPA).

77-8.90) 7.80) 7.57-5. and as polymerization catalysts.80 (8.72-7.40-5.90-10.3-13. the body half-life is estimated to be 70-109 days based on 137Cs exposures.20-5.7) 10. interval) 4.84) 5. see Data Analysis section) for Survey years 99-00.95 (3.0) 12.50-7.8) 11.10 (8.10-5.71-8.94 (4.80-13.20) 5.60 (7.50 (6.52-9.59-5.96 (6.2-14.5) 9.25) 4.10-7.53-11.90-8.3) 10.42) 6.37) 7.8-13.4 (9.86 (7.60) 7.30 (6.90 (4.43-8.27 (7.2.60-6.36 (3.47-4.8) 11.60-5.24) 4.9 (11.7 (10.56-11.4) 10.99-11. although cesium was generally of low toxicity when given to animals.9 (11. Whether cesium compounds are carcinogenic is unknown.71 (4.44 (8.00) 4.73-5.23) 9.7 (11.87) 5.25 (3.77 (9.87 (4.50) 9. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.10 (6.50) 5.5) 12.64-10. photographic emulsions. soil.17) 4.21 (4.69-6.91-8.70 (4.00) 6.8 (10. 2004).81) 4.17-6.71) 4.90 (6. and 03-04 are 0.9 (10.97) 4.94 (4.5-13.70) 7.67 (4.01) 7.84) 8.86-12. and 0.29 (4.49) 75th 7.Metals Cesium CAS No. infrared lamps.4) 10.33 (5.46) 7.0) 11.0 (9.32) 4.71-9. 7440-46-2 General Information Cesium is a silver-white metal that is found naturally in rock.7 (9.35 (4.04) 7.94-4.90-10.10-8.64) 4.62) 4.40) 5.81) 4.0-13.6) 11.87 (4.79 (4.7-14.17 (6.66 (7.70 (6.4 (9.70 (9.1) 9.3 (8.27-5.98 (7.7 (9.55 (4. scintillation counters. For absorbed cesium salts.56 (4.9 (10.60-6.97-7.80 (4.9) 12.22 (4.31-8.6 (9.0) 9.8) 12.87-7.64) 5.02 (4.20 (6.6 (11.8) 9.80-10.27) 4.4) 95th 11.37) 5.2-13.76-6.71-5.00) 7.00-10.3-13.40 (4.52) 7.3) 12.07-11. Little is known about the health effects of this metal.59-5.1) 9. However.20) 8.49) 4.2) 12.62 (5.74) Selected percentiles ( 95% confidence interval) 50th 4.87 (4.08 (7.5-14.42) 7.08 (6.80-10.40) 7.1-13.08-5.54-11.39) 7.32 (3.89) 5.00-8.01-6.9) 8.1-12.5-16.00-8.3 (8.8 (11.36 (6.03 (4. Human health effects from cesium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.30-10.74 (4.59) 7. Inorganic cesium compounds are used in photomultiplier and vacuum tubes.20-4.77 (9.90-12.21) 90th 9.13-8.10 (8.70 (6. Fourth National Report on Human Exposure to Environmental Chemicals 205 .6 (9.8 (10.80-10.14. Case investigations of ingestions of large doses of cesium chloride have reported decreased appetite.0) 11. nausea.05) 5.0-15.5 (10.40-5.26 (3.4 (10.32-5. diarrhea.7 (8.56) 5. Most human exposure to cesium occurs through the diet.90-10.92-13.34 (4.12 (4.93 (4.9 (11. and high-power gas-ion devices.39-4.40-5.56 (4.4) 11. Radioactive 137Cs has been used medically to treat cancer.90) 5.4) 12.55-11.40-5.99) 9.55 (7.1-12.95-4.83) 6.70 (8.01-8.22-4. 0.6 (9.94) 4.80-11. population from the National Health and Nutrition Examination Survey.63 (4.91 (7.13 (8.1 (10.53 (6.16-6.2 (9.77 (4.14 (4.70-8.03 (4.20) 4.50 (4.10 (6.90) 4.S.47-8.30) 7.61) 7.59 (5.60-12.05-5.70) 5.7) 11.71 (8.70 (8.62 (5.34) 9.40-11.50 (7.89-5.6 (9.5) 10.33-5.40-7.63-4.4) 9.10-9.30 (6.64) 5.38) 5.40-11.3) 10.99) 7.05) 5.63) 6.35-5.84 (4.03-4.64-5.59-5.61-6.00-9.8) 9. Workplace guidelines for cesium hydroxide are available from ACGIH and NIOSH.26) 4.99-6.70-5.68 (7.80 (8.70 (5.20-7.81) 9.90) 9. respectively.12-11.00-4.90) 5.60) 5.7 (9.4-13.82-4.80 (8.86-11.13 (7.4) 12.09) 5.9 (11.3) 10.82) 5.45-8.68) 9.80 (4.42-7.05-5.6) 10.49 (5.8) 12.9) Total 4.3) 9.64 (4.0) 12.15-8. 01-02.3-15.5 (8.7) 10.36) 3.35 (4.1 (11.72) 4.26) 7.0 (10.95) 5.2-13.7) 11.13 (5. and clay.23-4.9) 11.50 (4.12-5.54) 4.81-14.25-5.7 (10.88 (8.20) 7.45-5.7 (10.1) 11.20-8.97) 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 4.09-5.3) 10.08) 7.20 (4.80-6.5-14.33 (6. semiconductors.80 (4.0) 12.6) 1226 1335 1281 1238 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 4.26-11.08-5.84-9.7) 884 683 618 568 667 723 821 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.8) 12.83-4.60 (8.43 (5.1) 10.60-7.89) 4.2) 11.73-11.74-5.1) 11.81 (4. cesium hydroxide is corrosive and irritating at high concentrations.00 (7.07) 4. Urinary Cesium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.97 (7.12) 5.98 (7. and cardiac arrhythmia (ATSDR.30) 5.2-13.1 (9.29) 4.2 (9.2-12.99-11.6 (11.60) 7.30-5.49 (4.16-6.90-12.0) 10.60-7.70) 5.84-5.14.40) 5.9) 340 368 290 718 762 725 1406 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 4.04 (4.50 (4.

54 (5. (2000) found urinary cesium levels that were slightly lower than those reported for the U.58-5.28) 7. Komaromy-Hiller et al.99-9. population from the National Health and Nutrition Examination Survey.43) 8.51 (3.08) 4.22 (3.53) 6.43 (4.38) 10.84-7.9) 10.44 (4.76-6.50) 4.2) 11.87) 5.17 (6.56) 4.6) 6.36-6.82-4.91) 5.42-4.92) 3.39) 5.30 (3.03) 6.64 (8.41) 9. Minoia et al. 1990). Urinary cesium levels were similar in a group of forest fire fighters and residents living near the fire area (Wolfe et al. interval) 4.27-4.24-10.66 (5.27-6.16-8.92 (5.74) 3.05 (4.06 (5.99-9.50) 4.8) 10.74) 75th 5.84-9.94) 7.98) 5.14 (6.93-9.13) 7.14) 4.4) 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.88-10.0 (7.28 (4.14) 4.57) 3.56) 4.5) 7.40) 6.02-4.05-3.95) 4.50 (5.86 (4.16-5.08) 3.27 (6.52-5.3-15.17) 4.27 (6.14-6.77 (7.95) 10.54 (4.90 (7.73 (3.31-4.31-6.25) 4.78) 4.65 (6.30 (7.41) 4. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.79) 4.2 (8.09) 4.00-5.08 (6.42 (4.98 (7.68 (4.09 (4.62) 5.78 (3.43-6.99) 4.68) 6.46 (8.97-4. Using clinically submitted specimens.37-3.79 (5.10 (3.21-5.63 (6.42 (5.16-8.60 (5.95-6.91 (5. Finding a measurable amount of cesium in the urine does not mean that the levels of cesium cause an adverse health effect.61-3.35 (4.01-8.72-5.08 (5.96-4.07) 8.7) 10.00-10.40) 7.35-11.95-12.S.20-4.5) 9.96-4.89-4.63 (4.10 (5.47) 7.75 (7.00 (8.18-7.43 (3.78) 4.66-6.44) 3.06) 5.79) 6.20-8.68) 3.37) 4.83-6.95 (5.91 (5.51 (4.28) 8.06) 4.3 (9.70) 6.38-12.13-9.46 (7.14-7.73-4.8) 6.70) 7.91-6. population results shown in this Report (Alimonti et al.04-11.7) 10.09) 8.36-3.38 (3.51) 4..36-10.67 (5.97) 8.20-4.99-4.71 (7.8) 5.21 (2.7-12.29-3.47) 6.44-9.34 (5.95) 8.96) 4.30-4. population.48-6.53 (6.51 (3.65-4.3) 11.81 (4.75 (6.68) 4.81 (4.42-4.60-20.74 (5.72) 4.70 (7.22-11.9 (9.47 (4.94 (5.Metals Biomonitoring Information Urinary cesium levels reflect recent exposure.79) 9.51 (7.47) 4.63 (7.82) 7.00) 6.41 (4.50 (7.13-9.55 (3.41-4.15-11.54 (3.90-8.08-7. Urinary Cesium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.75-11.30-4.46-8.3) 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 3.43-11.66 (6. 2005.39) 8.20) 5.45-6.30) 10.46) 6.35-7.76-9.96) 4.9 (10.08 (3.59-8.66 (5.74-11.2 (8.20-4.43 (4.63) 6.67 (6.26-6.17) 9.04) 6.24-4.0) Total 4.87 (5.41-7.44-5.50 (6.85) 4.60-10.74 (4.1) 11. Two small studies of European populations reported urinary cesium levels similar to 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 .41 (5.04) 5.00-4.77-5.56) 3.00-8.84-9.50) 4.60) 3.28 (5.48) 7.99 (3.58 (6.10) 7.65-3.07 (5.93-7.13 (3..84-7.97-5.19-6.64-6.61 (7.54 (4.77 (4.16) 5. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.77 (6. 2004).39 (5.47) 6.S.30) 10.38 (3.44 (8.64) 4.12-6.15 (7.33-3.84-11.11 (5.25) Selected percentiles ( 95% confidence interval) 50th 4. and were also roughly similar to those in this Report.98) 5.67) 5.90-3.91) 4.06 (3.03-5.31 (4.3 (10.05-3.53 (4.21-3.33 (5.29) 4.59) 4.19-3.15) 95th 8.11 (5..64) 5.40-5.18) 8.71) 6.45 (4.55) 4.88-4.87) Sample size 2464 2689 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 5.47 (7.91-7.29) 5.80) 6.5) 9.04-5.00-9.6 (9.95 (3.58 (4.3 (8.48) 90th 7.77) 4.72 (4.98 (6.50) 8.87-4.58) 3.26 (3.63-6.41 (8.29) 4.29-3.35 (3.85-4.56-10.38-7.27) 4.49) 3.96 (4.08) 4.85) 5.00-5.53) 3.55-5.63-6.17-4.15-4.8 (9.64 (4.21-4.50-5.26 (4.91) 5.07-4.68-11.42-6.90-8.18-6.07) 8.18 (7.46-4.08-3.22) 6.51 (4.05) 6.64) 9.24 (3.S.62-8.35) 3.14-4.03-6.2) 340 368 290 718 762 725 1406 1559 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 3.05-4.60 (3.10 (3.33 (5.02 (5.5 (9.31 (4.43 (8.83) 8.33-8.0) 7.58) 8.79-5.78 (3.12) 3.27 (8.56 (4.91-9.10-4.03) 5.83-7.3) 9.05) 3.30 (4.6 (9.12 (3.23 (7.

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

450) .850) . It is emitted into the environment from burning coal and oil and car and truck exhaust.340-.300 (.47 (1.620-.670 (.620-.550) 90th .950 (.32) 1.487) .740-.08.810) .530) .530 (.390-.410-.92) 1.S.900) .420 (.330 (.81) 1.540-.53) 1. 7440-48-4 General Information Cobalt is a magnetic element that occurs in nature either as a steel-gray.435 (.434 (.570-.07-1. see Data Analysis section) for Survey years 99-00.50) 1. steel-belted radial tires.338-.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 .410) . and in synthesizing polyester and other materials.359 (.350-.870 (.08) .06-1.64) 1.04-1.46 (1.680 (.690-.301 (.520 (.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 .28 (1.600 (. and magnetic recording media. interval) .379 (.07-1.920) 1.67) 1. Usual human exposure is from food sources.660) .630-. automobile airbags.430 (.01 (.319) .581) .880-1.950-1.790) .05) 1.290-.23) .810) .45 (1.270-.590-.16) 1.32 (1.17 (.550 (.890) 95th 1.480 (.690-.460 (.04 (.377-. respectively.740 (.371 (.850-1.394) .930 (.340-.370-.710) .424) .03-1.17 (1.890-1. Cobalt is used as a drying agent in paints.334) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.81) 1.540-.583) .300-.75 (1.650 (.520 (.890-1.310 (.42) 1.580 (. and soil.00) .750 (.16) 1.380 (.05 (.22-1.22 (1.26) Total .590) .410) .32 (1.404) .316-.04) 1.630 (.386) .510) 1.790-.33-1.369 (.01-2.980-1.01-1.980) .600) .12) 1.327-.348-.24 (1.333-.390) .15 (1.450) .519 (. 01-02.19) .830-1.490-.399) .460) .65) 1.06 (.60 (1.710 (.360-.570) .23-2.650-. 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.500) .26-1.900) .28-2.331-.270-.520-.52 (1.20 (1.360-.450) .523) .410-.398) .670 (. and 0.800-.370-. hard metal or in combination with other elements.428-.452 (.308-.960-1. diamond-polishing wheels.373) .336-.680 (.393-.660) .14-1.760 (.28 (1.520-.620-. varnishes.850-1.740-.350-.820 (.590-.03) 1.364-.285 (.710) 1.352 (.610-.860 (.610) . The cobalt used in U.700) .880 (.73) 1.920-1.07.316 (.419) Selected percentiles ( 95% confidence interval) 50th .07.48) 1.420) .380-.414) .03 (.16 (.340) .29 (1.469-.03 (.418 (.520 (.550-.440-.09 (.450-.750 (.39) 1.03) .465) .370) .S.Metals Cobalt CAS No.08-1.310-.350 (. Cobalt compounds are also used in manufacturing battery electrodes.330-.460) .48) 1.950 (.431) .420) .313) .13) 1.950-1.470 (.21) 1.06 (.520-.543) .47) 1.490-.343 (.670 (.770) .259-.16-1.372) .16 (1.570-.520) .520-.280-.340 (.340) .56) 1.12) 1.610 (. large appliances.496) . and fertilizers.910-1.500 (.32-2. Medical uses include joint and dental prostheses and radioactive cobalt in cancer chemotherapy.398 (.410 (.940-1.375 (.390 (.17-1.480-.570) .900-1.930) .44) 1.16 (1.294 (.24 (.305-.348-.540-.430) .370 (.405-.470) .360-.380 (.47 (1.09) . seawater.417) .450-.16-1.840) .04-1.28 (1.690 (.410 (.560 (.350-.427-.388-.373-.25-1.454 (.04-1.339 (.36) 1.09 (.26) 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.499 (.410-. blue-colored pigments.02-1.850) 1.900-1.750 (.379 (.333-.580 (.291-.890-1.400-.640) .650 (.502) . Cobalt compounds are used as catalysts in producing oil and gas.430) .32) 1.460) .580 (.59 (1.680) .890) .940-1.07 (.330) .820 (.14) .700) .730) 1.800-. industry is imported or obtained by recycling scrap metal that contains cobalt. 208 Fourth National Report on Human Exposure to Environmental Chemicals .620) .660-.564) .760) .610) .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 .355-. shiny.820 (.431) .17 (1.540-. population from the National Health and Nutrition Examination Survey. and inks.03) 1.530-.750-.480 (.374 (.630 (.800) .33 (1.380-.410 (.570 (.810-.01 (. hard metal (alloys of cobalt and tungsten carbide).430 (. It is also a component of porcelain enamel applied to steel bathroom fixtures.670-.680) .15-1.590 (.870-1.370-.410 (.515 (.47) 1.430-.367 (.390 (.99) 1.390 (. and kitchenware.410 (.463-.461 (.870 (.520) .640) .450) .37-1.22) 1.900) .600-.940 (.416) .790 (.460 (.68 (1. Among its many uses are manufacturing superalloys used in gas turbines in aircraft engines.430 (.950) .270-.26) 1.930-1. Cobalt occurs naturally in airborne dust.350) 75th .670-.540) 1.460-.50 (1. 0.640) .380 (.320 (.05 (. and 03-04 are 0.26-2.520 (.

274-.372) .673-.476-.471-.342-.857-1.394) .487-.29 (1.293 (.444 (..469-.35) 1.248-.505) .608 (.533 (.955) .339-.391 (.257 (. or using diamond-polishing wheels that contain cobalt metal. A nutritional requirement for cobalt other than that contained within dietary cobalamin has not been established.833-1.547 (.563-.400 (.861 (. Urinary Cobalt (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.33) .278-. 1994.358 (.259) .848 (.452-.428-.662) .792-1.513) .738 (.313-.323) .744) 1.391) Selected percentiles ( 95% confidence interval) 50th .309) .753) 1.00) .963-1.16 (.500-. Smith et al.824 (.844 (.542 (.362-.50) 1. Cobalt constitutes 4% by weight of vitamin B-12 (cobalamin).479) .337 (.838 (.457-.640) .728 (.378 (.552 (.983) .691 (.381) .15) 1.333 (.461) .647) .380-.329-.438) . 1972).402 (.304) .433) .495 (.515 (.250) . refining or processing alloys.523 (.938-1.630-.277-.10-1. A portion of cobalt retained for long periods is concentrated in the liver.425-.387) .937 (.396) .990) .785) .275-.251-.707) .333-.346 (.548 (.728) .426 (.282-.271 (.384) .826-1.593) .275-.606 (.404-.481) 90th .774 (.234 (.529 (.368) .393-. an essential human nutrient.316 (.349) .396) .756 (.600-. 1979).17) .449) .895-1.328 (.534-.938) .753-.363) .243-.02 (.585) .324) .50) 1.16 (1.10) 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 .278 (.861-1.327 (.467-.522) .361 (.297) .704-.421) .314 (.303-.417) .310) .00) .386 (.27) 1.407) .757-1.326-.215-.35) .337) . 1994).298 (.44 (.256-.301-.554 (.382-.644 (.804) 1.313 (.952 (.905) ..361-. Workplace standards and guidelines for external air exposure to cobalt and several of its compounds have been established by OSHA and ACGIH.895-1.534 (.708) .425) .550-.09) 1.683-.365) .594) .475 (.313-.409) .393 (.949) . population from the National Health and Nutrition Examination Survey.00 (.272-.29 (1.329 (.408 (.16) .23 (1.00 (.667-1.630-.457) .14 (.83) 1.344-.378-.513 (.00 (.615) .343 (.750) .24) .611) .457 (..12-1.689 (.378-.325) Sample size 2465 2689 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .352 (. Once absorbed and distributed in the body.439) .00 (.407 (.700 (.537 (.259 (.290 (.976 (.508-.781-1.626-.259-.25 (.388 (.00-1.27) 1.733-1.302-.635 (.33) 1.523 (.429) 1.327-.36) 1. Elimination reflects a multi-compartmental model dominated by compartments with half-lives on the order of several hours to a week.561) .273 (.932-1.669) .455 (.562) .990-1.463-.12 (.282 (.503-.842) .581) .703-.60) 1.365-..Metals fabricated from cobalt alloys (Lhotka et al.55) .611) .57) 1.694) .360) .679-.353-.879-1.634-.353 (.595) . Cobalt is absorbed by oral and pulmonary routes.333-. using hard metal cutting tools.929) ..54) 1.369 (.368) .10 (.49) 1.50 (1.301) .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 . and to a lesser extent.737 (.362 (.290 (.560-.829-1.900-1.700 (.500 (.723 (.435-.291 (.343-.25 (.582-.760-1.786-.872 (.616-.963-1. Lung retention of relatively insoluble cobalt compounds such as cobalt oxide may be prolonged.964 (.297-.598 (.660-.19) .10) .03-1.574-.333-.898 (.392 (.471 (.29) 1.306 (.331-.850-1.328 (.847) . respectively.28) 1.500-.36) 1.750-.248-.268 (.388 (.821 (.281) .829) .554 (.319-.247 (.442-.983-1.296-.355) .30 (1.960 (.306) 75th . with pulmonary clearance half-lives of from one to two years (Hedge et al.417 (.975 (.10) Total .488) .313-..632-.286) .955) .609) .16 (.850 (.335 (.543) .280-.487-.04 (.963) . cobalt is excreted predominantly in the urine. interval) . 1972).911-1.289) .361 (.462) .591 (.324-.239-.279 (. Exposure in the workplace may come from electroplating.300) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.04-1.851 (.727 (.449-.513-.06 (.296) .29 (1.434-.352) .368 (.830 (.777-.294-.361-.479-.963) .419) .03 (.599) .362) .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 .29) .11-1.15 (.317 (.290 (.313-.468) .435 (.562) .821-3.304-.S.792 (. in the feces.60) 1.667-1.740-1.257-.736-.376 (.638-1. Human studies with 60Co administered as soluble cobalt chloride have reported oral absorption ranging from approximately 1 to 25 % (Smith et al.313-.781) 95th 1.73) 1. Recent inhalation exposure to soluble cobalt compounds can be monitored by measuring cobalt in urine or blood (Lison et al.279) .237-. 2003).348) .11-1.917) .334) . but with a minor fraction (10-15 %) exhibiting a half-life of several years (Mosconi et al.352 (.378-.471-.738 (.328) .

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

Gross RT. Vitali MT. Metal ion levels after metal-on-metal proximal femoral replacements: a 30-year follow-up. Diepgen TL. Ichikawa Y. Metal-on-metal versus polyethylene in hip arthroplasty: a randomized clinical trial. Mutat Res 2003. Dunstan E. Lison D. Lison D. J Bone Joint Surg Br 2005.Metals effects of cobalt. Am J Ind Med 2003. Kriss JP. Dunning SP. Industrial Chemical Exposure: Guidelines for Biological Monitoring. Chest 1989.58(10):631-634. and hard metal dust. Hammon E. Kato M. et al.36:732-734. et al. The release of metals from metal-onmetal surface arthroplasty of the hip. et al. Blunn G.” Contact Dermatitis 2001. Alessandrelli M. Occupationallyinduced “isolated cobalt sensitization. a study of 13 elements in blood and urine of a United Kingdom population. Lisi P. Kusaka Y. Boca Raton (FL): Lewis Publishers. Salama A. Heki S. Weyher I. Angerer J. Biological monitoring of workers exposed to cobalt metal. Bourne RB.88(4):443448. Shirakawa T. Fujimura N. The effect of the diameter of metal-on-metal bearings on systemic exposure to cobalt and chromium. Romazini S. Hoet P.20(1):25-31. Kiilunen M.45:246-247. Zobelein P. Exposure assessment in the hard metal manufacturing industry with special regard to tungsten and its compounds. Science 1988.204:147-160. et al. HoffmannB. McMinn DJ. Toxic trace element reference levels in blood and urine: influence of gender and lifestyle factors. Linnainmaa M. Cobalt and antimony: genotoxicity and carcinogenicity.95:29-37. J Trace Elem Med Biol 2006. Kristiansen J. Sabbioni E. Hoher T. Weber A. Buchet JP. Cannon SR.22:359367. et al. oxides. Dickel H. De Boeck M.34:620-626. Lauwerys R. Schank M. Thomassen H. 1985. Edmonds CJ. Goldberg MA. DeSantis V. Moulin JJ. Kraus T. Peltier A.150(1-3):167-171. Occup Environ Med 1994.(1-3):133-139. Hedge AG. Thabe H. Roto P. et al. Am J Epidemiol 1998.48:172-173. Bacis M. Int Arch Occup Environ Health 1997. J Bone Joint Surg Br 2006. J Orthop Res 2003. Lauwerys R. Uitti J. Linna A. Rorabeck CH. Meyer zum Buschenfelde K-H. Goto S.406:282-296. Oksa P. Lung cancer risk in hard-metal workers. Unwin P.148:241-248. J Rheumatol 2001. Kuska Y. Tilley S. cobalt salts. Palmroos P. Swennen B. Bunn HF.69(3):193-200. MacDonald SJ. Stanescu D. Sabbioni E. Lhotka C. Lison D. Hypothyroidism and thyroid hyperplasia in patients treated with cobalt JAMA 1955. Steffan I. Kirsch-Volders M. Clin Orthop Relat Res 2003. Lasfargues G. Daniel J. Zweymuller K. Laippala P. Jarvis JQ. Trace element reference values in tissues from inhabitants of the European Union.150. 3rd ed. Barnaby CF. Health Phys 1979. Schaller KH. Br J Ind Med 1993. Biological monitoring of cobalt exposure based on cobalt concentrations in blood and urine. Co-sensitivity between cobalt and other transition metals. Buchet JP. Carnes WH.44:124-132. Cobalt excretion in urine: results of a study on workers producing diamond grinding tools and on a control group. Four-year study of cobalt and chromium blood levels in patients managed with two different metal-on-metal total hip replacements.242:1412-1415. Schramel P. Ghat IS. Cleland D. Outcome of occupational asthma due to cobalt hypersensitivity.216:253-270. Fourth National Report on Human Exposure to Environmental Chemicals 211 . Pisati G. Falcone G. Occupational asthma from cobalt sensitivity in workers exposed to hard metal dust.87(5):628-631. 2001. and cobalt metals. Cresti R. Molders J. Epidemiological survey of workers exposed to cobalt oxides. Salvatori S. Szekeres T.28(5):1121-1128. Swennen B. Sabbioni E. Sci Total Environ 1994. J Occup Med 1992. Radulescu M. Cobalt cardiomyopathy. Cobalt-specific T lymphocytes in synovial tissue after an allergic reaction to cobalt alloy joint prosthesis. Int Arch Occup Environ Health.150:177-183.533:135-152.21(2):189-195. Iversen BS. Wild P. Chess DG. Ziaee H.55(4):269-276. A report of two cases from mineral assay laboratories and a review of the literature. Bozec C.50(9):835-842. Smith T. Occup Environ Med 2001. X.157:117121. Mosconi G. Pradhan C. Sci Total Environ 1994. Regulation of the erythropoietin gene: evidence that the oxygen sensor is a heme protein. White MA. Zedda S. Urinary cobalt as a measure of exposure in the wet sharpening of hard metal and satellite blades. Iavicoli I. Zhuber K. Long-term clearance of inhaled 60Co. Goto S. Robinson C. Sci Total Environ 1998. Arch Intern Med 1990. Absorption and retention of cobalt in man by whole-body counting. Contact Dermatitis 2003. Respiratory health of cobalt production workers. Christensen JM. Lauwerys RB. salt. Sanghrajka AP. Sci Total Environ 1997. McCalden RW. Thakker DM.51(7):447450. Leghissa P. Health Phys 1972. Meier R.

30 (4.60-1.800-1.20) 1.90) 1.86) 1.40-1.70 (1.90) 2.25) 1.70 (2.90 (3.00-2.50-2.00 (6. Lead was used in plumbing for centuries and may still be present.50-2.00) 6.30-4. Lead has a variety of uses in manufacturing: storage batteries.50-2.52 (1.10-4.65 (1.60 (1.81) 1.60 (2. respectively.10 (1.00) .70-4.89) 1.90-4.80 (1.50-1.60) 723 898 911 905 1044 856 2135 2231 2081 4207 4772 4525 6-11 years 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 2.50-4.10) 5.90 (3.55-1.10) 2.20 (3.71-1.90-2.55 (1.30 (1.00-4.30-2.20 (1.60-4.30) 2.40-6.30 (1.80) 3.70) 1.20-3.00 (5.80) 2.70 (5.70) 1.80 (1.30) 2.60-3.60) 2.36) 1.40-6.70-1. malleable.70) 4.20) 3.60 (1.40-1.80 (1.10-3.70) 4.30) 1.40) 1. leaded glass.43 (1.20-2. solders.10) 1.10-2.20 (2.60 (1.60 (1.60 (2.80 (2.70 (2.40) 1.60) 5.50) 5.53) 1.40) 1.56 (1.60 (3.40 (1.36-1.00) 1.40 (5.40) 5.48) 1.10) 3.60) 1.946 (.75) 1.19 (1.60) 1.30-1.10) 1.40) 2. see Data Analysis section) for Survey years 99-00.50) 2.50) 4.70 (1.46 (1.10-1. Elemental lead can be combined with other elements to form inorganic and organic compounds.00 (1.60 (1.87 (1.60-2. and 03-04 are 0.10) 1.40-3.Metals Lead CAS No.40 (2.30-6.00-6.90-3.60) 4.40) Total 1.34-1. metal alloys (e.30) 2.70 (1.60 (4. antique-molded or cast ornaments.30 (3.90 (2.30) 95th 5.40-1. population was aerosolized lead emitted from combustion engines that used leaded gasoline.10-3.93-2.80 (2.20 (1.60) 1.80-2. Since lead has been eliminated from gasoline.10 (3. and for radiation shielding.60) 3.50 (1.50-1.00) 2.40 (3.60-6.52-1.S.60) 2. brass.45-1.80) 1.70) 3.50) 75th 2.20 (2.00) 3.20-3.30-2.51) 1.23 (1.60 (2.20-3.10 (1.60) 1.50 (4.10-2.62) 1.50-4.30 (2.37 (1.50 (1.80) 2.70-3.10-6.80) 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 1.80 (4.00) 2.70-2.50-5.90-2.20 (1.90) 1.60) 4.25 (1.70-1.37-1.50 (1.40-2.32-1.43-1.50-3.00) 2.70-2.30 (2.20 (1.00) 1.90-2.60-2.75-2.69) 1.66 (1. ammunition.55-1.50) 5. 212 Fourth National Report on Human Exposure to Environmental Chemicals .60 (2.20) 3.900 (.32-1.00-1.30) 5.20-1.70-6.30 (1.70-5.50-5.30-2.10) 3.60) 2.10-2.40-1.30-1.70) 1.30 (2.60-1.90) 2.12-1. population from the National Health and Nutrition Examination Survey.00-4.40 (1.51 (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.69 (1.70) 4.43 (1.30 (1.83 (1.20) 3.00) 1.60) 3.20 (3.43) 1.77 (1.80) 2.80 (4. Lead is most often mined from ores or recycled from scrap metal or batteries.50-1.69) 1.70 (1.70) 1. Before the 1980’s.50-2.80) 2.60-1.90 (1.50 (3.60) 4.00 (3.20) 2.60) 4.30-1.80) 1.80 (1.S.80-3.00) 4.01 (1.00 (2.70) 1.90 (3.02) 1.70) 3.17) .20-2.00) 1.90) 1.10-2.31) 1.50-1.50 (1.00 (1.20) 3.00) 3.40-2.14-1.00) 4.49-1.899-.75-1.62-1.22 (1.90 (1.50) 1.80 (5.80-4.10-2. such as lead phosphate and tetraethyl lead.20-6.20 (3.60) 3.60) 5.10-2.50 (2.50-1.g.10-3.900-1.40-5.30-1.20 (3.40 (4.40) 3. 0.40-1.50 (2.90-4.60 (2.20) 5.75 (1.30 (2.50 (2.60 (2.10) 4.80-4.80 (2.70) 2.60 (3. Aerosolized lead is either inhaled or ingested after it is deposited on surfaces and food crops.91) 1.90) 3.20) 90th 3. lead was added to gasoline and residential paints and used in soldering the seams of food cans.80-3.50) 7.50) 2.60 (3.70 (3.10-1.20-3.90 (3.900 (.68-1.80) 1. the main source of lead exposure for the general U.60-1.70) 4.90 (4.10-4.40-2.20 (4.40 (2.3.45 (1. ceramic glazes.00-4.36-1.90-4.00-1.20) .60) 2.60) 3.10) 3.20 (3.66) 1.20 (3.40-4.80 (3.39-1.40 (1.30-1.60-4.14-1.96-2.80) 1.00) 1.43) 1. interval) 1.50 (2. and 0.40-3.90-6.20 (1.80-5.50-6.10 (2.90 (3.40-1. plastics.04-1.90) 3.10) 2.80 (1.50-3.00) 2.90-4.40) 2.80-3.25 (1.40-3.80 (1.986) .50) 4.70-2.28.90) 2.80) 1. blue-gray metal that occurs naturally in soils and rocks.50) 1.00) 5.10 (4.00 (4.60) 2.78 (1.3.20-1.14-1. bronze).942 (.40) 2.70-1.10 (1.52-1.39) 1. dense.70 (2.20) 4. 01-02.20) 4.62 (1.10-8.90) 2.80-4.90) 2.20 (3.00 (4.30 (2.50) 3.30 (2.20-4.70) 3.50 (4.50) 1.80-3.10-3. In the past. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.10-6.40) 2.60 (1.30-2.72) Selected percentiles ( 95% confidence interval) 50th 1.30-5.95) 1.90-2.50 (2.80 (5.00-5.30-1.90) 5.90 (2.878-1.50) 1. 7439-92-1 General Information Elemental lead is a soft.30 (4.10 (2.60 (1.70 (3.69 (1.60 (3.87) 1.30 (4.10-1.09) 1.10 (2.50) Sample size 7970 8945 8373 Age group 1-5 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 2.30) 2742 2268 2085 1842 2219 2293 2716 3806 3478 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.40) 4.30 (2.60) 1.40 (1.37 (1.50 (3.

70-3.900) .90-2.80) 2.52-1.700-.20 (2.900) .33-2.910-.70) 3.89) 2.14-1.661-.20-2.40 (1.90) 1.700 (. population from the National Health and Nutrition Examination Survey.97) 4.90-2.940 (.700-.613) .730 (.700 (.642 (.753 (.800-1.10 (1.808 (.80-2. 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.30) 2.30) 1.625-.00 (1.30-3.800-.688 (.41) 2.900-1.20 (1.14 (1.02) 1.30) 1.731 (.40) 2.11) 2. 2007.72) 1. and contact with soil.75) 3.40-1.990) 1.591 (.900) .850 (.691-.10-3.10) 2.04) .600-.900-1.91) 2.20 (2.40-5.86) 95th 2.820-1.80) 2.73 (1.749) .766 (.10-1.70) 1.07-1.17 (1.604 (.90 (1.78-2.500-.526-.558 (.10) .80) 3.572-. Lead is absorbed into the body after fine lead particulates or fumes are inhaled.82 (1.970-1.30) . In the blood.30) 2.60-2.50 (1.20) 1.20 (1. see Data Analysis section) for Survey years 99-00.90 (1.70 (2.600 (.31-3.800-1.10-3.60 (2.800) .553-.20 (1.40) 1.00) .80) 1.10 (.00) 2.941) .700 (.70 (2.757-.00) 1.640-. dust.800 (. and 03-04 are 0.00-2.857) .595-.20) .40-1.30) 1.50-1.04) 2.20) 1.49 (1.07 (.20 (1.960-1. or after soluble lead compounds are ingested. absorbed lead is bound to erythrocytes and then is distributed initially to multiple soft tissues and eventually into bone.09) 1.535-.590 (.g.20 (1.10-3.30-1.671-.915-1.960-1.78-2.23) .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 .50 (1.10 (.641-.04-2.02 (.59) 1.10-1.600 (.27) 1.00 (2. However.600) .828) Selected percentiles ( 95% confidence interval) 50th . battery and radiator manufacturing) and recreational sources.90 (1.833-1. or water contaminated by mining or smelting operations.70-2. lead-contaminated dust in indoor firing ranges.900-1.556-.50-2. and 0.86 (1.21 (2.40) 3.560-.40 (1.S.00) .738) .10) 1.00 (1.800) . pewter utensils and drinking vessels.700-1.12) 90th 2.70) 1.90-3.677 (.20-1.50-2.75) 4.70 (2.Metals occupational (e.708-.700 (.90) 2.20) .920 (.86) 1.800-.625 (.10-1. which is the site of approximately Urinary Lead Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.20-1.40 (1.630 (.822-1. Less common sources of incidental or unique lead exposure are numerous: lead-glazed ceramic pottery.620) 1.785) .80 (2.600) .900 (.60) 2.40 (1.24-1.90) 2.900 (.80) 2.660) .10 (1.18-1.11 (1.10 (1. 01-02.03-2.30-1.718) .700-. bullet fragments retained in human tissue.580-.19 (1.800) .00-2.40) 2.30 (2.659 (.86-2.40 (2.600-.00) .35 (.570-.40 (1.900) .30 (1.03 (1.564 (.32 (1.10 (1.573 (.920 (.680) .50-3.62) Total .82 (2.10) 2.790 (.695 (.10 (.680-.29 (2.40) 2.506-.10-1.90) 2.00) .610 (.13-3.66 (2.579-.605) .59-2. respectively.636 (. interval) .20) .66 (2.900) .60 (1.616) .800) .1.50) 1.30-1.60-3.00-1.680) Sample size 2465 2690 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.935) 1.40 (2.840 (. Small amounts of environmental lead also may result from burning fossil fuels (ATSDR.752 (.745-.90 (2.960 (.20 (3. CDC.31 (1.40) 1..60-2.90-3.70 (1.20) .862) .50) 2..70) 2.800 (.70 (2.900) .815 (.60-1.52 (1.700) 1.90 (2.70) 1.52-1.589-.80) 2.540 (.00-2.80-3.33.60-3.40-1.50) 1.50 (2.628) 1.800) .50-2.620 (.30) 1.923 (.20-1.579-.40) 2.710-.40 (2.600-.900-1.30) 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 1.795 (.10) . lead-containing folk remedies and cosmetics.40-1.29) 2.674) 1.14 (1.50 (2.700) .62-4.773) .80) 1.40) 1.690) 75th 1.650) 1.23-4.13) .20-2.800 (.06) .480-. 0. 2000).833 (.20) 1.800 (.40 (2. Children may also be exposed to lead brought into the home on the work clothes of adults whose work involves lead.700-.00 (1.651) .1.80 (1.40-3.40) 1.04 (.00-1.600-.80) 2.600-.30) 2.60 (1.30-5.80) 3.70) 3.20 (1.33 (2.20 (2.40-2.848 (. older plumbing systems with leaded pipes or lead soldered connections.986) .00) 2. lead-based painted surfaces undergoing renovation or demolition.80 (1.700-. imported children’s trinkets and toys.90-2.700 (.90 (2.701) .90-4.78-2.00 (1.640 (.729-. 1991).44-2.50) 2.680-.30-1.30) 1.40) 1.22) 1.637-.931) .51) 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.710-1. Approximately half of the absorbed lead may be incorporated into bone.10-1.30-2.50) 3.900 (.700 (.30 (3.955-1.540-.810-1.990) 2. the primary source of exposure in children is from deteriorated lead-based paint and the resulting dust and soil contamination (Manton et al. stained glass framing.04 (.00-1.90-2.50) 1.60 (1.80) 1.50 (2.00 (.27 (1.80-2.64) 2.818) . Fourth National Report on Human Exposure to Environmental Chemicals 213 .10-5.60 (1.

28) .38 (2.721 (.979 (.702) .89-2.739) .23 (1.52) 1. Lead is cleared from the blood and soft tissues with a half-life of 1 to 2 months and more slowly from the skeleton.31 (1.97) 1. population from the National Health and Nutrition Examination Survey.975-1.04) 2.62) 2.635 (.559-.33) 1.11 (.61) 1.66 (1. Large amounts of lead in the body can cause anemia.03) .00 (1.657) 1.04-3.72-2.62-3.940 (.681-.26) 2.01 (.639 (.01) .618 (.44 (1.94 (1.43 (1.639 (.615 (.15-2.796-1.712 (.604-.722 (.746) .10 (1.73-2.601-.652 (.677-.18) 1.22-1. based on prospective population studies.793-1. Staessen et al.31 (2.673) .742) Selected percentiles ( 95% confidence interval) 50th .28-1.Metals 90% of the body lead burden in most adults.61) 1.00) .08-2. In 1991.89-5.36-2.621 (.88) 1.08) . The skeleton acts as a storage depot.594-.569 (.67-4.612-. 1993.606-.85-2.78 (2. seizures.898) .988 (.03 (.17-1.648 (.571-.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 .625 (.24 (1.615 (.668-.686) .97 (1.997-1.94-2.41 (1.82) 1.383-.623 (. 1995).03-2.66 (1.720 (.655) 75th 1.33-1.742) .720 (. The toxic effects of lead result from its interference with the physiologic actions of calcium.00 (1.31) 1.609 (.658 (.20) .496 (.05 (1.763) .22) .79) 1.53) 1.22) 1.876-1.56) 3.25-1.00 (1.938-1.682) .588-. Additional mechanisms include generating reactive oxygen species and altering gene expression (ATSDR. kidney injury.718) 1.51) 1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.56 (1.09-1.10) 1. Schwartz.46 (2.607-.17 (.561-.63) 1.11 (1.09) 1.56-2.06) 1.655-. through the inhibition of certain enzymes.50-1.436) .529-.19-5.55 (1.06 (1.707 (.644 (.977) 1.914 (.679-.696 (.677 (. 1995.45 (1.698) . Equilibrated blood lead levels (BLLs) after chronic intake are associated with certain toxic effects.88) 2.693 (..957-1.828) .583-.701 (.98) 2.88 (1.670) 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 1.676) .946-1.61) 1.851) .683-.15) 1.790) .64 (1.50-2.461) .571-.605-.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 .404 (.75 (2. 2007).655) .40-1.758) .20-3.681-.641 (.15-2..06) .18 (1.85-2.838) .85) 1.11) 1.09-1.632 (.98 (1.88-2.39-1.06 (.432 (.79 (1.608-.702) .07-1.S.639 (.893) .52 (1.667) .617-.46 (1.62-1.703) . zinc. 2003.35) 2.87) 1.698) .49 (1.914 (.88) 2. BLLs near 10 µg/dL can affect blood pressure in adults and neurodevelopment in children (Bellinger.645-.79) 2.679) 1.992-1.72) .44) 1.50) 1.608 (.51 (1. Nash et al.722 (.37-1.05-1.992-1.639) .659-.404 (.08) .774 (.12-1.03) 90th 1.31) 1.97) 1.22-2.97-18.86 (1.988-1.83 (2.579-.375 (.64) 2.62-2.15) 1.812-1.02-1.44 (1.31 (1.428) .667-.26) Total .11 (1.41) .61) 1.48 (1.701) .65-2.588-..718) .933) .11 (. Approximately 70% of lead excretion occurs via the urine.492-.708 (.00 (.47 (1.20) .725) .380-.404-.603-.510-.918-1.71 (1.853-1.963-1.03) .862-.400) .07 (.29 (1.64-2.12) 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 .05-1.920-1.633 (.55 (1.53-1.810 (. Lead can cross the placenta and enter the developing fetal brain.469 (.03 (.03) 1.702-.644) .28) 2.594-.870 (. 2004.14) 1.587-. 1996).730) 1.03 (.938 (.50-2.38 (2.27 (1. O’Flaherty.800-.33 (1.603 (.623 (.74 (1.603-. and nails (Leggett.07) .72-2. For instance.56-3. 1993). hair. with a half-life of years to decades.753) .900 (. scant amounts are lost through sweat.14 (1.990 (.78-4.18) 1.03 (1.981-1. abdominal pain. 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.887 (.841-1.37-1.71-2.09-1.65 (1.10 (.68 (1. and iron.828-1.43) 1.622 (.649 (.22) 1. with lesser amounts eliminated via the feces.50-2.0) 3. and paralysis.25-1.667-. and through binding to ion channels and regulatory proteins.535) .755 (.98-2.77) 2.645-.92) 2.38 (2.700-.734) .03) 2. encephalopathy.677) . and approximately 40 to 70% of lead in blood comes from the skeleton in environmentally exposed adults (Smith et al.586-.593 (.43 (2.408-.654) .73) 2.671 (.05 (.96 (1.933-1.11-1.63) 4.688) .43-1.59-3. 1991.19) 1.75-2. interval) .11) .69 (1.58) 1.18) 2.971 (.962 (.460-.41-1.15-3.765) .926 (.03) 1.592-.64) 95th 2.731-.61) 3.725) .02) 1.03) 2.50 (1.781-1.47) 1.70 (1.85 (1.508) .551-.541-. CDC.709 (.638 (.43) 2.18) .33) 2.66) 2.34-1.917-1.47 (2.710) .882-1.914-1.918 (.342-.83) 1. BLLs and associated toxic effects differ in children and adults.

S.. particularly in the skeleton. 2001).cdc.xls). 2003. adult population has similar or slightly lower BLLs than adults in other developed nations (CDC.4% of children had BLLs of 10µg/dL or higher (CDC. The U. 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. Workplace standards and guidelines for lead exposure and monitoring have been established by OSHA and ACGIH. reduce sperm count. 1996.. 2006). urban residence. adults in the 1999-2000 NHANES sample.. the geometric mean BLL was 3. Urine levels may reflect recently absorbed lead. Fourth National Report on Human Exposure to Environmental Chemicals 215 . approximately 11. adult residents. and decrease fertility (Alexander et al.6%) were lower than those from NHANES 1991-1994.0 µg/dL in females (Soldin et al. including minority race or ethnicity. respectively.. Jones et al (2009) showed that the prevalence of BLLs of 10 µg/dL or greater decreased from 8. Data submitted through state public health programs from 2006 showed that 1.S. Telisman et al.gov/toxpro2. and peripheral neuropathy generally occurring at much higher levels (e.S. 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.. Surveillance data reported by U.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. 2003. 2002. and low family income (CDC.000 adults. For example.9 µg/dL) and percentage of children with BLLs greater than 10 µg/dL (1. BLLs reflect both recent intake and equilibration with stored lead in other tissues.. However. 1999). At low environmental exposures.. the national prevalence rate for adults with BLLs 25 mg/dL or higher was 7.e. 1996.cdc.html. 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... 2005a). 2002). Temporal declines in children’s BLLs have been found in other developed countries (Wilhelm et al.. 1999). Korrick et al. Recent studies have suggested that neurodevelopmental effects may occur at BLLs lower than 10 µg/dL (Canfield et al. and spontaneous abortion (Baghurst et al. Muntner et al. A general population survey of adults Germany in 1998 reported a geometric mean blood lead concentration of 3. 2003). Schwartz et al. EPA. Lanphear et al. and organic lead compounds not classifiable with respect to human carcinogenicity.. 1987. 2007).. Borja-Aburto et al. the prevalence rate has declined annually since 1994 (CDC.21% of approximately 3.75 µg/dL in U. More recently. 1995. residing in housing built before the 1950’s. Pirkle et al.7 µg/dL and 4. In occupationally exposed adults.. 1998). 1984.. 2000).gov/nceh/lead/surv/database/State_ Confirmed_byYear_1997_to_2006.4% in NHANES 1999-2004. NTP considers lead and its compounds reasonably anticipated to be human carcinogens. 2000). Payton et al. which is an 84% decline. High dose occupational lead exposure..S..S.. with overt encephalopathy. 2002a).5 per 100. lead in women may be associated with hypertension during pregnancy. 1995) and associations between increased bone lead concentrations and blood pressure (Hu et al. both the geometric mean (1. 2003. A general population survey of adults in Italy tested in 2000 found BLLs slightly more than double those reported for U... 2009). 2005b. Information about external exposure (i. Biomonitoring Information Blood lead measurement is the preferred method of evaluating lead exposure and its human health effects.. 2005b). Schwartz.07 µg/dL (Becker et al..g. higher than 100-200 µg/dL). environmental levels) and health effects is available from ATSDR at: http://www. Staessen et al. CDC. In NHANES 1999-2002 in children 1-5 years old.3 million children tested had BLLs of 10 mg/dL or higher (http://www. when the geometric mean BLL was 2..Metals µg/dL or higher as the level of concern in children. IARC considers inorganic lead compounds probable human carcinogens. 1991. premature delivery. 1996. Overall. subtle or nonspecific neurocognitive effects have been reported at BLLs as low as 20-30 µg/dL (Mantere et al.S. Bellinger 2005. usually with BLLs greater than 40 mg/dL. may alter sperm morphology. though there is greater individual variation in urine lead than in blood and greater potential for contamination. 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.atsdr. Many animal studies have established the multiple neurotoxic effects of lead (ATSDR.. Jones et al.6% in NHANES 1988-1991 to 1. A decrease in BLLs is evident also in adult NHANES results reported over past decades (CDC. adults in the 19992000 NHANES sample (Apostoli et al. seizures. 1994).2 µg/dL in males and 3. 2006). almost double the geometric mean of 1. BLLs greater than 10 µg/dL continue to be more prevalent among children with known risk factors. Low level environmental lead exposure may be associated with small decrements in renal function (Kim et al. Both drinking water and ambient air standards for lead have been established by the U.

et al.55(32):876-879. et al. Neurodevelopmental effects of postnatal lead exposure at very low levels.150(6):590-597. N Engl J Med 2003. 1988-2004. Intellectual impairment in children with blood lead concentrations below 10 µg/dL. McMichael AJ. 2005. Hertz-Picciotto I. Becker K. Reese YR. Brody DJ.275:1177-1181. Recommendations from the Advisory Committee on Childhood Lead Poisoning Prevention. Atlanta. Sparrow D.1542/peds:2007-3608. Stanek KL. Neurotoxicol 1987. 2003-2004. Managing Elevated Blood Lead Levels Among Young Children. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Ga. Blood lead levels measured prospectively and risk of spontaneous abortion.cdc. Atlanta (GA). 4/14/09 Centers for Disease Control and Prevention (CDC). Public Health Rep 2000.cdc. Blood lead and chronic kidney disease in the general United States population: 216 Fourth National Report on Human Exposure to Environmental Chemicals . Dietrich K. Blood lead levels—United States.atsdr. JAMA 1996. et al. Centers for Disease Control and Prevention (CDC). Cory-Slechta DA. Vimpani FB. Ronchi L. Baj A. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Neurotoxicol Teratol 2004. IARC Monogr Eval Carcinog Risks Hum 2006. Occup Environ Med 1996.Metals Biomonitoring studies on levels of lead provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of lead than are found in the general population. Cognitive deficits with blood lead concentrations < 10 µg/dL in US children and adolescents. Acquisition and retention of lead by young children. Available at URL: http://www. Lanphear BP. Hänninen H. gov/mmwr/preview/mmwrhtml/mm5420a5. Jusko TA. Manton WI. The Port Pirie cohort study: lead effects on pregnancy outcome and early childhood development. Hu H.htm. Blanco J. Blood lead reference values: the results of an Italian polycentric study. Seiwert M.cdc. 1991 [online]. 2002 [online]. Kaus S. Caldwell KL. Hu H. 4/14/09 Centers for Disease Control and Prevention (CDC). Payton M. Canfield RL. MMWR Morb Mortal Wkly Rep 2005a. Aug 2007 [online]. MMWR Morb Mortal Wkly Rep 2006. 2005b. Kaufman JD.115:521-529. Weiss ST. Ganzi A.gov/toxprofiles/tp13. Homa DM.348:15171526. 4/14/09 Centers for Disease Control and Prevention (CDC). Kuehnemann TJ.gov/mmwr/preview/mmwrhtml/ mm5532a2.53:411-416. Teratogen update: lead and pregnancy.123:e376-e385. doi:10. Rotnitzky A. The relationship of bone and blood lead to hypertension.82:60-80. Wigg NR. Wager C. Environ Health Perspect 1993. Jacobson JL. Bellinger D.54(20):513-516.87:1-471. Muntner P. Roberts RR. Preventing Lead Poisoning in Young Children.205:297-308.101(7):598-616. Kim R. Angle CR. van Netten C.26:359-371. Inorganic and Organic Lead Compounds. Leggett RW. Batuman V. Rotnitzky A. Birth Defects Research (Part A). Farias P.cdc. 4/14/09 Alexander BH. Henderson CR. Baghurst PA.10:43-50. Luukkonen R. Hunter DJ. Bellinger D. Int J Hyg Environ Health 2002. 1999-2002. Jacobson SW.8(3):395-401. Atlanta (GA).htm. Korrick SA. Sci Total Environ 2002. Weiss ST. Cox C. Chiodo LM. Aro A. Adult blood lead epidemiology and surveillance—United States. Auinger P. Apostoli P.113(4):1016-1022. Ewers TG. Muller CH. Meyer PA.htm.275(15):1171-1176. Trends in blood lead levels and blood lead testing among US children aged 1 to 5 yeas. Korrick S. CDC.287:1-11.gov/nceh/lead/publications/ books/plpyc/contents. Borja-Aburto VH. A prospective follow-up study on psychological effects in workers exposed to low levels of lead. Available at URL: http://www. Available from URL: http://www. Pirkle JL. Available at URL: http://www. Coresh J. 4/14/09 Centers for Disease Control and Prevention (CDC). Sparrow D.cdc. Lepom P. Lead. Lead and hypertension in a sample of middle-aged women. Neri A. Scand J Work Environ Health 1984. Rios C.89:330-335. Pediatrics 2004. Am J Public Health 1999. Toxicological profile for lead. JAMA 1996. Hernberg S. Age-specific kinetic model of lead metal in humans. Checkoway H. Mantere P. Krause C.html. Jones RL. Bavazzano P. Semen quality of men employed at a lead smelter. A longitudinal study of low-level lead exposure and impairment of renal function: the Normative Aging Study. Speizer FE. Am J Epidemiol 1999. Pediatrics 2009. Schulz C. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population.gov/nceh/lead/ CaseManagement/caseManage_main. et al. Third National Report on Human Exposure to Environmental Chemicals. References Agency for Toxic Substances and Disease Registry (ATSDR).73:409-420. Hu H. Cox C. et al. Vupputyuri S. Available at URL: http://www.htm. Environ Res 2000. Rojas LM. Lanphear BP. Robertson EF.

Osterloh JD. Low-level lead exposure and renal function in the Normative Aging Study. Soldin OP. Use of endogenous. O’Flaherty EJ. Weiss ST. Lustberg M.153(5):453464. et al. Sherwin R. Paschal DC. Environ Health Perspect 2000. Rubin R. Physiologically based models for bone-seeking elements. Smith DR. Hwang KY. J Hum Hypertens 1995. Revised and new reference values for arsenic.327:109-113. blood pressure and cardiovascular disease in men. Am J Epidemiol 2001.9:303-327. Pizent A. Semen quality and reproductive endocrine function in relation to biomarkers of lead.108(1):45-53.Metals results from NHANES III. Nash D.140:821-829. Lauwerys RR. Lee SS. Cvitkovic P. Schwenk M. and tibia lead with neurobehavioral test scores in South Korean lead workers. Pirkle JL. Hanak B. dimercaptosuccinic acidchelatable lead. Brody DJ.209:301305.118:16-29. Gavella M. Low-level lead exposure and blood pressure. Hu H. Telisman S.S. Clin Chim Acta 2003.104(1):60-66. Am J Epidemiol 1994. 50:31-37. Kidney Int 2003. et al. Blood lead concentrations in children: new ranges. stable lead isotopes to determine release of lead from the skeleton. Fourth National Report on Human Exposure to Environmental Chemicals 217 . zinc. Hickman T. and hypertension in perimenopausal and postmenopausal women. Staessen JA. Int J Hyg Environ Health 2006. Lee GS. Gunter EW. Payton M. Blood lead. Jurasovic J. Environ Health Perspect 1996.63:1044-1050. Association of blood lead. population to lead: 1991-1994. Exposure of the U. cadmium. Rocic B. Sparrow D. Schwartz BS. Flegal AR. Toxicol Appl Pharmacol 1993. Magder L. Soldin SJ. Kaufmann RB. Arch Environ Health 1995. Schulz D. Environ Health Perspect 1998. lead. blood pressure. Roels H. JAMA 2003.106:745-750. Stewar WF. Lee BK. Lead. and copper in men. Kaufmann R.289(12):1523-1531. Schwartz J. cadmium. IV. Kinetics of lead disposition in humans. Wilhelm M. Amery A. and mercury in blood or urine of children: basis for validation of human biomonitoring data in environmental medicine.

70 (1.50) 5..800-1.40-3.40-1. 1980.80) 3.400-. Apart from methyl mercury. 1999 .80 (1. 218 Fourth National Report on Human Exposure to Environmental Chemicals .60 (2.800-1.00) 4. Inorganic mercury compounds such as mercuric oxide are used in producing batteries and pigments and in synthesizing many organic chemicals.Metals Mercury CAS No.800 (.886) . Poorly absorbed from the gastrointestinal tract.797 (. Elemental mercury is used to produce chlorine gas and caustic soda for industrial applications.689-.30-2.50-3.60-3.40 (3.80) 4.30) 1.00 (2.30) 3.20-4.700 (.12) .900) 75th 1.00-5..90) 3. thermostats and switches).00 (.50) 4.927) .70 (3.50-2. population from the National Health and Nutrition Examination Survey.500 (.00 (2.700) .. The ingestion of methyl mercury.70-2.90 (1. and mercury compounds are still used as preservatives (e.900) 1.90 (4. Imported folk and alternative medicines occasionally are contaminated with inorganic mercury.80) 1. 1998.70 (4.400 (.500-.00) 1.326 (.300-.10) .00 (.60-6.40) 1.472-. to form inorganic mercury compounds or salts.60-5. which can bioaccumulate in aquatic and terrestrial food chains.30) 5. sphygmomanometers and barometers.903) Selected percentiles ( 95% confidence interval) 50th .80 (3.90 (1. IARC.300) . Accidental spills of elemental mercury.30-5.00 (1.00) 3.40 (4.574) .753-1. and organic forms.400-.700) .900) 1.20) 2. and is distributed to most tissues.40-2.80 (1.700-.00 (.g.700-.30-4. Inorganic mercury exists in two oxidative states (mercurous and mercuric) that combine with other elements. may contain inorganic mercury.703-.800 (.700-.20 (2.90) 95th 4. Also. mercuric chloride). Woods et al.g.60) 1.60 (1.800 (.30) 1. 1994.60-6..800-1.672) . water can be contaminated by the direct release of elemental and inorganic mercury from industrial discharges.655-. with the highest concentrations occurring in the kidneys (Barregard et al..700-.40 (3. Metabolism of mercury by microorganisms in aquatic sediments creates methyl mercury.285-.g.00) 1.900) 1. thimerosal.30 (1.20-3. solid-waste incineration. inorganic.490 (.60) 1.60-2.50-1.776 (.500) . In addition.419 (. The kinetics of the different forms of mercury vary considerably.363-.60) 2085 2293 3478 Limit of detection (LOD.S. Survey years 03-04 Geometric mean (95% conf.979 (.70) 911 856 2081 4525 03-04 03-04 .814 (.418-.877 (.800-1.50) 2.600 (. thermometers.563 (.372) .. synthetic organomercury compounds were once used in pharmaceutical applications. 1993). merbromin).500 (. 7439-97-6 General Information Mercury is a naturally occurring metal that has elemental (metallic). and mining and smelting. or oxygen. After elemental mercury is absorbed.700-. Inhalation of elemental mercury volatilized from dental amalgam is a major source of mercury exposure in the general population (Halbach.30) 3. 2002). Kingman et al.500-.S.900 (.30 (2.g. interval) .10-3.40-1.40-2.00 (2.40) 3.30) 4132 4241 03-04 03-04 03-04 ..800 (.. such as chlorine (e..860-1. Elemental mercury is a shiny.80 (1. elemental mercury is absorbed mainly by inhaling volatilized vapor.90) 90th 3.00 (.20-4. constitutes the main source of dietary mercury exposure in the general population. it is oxidized in Total Blood Mercury—2003-2004 Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U.2. Hursh et al. an organic form of mercury.00-1. silver-white liquid (quicksilver) obtained predominantly from the refining of mercuric sulfide in cinnabar ore. elemental mercury is used in rituals practiced in some Latin American and Caribbean communities.40 (4. electrical lamps.00) . which create an episodic potential for volatization and inhalation of mercury vapor.50) 1.919) . Some cosmetic skin creams from countries other than the U.300 (.600) 1. phenylmercuric acetate) or topical antiseptics (e. predominantly from fish and other seafood.02) . 2007). see Data Analysis section) for Survey year 03-04 is 0. Other major uses include electrical equipment (e. Atmospheric elemental mercury can be deposited on land and water.90-3.484) . Elemental mercury is released into the air from the combustion of fossil fuels (primarily coal).800-1. and dental amalgam.714-.900) .30-6.60 (1.70 (1. sulfur. have often required public health intervention (Zeitz et al.781 (.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 .

40) 1.317 (.800 (.30-4.70-3.60) 3.00 (2.60 (2.90) Sample size 705 872 318 432 387 440 1709 1928 Age Group 1-5 years (females and males) Females Males 16-49 years (females only) 99-00 01-02 99-00 01-02 99-00 01-02 99-00 01-02 .500-.800) 1.90) 90th 1. 1993).00) .60 (3. 1999-2002. 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..500-. 1998). 1973). McDowell et al.50 (1.200-.369) 1. 2003)..40 (1.300 (. After exposure to elemental mercury..10 (1.833 (.30 (.500 (.90) 2.00 (2.60) 2.20-3.800) .00 (1. 1998).14.01) .30-6.50) 2.10 (1.30-3.800-1.700-.00-3.726-1. excretion of mercury occurs predominantly through the kidney (Sandborgh-Englund et al. Jonsson et al.. 1971). population.256-.60 (1.50-3. Methyl mercury is incorporated into growing hair.300 (.329 (.300) .00-2.50-2.02 (...06 (.20) .20-11.00) 6.30-11.80) 579 527 370 436 588 806 Limit of detection (LOD.50) 95th 2. 1991. thereafter.90 (4.. 1975.80-3.700-1.374) .944 (.35 (1.90) 2.10 (1. Excretion occurs by renal and fecal routes.697-.500 (.20-3..40-2.80 (1.00) 1.70) 4.200 (.919) .60 (3.40 (1.500-1. urinary mercury levels decline with a half-life of approximately 1-3 months (Roels et al.90 (1.20 (. 1999). 1990).30 (1.541-.700-1. Transplacental transport of methyl mercury and elemental mercury has been demonstrated in animals (Kajiwara et al.824) 1.307 (.825-1. 1992).7) 4.70-3.90) 3.400-.73) 1.10 (3. 1996). 2005).395) .269-.700) 2.10) .10) 1.30-2.667 (..940) Race/ethnicity (females.00-1.200-.50) 3.700 (.29) . and peak urine levels can lag behind peak blood levels by days to a few weeks (Barregard et al.300) . Vimy et al. 1996..70 (1.90 (1.600) . 1992 and 1999.700-. Smith and Farris. 1993).900-1. interval) Selected percentiles (95% confidence interval) 50th .30 (1.265-.300) .60 (1. 16-49 years) Mexican Americans Non-hispanic blacks Non-hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 . with most elimination occurring through in the feces (Sherlock et al. The half-life of inorganic mercury in blood is similar to the slow-phase half-life of mercury after inhalation of elemental mercury.30-6.297-.900 (. Geometric mean Survey years (95% conf.300 (.800-1. Blood concentrations decline initially with a rapid halflife of approximately 1-3 days followed by a slower half-life of approximately 1-3 weeks (Barregard et al.700 (.200-.300) . 1994).475) .80) 1.50) 1. The slow-phase half-life may be several weeks longer in persons with chronic occupational exposure (Sallsten et al. Sandborgh-Englund et al.23) .. Mercury levels in the cord blood are higher than in the mother’s blood (Stern and Smith.300 (.. Lesser penetration of inorganic mercury occurs through the bloodbrain barrier than occurs with either elemental or methyl mercury (Hattula and Rahola.30) 3.407) .27) .00 (2.40-2.300) .738-.800 (.20) 1.3) 4.800-1.90 (3.800) 1.200 (.Metals the tissues to mercurous and mercuric inorganic forms.200-..14 and 0. Human pharmacokinetic studies indicate that methyl mercury declines in blood and the whole body with a half-life of approximately 50 days.300) .377) . 1994.50) 1.60) 1. The fraction of methyl mercury absorbed from the gastrointestinal tract is about 95% (Aberg et al.600 (. National Health and Nutrition Examination Survey.20 (2. Vahter et al. a measure of accumulated dose (Cernichiari et al.00) 7.00) 4.00) 1. and a useful marker of exposure in epidemiologic studies (Grandjean et al..900-1.50 (2..700 (.00-2.50-12.820 (.343 (..318 (.10) .500-.70-5.40-1.30-6.60) 1. and the newborn’s levels decline gradually over several weeks (Bjornberg et al.. 1969.800 (.60 (1.00-6..664-1. 1984. Suzuki et al.80 (3.90) 5. 1995.S.00 (3. Miettinen et al.70) 1.377 (.30-5.06-1. Smith et al. 2004.500-.30) 1.871-1.900 (.40) 5.70-6.268-.700 (..800) .. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.10 (5.0) 4..40) 2.00-2.500-.90 (4.10 (. Less than 15% of inorganic mercury is absorbed from the human gastrointestinal tract (Rahola et al. 2003).10 (.30-4.20) . Methyl mercury enters the brain and other tissues (Vahter et al.30) 1.70-5.70 (1. 1992. Myers et al.20-2.600) .10-1.00) 2.70) 4.900 (. Inorganic mercury and methyl mercury are distributed into human breast milk in relatively low concentrations. for both acute and chronic exposures.200-.10-3..30 (1.200-.299-.20-3. 1994) and then undergoes slow dealkylation to inorganic mercury.800) 75th .70 (1. Fourth National Report on Human Exposure to Environmental Chemicals 219 .

700) 2007 2240 3406 Limit of detection (LOD. and progressive constriction of the visual fields.600 (.600 (. typically after a latent period of weeks to months.600 (. 1996).500 (<LOD-.800) 4015 4132 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD . Factor-Litvak et al.600) * 03-04 03-04 03-04 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .800) . 2002.800) . gingivitis. 220 Fourth National Report on Human Exposure to Environmental Chemicals . At levels below those that cause acute lung injury. and cerebral palsy (NRC. insomnia.600) . sensory impairments.600-. 2004.700-. 1995.600) . interval) Selected percentiles ( 95% confidence interval) Sample 95th .500-. population from the National Health and Nutrition Examination Survey.500-. overt signs and symptoms of chronic inhalation may include tremor..600 (.700 (. altered physical growth.600) . 2000.600 (.700 (.700 (. 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. 2005. Once absorbed.500-. irritability.. < LOD means less than the limit of detection. In recent epidemiologic studies.. 2004. Low-level exposure from dental amalgams has not been associated with neurologic effects in children or adults (Bates et al. Survey Geometric mean (95% conf. 1993).600) . Salonen et al. Inorganic mercury exposure usually occurs by ingestion.. Large amounts may cause irritant or corrosive effects on the gastrointestinal tract (Sanchez-Sicilia et al. 1963).500-. Acute.. ataxia.. Although recent investigations have suggested a possible link between chronic ingestion of methyl mercury and an increased risk for cardiovascular disease.700) .600 (.500 (. and neurocognitive and behavioral disturbances. High-level prenatal exposure may result in a constellation of developmental deficits that includes mental retardation. Stern 2005. 1983).700 (. fatigue..500-. the existence of a causal relation is unresolved (Chan and Egeland. Mercury levels in breast milk also decline in the weeks after birth (Bjornberg et al. 2004).500 (.. 1998. hearing impairment. maculopapular rash. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 2000.500-.600) . and a drinking water Inorganic Blood Mercury Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U. the most prominent effect is on the kidneys where mercury accumulates and may lead to renal tubular necrosis. 1987). anorexia. short-term memory loss. Drexler and Schaller..600) .600) .S. Smith et al. lower levels of prenatal exposure due to maternal seafood consumption have been associated with an increased risk for abnormal neurocognitive test results in children (NRC.500 (<LOD-.600) .600 (. Acrodynia is a sporadic and predominantly pediatric syndrome historically associated with calomel (mercuric oxide) in teething powders and occasionally other inorganic forms of mercury.500-. and pinkish discoloration of the hands and feet (Tunnessen et al. high-dose exposure to elemental mercury vapor may cause severe pneumonitis. Sakamoto et al.600-. 2004).. Sakamoto et al.500-. Overt poisoning from methyl mercury primarily affects the central nervous system..700 (. 1951. 1970.600-. Vupputuri et al.700) size 8147 Total Age group 1-5 years 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th 90th . The constellation of findings may include anorexia. cerebellar ataxia.500) .700-.600-. 2000)..800) 792 842 2060 4453 03-04 03-04 * * < LOD < LOD < LOD < LOD . pain in the extremities. Workplace standards for inorganic mercury exposure have been established by OSHA and ACGIH. 2005)..700-. causing parasthesias.500-. dysarthria. Oskarsson et al. Rissanen et al. Bellinger et al. Rice. DeRouen et al. which may vary for some chemicals by year and by individual sample. depression.600) . 1995. particularly irritability. see Data Analysis section) for Survey year 03-04 is 0... Smith et al.700 (.600 (.. and sleep disturbance (Bidstrup et al. hypertension.Metals may be more efficient for inorganic mercury (Grandjean et al. limb deformities. dysarthria.42. 2006. 2006. 2003)... Occupational exposure to elemental mercury vapor has been associated with subclinical effects on biomarkers of renal dysfunction (Cardenas et al.

gov/mercury and from ATSDR at: http:// www.09 (2. who participated in a 1998 representative population survey (Becker et al.78 µg/L for adults and 0.atsdr.30) 3.370) .410-. the total blood mercury concentration is due mostly to the dietary intake of organic forms.S.S.19 (1. average age 33 years. Schober et al. 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. In NHANES 19992002. total blood mercury geometric mean levels in females aged 16-49 years did not change.530) .580) .408) .18) 2. (2000) studied 1216 blood donors in the Czech Republic (896 men and 320 women.406-.840-1.430 (.39-3. 2009). 2001. aged 18 to 69 years.413-.330-.700-1.01 (.07 (. From 1996 through 1998.13-2. 2002).76-3. These men had no occupational exposure to mercury but previously had received dental amalgams at military facilities (Kingman et al. Among the three racial/ethnic groups. environmental levels) and health effects is available from the U.534) . Biomonitoring Information In the general population.530-.89) 3.492) Selected percentiles ( 95% confidence interval) 50th . Sanzo et al.52) 2. 2003). particularly methyl mercury.382-.330 (.14-2. Urinary mercury consists mostly of inorganic mercury (Cianciola et al. 1997.60-2.480 (.420 (..46) 3.19 (2.960 (.85-2.405-.840) 1. the developing fetus may be the most susceptible to the effects of ongoing methyl mercury exposure (NRC. 1998)... and increased slightly in non-Hispanic white children (Caldwell.24 (2.213-.23) 2.254 (. IARC considers methylmercury to be a possible human carcinogen and elemental and inorganic mercury to be unclassifiable with regard to human carcinogenicity. total blood mercury increased with age.160-. population from the National Health and Nutrition Examination Survey.360-.840-1.33 (2. 1995.S.00) 1.03-4.76-3.05) 3.31) 2.54 (2. average age 9.68 (2. These distinctions can help interpret mercury blood levels in people. et al.441 (.350-.58 µg/L for 4645 adults.476 (.460 (.700 (.28) 1. Benes et al. Survey years 03-04 Geometric mean (95% conf.358 (.200 (.340-.360 (..396-.gov/toxprofiles.08 (1.20 (1. Mahaffey et al.65) 1.9 years).S.97) 2. During the same survey periods. 1998).66) 3.610-1.S.90) 2.34-3..23) .304) .67-2.442-. 2000).16 (1. although non-Hispanic black females had higher levels than non-Hispanic white or Mexican American females.430) . the median concentration of blood mercury was 0.42) 95th 3.88) 287 722 1529 03-04 03-04 .00 (.. Total blood mercury levels increase with greater fish consumption (Dewailly et al.770-1.509) . see Data Analysis section) for Survey year 03-04 is 0.460) .e.330-. 2004. total blood mercury levels declined slightly in non-Hispanic black and Mexican American children.Metals standard for inorganic mercury has been established by U.14) 90th 2. Clinically observable signs of ataxia and paresthesias may occur when blood mercury levels increase to approximately 100 µg/L after methyl mercury poisoning. interval) .330-.31) 1266 1272 03-04 03-04 03-04 .420 (. military veterans (mean age 52. Over the NHANES 1999-2006 survey periods. range 40 years to 78 years) had an average total blood mercury concentration of 2.cdc.26 (1. A cohort of 1127 U.. EPA at: http://www.96 (1..63-2.313-.16 (. slightly higher total blood mercury levels were found in U. EPA. In Germany the geometric mean for blood mercury was 0..77-2. and the age-related changes differed across the groups (Caldwell et al.60 (1.76-4.08 (1.430 (.570) .290-.67-3.8 years.epa. Fourth National Report on Human Exposure to Environmental Chemicals 221 .870-1.520) .890 (. 2009).930-1.440 (. Kingman et al.416 (. Urinary Mercury—2003-2004 Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.280-. Urine mercury levels increase as more occlusal surfaces of teeth are filled with mercury-containing amalgams (Becker et al..870-1. Information about external exposure (i.509) .14.549) .99-6.55 µg/L.05) 1.61) 1.463) .88-3.88 (1.78-2..360-. 758 children.447 (..93 (1.433 (. Grandjean et al. 2003).480) 75th 1. However.940 (.60) 619 713 1066 Limit of detection (LOD.96 (1.46 µg/L for children. 2001. adult women in several ethnic subgroups (Hightower et al.400 (.29) 1.12 (..555) . 2006).250) .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 .24) 1.530) .495 (..

S.347) . reversible increase in urinary N-acetyl-glucosaminidase.32-2.06 (.909 (.79) 1.11) 2.40-1.368) .00) 90th 1. Department of Health and Human Services noted that several studies have observed a modest.265-.508 (. women of childbearing age have generally been much lower than these levels (CDC.599) .39) 1...64-2. and Italian (Apostoli et al.67 (1.970 (.498) 75th .11) 1.587 (. 1988. not to imply a safety level for general population exposure.301-..13-2.21) 1.417) . 1992).714-1.630) . 2003).56) 1266 1271 03-04 03-04 03-04 .78-4.79 (1. et al. Urinary Mercury (creatinine corrected)—2003-2004 Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.23-2. In the study of U.343 (.44) 1.532 (.61) 1.447 (. 2006. Langworth et al.280-.46-2.65 (1.306 (.90) 618 713 1066 222 Fourth National Report on Human Exposure to Environmental Chemicals .522-.768 (. Finding a measurable amount of mercury in blood or urine does not mean that the level of mercury causes an adverse health effect.535) 1. 2009)..85) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites Sample size 2537 03-04 03-04 03-04 .07) 1. 2002). Levels in U.40 (1.404-.875-1.217 (.275) .196-.365 (.13 (1.309-.447-.385-.400) .86) 95th 2. 2009).30) 1.455-.225-.09) 1. 2002) adult population surveys were similar to those in a U.289) .620-.41-2. Urinary mercury levels in recent German (Becker et al. representative sample of women aged 1649 years reported in NHANES 1999-2006 (Caldwell. interval) .S.480) .472-..362 (.969-1. Urine mercury and the number of dental amalgams were correlated.S.455-. The ACGIH (2007) currently recommends that urinary inorganic mercury in workers not exceed 35 µg/g of creatinine..391-.652) .00 (.25 (.376-.476 (.88 (1.537) .616) .784) 1.400-.391) . 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.06 (.04-3.964-1. DeRouen et al.785-1.255 (.619-.384 (. military veterans with dental amalgams.12-3.566) .464 (.51-2.545 (.687) . 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.16) 1. 2005).297 (.486) Selected percentiles ( 95% confidence interval) 50th .667-1.54 (2.525 (.35 (1.443 (.208-.30) 2.77 (2. ACGIH recommends that the blood levels due to inorganic mercury exposure in workers not exceed 15 µg/L.. a biomarker of perturbation in renal tubular function. population from the National Health and Nutrition Examination Survey. An expert-panel report recently prepared for the U.307-..455) .696 (.588) .276 (.03) 2.00) 286 722 1529 03-04 03-04 .32 (1.62 (1.392-.333-. among workers with urinary mercury concentrations of 25-35 µg/L or greater (Barregard et al. 2006).28 (.67 (1.990) .800-1. 1998). Information about the biological exposure indices is provided here for comparison..63) 1.365 (.1 µg/L for each surface with a dental amalgam (Kingman et al.18-1.76 (1.88-2.485 (.01) 2.87 (1. and on average.87) 2.358) .S. mean urinary mercury was 3..246-.463 (. Czech (Benes et al.Metals 2000). Blood mercury levels of women and children in NHANES 19992006 were also below levels established as occupational exposure guidelines (Caldwell. et al.1 µg/L.11-2.88-2. Survey years 03-04 Geometric mean (95% conf. Biomonitoring data will also help scientists plan and conduct research on exposure and health effects. the urine mercury increased by approximately 0.S.31 (1.

719 (.846) .578-.540 (.87-4.508-.426-.14) 3.699) 1.28 (1.77) 2.53-3.07) 1.18) 3.606 (.76-5.91-7.54) 595 531 381 442 594 826 Limit of detection (LOD.45) 95th 3. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.501-. population.553-.686) .909-1.35 (1.450-.37) 1.68-3.04-1.540-.83-3.46-4.97 (1.710 (.06 (.579-.72) 1.656-.46 (1.624-.23-1.710 (.569-.580-. interval) Selected percentiles (95% confidence interval) Survey years 50th .32) 2. 1999-2002 Geometric mean and selected percentiles of urine concentrations (in µg/L) for females aged 16 to 49 years in the U.616-.97) 2.560-.79) 1.582-.18 (3.631-.30-2.50 (1.772 (.870) .89 (2.55-3.664) Mexican Americans Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .22 (.46) 3.92) 3.500-.892) .94) 1.22-3.790) .14-1.61-6.520-.810) .592 (.655 (.596 (.05 (2.09-1.59-5.410-.420-.723 (.605-.580 (.516 (.45-2.706 (.79) 3.45 (1.03 (.32-3.664) .557-.30 (2.42) 90th 2.709) .68 (3.658 (.41-6.70 (2.76 (1.81 (3.09-1.03-2.636-.3) 5.30 (1.799) .21 (2.99) 1.615 (.45) 2.95 (2.709) 75th 1. 16-49 years) 99-00 01-02 .68) 3.620 (. Geometric mean Survey years (95% conf. population.650 (. Geometric mean (95% conf.10-4.S.03 (.526-.50-4.21-3.824) .61) 1.14.65) 1.27 (2.47) 1.69 (1.13 (2.53) 595 531 381 442 594 826 Fourth National Report on Human Exposure to Environmental Chemicals 223 .27-1.502-.92) 2.560 (.00) 2.23-1.14 and 0.10-2.99-2.41 (1.45) 2.650) 1.930) .03) 1.721 (.00 (3.98 (5.15 (2.665) .04-10. 1999-2002.76) 2.85) 4.39) Sample size 1748 1960 Age group (females) 16-49 years Race/ethnicity (females.32 (1.24-1.69-3.37 (1.831) . National Health and Nutrition Examination Survey. Urinary Mercury (creatinine corrected)−Females Aged 16-49 Years Old.24) 6.387-.99 (2.740 (.665) Mexican Americans Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .806) .43-1.42-3.56 (1.41 (2.55) 90th 3.21 (1.17) 95th 5.50 (2.51 (3.81-6.91 (2.Metals Urinary Mercury−Females Aged 16-49 Years Old.831) .51) .84 (2.63) Sample size 1748 1960 Age group (females) 16-49 years Race/ethnicity (females.650 (.760 (.833) .639 (.99 (3.05 (3.632 (.39-3.85-3.30 (2.62 (4.41 (1.670) 75th 1.657 (.07-5.47) 1.52) 3.56) 3.97) 2.45-3. 16-49 years) 99-00 01-02 .92) 4.742-1.16) 5.44) 3.65-4.97) 2.850-1.31 (1.35) .910) .520-.25) 2.07-2.600 (.S. interval) Selected percentiles (95% confidence interval) 50th .16-5.710) 1. National Health and Nutrition Examination Survey.832-1.809) .84 (2.57-4.27 (1.48 (2.691) .00 (2.522 (.42) 2.31-1.966) .622-.475-.62 (3.15-1.637) .610-.565 (.38) 4.13-4.685 (. 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.774) .14-2.77) 1.62 (1.56) 4.724 (.744) 1. 1999-2002.

Woods JS. Martin MD. Niklasson B. Dewailly E.149:301-305.295(15):1775-1783. Cerna M. Fawcett J. Hasselgren G.47(3):185-195. Barregard L. Videro T. Arch Environ Health 1969. Ekman L. population: 19992006.33:1-9. Arch Environ Health 1992. Am J Epidemiol 1999. Mercury derived from dental amalgams and neuropsychologic function.62(2):68-72. Bellinger DC.77(2):124-129. Barregard L. Martin MD. Becker K. Mortensen ME. 2007 TLVs and BEIs. Ayotte P.56(4):350-357. Centers for Disease Control and Prevention (CDC). Schuzt A. Enzymuria in workers exposed to inorganic mercury. Barregard L. and lead. Bruneau S. Persson G. Locket S. Lauwerys RR. Methylmercury exposure biomarkers as indicators of neurotoxicity in children aged 7 years. Neurobehavioral effects of dental amalgam in children: a randomized clinical trial. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. 52:19-33. Int JHyg Environ Health 2002. Cardenas A. Debes F. Neurotoxicology 1995. Martins IP. Brewer R. Tissue levels of mercury determined in a deceased worker after occupational exposure. Nutr Rev 2004. Snihs JO.111:719-723. Environ Health Perspect 2003. McKinlay S. Arch Environ Health 2001. Buchet JP. Trachtenberg F. Daniel D.S. Lapham LW. Factor-Litvak P. Skerfving S. Cernichiari E. Spevackova V. DeRouen TA. Myers GJ. Egeland FM. Jacobs D. White RF. Jones RL. Sci Total Environ 2002. Garrett N. Falk R.72:169-173. Arch Environ Health 1992. Begg M. et al. Int J Hyg Environ Health 2009. Weihe P. Int J Hyg Environ Health 2003. Sandborgh-englund B. Attewell R.16(4):705-710. Rosenbaum G. Townes BD. et al. Cutress T. and Se in blood of the population in the Czech Republic. Transport of methylmercury and inorganic mercury to the fetus and breast-fed infant. Luis H. Atlanta (GA). Int Arch Occup Environ Health 1999. Gagliardi T. Osterloh JD. Cox C. Zn.2:856-861. The mercury concentration in breast milk resulting from amalgam fillings and dietary habits. Schutz A. Grandjean P. Int Arch Occup Environ Health 1988. Jorgensen PJ. et al. Sallsten G. Greitz U. et al. I. Chronic mercury poisoning in men repairing direct-current meters. Geier J. Berglund B. Echeverria D. Cernichiari E. Impact of maternal seafood diet on fetal exposure to mercury. Benes B. Woods JS. Leroux BG. Subrt P. Int J Epidemiol 2004. Kaus S. Kline J. Grandjean P. et al. Becker K. Bonnell JA. Schaller KH. Castro-Caldas A. Total blood mercury concentrations in the U.7(3):176-184.205:297-308. Kjellstrom T. Levallois P. Jorgensen PJ. Assessment of reference values for mercury in urine: the results of an Italian polycentric study. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Lepom P. Sallsten G. Tavares M.19:478-484. Neuropsychological and renal effects of dental amalgam in children: a randomized clinical trial.50:17-27. 2005. Schulz C. Vahter M. and heart diseases. Cianciola ME. Cernichiari E.61:65-69.Metals References Aberg B. Budtz-Jorgensen E. Cu.289:1324. Jarvholm B. Seifert B. 206:15-24. Harvey DG. Markers of early renal changes induced by industrial pollutants. Aposian HV. Bernard AM.212:588-598. Cejchanova M. Lancet 1951. Krause C. JAMA 2006. Weihe P. Schulz C. Fish consumption. Caudill SP. Drago I. Cortesi I. Cent Eur J Public Health 2000. The concentration levels of Cd. selenium. Caldwell KL. mercury exposure. Bjornberg KA. Monitoring methylmercury during pregnancy: maternal hari predicts fetal brain exposure.295(15):17841792. Lebel G. Smid J. Conradi N. Bates MN. Elia G. JAMA 2006. Drexler H. Health effects of dental amalgam exposure: a retrospective cohort study. Exposure of the Inuit population of Nunavik (Arctic Quebec) to lead and mercury. Mangili A. Seiwert M. Marsh DO. Environ Res 1998. et al. Br J Ind Med 1993. Pb. Weber JP. Bidstrup PL. 224 Fourth National Report on Human Exposure to Environmental Chemicals . Clarkson T.8(2):117-119. Bernardo M. Application to workers exposed to mercury vapour. Leitão J. Apostoli P. Barbon R. Seiwert M. Kaus S. Barregard L.113(10):1381-1385. ACGIH. Kinetics of mercury in blood and urine after brief occupational exposure. Sallsten G. Epidemiologic assessment of measures used to indicate lowlevel exposure to mercury vapor (Hgo). Hg. J Toxicol Environ Health 1997. Chan JM. Third National Report on Human Exposure to Environmental Chemicals. et al. Hultberg B. Metabolism of methyl mercury (203Hg) compounds in man.. Based on the Documentation of the Threshold Limit Values for Chemical Substances and Physical Agents and Biological Exposure Indices. Cincinnati (OH): Signature Publications. Roels H. Environ Health Perspect 2005. Biennow M.

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Acrodynia: exposure to mercury from fluorescent light bulbs. Schober SE.31:687-700. Sinks TH.128(2):25125-25126. The hair-organ relationship in mercury concentration in contemporary Japanese. Hislop D.115(10):1527-1531. Dorronsoro M. Environ Health Perspect 2002. Zeitz P.97(2):195-200. McDowell M. Effects of exposure to mercury in the manufacture of chlorine. Environ Res 2005. Estimation and validation of mercury intake associated with fish consumption in an EPIC cohort of Spain. Baser M. Vahter M. Guo S. Takahashi Y. Turner MD. Fisher HL. Vupputuri S. Environ Health Perspect 2003. Kaye WE. Patil LS. Nakazawa M. Newton G.4(5):981-988. Smith RG.2:117-131. JAMA 2003. Suzuki T. Daniels JL. Farris FF. Toxicol Appl Pharmacol 1994. 226 Fourth National Report on Human Exposure to Environmental Chemicals . Amiano P.289(13):1667-1674. Pediatrics 1987. An assessment of the cord blood: maternal blood methyl mercury ratio: implications for risk assessment. Amurrio A. Friberg L.40:413-419. Sherlock J. Stern AH. Whittle K. Smith PJ. Bolger PM. Mooney TF.124:221-229. Lind B. Toxicol Appl Pharmacol 1996. Allen PV. Smith JC. Elevation of mercury in human blood from controlled ingestion of methyl mercury in fish.79:786789. Tunnessen WW. Goldberg J.98(1):133-142. Hum Toxicol 1984. Public Health Nutr 2001. Leroux BG. Leitao JG. Am Ind Hyg Assoc J 1970. Lorscheider FL. Yoshinaga J. Vimy MJ. Br J Ind Med 1983. A review of the studies of the cardiovascular health effects of methylmercury with consideration of their suitability for risk assessment. Bernardo MF. Azpiri MA. Vorwald AJ. Maternal-fetal distribution of mercury (203Hg) released from dental amalgam fillings. Osterloh J. DeRouen TA. Sandler DP. Speciation of mercury in the primate blood and brain following long-term exposure to methyl mercury. Shen DD. Hall LL. Longnecker MP. Smith AE. Martin MD.110:129-132.37:245-252. Burbacher T. Blood mercury levels in US children and women of childbearing age. Aguinagalde FX. 1999-2000. Environ Res 2005. Methyl mercury pharmacokinetics in man: a reevaluation.258(4 Pt 2):R939-945. Mottet NK. McMahon KJ.111(12):1465-1470. Arch Environ Health 1993.Metals Sanzo JM. et al. Environ Health Perspect 2007. The kinetics of intravenously administered methyl mercury in man. Am J Physiol 1990. Smith JC. Imai H. Topping G. Jones RL. et al. The contribution of dental amalgam to urinary mercury excretion in children. 1993-1998. Stern AH. Woods JS. Orr MF. Hongo T. Public health consequences of mercury spills: hazardous substances emergency events surveillance system. et al. Langolf GD. Blood mercury level and blood pressure among US women: results from the National Health and Nutrition Examination Survey 1999-2000. Toxicol Appl Pharmacol 1994. Most B. Effects of occupational exposure to elemental mercury on short term memory. Matsuo N.48(4):221229.

1-55.8.7 (50.1-44.7) 86.4) 41.1-52.5) 44.8-94.2) 52.8.8) 44. chemical reagents in hospital laboratories.5 (43.7-51.0) 55.7-91.1 (34.3-75.7-96.8) 46.5-68.0-62..6 (40.2-37. Gastrointestinal absorption of molybdenum averages 8893% for dietary intakes of 22-1490 µg/day.2 (40.6 (40. More recently.2 (49.1) 59.1) 60.7-47.2 (55.5-91. Compounds of molybdenum are also used as corrosion inhibitors.0) 45.3 (37.4) 52. The recommended dietary allowance for adult men and women is 45 µg/day (IOM.S.7) 46.7-105) 69.2-59.6-46.9-109) 97.9 (44.2) 48.5 (49.8) 75.8 (67.1 (91.8-49.7 (73.0) 62.3 (73.9-85.2 (38. see Data Analysis section) for survey years 99-00.6-96.3 (38.9-55.5) 80.2) 37. hard metal widely used to add strength and hardness and retard corrosion in metal alloys.8-106) 88.7-92. 0.0 (81.0 (42.6 (43.3-47.1) 46.9) 62.7-73.0) 54.3 (79. WHO.6-72.0 (41.9) 34.3 (71.2-91.9 (78.0 (42.3-108) 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 47.0-56. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. Excretion occurs predominantly via the kidneys.3) 85.3) 37.6-82.9 (40.9-56.6-55.1-59.7) 45.3 (46.1) 82.7 (36.0-100) 63.0 (43.5 (48.0-110) 90.5 (67.0-77. aldehyde dehydrogenase. Molybdenum is a nutritionally essential trace element that enters the body primarily from dietary sources.8 (85.3) 41.4 (48.6 (73.6) 53.2) 53.3-115) 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.2) 150 (128-187) 130 (120-141) 119 (112-130) 119 (105-138) 115 (104-128) 101 (97.5 (74.6-111) 267 (159-840) 197 (161-291) 181 (138-235) 188 (146-216) 179 (155-227) 143 (130-156) 168 (143-206) 150 (130-166) 133 (119-144) 310 368 290 648 762 725 1299 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 52.2-59.7) 57.6 (55.3 (55. Fourth National Report on Human Exposure to Environmental Chemicals 227 .2-53.4-75.4-82.5 (41.0-53.5) 60.6-42.2 (69.5-46.8) 39.5 (37.3 (84. 7439-98-7 General Information Elemental molybdenum is a silver-white.6) 51. In humans.9-83.7) 77.1 (71.7-60.6) 71.4 (80.9 (52.5-124) 108 (92. lubricants.0) 84. and 03-04 are 0.9 (33.9 (32.5) 47.5-41. Molybdenum occurs in natural waters and may be present in concentrations of several hundred micrograms per liter or higher in ground and surface water near mining operations Urinary Molybdenum Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.6) 93.3) 54.4) 42. and the average dietary daily intake of molybdenum is approximately 100 µg/day (IOM.2) 40.8-108) 87. At a daily oral molybdenum dose of 24 µg.7 (51.5) 85.2) 41.5-65.1 (38.1) 35.9-55.7) 75th 84. urinary excretion over six days CAS No. 01-02.6) Selected percentiles ( 95% confidence interval) 50th 50. and in pigments for ceramics.5-66.3-91.3) 83. and xanthine oxidase (Kisker et al.0) 60.1-63.3 (64.9) 67.0) 97. inks.4 (48.4) 56.5-52.2 (63. and paints.8) 40.0-65.6-62.2-42. 1996). hydrogenation catalysts.7 (44.0 (48.0 (46.8-46.4 (34.7-84.0 (76.3 (47.2 (83.1-88.6 (55.4) 76.8 (82.2) 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 (98.2) 79.5. population from the National Health and Nutrition Examination survey.0-38.7) Sample size 2257 2690 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 78.2-79.6) 71.4 (79.3 (53.7-41. respectively.7-50.7) 78.9 (73.Metals Molybdenum or ore deposits.8-90.6) 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 (99.3) 47.1-48.1) 126 (106-147) 109 (94.1-52.2 (49. 2001.4 (72. 2001).2 (61.9 (37.9 (34. interval) 45. molybdenum is a cofactor for three enzyme classes— sulfite oxidase.5-52. and 1.4-61.0-85.4) 49.5) 80.7) 78.7 (71. which exert homeostatic regulation over molybdenum balance.1-51.2 (56.4) 45.6 (52.0) 39.0-71.5 (81.3-44.8) 48. 1997).3) 90th 135 (125-146) 124 (117-130) 111 (105-118) 95th 180 (154-216) 165 (145-176) 138 (133-146) Total 45.6-58. semiconductor and battery industries have begun to use molybdenum.7 (45.3 (55.7-68.3) 65.0-101) 82.2-70.1) 57.9-82.5 (41.7 (58.4-52.7) 51.7-39.8 (42.7 (37.7-122) 93.

6) 36. 1997).Metals was 18% of the ingested dose.4-107) 85.4-106) 85.5 (40.5) 214 (154-1040) 185 (165-219) 160 (129-257) 112 (78.9) 92.8 (36.3) 56.4) 122 (107-133) 109 (99.3-59.6 (42.4) 44.8) 37.8 (57.3-56. Based on studies finding adverse reproductive effects in rats and mice.5-46.1 (38.3-45.3 (58.7-52.3-141) 109 (81.8 (56.4 (56.7 (75. dust and other fine particles produced during refining or shaping of molybdenum or molybdenumcontaining alloys are inhalational pathways of exposure.2-80. interval) 43.6-45.9-45.0-46.1-81.3 (37.4) 40.4) 47.4) 58.9 (36.6-88.5 (34.5-69.2 (37.4-185) 106 (94.1 (39.8) 39.0-103) 103 (90.5 (78.2-103) 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 42.8) 38.6 (59.2 (40.6 (57.7) 112 (95.2-65.1) 56.3) 64.5 (50.4) 61.0) 38. 1961.1-100) 86.2) 55. 2001).5 (37.3 (36. 1993).4 (59.8-42.0) 39.5) 71.8-47.5 (39.4 (37.2 (43.9-96.0 (80.3-115) 98.6) 39.5-50.7-43.7 (77.3 (71.5 (65.5 (59.1 (33. Molybdenum is generally considered to be of low human toxicity.1-79.3 (53. and urinary levels reflect intake from all sources.5 (79.5) 63.5) 90th 108 (97. Human health effects from molybdenum at low environmental doses or at biomonitored levels from low environmental exposures are unknown.1) 101 (83.4) 89.6-61.5 (36.0-41.3) 43. at daily oral doses of 95 µg and 428 µg.0-38.9) 40.0) 62.5 (37.4-118) 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) 44.6 (36.8-47. EPA.1-38.3-44.0) 39.9 (64.1 (30.0) 53.8-84.7) 62.5 (35.2-41. 1999). 1995).6-63.7-62.9) 31.2-96.0) 44. U. but available epidemiologic data are scant. A long term inhalation bioassay of molybdenum trioxide in mice yielded “some evidence” of carcinogenicity (NTP.9 (39.5-62.8) 79.4-42.2) 42.9-71.5-99.4 (78.4 (40.3-46.0) 33.2-49.9) 79.3-102) 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 40.2-121) 107 (92.6-76.2-47. One case-control study suggested a possible link between occupational exposure to molybdenum and lung cancer (Droste et al.9-87.8) 45.7-137) 129 (109-155) 112 (97.1-45.2 (40.3-52.6 (38.4) 116 (101-126) 104 (88.5-70.2 (36.3) 44.7-93.9 (73.6-61.8-66. Levels of molybdenum Urinary Molybdenum (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.1-43.9-68.1) 37.3 (37.3 (71.4-66.9 mg/kg/day and established a tolerable upper intake level of 0.4) 48.4 (67.3) 37.3 (51.1-40.1 (49.7-100) 77.1-112) 78.5 (80. the Panel on Micronutrients of the Institute of Medicine identified a no observed adverse effect level (NOAEL) of 0.4 (44.8) 62.9-42.6 (36.2 (73.. population from the National Health and Nutrition Examination survey.3) 40. of the ingested dose (Turnlund et al.6-41.5-60.9 (64.1 (38.1) 37.8-67.5 (39.8) 38.5-48.2 (33.6) 43.2) 39.5) 73.0) 72.1 (42.6) 39.9-61.7) 53.8-52.0 (58.1-41.3-68.5 (40.0-56.1 (82.7) 45.9 (79.5) 72.1-34..8) 61. In industry.2 (40.0-46.9-41.5 (41.2) 39.7) 42.3-43.4 (53.3) 41.3 (83.3) 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 85.5 (38.4-120) 101 (84.7-38.8-65.2 (50.0-133) 119 (88.9 (40.1) 65.3 (36.7) 115 (93.8-46.4-39.9-117) 57.1 (44.5-45.9) 41.0) 95th 144 (125-171) 130 (120-149) 120 (107-135) Total 42.1 (37.9 (49.1-39. respectively.9-45. and clinical or epidemiologic evidence of adverse effects is limited.8 (37.4 (55.2) 38.6) 48.0 (74. Biomonitoring Information Molybdenum is an essential element for health.4-76.1) 43.0-120) 85.S.0) 36.2 (69.1-43.8) 71.6-78.8 (75.9-118) 91.2) 43. urinary excretion over six days rose to 50% and 67%.2) 58.9 (39.8 (90.3) 57.5-44.7) 75th 63.2-40.1-109) 89.9-40.6 (71.9 (35. and molybdenum has not been systematically evaluated for carcinogenicity by IARC.1-39.2) 37.7-44.03 mg/kg/day in humans (IOM.1 (40.1-67.2 (52.6-63.5 (65.7-40.2) 37.8-118) 81.7 (66.9) 173 (130-243) 159 (129-170) 132 (107-158) 85.5 (35.5-97.5 (83.4) 60.2 (57. Chronic exposure to very high levels may result in higher serum uric acid levels and a gout-like illness (Koval’skiy et al.1-127) 90.5-92.1 (54.7) 41.3) 61.4-41.7) 57.7 (30.0 (35.5-35. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.2-96.6) Selected percentiles ( 95% confidence interval) 50th 41.5) 60.0) 88.3 (55.4) 77.7-120) 87.5 (54.5-119) 90..5 (41.S.1) 40.2) 42.2-46.

Droste JHJ. Turci R. Menne C. Institute of Medicine (IOM). and zinc: a report of the Panel on Micronutrients. pp. Geneva: WHO. Urinary molybdenum concentrations in infants may be slightly lower than those in other age groups (Sievers et al.S. 144-154. Environmental Protection Agency (U. U. Turnlund JR. Schleyerbach U. iron. 2001. Sci Total Environ 1998. White and Sabbioni. Available at URL: http://ntp. 2005. Molybdenum-cofactorcontaining enzymes: structure and mechanism. copper.. X. Molybdenum absorption. Atlanta (GA). In: Trace elements in human nutrition and health. Trace element reference values in tissues from inhabitants of the European Union. Weyler JJ. Aprea C. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Sabbioni E. 4/14/09 Sievers E.epa. Peiffer GL. Am J Clin Nutr 1995. vitamin K. White MA. Schaub J. Inductively coupled plasma mass spectrometric determination of molybdenum in urine from a Danish population. Minoia et al. A study of 13 elements in blood and urine of a United Kingdom population. National Toxicology Program (NTP). (DC): National Academy Press. World Health Organization (WHO). Molybdenum 1993 [online]. silicon. Kristiansen J...gov/iris/ subst/0425. Rees DC. Occupational risk factors of lung cancer: a hospital based case-control study. Ronchi A. molybdenum. Zhurnal Obshchey Biologii 1961. Sciarra G. Molybdenum.216:253-270. et al. Finding a measurable amount of molybdenum in the urine does not mean that the level of molybdenum causes an adverse health effect. Third National Report on Human Exposure to Environmental Chemicals. 1998.gov/index. Koval’skiy GA. Available at URL: http://www. population were well characterized in NHANES 1999-2000 and 2001-2002 (CDC. edu/openbook. 1313-27-5) in F344 Rats and B6C3F1 Mice (inhalation studies) 1997 [online]. Ann Rev Biochem 1997. Yarovaya GA. Changes of purine metabolism in man and animals under conditions of molybdenum biogeochemical provinces. and retention studied with stable isotopes in young men at five intakes of dietary molybdenum. 2001). 1998). 16:1313-1319. Shmavonyan DM.123(1):81-85. References Centers for Disease Control and Prevention (CDC). Fourth National Report on Human Exposure to Environmental Chemicals 229 . Keyes WR. Standing Committee on the Scientific Evaluation of Dietary Reference Intakes. Sabbioni E. nickel.15(2-3):149-154. iodine.nap. Available at URL: http://books. vanadium. 1996.niehs. Kisker C. van Sprundel MP. TR-462.22(3):179-191. Occup Environ Med 1999. Rapid Comm Mass Spectrom 2002.htm.php?record_id=10026&page=420. Analyst 1998. Molybdenum in infancy: methodical investigation of urinary excretion. chromium. 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. 2002.66:233-267. 4/14/09 Iversen BS. J Trace Elem Med Biol 2001. these levels were comparable to those reported for adults in smaller European population surveys (Iversen et al. Toxicology and carcinogenesis studies of molybdenum trioxide (CAS No. 56:322-327. 4/14/09 White MA. Food and Nutrition Board. Dietary reference intakes for vitamin A.Metals in urine for the U. Minoia C. arsenic.S. manganese. pp. Christensen JM. Inductively coupled plasma mass spectrometric determination of molybdenum in urine. EPA). Washington. excretion.S. Vermeire PA. Gatti A. boron. Schindelin H. cfm?objectid=070A72C6-E9C1-AE67-4BFAB97AD0F427E8. 2005). Van Meerbeeck JP.nih.62(4):790-796. 420-441.

and 0. and 03-04 are 0. population from the National Health and Nutrition Examination Survey. 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. however. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Higher environmental soil concentrations of platinum from vehicular emissions have been found near roadways (Farago et al. 01-02.04.07. 1998).Metals Platinum CAS No. as oxidation catalysts in chemical manufacturing. 0. respectively. strength at high temperatures. carboplatin) in the treatment of cancer. which may vary for some chemicals by year and by individual sample. Platinum-rhodium compounds are also used in glass and glass-fiber manufacture and in hightemperature thermocouples. jewelry. thick-film circuits printed on ceramic substrates. Important properties of platinum are resistance to corrosion. lustrous metal found naturally in extremely low amounts in the earth’s crust and is typically associated with sulfide-ore bodies of nickel. Platinum-rhodium and platinumpalladium crystals are used as catalysts in petroleum refining and in vehicular catalytic converters to control exhaust emissions. 230 Fourth National Report on Human Exposure to Environmental Chemicals . copper. 7440-06-4 General Information Platinum is a silver-gray. see Data Analysis section) for Survey years 99-00. < LOD means less than the limit of detection. and as drugs (e. Platinum compounds are used in electrodes.S. dental alloys.04. and high catalytic activity. and iron. 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... Human health effects from platinum at low environmental Urinary Platinum Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. cisplatin.

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

Biomonitoring studies on levels of platinum provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of platinum than are found in the general population. Herr CE. Schulz C. Int Arch Occup Environ Health 2003. Cohrssen B. Platinum-industry and precious-metal workers had urinary concentrations about one-thousand times higher than general populations (Schierl et al. Ensslin AS. 2004. International Journal of Hygiene and Environmental Health 2003. Moore W Jr. Campbell K. et al. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Saindelle A. Boos KS. Hall L. Petrucci F. 5th ed. Schierl R. Fries HG. 1998). 3/31/08 Moore W Jr. Part 1: monitoring of urinary concentrations. Several studies have shown that background concentrations in general populations were usually less than 0. Uptake of antineoplastic agents in pharmacy and hospital personnel. Kaus S. Ruff F: Histamine release by sodium cholorplatinate. Gromiec JP. Pethran A. and in blood and urine in the United Kingdom. Occup Environ Med 1998. Urinary platinum levels associated with dental gold alloys. Stilianakis NI. 2003. Schierl R. Hysell D. and gold excretion of patients after insertion of noble-metal dental alloys. Kuster W. International Programme on Chemical Safety (IPCS). population were below the limit of detection (0. Duneman L:Long-term urinary platinum. Biomonitoring of traffic police officers exposed to airborne platinum.inchem. Bocca B. Kulka U. 2003. New York: John Wiley & Sons. Schierl R.13(1):24-30. Revised and new reference values for some trace elements in blood and urine for human biomonitoring in environmental medicine. 1997. Biomarkers 1999. Int Arch Occup Environ Health 1997. palladium. Begerow J. Parrot JL. palladium. et al. Iavicoli I.. 2004) or less than 0.70(3):205-208.56(3):283-286. J Expo Anal Environ Epidemiol 2003. Blanks R. Int J Hyg Environ Health 2004. Environmental Health Criteria 125.35:313-321. 206:15-24. van de Weyer C. Biological monitoring of hospital pharmacy personnel occupationally exposed to cytostatic drugs: urinary excretion and cytogenetic studies.. ruthenium. References Becker K. Neuendorf J. Angerer J. Levels of platinum in urine for the U. Kavanagh P. Huber R. Patty’s Toxicology. Gieler U. 1999. Ruff F: Platinum and platinosis. Kazantzis G. Seiwert M. Senofonte O. and platinum. 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. Ewers U.01 µg/L (Becker et al. Environ Res 1975a. Crocker W. Pethran et al. Saindelle A. Platinum concentrations in urban road dust and soil. Allergy and histamine release due to some platinum salts. 1998). which elevate urinary platinum by five to twelve-fold (Begerow et al. Nickel. Br J Pharmacol 1969. Pethran A. 2004).4(1):27-36. Biomonitoring Information Urinary platinum levels reflect recent exposure. Analyst 1998. Rommelt H. Seifert B.9:152-158. Wilhelm et al. Powell CH.. Turfeld M. Farago ME. Arch Environ Health:1969.61(7):636-9. Alimonti A. Schierl..76(1):5-10. Occup Environ Med 2004. Available at URL: http://www.005 µg/L (Iavicoli et al. Carelli G. et al. 232 Fourth National Report on Human Exposure to Environmental Chemicals . 289-380. Schierl R.. rhodium. 2003). 1991 [online]. Czerczak S.19:685-691. Finding a measurable amount of platinum in the urine does not mean that the level of platinum causes an adverse health effect. Stara J: Preliminary studies on the toxicity and metabolism of palladium and platinum.55(2):138-140.123(3):451-454. et al. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Hebert R. Hysell D.inchem. Fruhmann G. pp. Nowak D.04 µg/L) in this Report... Herr et al. eds. Raab W. Herr et al.htm..org/documents/ehc/ehc/ehc125.207(1):69-73. In: Bingham E. Influences on human internal exposure to environmental platinum. 2003. Grimm CH. Kelly J.. Wilhelm M..Metals the International Programme on Chemical Safety at http:// www. Jankofsky M..S.10:63-71.htm. Urinary excretion of platinum from platinum-industry workers. osmium. Environ Health Perspect 1975b.org/documents/ehc/ehc/ ehc125. 2000. One study found that traffic-control officers had no greater urinary platinum concentrations than office-based control subjects (Iavicoli et al. Stara J: Biological fate of a single administration of 191Pt in rats following different routes of exposure. Thornton I. Hauff K. Schierl et al. Schulz C. 2001). Arch Environ Health 2001. Platinum. Gold-platinum dental restorations were correlated with increased urinary platinum concentrations.

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 .370) .290) .290 (.350-. Thallium exposure occurs primarily from industrial processes such as coal-burning and smelting. Human health effects from thallium at low environmental CAS No.360-.340-.230) .340 (.200 (.370-.173) .350) .200-.250-.160 (.370-.590) .310) .220) .410-.590) .420) .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 .220 (.310 (.350-.200) .370 (.160-.170-.300 (.310-.390-.220 (. thallium readily crosses the placenta and also distributes into breast milk.225) .147-.330-.380-.02.420-.220) .156-.400) .200) ..420) .135-.450 (.182-.260-.430) .510 (.173-.210) .350 (.390 (.430 (.370) .290 (.157-.250-.250-.360 (.147-.220) .450 (.400-.450 (.200 (.02.340) .280) .390-.201 (.290-.183) .420) .450 (.370 (.360) .360-.340-.170 (.179-.480) .270 (.184 (.290) .320 (.230) . 01-02.215) . In addition.240) .170-.250-.172 (.153-.310 (.188) .220 (.167-.300 (. 7440-28-0 General Information Elemental thallium is a blue-white metal found in small amounts in soil and in sulfide-based minerals.200) .140-.270) . Elimination from the body tissues occurs slowly through urine and feces (Blanchardon et al.280 (.150-.420) .260-.243) .Metals Thallium depilatory cosmetics.420) .177) .230-.490) . and 03-04 are 0.410 (.400) .149 (.180-.250) .185 (.190 (.230-.440 (.470 (.400 (.150-.146 (.320-.159 (. and 0.450 (.187-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.230) . it has not been specifically mined or refined in the United States since 1984.170-.200) .460 (.178) .159 (.480) .220-.250-.200) .210 (.230 (.300) .500) .330) .400 (.160 (.196) .420-.410-.240-.197 (.170 (.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 .440 (.330) .330-.520) .360-.400 (.170) .147-.170-.330) .440) .430) .310 (.360-.350-. population from the National Health and Nutrition Examination Survey.180 (.290) 90th . 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.167 (.134-.470) .400) 95th .560) .220 (.200-.160-.270-.270) .400 (. respectively.156) .300) .420-.270 (.160 (.410 (.320) .181-.440) .410-. thallium is produced in a fine particulate form that can be absorbed through inhalation or ingestion.176 (.239) .260 (.160 (.390) .470) .159 (.480) .218) .154-.150-.250-.270 (.162-.170) .200-.02.137-.260) .390) .183) .290 (.197-.206) .470 (.480) .340) .172) .430-.440) .320) .280-.490) Total .690) .410 (.250 (.410-.155 (.380) .145 (.420) .330-.300) .175) .230-. It is still used in relatively small amounts in pharmaceutical and electronics manufacturing.171 (.390) .150-.280-.440 (.210-.390 (.240-.180 (.200 (.156) .290) .165 (.330-.290 (.250 (.500) .340-.202 (.133-.170 (.190 (. 2005).218) .240) .450 (.200 (.410 (.290-.370 (. Thallium disappears from the blood with a half-life of several days.390) .400) .200-.170-.148-.430 (.430 (.410 (.410-.200 (.290 (.217) .167-.190 (.460) .240-.420 (.260-.280) .420-.160-.370-.180-.450 (.490) .190 (.200) . Fourth National Report on Human Exposure to Environmental Chemicals 233 .520) .144 (.180) .250-.210 (.200 (.380 (.300-.280 (.330-.150-.280) .390-.173) .450) .260-.440 (.192) Selected percentiles ( 95% confidence interval) 50th .260 (.230) .380-.163) .320) .400-.500 (.180) 75th .400-.202) .180 (.360 (.172 (. interval) . 0.300 (. In the past.350-.145-.290 (.170) .450 (.270-.550 (.160 (.360-.S.330-.400) .260-.410) .201 (.220 (.430-.360 (.350-.160-.480) .490 (.260 (.280 (.290) .470) .270 (. In the United States.270 (.370 (.630) .430 (.420) .370 (.520) . the latter being the current major industrial consumer of thallium in this country.410-.330) .220) .180-.340-.440-.190 (.410 (.460) 861 675 618 561 657 723 801 1114 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.196) .510) . representing distribution into other tissues. however.220) .400-.640) .370 (.350 (.390-.180-.190-.145-.217 (.490) .500) .160-.170-.330-.220) .202 (.185-.370-.380 (.170-.350-.370 (.520 (.300) .190 (.460-.360 (.150-.191 (.240) . see Data Analysis section) for Survey years 99-00.270-.250-. thallium was obtained as a by-product of smelting other metals. From these and other sources.430-.158) .450 (.350) .400-.400 (.

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

Wiegand H. et al. Long term retention and excretion of 201Tl in a patient after myocardial perfusion imaging. 1980.95:89-105. Martin J-C. Apostoli P.. Marcus RL. These urine levels are generally comparable to levels observed in earlier studies of general populations (Brockhaus et al. Minoia C. White and Sabbioni.html. Challeton-de Vathaire C. Pietra R. Sci Total Environ 1990.1 mg/m3 (Marcus. 1998). Schaller KH.113(1):47-53.gov/toxprofiles/tp54. Sci Total Environ 1998..47(3):223-231. Brockhaus A. 1981.. Sabbioni E. Ting BG. Investigation of a working population exposed to thallium. Available at URL: http://www.35(1):4-9. Pozzoli L.Metals (CDC. Trace element reference values in tissues from inhabitants of the European Union. 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. Finding a measurable amount of thallium in urine does not mean that the level of thallium causes an adverse health effect. Toxicological profile for thallium.cdc. et al. Third National Report on Human Exposure to Environmental Chemicals. Jackson RJ. Sampson EJ. with concentrations ranging up to 76. Schmidt M. Trace metals in urine of United States residents: reference range concentrations. A study of 13 elements in blood and urine of a United Kingdom population. Schaller et al. Valentin H. Gallorini M. Sabbioni E. Nearby residents were exposed by eating garden plants that had been contaminated by the thallium.76(1):53-59. Intake and health effects of thallium among a population living in the vicinity of a cement plant emitting thallium-containing dust. Fourth National Report on Human Exposure to Environmental Chemicals 235 . J Soc Occup Med 1985. Cassot G. Centers for Disease Control and Prevention. Int Arch Occup Environ Health 1981. 7/15/09 Blanchardon E. Boisson P. Soddemann H. Trace element reference values in tissues from inhabitants of the European community I. Brockhaus et al. 2005.48(4):375-389. population) are thought to correspond to workplace exposures at the threshold limit value of 0. Pirkle JL.atsdr. A study of 46 elements in urine. Manke G.216:253-270. 2005. Paschal et al. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 1990. X. Celier D. White MA. Raithel HJ.. Morrow JC. References Agency for Toxic Substances and Disease Registry (ATSDR). Buhlmeyer G. Investigations of thallium-exposed workers in cement factories. Minoia et al. blood. Dolger R. and serum of Italian subjects. 1998. Environ Res 1998. 1985). Kramer U. Int Arch Occup Environ Health 1980. Paschal DC. Atlanta (GA). Radiat Prot Dosim. Ewers U. Urinary concentrations of 100 μg/L in asymptomatic workers (500 times higher than median levels in the U.265 people living near a thallium-emitting cement plant in Germany. 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. 2005) and are shown with results from NHANES 2003-2004 in this Report. (1981) studied 1. 1992 [online].5 μg/L. Seventy-eight percent of the urine specimens in that study contained greater than 1 μg/L. et al.S.

236 Fourth National Report on Human Exposure to Environmental Chemicals .080-.160 (.100 (.380-.140) 90th .080) .180-.460) .160-.360 (.190 (.380 (.084-.510-1.800) . and for producing ferrotungsten.530 (.400 (.120) .380-.090-.100) .070) .250-.070-.370-.550 (.122) .071 (.320 (.090 (.133) .140 (.065 (.210 (.120-.084 (.110 (.070) .069) .060 (.590) .250) . Evidence is lacking for the carcinogenicity of tungsten.116) .100 (. Occupational exposure is from dusts released during grinding or drilling of hard metals.510 (.073-.190 (.950) . population from the National Health and Nutrition Examination Survey.080 (.100) Selected percentiles ( 95% confidence interval) 50th .470 (.Metals Tungsten CAS No.560) .160 (.520) .260-.370 (.130-.460 (.220 (.390 (.120) .170) .110-.110-.135) .110 (.062 (.530 (.113 (.270 (.410) 790 680 618 562 649 723 802 1117 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.810) .130) .050-.101-.132) .056-.310-.320-.300) 95th .105) .076 (.100) . which is used in the steel industry.120-.790) .120-.100) .00) .150 (.360 (.470-.400 (.120-. and 03-04 are 0.460 (.130-.420-.095-.250) .073) .056-.090) .400 (.550) .120) .350 (.620) .360 (.050-.350) . Tungsten is used mainly for producing hard metals. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.060-.081 (.090) .290-.450-.380-.150 (.160-.160) .320) .120-.330 (.069-.830) .290-.280 (.220) .060-.060-.240-.220) .310-.430-.110 (.350) .570 (.096 (.270 (.130) . and as catalysts in the petroleum industry.520) .390) .160 (.080) 75th .340) .280-.070-.130) .084) .080 (.330) .470) .490) .090-. and it has not been classified with respect to its carcinogenicity by either IARC or NTP.091) .690) .050-.470) .073-.170 (.180-.110-.113 (.100 (.097-. 01-02.090-.120) .090-.370 (.630) .120) .110 (.500) .550) .520) .071-.190-.300 (.250) .062 (.080 (.230) .410-.090) . Tungsten compounds are used as lubricating agents.580) .107 (.300-.070-.150 (.086 (.360-.150) . mainly as scheelite (CaWO4).320-.090-.310) .220) .270-.180-.330-.050-.490 (.060 (.300 (.04.090-.095-.096-.560) .370 (.330-.270 (.530 (.230-.074-.130 (.310 (.087) .110) .080 (.260 (.120) .190-. their illness may stem from exposure to cobalt mixed with tungsten carbide rather than to tungsten alone.500 (.158 (. see Data Analysis section) for Survey years 99-00.450 (.109) .230-.380 (.170) .400-.137 (.370-. Urinary Tungsten Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.060-.160) .200-.260-.093) .120-.073 (.260-.104) .250) .360-.111-.070) .087-.060 (.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 .460) .065-.093 (. and 0.110 (.070 (.300) .140 (.53) .082 (.250-.140-.510-. filaments for incandescent lamps.250) .260 (.130) .160-.077-.340-.360) .126) .070) .170 (.070-.410 (.640 (.190-.070 (.170) .430 (.113 (.130) . Human health effects from tungsten at low environmental doses or at biomonitored levels from low environmental exposures are unknown.140 (.370) .560) .105 (.420-.100-.340-.160 (.190-.130-.430 (. interval) .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 .082-.060 (.160 (.092) .230) .093-.180 (.210 (.300 (.340-.440) . which are used in rock drills and metal-cutting tools.290-.280 (.560 (.230-.076 (.200) .270-.082) .290 (.380) .130 (.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 .260) . bronzes in pigments.620) .250) .310-.04.090-.080-. 0.100) .310-.060-. Although workers occupationally exposed to tungsten carbide may develop serious lung disease (“hard metal disease”).078-. Most background environmental exposures to tungsten are from the soluble forms such as tungstate salts that may occur in drinking water.080-.550) .180-.200 (.480) Total .430 (.060 (.180) .04.270-.080) .620 (.092 (.120 (. respectively.088) .170) .800) .350) .160-.066-.060 (.100-.310-.670) .090-.070 (.070-.090 (.088 (.123-. 7440-33-7 General Information Tungsten is a steel-gray to tin-white metal that occurs naturally in the earth’s crust.400 (.210 (.290) .140-.204) .210) .080) . Little information is available on the toxicity of tungsten.400) .180) .240 (.060-.380-.100) .500 (.230-.180) .770 (.080 (.290) .068) .210 (.100-.210-.082 (.460 (.058-.190) .110) .470 (.113 (.270-.064-.090 (.180 (.330) .151) .170-.100 (.101 (.150-.090) .092 (.210 (.430) .430-.S.220-.560) .320 (.180) .130-.570 (.650) .140 (.230 (.350-1.

167) . 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.136 (.453) .124-.079 (.073 (.069 (.300) .117 (.098 (.067-.133) 90th .279 (.215 (.359 (.144-.064-.186 (.131-. population from the National Health and Nutrition Examination Survey.250 (.084) .151 (.059-.069 (.727) .431) .158 (.605) .138) .093) .231-. A were more than 900 times higher than the overall geometric nonrandom subsample from NHANES III demonstrated mean of the U.154) .169 (.358) .085) .078) .071) .095-.073 (.111 (.086) .170-.080-.353 (.120) .300 (.436) . In whereas the tungsten-worker group had mean urine levels a Nevada community where tungsten was measured and 35 times higher.308) .538) .385 (.255 (.136-.077) .130 (.080 (.091) .S.150-.197) .431) .265 (.072-.739) .084 (.198) .071) .153) .054-.216-.082) .088) .090-.240-.354) .074-.065 (.179-.148 (.063-.272-.459) .089) .197 (.237) .333 (.067 (.497 (.383 (.150 (.109-.130-.317 (.069-.086) .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 . interval) .082 (.233-.317-.315-.091) .100 (.439 (.126-.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 .077) .063-.253) 95th .075) .078 (.287) .125 (.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 .074) 75th .083-.073 (.224) .136-.139) .089 (.190) .354-.136-.333-.300-.074) .145 (.057-.095) Selected percentiles ( 95% confidence interval) 50th .138 (.214) .071 (. or exposure that a control group of non-metal workers had mean levels differences.301) .063 (.200-.439) Total .308) .092) .071 (.091) .Metals Workplace air standards for external exposure have been established by ACGIH and recommended by NIOSH.098) . 1997).187) .302-.217-.426) .174 (.148) .071) .116) .078) .270 (.253 (.070 (.217-.055-. 2003.294 (.880) .105 (.152-. A study of 14 unexposed adults yielded values that were similar to the 95th percentiles in this Report. Biomonitoring Information median urinary levels were as much as 15-fold higher than median levels in the U.108-.439 (.080-.258 (.053-.582) .267-.083 (.063 (.082) .222-.199 (.341 (.083) .255-.301) .079) .237) .465) .199 (.329-.074 (.339 (.331-.482 (. measure urinary tungsten.344-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.500) .353 (.484 (.139-.078-.081 (. Patients with medically-inserted tungsten found at increased levels in drinking water.100) .245-.184 (.359 (..150-.278-. similar to those in this Report (Schramel et al.075-.555 (.091 (.063-.197) .231 (.340 (.333) .054-.237-.. 1998). population in the NHANES 1999-2000 slightly higher values than those found in NHANES 1999.056-. 2001).317) .554) .216 (.075) .125) .167-.091 (.121 (.120) .071 (.075 (.091) .216-.267) .060 (.216 (.S. population.797) .431) .061-.094) .065-.279 (.174) .165) . 2001-2002.253-.108) .086) .081-.285) .283) .105 (.066 (.375) .364 (.049-.144 (.333 (.078 (.056-..079) .222) .167-.205-.068-.065-.079 (.414) .436-1.098-.074-.084) .667) .103-.079) .070 (.083 (.122-.139 (.058-.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 .484) .181 (.216-.090-.075 (.176-.063-.198-.066 (.339 (.333 (. (1987) found possibly due to methodologic.208-.28) .094) .347 (.124 (.062 (. Nicolaou et al.169) .083) .065 (.077-.426) .386) .059-.209-.096) .301) .067 (.060-.158) . 2005).061-.176-.279 (.201 (.057-.452-.143-.258-.106 (.087) .154) .084 (.218 (.136-.155-.326) .075-.072 (.081) .086-.153-.462) .179-. and 2003-2004 (Paschal et al.098-.064-.286-.085 (.099-.061-.S.275 (.098-.823) .299 (.250 (.133) .(Kraus et al.138 (.284) .211 (.116-.255 (.634 (.146 (.203-.250-.065-.068 (.392) .146 (.109 (. population (CDC.410-.094-.060-.215) .100) .119 (.059-.071-.093-.119-.080 (.122-.333) .077-.107-.158) .073 (.116 (.088) .122 (.412 (.329 (.261-.293 (.065) .188-.206-.201) .117) .161) .121-.379 (.302-.197-.158) .164 (.167) .465) .081 (.306) .146) .214-. Using neutron activation analysis to 2000.143 (.300-.180-.085-.104-.079) .381) .157) .333 (.133) .200-.072-. Workers involved in grinding operations that released tungsten metal into the air had elevated urinary levels that Levels of urinary tungsten reflect recent exposure.168 (.360 (.087 (.059 (.333-.667 (.

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

012-.019-.017-.021 (.010) .009) .027-.024-.010-.008-.007-.013 (. and 234U.023-.027 (. see Data Analysis section) for Survey years 99-00.008 (.016-. Thus.009 (.031 (. in some ceramics.005-.009) .007-.066) .036 (.021 (.009-.017) .018 (.012) .006-.009-.019-.009-.018-.031 (.158) .036-. or processing.055 (.007-.008) .008 (.027 (.016-.016 (.008-.031 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.045) .020-.024-.046 (.008) .049) .031-.011) .007-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.014 (.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 .028-.013-.023 (.029 (.005-.016) .043) .006-.034) .023) .011-.007 (. interval) .012 (.004.007-.010-.006-.010) * .062) .009) .048) .040) .006-.050) .011-.065) .006 (.008 (.030 (.007-.018) .012) .009 (.008 (.009) .027) .020-.008 (.007 (.012-.009-.027 (.019-.015) .010) .007-.067) .009) .023-.008 (.012-.023) .017) .006-.009) .018) .037) Total .006 (.040-.038) 340 368 289 719 762 725 1405 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .009 (.016) .033 (.279) .020-.026) 95th .017) .065) .021-. including nuclear weapons.023-.013-.010) . Uranium has many commercial uses.044 (.013 (.023-.012-.041 (.007 (.008 (.028 (.012) .039-.016) .009 (.007 (.073) .016-.046 (.035) .009) .041 (.011-.008-.006-.051) .017-.054-.025-.036 (.027) .013 (.054) .011-.017-.008 (.008-.006-.031 (.008 (.018 (.007-.008) .Metals Uranium CAS No.020-.010 (. the primary exposure sources for nonoccupationally exposed persons are dietary (especially root vegetables) and drinking water.027) .020-.005-.010) . and as an aid in electron microscopy and photography.028-. 235U (about 0.036-.035-.015 (.026-.010 (.049) .022-.007-.012 (.047 (. It usually occurs as an oxide and is extracted from ores containing less than 1% natural uranium.036) .046) .040-.050) .006-.015 (.037) .017-.020) .008-.037) .009 (.037-.012 (.005-.009 (.007-.008 (.008 (.009) .069) .009 (.007) .009) .011) .013 (.010-.013) 90th .021-.017 (.035) .017) .010) .011) .014 (.017-.007 (.045) .038) .016) . 01-02.015 (.009 (.008 (.028 (. 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. and 03-04 are 0.063) .018) .006 (.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.053 (.008 (.010) . Variable concentrations of uranium occur naturally in drinking water sources.008-.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 .011) .004.015) .026 (.009-.023 (.015 (.029-.008 (.067) .013-.007-. Since the 1990’s.014 (.016) .006-.011) .027-.127) . human exposure occurs primarily by inhaling dust and other small particles.014 (.007) .009 (.010) .007) .064 (.007-.019-.040 (.007 (.009-.012 (.009) .013 (.010) * .114 (.027-.034-.008) .006-.013 (.007-.010-.022) .009-.030-.008-.013 (.024-.026) .019 (.033) .016) .007-. Natural uranium is a mixture of three isotopes: 238 U (greater than 99%).011 (.022-.010-.021) .008 (.012-.072) .009) .027) .007 (.017-. respectively.007) 75th .72%).010 (.020 (. milling.007) .S.053) .022 (.056) .005-.011-.088) .039) .021) . In workplaces that involve uranium mining.006 (.034-. 7440-61-1 General Information Uranium is a silver-white metal that is extremely dense and weakly radioactive.048 (.026 (.020) .007-.038 (.030 (.033 (.012 (.009) .007 (.032 (.027 (.011) .010 (.026 (. Fourth National Report on Human Exposure to Environmental Chemicals 239 .014 (.009-.043 (.036) .008 (.008-.014 (.007 (.008) .012 (.012-.007) .046 (.017 (.010) .036) 883 683 618 568 667 722 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.017) .056) .052 (.040) . DU has been used by the military in armor-piercing ammunition and as a component of protective armor for tanks.011-.026-.009-.006-.010 (.022-.029-. population from the National Health and Nutrition Examination Survey. 0.031 (.006-.028 (.030) .015-.006-.012) .030 (.008 (.007-.013) .007 (.026) .033-.021 (.009) * .037) .042 (. nuclear fuel.011 (.040 (. and 0.024 (.039) .046-.007-.046 (.007 (.054) .010-.005.023 (.007-.011-.009) Selected percentiles ( 95% confidence interval) 50th .011) .042) .023) .060 (.021) .009-.018) .037 (.009 (.

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

Boyd P. with emphasis on quality control.S... 28 soldiers who may have been exposed to DU by inhalation. Six workers in a depleted uranium program showed concentrations of 0. in that the levels were below their respective detection limits (Byrne et al. Kent (England): Nuclear Technology Publishing. Uranium content of blood. and no consistent effects on multiple endpoints of kidney function were found.. 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.S. population.. Hamilton et al. Nuclear Regulatory Commission (NRC) has set an action level of 15 μg/L urinary uranium to protect people who are occupationally exposed (U. Workplace air standards and guidelines for external exposure to soluble and insoluble uranium compounds have been established by OSHA and ACGIH.html. Recent studies of veterans have been conducted to examine concerns about DU exposure during military conflicts. environmental levels) and health effects is available from ATSDR at: http://www. 1999) and other small populations have shown urinary concentrations that are similar to those in NHANES 1999-2000. 2006). Drinking water and other environmental standards have been established by U. 2004).. In the same study. References Bhattacharyya MH. had a mean urinary uranium concentration of 0. Benedik L. Dietz LA. during. Squibb K. McDiarmid M. The U. A cohort of 46 U. 2004). Pullat VR. Biomonitoring Information Levels of urinary uranium reflect recent and accumulated exposure. 2004). 41 (1). soldiers who had been injured and had embedded DU shrapnel for as long as eight years.. the geometric mean urinary uranium concentration was 0. Vol.107:143-157.. but in whom no shrapnel was embedded. Fourth National Report on Human Exposure to Environmental Chemicals 241 . A previous nonrandom subsample from NHANES III (n = 499) (Ting et al. 1991. Zimmerman I.55 μg/L (median 0. 2006. Determination of the isotopic composition of uranium in urine by inductively coupled plasma mass spectrometry. the median urinary concentration was 0. although slightly increased during and after deployment. Older studies have demonstrated urinary uranium concentrations that are consistent with levels in the U. Pillai KC. Atlanta (GA).e. Health Phys 2000. 2003. Ejnik JW. IARC and NTP have no ratings for uranium human carcinogenicity.1992. 1978)..Metals injury associated with elevated urinary uranium levels (Kurttio et al. urinary levels of uranium were as high as 9.atsdr.S. NRC. In a much larger study of 446 Gulf War veterans who were concerned about past exposure to DU. and 2003-2004 (Dang et al. Urinary uranium measurements in 103 Canadian military personnel showed mean urinary levels slightly less than geometric mean in this Report (Ough et al. 2002. soldiers evaluated before. Dang HS.. 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. ingestion. et al. Guidebook for the treatment of accidental internal radionuclide contamination of workers. Finding a measurable amount of uranium in urine does not mean that the level of uranium causes an adverse health effect. 2006). 2006). Muggenburg BA. or wound contamination. 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. Determining the normal concentration of uranium in urine and application of the data to its biokinetics. 2004)... 2000). 2005. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 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.. Thomas RG. (May et al. Metivier H.1996.S. Galletti.. 2000).S.S. Mil Med 2003. Durakovic A.110 to 45 μg/L (Ejnik et al. Radiation protection dosimetry. In two studies of a Finnish population with high natural uranium concentrations in their drinking water. respectively. Komaromy-Hiller et al.011 μg/L (McDiarmid et al. 1-49. Horan P. Hamilton MM.. EPA.066 μg/g creatinine (Gwiazda et al. Breitenstein BD. Carmichael AJ. pp.. Eighty-five percent of those levels were above the 95th percentile of the NHANES 1999-2000 population. Third National Report on Human Exposure to Environmental Chemicals. Stradling GN. 2006). In 17 U. Karpas et al. the median urinary uranium concentration was 2.62:562-566. In a study of 105 persons exposed to natural uranium in well water. urine and hair of exposed and non-exposed persons determined by radiochemical neutron activation analysis.gov/ toxpro2. Sci Total Environ 1991.. 1992. Information about external exposure (i.162 μg/L) (Orloff et al. 1994...078 μg/L (ranging up to 5. eds.61 μg/g creatinine. McDiarmid et al.cdc. Volf V.168(8):600-605. 2002). Byrne AR. Health Phys 1992. Tolmachev et al.65 μg/L).78:143-146. 2001-2002. In: Gerber GB. Centers for Disease Control and Prevention (CDC). (Kurttio et al.

July 1978. Human exposure to uranium in groundwater. Shelly T. Kurttio P. Paschal DC. Gwiazda RH. Bennett LG. Ting BG.S. et al. Squibb K. Health Phys 1996. Clin Chim Acta 2000. Heller J. Karpas Z. rapid. Saha H. Costa R. Van der Venne MT. Comparison of representative ranges based on U.22–Bioassay at uranium mills. Engelhardt SM. Squibb K. Noguchi H. Cremisini C. McDiarmid M. Health Phys 2004. Hancock RG.91(2):144-153. Kurttio P.S.296(1-2):71-90. Review of elements in blood. Howerton K. Health Phys 2006. Hamilton EI. Kidney toxicity of ingested uranium from drinking water. Sabbioni E. Englehardt SA. Ough EA.Metals Galletti M. Harmionen A. Radiat Environ Biophys 2005. McDiarmid MA. Smith D. Paretzke HG. Charp P. Sci Total Environ 1994. Hollriegl V. et al. D’Annibale L. Scott K.82(4): 527-532. Biologic monitoring for urinary uranium in Gulf War I veterans. Kalinsky V. Komulainen H. Salonen L. NRC). Health Phys 2003. Uranium and thorium in urine of United States residents: reference range concentrations. Environ Health Perspect 2002. Roiz J. Am J Kidney Dis 2006. Environ Res 1999. Roth P. Oeh U. Salonen L. et al. Oliver M. Cordero S. VI. Environ Res 2004. Andrews WS.67(8-10):697-714. U. Kane R. Pinto V.47(6):972-982.94:319-326. Nuclear Regulatory Commission (NRC) Guide 8. Metcalf S. May LM. Katorza E.85:228-235. Makelainen I. Washington (DC): NRC. patient population and literature reference intervals for urinary trace elements. Saha H. Jackson RJ. U. Renal effects of uranium in drinking water. Health Phys 2002. McDiarmid MA.44:29-40.87:51-56. Ash KO.S. Li WB. plasma and urine and a critical evaluation of reference values for the United Kingdom population. Uranium daily intake and urinary excretion: a preliminary study in Italy. et al. Wilson PD. Lorber A. Kuwabara J. Jarrett JM.81:45-51. 242 Fourth National Report on Human Exposure to Environmental Chemicals . Mistry K. Oberbroekling KJ.110(4):337-342. Wahl W. Detection of depleted uranium in urine of veterans from the 1991 Gulf War. concentration and daily excretion of uranium in urine of Japanese. Int Arch Occup Environ Health 2006. Nuclear Regulatory Commission (U. Lewis BM. Ejnik J. Tolmachev S.71(6):879-85. Marino R. Orloff KG.79(1):11-21. Biological monitoring and surveillance results of Gulf War I veterans exposed to depleted uranium.86:12-18. Health Phys 2004. Sampson EJ. Pirkle JL. et al.S. Element reference values in tissues from inhabitants of the European community. Pekkanen J. Marko R. Military deployment human exposure assessment: urine total and isotopic uranium sampling results. An examination of uranium levels in Canadian forces personnel who served in the Gulf War and Kosovo. Karpas Z.158:165-190. and inexpensive method for determination of uranium in urine and fresh water: comparison with LIF. Auvinen A. Biokinetic modeling of uranium in man after injection and ingestion. Halicz L. Gucer P. et al. Inductively coupled plasma mass spectrometry as a simple. Komaromy-Hiller G. Auvinen A. J Toxicol Environ Health A 2004.

18-3.0) 708 617 681 652 1228 1092 Limit of detection (LOD.10 (5.76) 4.0-15.51 (3.05. In addition.0-17.0-19.62 (3.38) 5.67-5.0) 10.10) 5. Survey years 01-02 03-04 Geometric mean (95% conf.50) 11.0 (11.70-5.0) 8.0) 13.22-5.10) 3.11) 4.40) 3.20-4.40-7.30-7.Perchlorate Perchlorate (Urbansky.05 (2.90 (5.00) 3.70-9. leather tanning.0 (13.80) 75th 6.70) 3.65) 3.0-17.30 (5. Perchlorate was added to the U.39-4.20-4. Perchlorate has been characterized as a mobile and persistent ground and surface water contaminant.00-5.20 (4.40-4. 2005).90-3.84) 14.0) 13.90) 6.20 (2.0-14.0 (9.26 (2. matches.0) 9.80-6. and certain plants with high water content (e.70-3.0-18.0 (9.90-6.0) 11.S.30 (2.09) 3.0-17.5 hours and has a small estimated volume of distribution (Crump and Gibbs.0 (12.0) 1335 1229 1485 1293 01-02 03-04 01-02 03-04 01-02 03-04 4.20 (5.40) 4. Inhibition of iodine uptake by competition for the sodium/iodide symporter in the thyroid can be estimated in humans by measuring radioiodine uptake CAS No.90) 5.10) 12.00-6.0 (11.40 (4.20 (2.0 (8.0) 9.76 (3. 2002).0 (10.80 (3.10 (2.75-3.0 (8.81) Selected percentiles ( 95% confidence interval) 50th 3.70-11.90 (5.90-3.60) 5. lettuce) can be the main sources of intake for humans (FDA. and electroplating. 1998).0-18.0 (11.g.0) 11.40-4.30-7.32 (3.12) 3.0-23.0) 14.50) 5.50 (8.0-17.0 (12. but has strong oxidant properties in the presence of concentrated acids.10-11.40) 2.80-4.90-11.0 (11.0 (11. 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.90-10.40) 90th 10.0) 10.0) 12.47-4. EPA’s Contaminant Candidate List (CCL) for drinking water in 1998 following discoveries of its presence in drinking water supplies throughout the southwestern United States (U.21 (2.0 (9. Animal and human studies have shown that perchlorate can inhibit thyroid hormone production (NAS.55) Sample size 2820 2522 01-02 03-04 01-02 03-04 01-02 03-04 4.. Other manufactured uses include fireworks.66) 3.81-16.0) 374 314 828 721 1618 1487 01-02 03-04 01-02 03-04 4.29-3. Drinking water.70-6.30-17. Perchlorate is excreted unchanged from the human body with an estimated elimination half-life of about 7.40 (5.00) 4.50) 6. interval) 3. Large doses of perchlorate have been used as a medicine to treat hyperthyroidism and to diagnose disorders related to thyroid or iodine metabolism. certain catalytic metals.0) 14.20-11.60-6.40-5.0-18.87-3.10 (6.0) 15.60) 3.90-12.11) 3.50-3.19-4.0) 8.56) 3.0 (9.50 (3.40-6.S.0-17.70-7.60 (4.30 (2.90 (4..0 (8.10 (6.0) 9.16) 3.70 (3.30-19.20-12.20) 7.0 (11.20 (4.0 (11. 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.0) 13.10-4.0) 13.80 (3. 2001-2002 performed on surplus samples (variable unavailable of NHANES website) Fourth National Report on Human Exposure to Environmental Chemicals 243 .50 (5.0) 14.0) 13.51 (3. Perchlorate is stable under most environmental and physiological conditions.80-12.0-29.0) 9. 2007).0 (11.88) 3.0) 19.30-6.70 (3.0) 11.19 (3.70-3.60 (4.80) 7.0) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites 3.0-20.0 (9. or ammonium salt.90-9.44-4.22 (2.03) 3.30) 6. population from the National Health and Nutrition Examination Survey. 7601-90-3 General Information Perchlorate is an inorganic chemical containing one chlorine and four oxygen atoms.10) 3.00) 3.50-11.90 (2.30) 6.93-3.0) 9.30 (5.93-4. see Data Analysis section) for Survey years 01-02 and 03-04 are 0.0) 13.0) 16.10) 5. It is normally found and produced as the anion of a sodium.89-3.90 (5.20) 3.50-4.74-3.00) 5.20 (7.40) 3.0 (9.45-4. small amounts of perchlorate can form naturally in the atmosphere (Dasgupta et al. and reducing agents.00) 7.0) 15. 2005).60 (7.60) 8.0 (11.40 (3.54 (3.68) 4.80-8.93 (4.50) 3.05 and 0.90 (3.75 (3.60-7. milk.40) 3.EPA.20 (6.0) 10.40 (8.80) 3.10-12.07-4.40 (5.80-4.S.0-17.20-3.0) 13.96 (3.80-15.08-3.40 (4.80 (7. and limited applications in pharmaceutics.00-6.35 (3.46) 3.10-11. fabric dyeing.80 (6.0-15. laboratory analysis. potassium.90-9.40-13.40 (3.80) 12.49-3.31) 2.70-12.10-7.50-7.02 (3.0 (8.0 (12.0) 95th 14.0 (12.90-11.0) 9.79 (2.40-11.40) 6.70 (3.0 (11.50) 5.10 (7.0 (8.40 (5.0 (9.20) 4.0) 13.50-4.20 (8.01 (2.

90 (7.0-14.50) 2.50 (3.90) 5.04-3.66) 3.35) 3.3) 8.80 (7.20) 3..10) 13.90-3.S. chronicity of exposure. but without effects on serum levels of thyroid stimulating hormone or thyroxine (Braverman et al.87 (5.82 (5.14 (2.30 (3..10 (6.47) 2.25) 5. Lawrence et al.33-12.83 (5.50-3.76 (3. gender. Li et al.45-2.60-3.4 (11.20-10..26) 4.6-17.61-5.93-5.g.19-10.52-9. 2002.51 (3.0) 1335 1220 1483 1284 01-02 03-04 01-02 03-04 01-02 03-04 3.05 (4.S. Short term human studies of the effect of perchlorate on RUI have been used for risk estimation (Greer et al.50) 9. 2005.10 (2. age.60-8.40 (3.60) 3.60-6.40) 3.0) 9. 2005).12-2.77 (3.0 (11.84) 2.08 (3.22-4.87 (7.56 (3..4 (10.3 (10.26 (3.0 (11.02) 3. population from the National Health and Nutrition Examination Survey.60) 8.15-12.25 (3.34-3. and the presence of other substances known to affect thyroid function (e.46 (3.00 (6.70 (2.87) 2. Greer et al. medications).60-15.18-3.30) 75th 5.93-7.6) 20. suggesting its tumorgenic effect is a result of a chronic increase in thyroid stimulating hormone indirectly resulting from iodine uptake inhibition.4 (11.0 (9. In the U.20-9. Though it produces follicular cell thyroid tumors in animal studies at goitrogenic doses.80-3.Perchlorate inhibition (RUI).35 (2. although iodine intake was higher than U.60-11.30-10.54 (2.40 (3.72 (3.12 (6.1-14.00 (4.0) 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 .21 (2. Steinmaus et al.98) 3.80) Selected percentiles ( 95% confidence interval) 50th 3.20-4.EPA.00 (2.46-13.20 (4.32) 5.93-8.09 (7.3) 12.44) 3.0) 12.0 (8.52 (8.30-5. 2000).4) 8.10-7.0) 9.80 (4.5) 8.0-17.08) 3.24-2.30) 90th 9.40) 17.20-3. 2002.S.51-4. in a representative sample of U.20 (3.02-4. 2005.10) 4.90-15.03 (2.58) 2.10) 6.87-3.99 (5.70-5.60-8.3) 11. However.0 (8.10 (4.10 (1.60-5.0) 14.50) 95th 12.0-19. 2007).50 (6.36 (8.00-11. menopausal status.22-6.00) 4.41) Sample size 2818 2504 01-02 03-04 01-02 03-04 01-02 03-04 5. Lamm and Doemland. perchlorate is negative in most genotoxic assays (U.43) 6. 2006.0-14.39) 2. 2003. up to 68% RUI has been demonstrated.70-15.50) 2.0 (10.0) 6.EPA. 2002).29-6.S. Survey years 01-02 03-04 Geometric mean (95% conf.0) 10.56-3.0) 12.07 (2.80 (7.20 (7..30 (6. Also. Many factors may be important in consideration of perchlorate action on the thyroid: dose.45) 3.00) 9.24 (4.S.20 (6.20) 8.40 (4.6) 12.0) 4.90-11.0-44.59) 3.90-9.70-4..5 (13.89 (2.90-2.70) 10. interval) 3.1 (8.7 (11.0 (9.86) 4. 2005).4-16.8 (11. women with urinary levels of iodine less than 100 micrograms per day.1-16. NAS.37-13.35 (4.60-11. congenital hypothyroidism is a condition for which nearly all newborn blood is screened.50-5.1-13.73) 3.0 (11.60-5.0) 13.74) 7.97-5. it is known that maternal and congenital hypothyroidism adversely effects neurological development and decreases learning capability.39-4.40 (7.50-9.2) 8.4 (8.19-6.20 (2.76-3.29) 2.1 (11.75) 3.1-22.46-4. urinary perchlorate at environmental exposure levels were inversely associated with thyroxine levels and positively associated with levels of thyroid stimulating hormone (Blount et al.50) 6.0) 12. 1999.25) 5.80-3. 2001.93-5.04-3.00-2.67) 5.41-9.89-3. levels and sufficient in most participants (Tellez et al.30) 3.4) 13.22-4. nitrate.42 (3.54 (3.71 (5.16-3.70 (4.0) 12.90 (4.60) 10.90 (2. levels..40) 5. Follicular cell thyroid tumors would Urinary Perchlorate (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. 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.90 (2.60 (3.0) 7.00-3.00) 3.33 (7..10 (4.3-14.99-3. During gestation and infancy.61 (5.81-3.50) 5.93) 3.0) 13.22 (2. 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.25) 5.33-6.64-3.64) 5. dietary iodine intake.2) 8.30) 5. 2005).44-6..30-5.S.70 (2.0) 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 3.09) 3.0) 11.87) 7.90-20.61-10.40-10.1) 8.96) 2.70) 2.10-3. U.37 (4.20-3.S.39 (3.70-3.10) 3.91) 4.95 (2.30 (5..53 (2.0 (9.0) 374 313 827 715 1617 1476 01-02 03-04 01-02 03-04 3. thiocyanate. 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.

Biomonitoring Information Urinary perchlorate levels reflect recent exposure. He X.fda. Food and Drug Administration (FDA).46(5):509. Low dose perchlorate (3 mg daily) and thyroid function. Washington (DC): National Academy Press. Lamm S.. Primary congenital hypothyroidism. J Clin Endocrinol Metab 2005. Tellez RT. Has perchlorate in drinking water increased the rate of congenital hypothyroidism? J Occup Environ Med 1999. Rutherford GW.110(9):927-937. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Preliminary Estimation of Perchlorate Dietary Exposure Based on FDA 2004/2005 Exploratory Data.11(3):295. (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. Health Implications of Perchlorate Ingestion. Braverman LE.45(10):1116-1127. the women in the community with the highest drinking water levels had mean urinary perchlorate levels about 40 times greater than the geometric mean for participants in NHANES 2001-2002 aged 20 years and older (Tellez et al. Perchlorate in the United States.gov/Food/FoodSafety/ FoodContaminantsAdulteration/ChemicalContaminants/ Perchlorate/ucm077653. Neonatal thyroxine level and perchlorate in drinking water. Finding a measurable amount of perchlorate in urine does not mean that the level of perchlorate causes an adverse health effect. Richman K. Pino S.114(12):1865-1871. Dasgupta PK. J Expo Sci Environ Epidemiol 2007. Thyroid 2000. Erratum in: J Occup Environ Med 2004. Braverman LE.42(2):200-205. 2005). Additional information about exposure and health effects is available from the U.gov/safewater/ccl/perchlorate/perchlorate. Pino S.atsdr. Skeels MR.17(4):400-407. Environ Health Perspect 2007. Dyke JV. Page Last Updated: 05/28/2009. Pirkle JL. Cross M. Daaboul JJ. 2007).html and from ATSDR at: http://www. Li FX. National Research Council of the National Academies. Chacon PM. epa. Lawrence J. Pirkle JL. 2001-2002. newborn thyroid function. Valentin-Blasini L.html. CFSAN/Office of Plant & Dairy Foods. References Blount BC. Abarca CR. and environmental perchlorate exposure among residents of a Southern California community. Li Z. Goodman G. et al.90(2):700-706. Benchmark calculations for perchlorate from three human cohorts. Lau EC. J Occup Environ Med 2000. most of the population is considered to be below the U.cdc. Environ Sci Technol 2006. May 2007. Landingham CB. Gibbs JP. When these NHANES 2001-2002 urinary levels of perchlorate are used to calculate daily oral intakes for the U.S. Environ Health Perspect 2002. J Occup Environ Med 2003. The effect of perchlorate. Perchlorate Exposure of the US Population.113(11):A732. Jackson WA.41(5):409-411. Kelsh MA.. Buffler PA.Perchlorate be unlikely to occur without overt perturbation of thyroid homeostasis. Greer SE. Mauldin JP. 2005. Byrd D.htm. Available at URL: http://www. Valentin-Blasini L. National Academy of Sciences (NAS). Urinary perchlorate and thyroid hormone levels in adolescent and adult men and women living in the United States. thiocyanate. Blount BC. population. Thyroid 2001. Doemland M.EPA at: http://www. Erratum in: Environ Health Perspect 2005. Blount BC.S. Miller MD. Health effects assessment for environmental perchlorate contamination: the dose response for inhibition of thyroidal radioiodine uptake in humans. 2005). 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. Compared to a previous study of pregnant women in three Chilean communities with varying perchlorate levels in the drinking water.115(9):1333-1338.gov/toxpro2. Lamm SH. Caldwell KL. et al.113(8):10011008. 6/2/09 Greer MA. Steinmaus C. Howd R. Sesser DE.10(8):659-663. Lamm SH. Crump KS.. Impact of smoking and thiocyanate on perchlorate and thyroid hormone associations in the 2001-2002 national health and nutrition examination survey. Kirk AB. Osterloh JD. Long-term environmental exposure to perchlorate through drinking water and thyroid function during Fourth National Report on Human Exposure to Environmental Chemicals 245 . Crump KS. Barnard JC.40(21):6608-6614. The levels seen in NHANES 20032004 show a similar pattern to NHANES 2001-2002. et al. and nitrate on thyroid function in workers exposed to perchlorate long-term. Analysis of relative source contributions to the food chain. Also. Magnani B. Deyhle GM. Environ Health Perspect 2005. Biomonitoring studies of urinary perchlorate provide physicians and public health officials with reference values so that they can determine whether or not people have been exposed to higher levels of perchlorate than levels found in the general population.S. Pleus RC. Braverman LE. Lamm SH. The effect of short-term low-dose perchlorate on various aspects of thyroid function. EPA reference dose (Blount et al. Osterloh JD. Lawrence JE. Environ Health Perspect 2006. Blount et al. et al.

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

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

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

80) 485 538 962 Limit of detection (LOD.400-1. Olsen et al.. Slightly higher levels of PFOS and PFOA in males than females have been noted in several other studies (Calafat et al. and other PFCs have not been classified as to human carcinogenicity by IARC or NTP.80) 640 1454 03-04 03-04 * * < LOD < LOD .400-1. Fei et al. Survey Geometric mean (95% conf.300 (<LOD-.500) 90th . 2004. At high but non-toxic maternal doses of PFOS.700) . developmental and teratogenic effects were demonstrated in offspring. 2005). 2003. EPA.500 (.10) .800) 1.500) .. 2001. reproductive.600 (. 2004).10 (. 2003..S.10) .S. elderly and children.400 (<LOD-. Roughly similar levels of PFCs in serum have also been measured previously in other samples of the U. 1992. see Data Analysis section) for Survey year 03-04 is 0.00 (. Thibodeaux et al.108 times higher than background serum levels in humans (Butenoff et al.800 (. Harada et al.900 (. 2005)..500-1.20) .600-2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 2007b. U.. EPA. 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.600 (. Two recent cross-sectional human studies observed a negative correlation of birth weight with serum levels of PFOA (Apelberg et al.. Olsen et al. PFOA. 1999..50) .. 2007b).800 (. Lau et al. 2003).900 (.400-1.400-1... monkeys. 2007). population.500-1. 2004.600 (. 2007a.00) . 2003a). 2004b).500) .. Fourth National Report on Human Exposure to Environmental Chemicals 249 . 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.500-1.3.800) 1.800 (.20) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD . 2007a. and there was no clear evidence of excess all-cause or diseasespecific mortality. the median PFCs values tend to be roughly similar in these age categories (Olsen et al.700 (.500 (<LOD-1.. population from the National Health and Nutrition Examination Survey.500 (. In such studies. Kennedy et al. Cook et al.500-1. Serum Perfluorodecanoic acid (PFDeA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U. In comparing three separate reports on adults.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 . possibly related to lung immaturity (Lau et al.S. Animal studies of PFOS have demonstrated weight loss. 2004). hepatotoxicity. development in offspring was stunted and hypothyroxinemia was observed.400-1. Serum PFOS levels associated with toxicity in test animals were 310-1550 fold higher than 95 percent of the levels found in a study of adults (Olsen et al. 2003)..500-. 2004a. 2003a.Perfluorochemicals and testicular tumors in high dose animal testing (Biegel et al.300 (<LOD-. However.400 (<LOD-. thyroidal). Due to marked intergender differences in the elimination of PFOA in rats and substantial differences in the half-life of PFOA in rats. < LOD means less than the limit of detection. At doses causing maternal toxicity. 2007.500) .10) * 03-04 03-04 * * < LOD < LOD < LOD . Biomonitoring Information Serum levels of PFCs (particularly PFOA and PFOS) tend to reflect cumulative exposure over several years. which may vary for some chemicals by year and by individual sample.S.00) .... and changes in thyroid hormone concentrations (Grasty et al. PFOS. interval) Selected percentiles ( 95% confidence interval) Sample 95th .400-.. Effects on serum liver enzymes in limited observational studies of human occupational exposures are unclear.400) . the potential to estimate risks to humans from animal doses is uncertain.400-. PFOA. U. Olsen et al. Twelve different PFCs were measured in the sera of NHANES 2003-2004 participants. A study of workers chronically exposed to primarily PFOA showed no biochemical evidence of hepatotoxicity or hormonal changes (adrenal. 2003. 2003).. Late gestational exposure to PFOS in animal studies has also demonstrated early neonatal lethality.40) . 2003a)..00) . 2003a.800 (. or increased cancer rates (Alexander et al. perfluorohexanesulfonate (PFHxS). PFOS.. and humans.900 (..300 (<LOD-.500-3. 2003a. animal and human serum PFOA levels have been compared: serum levels associated with toxic effects in animals are 66-11. and no substantial age trends were seen within adults ages 20-69 (Olsen et al.300-1.400 (<LOD-.500) .

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

400 (.3.500) 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 . 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) 485 538 962 Limit of detection (LOD.300 (<LOD-. 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.300-.500 (<LOD-. population from the National Health and Nutrition Examination Survey.S. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Serum Perfluoroheptanoic acid (PFHpA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.400) . < LOD means less than the limit of detection. Survey Geometric mean (95% conf. which may vary for some chemicals by year and by individual sample.900) < LOD .600) < LOD .600) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .0. < LOD means less than the limit of detection.S.400 (<LOD-.900) < LOD 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD .600 (. see Data Analysis section) for Survey year 03-04 is 1.400 (<LOD-. Survey Geometric mean (95% conf.300 (<LOD-. population from the National Health and Nutrition Examination Survey.Perfluorochemicals Serum Perfluorododecanoic acid (PFDoA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U. see Data Analysis section) for Survey year 03-04 is 0. Fourth National Report on Human Exposure to Environmental Chemicals 251 .500-. interval) Selected percentiles ( 95% confidence interval) Sample 95th .

50 (4.30-12.60-2.80-4.30-2.40) 640 1454 03-04 03-04 2.900-1.40) 1.70) 1.80-2. 252 Fourth National Report on Human Exposure to Environmental Chemicals .10 (4.50 (1.90) 90th 5.900) 1.10) 6.70-2.60 (1.80-3.72) 1.16) . Survey Geometric mean (95% conf.30 (3.20 (1.20) .80) 4.90 (4.5) 8.00-6.30) 3.17 (1.721-1.20 (1.40-3.50 (6.50 (2.900-1.04) .80) 3.10 (.60-2.90) 1.80 (4.70-5.60) 1.20 (1.80-8.10) 4.10) 1053 1041 03-04 03-04 03-04 .1) 485 538 962 Limit of detection (LOD.5) 5.09 (.00 (.40-1.3 (9.80-12.40 (1.00) 2.10 (.00 (1.10 (4.91) 2.20) 1.70 (2.00) 1.90) 3.50 (1.60-3.90 (1.6) 7.90 (2.900 (.1.05-2.912-1.40 (2.27) 1.30) 3.50-6.90) 1.50 (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 1.03) 1.93 (1. see Data Analysis section) for Survey year 03-04 is 0.73-2.900-1.90 (4.62-2.20) 1.852 (.60-4.70-7.70-10.80 (1.14) Selected percentiles ( 95% confidence interval) Sample 95th 3.80-4.10-5. population from the National Health and Nutrition Examination Survey.816-1.900-1.586-.50 (4.80-7.86 (1.30 (6.40-1.861 (.20 (1.70) 2.80 (1.44 (2.60) 2.80-3.50 (6.50-6.0) 1053 1041 03-04 03-04 03-04 1.60 (1.30 (7.20) 03-04 03-04 2.20-3.00) 3.30) .30) 03-04 03-04 .0) 8.50-3.01 (1.00 (1.30 (2.00-1.56-1.50) 2.00 (.90) 1.90-19.60) 9.10-9.800 (.50) 2.10) 8.30-6.00 (5.00-7.20-1.90) 8.30-9.30 (2.600-.80-8.80) 90th 2.10) 1.50 (1.54) .10 (.00-1.70) 2.60-4.70) 13.92 (1.10) 75th 3.30) 3.10) 1.50) 6.00-8.40 (1.40 (1.700-1.20-1.60-7.00 (2.20-1.70) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 1.10) 6.77-2.90-10.26) 2.700 (.70 (1.3.Perfluorochemicals Serum Perfluorohexane sulfonic acid (PFHxS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.20-2.20) 2.60 (6.16) Selected percentiles ( 95% confidence interval) Sample 95th 8.984 (.90 (1.50-10.40) 1.72 (1.689 (.20 (6.00 (1.80-6.S.60) 3.40) . population from the National Health and Nutrition Examination Survey.70-2.20 (6.60-8. Serum Perfluorononanoic acid (PFNA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.966 (.60-3.70) 3.70-6.00) 1.900 (.835-1.08) 2.51) 1.10) 75th 1.12) .80) 5. see Data Analysis section) for Survey year 03-04 is 0.S.80-4. interval) 1.10-9.67-2.900-1.14 (.40) 4.90-2.809) 1.80) 1.697-1.80-7.90 (1.963 (.40) 640 1454 03-04 03-04 1.10) 4.826-1.20-1.10 (1.70) 1.20) 485 538 962 Limit of detection (LOD.90 (1.30 (1.30 (1.00 (1. Survey Geometric mean (95% conf.30 (1.40) 2.834-1.30 (1.87-2.60-2.900-1.40 (1.60 (1.42 (1.800-1.10) 5. interval) .17-1.

2 (16.20) 7.80 (6.8-22.9) 9.7-30.2 (21.27) Selected percentiles ( 95% confidence interval) Sample 95th 9.90-12.0) 21.8) 32.4 (23.2 (27.30) 7.27) 4.2-57.1-33.5) 1053 1041 03-04 03-04 03-04 14.60-14.6-50. see Data Analysis section) for Survey year 03-04 is 0.84-3.7 (43.60) 03-04 03-04 3.1 (19.60 (5.4) 56.5) 8.21-3.60 (3.6-45.8-22.40-6.9 (22.4-25.30-3.10) 5.60 (6.3 (28.Perfluorochemicals Serum Perfluorooctanoic acid (PFOA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.9) 22.1-24.70) 3.20-4.6) 35.6) 21.7-33.6) 62.7 (19.10-3.80 (5.40-10.40-14.67-4.8-22.90) 6.4.0) 43. Fourth National Report on Human Exposure to Environmental Chemicals 253 .60 (6.70) 6.10 (6.1-35.6 (42.5-33.20 (4.8-78.7-53.7-23.8) 46.7-69.10 (3.5-62.6) 9.40) 90th 7.5) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 21.60-6.7 (35.6) 1053 1041 03-04 03-04 03-04 3.20) 5. interval) 3.3) 485 538 962 Limit of detection (LOD.60) 8.20) 10.37 (2.60 (7.20-5.3-22.80 (7.6 (19.7 (7.3) Selected percentiles ( 95% confidence interval) Sample 95th 54.9 (17.8 (45.00 (3. population from the National Health and Nutrition Examination Survey.4) 20.3 (44.90 (7.90 (7.5 (28.20) 5.80-4.0) 03-04 03-04 19.70) 4.5) 7.70-5.4) 640 1454 03-04 03-04 23.40) 3.5-21. Serum Perfluorooctane sulfonic acid (PFOS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.50) 4.47 (4.1) 15.70-10.6) 18.9) 22.4 (17.1) 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 (3.0 (20.40) 75th 5.00 (5.6) 42. Survey Geometric mean (95% conf. Survey Geometric mean (95% conf.20) 7.2) 30.50) 7.80) 8.0-20.1 (24.S.8-81.18 (3.60-13.5) 19.3 (35.8 (37.30-6.80 (6.70-7.40-17.4) 75th 30.65-4.7-49.3) 42.00 (5.5) 32.3 (35.11 (2.50 (3.5 (28.5) 9.0) 90th 41.70 (5.5) 57.70 (3.9-23.4-17.7 (13.4 (19.3-61.90-4.95 (3.2 (19.6-24.0) 23.40) 5.0) 36.90 (7.1-36.0-70.6 (35.30 (5.8) 27.80-12.0 (27.2) 45.91) 3.6 (44.4) 21.53) 3.85-4.5-23.00) 3.70-9.40-6.30-11.50-13.9 (19.9) 27.50 (4.8 (34.90-4.2) 640 1454 03-04 03-04 4.35) 3.0-66.6) 7.60-9.2) 30.20) 4.2 (28. interval) 20.8-35.4 (28.82) 4.2-22.1 (23.7) 39.4-42.20-9.9-19.30) 6.70 (5.1.3) 41.80-9.30 (3.30-5.7 (43.89 (3.8-30.60 (4.9 (13.79) 4.10 (3.1) 57.96 (3.40 (4.3 (17.30-8.7 (35.50-4.70-7.47-4.20 (4.99-3.1-25.0) 485 538 962 Limit of detection (LOD.S.90 (5.1-52.0) 21.2 (18.0-16.3) 28.9-38. population from the National Health and Nutrition Examination Survey.4 (19. see Data Analysis section) for Survey year 03-04 is 0.5) 18.40 (6.50-6.07-4.

300 (. which may vary for some chemicals by year and by individual sample.300) .300 (.300 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th < LOD 90th * 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .200-.300) .300) .300 (.500) < LOD 485 538 962 Limit of detection (LOD.300 (.400 (<LOD-.300 (.500) .2.300 (.300) . Survey Geometric mean (95% conf.200-. see Data Analysis section) for Survey year 03-04 is 0. Serum 2-(N-Ethyl-perfluorooctane sulfonamido) acetic acid (Et-PFOSA-AcOH) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.300) * 03-04 03-04 * * < LOD < LOD < LOD < LOD .300 (.300) .200 (<LOD-.200-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 254 Fourth National Report on Human Exposure to Environmental Chemicals .Perfluorochemicals Serum Perfluorooctane sulfonamide (PFOSA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.200-.200-.S. Survey Geometric mean (95% conf.300 (.200-.300-. which may vary for some chemicals by year and by individual sample.300) . population from the National Health and Nutrition Examination Survey. population from the National Health and Nutrition Examination Survey. interval) Selected percentiles ( 95% confidence interval) Sample 95th .300 (.200-.200-.200-. see Data Analysis section) for Survey year 03-04 is 0. < LOD means less than the limit of detection.300 (.500) .500) 485 538 962 Limit of detection (LOD.300-.S.500) .300 (.300-.200-.300 (.500) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD . < LOD means less than the limit of detection.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) 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD .300 (.300) .4.

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 .400 (<LOD-1.6.20) 1.900) 1.10 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.S.90) .40) 1.700 (<LOD-.900-1.300 (<LOD-. population from the National Health and Nutrition Examination Survey.600 (<LOD-1.30) .900 (.00 (.700 (<LOD-.700) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .Perfluorochemicals Serum 2-(N-Methyl-perfluorooctane sulfonamido) acetic acid (Me-PFOSA-AcOH) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.700) 1.30) 1.S.3.10-1.600) .00 (.10) * 03-04 03-04 * * < LOD < LOD .600 (<LOD-1.80) 1. Survey Geometric mean (95% conf.400 (<LOD-.10-1.30) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th < LOD 90th * 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD .00 (.700 (<LOD-.800) .900-1.10-1.800) . see Data Analysis section) for Survey year 03-04 is 0.30 (1.900) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.600 (<LOD-1.10 (.700) .80) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD .700 (<LOD-2.10) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.30 (1.10) .10 (1.600 (<LOD-.50 (1.00) < LOD .900-1.700 (<LOD-.900-1. Serum Perfluoroundecanoic acid (PFUA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U. interval) Selected percentiles ( 95% confidence interval) Sample 95th .00 (. < LOD means less than the limit of detection.700) 1.20-1.40) < LOD < LOD .800 (<LOD-.900-1.50 (1.700 (<LOD-.30 (1.40) 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD .10-1. see Data Analysis section) for Survey year 03-04 is 0.500 (<LOD-.700) 90th 1. < LOD means less than the limit of detection.900) 485 538 962 Limit of detection (LOD.300-2.300 (<LOD-1.60) 485 538 962 Limit of detection (LOD.80) 1. which may vary for some chemicals by year and by individual sample.900-1.70) 1.900 (<LOD-1. Survey Geometric mean (95% conf.10 (.30) 1. population from the National Health and Nutrition Examination Survey. Fourth National Report on Human Exposure to Environmental Chemicals 255 . which may vary for some chemicals by year and by individual sample.10) 1.700 (<LOD-.20 (1.00-1.60) 640 1454 03-04 03-04 * * < LOD < LOD .10-1.900-1.10) 1.

Bookstaff RC. and ex vivo studies. Biegel LB.46(2):141-147.S. Kennedy GL Jr. Keller JM. Yoshinaga T. Fillmann G. Frame SR. Cook JC. McLaughlin JK. Needham LL.115(11):1596-1602. Inoue K. Kuklenyik Z. Occup Environ Med 2003. Taniyasu S. Temporal trends of PFOS and PFOA in guillemot eggs from the Baltic Sea. Evans TJ. Taniyasu S.60(10):722729. Kannan K. Hurtt ME.60(1):44-55. Perfluorooctanesulfonate and related fluorochemicals in human blood from several countries. Effects of ammonium perfluorooctanoate on Leydig cell function: in vitro. Reidy JA. Butenhoff JL. Kuklenyik Z. Liu RC. Kannan K. Reidy JA. et al. Guruge KS.7(4):371-377. Mandel JH.179:99-121. Environ Sci Technol 2004. Regul Toxicol Pharmacol 2004. Edwards EA. Tarone RE. Ye Y. Environ Health Perspect 2007. Cook JC. Yamashita N. Mandel JH. Needham LL. Polyfluoroalkyl chemicals in the U. Day RD.104(2):322-333. Jarnberg U. Apelberg BJ.39(3):363-380. Perfluorinated chemicals in selected residents of the American continent. Witter FR. Cord serum concentrations of perfluorooctane sulfonate and perfluorooctanoate in relation to weight and size at birth. O’Connor JC. Mortality of employees of a perfluorooctanesulphonyl fluoride manufacturing facility. Dinglasan MJ. Seneviratne HR. J Environ Monit 2005.99(2):253-261. Induction of Leydig cell adenomas by ammonium perfluorooctanoate: a possible endocrine-related mechanism. Koizumi A. Environ Sci Technol 2007a. Morikawa A. Hurtt ME. Ingall GB.68(6):465-471. Bignert A. Fluorotelomer alcohol biodegradation yields poly. Calafat AM. Calafat AM. Corsolini S. Rodricks J. The toxicology of perfluorooctanoate. Environ Health Perspect 2007. population: Data from the National Health and Nutrition Examination Survey (NHANES) 1999–2000. Aguilar-Villalobos M. Grasty RC. sex and geographic factors on levels of perfluorooctanesulfonate and perfluorooctanoate in human serum over the last 25 years.38(17):4489-4495. Calafat AM. Tully JS. Toxicol Appl Pharmacol 1992. Chemosphere 2006b. Kudo N. Environ Sci Technol 2005. Loganathan BG. Rev Environ Contam Toxicol 2003. Kuklenyik Z. Toxicol Appl Pharmacol 1995.34(4):351-384. Burris JM. Needham LL. Seacat AM. Yamashita N. Perfluorochemicals in pooled serum samples from United States residents in 2001 and 2002. Mabury SA. Moore RW.124(2):119-132. in vivo. Chlorinated. Kumar KS. Characterization of risk for general population exposure to perfluorooctanoate. Mechanisms of extrahepatic tumor induction by peroxisome proliferators in male CD rats. Bandai N. et al. Serum concentrations of 11 polyfluoroalkyl compounds in the U. et al. 256 Fourth National Report on Human Exposure to Environmental Chemicals . et al. Katakura M. Olsen GW.39(23):9057-9063. Reidy JA. Watanabe T. de Voogt P. Perfluorinated chemicals and fetal growth: A study within the Danish National Birth cohort. Sasaki S. Hurtt ME. Environ Sci Technol 2005. Perkins RG. Laane RW. Toxicol Appl Pharmacol 1990. Renal clearance of perfluorooctane sulfonate and perfluorooctanoate in humans and their species-specific excretion.113(2):209-217. Androgenic deficiency in male rats treated with perfluorodecanoic acid. Kannan K. Perfluorinated compounds in the plasma of loggerhead and Kemp’s ridley sea turtles from the southeastern coast of the United States. Chem Biol Interact 2000. Perfluorinated organic compounds in human blood serum and seminal plasma: a study of urban and rural tea worker populations in Sri Lanka. Arendt MD. Butenhoff JL. Lau CS. Tully JS. brominated. and perfluorinated contaminants in livers of polar bears from Alaska. Harada K.38(10):2857-2864. Calafat AM.Perfluorochemicals References Alexander BH. Reidy JA.and perfluorinated acids. Wijeratna S. Moore JA.Koizumi A. Murray SM. Mandel JS. et al. Environ Sci Technol 2005. J Occup Health 2004. Kuklenyik Z.39(1):80-84. Yoshinaga T. Kawashima Y. Prenatal window of susceptibility to perfluorooctane sulfonate-induced neonatal mortality in the Sprague-Dawley rat. Environ Health Perspect.S. Grey BE. Frame SR. Gaylor DW. Olsen J. Peterson RE.63:490496.134(1):18-25.41:2237-2242. Environ Res 2005. Saito N. Hekster FM. Toxicol Sci 2001. Yun SH. Kamiyama S. Mohotti KM. Olsen GW. Falandysz J. Herbstman JB. Halden RU. Environ Sci Technol 2004. population: data from the National Health and Nutrition Examination Survey (NHANES) 2003-2004 and comparisons with NHANES 1999-2000. Needham LL. Birth Defects Res B Dev Reprod Toxicol 2003. Suzuki E. Wong LY. Caudill SP. 2007b. et al. Induction by perfluorinated fatty acids with different carbon chain length of peroxisomal beta-oxidation in the liver of rats.39(23):9101-9108. et al. Inoue K. Environmental and toxicity effects of perfluoroalkylated substances. Calafat AM. Caudill SP. Olsen GW. Holmstrom KE.1968--2003. Cook JC.115(11):1670-1676. Biegel LB. Crit Rev Toxicol 2004. Rogers JM. Fei C.115(11):1677-1682.40:21282134. O’Connor JC. Environ Sci Technol 2006a. Harada K. Saito N. The influence of time.

Pepper K. Taniyasu S. Kannan K. Sterchele PF. Olsen GW. Mandel JH. Biol Pharm Bull 2003. Olsen GW. Thibodeaux JR. Environmental Protection Agency (U. Horii Y. et al. J Occup Environ Med 2003b. Miller JP. Fourth National Report on Human Exposure to Environmental Chemicals 257 . fish. Larson EB. Burris JM.37(12):2634-2639. A survey of perfluorooctane sulfonate and related perfluorinated organic compounds in water. J Children’s Health 2004b. Subchronic toxicity studies on perfluorooctanesulfonate potassium salt in cynomolgus monkeys. Exposure to perfluorooctane sulfonate during pregnancy in rat and mouse. Reagen WK. et al. Olsen GW. Half-life of serum elimination of perfluoroo ctanesulfonate. Hansen KJ. Kannan K.111(16):1892-1901. Butenhoff JL. II: postnatal evaluation.) Tittlemier SA. Olsen GW. Lau C.54(11):1599-1611. Toxicol Sci 2003. et al.40(1):32-44. Toxicol Appl Pharmacol 2004. Huang HY. Burris JM.68(1):249-264. Mair DC. Biochim Biophys Acta 1993.45(3):260-270. Historical comparison of perfluorooctanesulfonate. Prevedouros K. Exposure to perfluorooctane sulfonate during pregnancy in rat and mouse. Buck RC. Barbee BD. et al. Environ Health Perspect 2005. Stanton ME. Seymour C.51(8-12):658-668. Olsen GW. Yamashita N. Hansen KJ. Hansen KJ. Preliminary Risk Assessment of the Developmental Toxicity Associated with Exposure to Perfluorooctanoic Acid and its Salts. Quantitative evaluation of perfluorooctanesulfonate (PFOS) and other fluorochemicals in the serum of children. Lundberg JK. Yamashita N. Case MT. Thomford PJ. Ehresman DJ. Olsen GW. The developmental toxicity of perfluoroalkyl acids and their derivatives. Coordinate induction of acyl-CoA binding protein.perfluorohexanesulfonate. et al. Nesbit DJ. Burris JM.1177(2):183-190. 2003.111(16):1900) Olsen GW.epa.41(9):799-806. A global survey of perfluorinated acids in oceans. Helzlsouer KJ. Toxicol Sci 2003. 1/15/06 Vanden Heuvel JP. Taniyasu S. Chemosphere 2004a. Thibodeaux JR. Hanson RG.55:3203-3210. htm. Church TR. Burris JM. Rogers JM. Grey BE. Kawashima Y.gov/opptintr/pfoa/pfoara. Burris JM. Induction of triglyceride accumulation in the liver of rats by perfluorinated fatty acids with different carbon chain lengths: comparison with induction of peroxisomal betaoxidation. Olsen GW. Froehlich JW. Environ Health Perspect 2003a. Epidemiologic assessment of worker serum perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) concentrations and medical surveillance examinations. birds. and perfluorooctanoate in retired fluorochemical production workers. Toxicol Sci 2002. Environ Sci Technol 2003. Seacat AM. Dietary exposure of Canadians to perfluorinated carboxylates and perfluorooctane sulfonate via consumption of meat. Sources. fish. and food items prepared in their packaging. Environ Health Perspect.. Lundberg JK. Cousins IT. Rogers JM. Zobel LR. Peterson RE. van Belle G. fatty acid binding protein and peroxisomal beta-oxidation by peroxisome proliferators. Serum perfluorooctane sulfonate and hepatic and lipid clinical chemistry tests in fluorochemical production employees.74(2):382-392. Available from URL: http://www. Lau C. Perfluorooctanesulfonate and other fluorochemicals in the serum of American Red Cross adult blood donors. J Occup Environ Med 1999.113(5):539-545. perfluorooctanoate andother fluorochemicals in human blood. Butenhoff JL. Burlew MM. Ehresman DJ. (Erratum in: Environ Health Perspect.74(2):369-381. Mandel JH. Serum concentrations of perfluorooctanesulfonate and other fluorochemicals in an elderly population from Seattle. Cao XL et al. Mandel JH. (Erratum in: Toxicol Sci 2004. Hanari N. Richards JH. U. Butenhoff JL. I: maternal and prenatal evaluations.115(9):1298-1305. Bronson R. fate and transport of perfluorocarboxylates. Grey BE. Butenhoff JL. Environ Sci Technol 2006. Petrick G. Horii Y. Moisey J. Olsen GW.68:105–111. Rogers JM. 2007a.S. J Ag Food Chem 2007. Hansen KJ. Hansen KJ. Ellefson ME. 2003a. Seacat AM. Butenhoff JL. Korzeniowski SH.198(2):231-241. Preliminary evidence of a decline in perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) concentrations in American Red Cross blood donors. Mar Pollut Bull 2005. Gamo T. Washington.Perfluorochemicals Kudo N.2(1):53-76. Mandel JH.S. fast foods. and humans from Japan. Church TR.26(1):47-51. Butenhoff JL. et al. Hanson RG. Church TR. EPA).82(1):359. Chemosphere 2007b.

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

Kessler et al. 2002).. Springer. Phthalate urinary metabolite levels in men evaluated at an infertility clinic were associated with several measures of sperm function and morphology (Duty et al. 2003. Assessment of critical exposure pathways.. Cousins IT. 2000a. 2001. Anderson WA. Variation occurs from person to person in the proportions or amounts of a metabolite excreted after similar doses (Anderson et al. High doses of di2-ethylhexyl phthalate (DEHP). The proportions of each metabolite for a given phthalate may vary by differing routes of exposure (Liss et al. variation also occurs in the same person during repetitive monitoring (Fromme et al. Herbert AR. Scotter MJ.. Albro PW and Lavenhar SR.Phthalates and metabolites have been tested.cdc. dibutyl phthalate (DBP).3. Toxicological profile for di(2-ethylhexyl)phthalate update [online]. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 2002). Toxicological profile for di-n-butyl phthalate update [online]. Dirven HA.atsdr. In Staples CA (ed). References Agency for Toxic Substances and Disease Registry (ATSDR). J Chromatogr B 2004.. Drug Metab Rev 1989. 4/20/09 Agency for Toxic Substances and Disease Registry (ATSDR). 1982). 2005). efficiency of intestinal absorption. at higher doses..html). 105:734-742.gov/toxpro2. Lovekamp-Swan and Davis. Springall C. phthalates produced anti-androgenic effects by reducing testosterone production and. Dave M.. but similar findings were not present in young Swedish men with comparable or higher median levels of urinary metabolites (Jonsson et al..gov/ toxprofiles/tp9.45:19-25. 2000c. gender.html. Jongeneelen FJ.e. and extent of metabolite conjugation to glucuronide (Albro et al. Rhodes et al. 1986). 2007). Silva MJ. Jordan S. peroxisomal proliferation may not be a relevant pathway in humans (Rusyn et al. 2003. 2000b. Connor C. environmental levels) and health effects is also available for some phthalates from ATSDR at: http://www. which may be a pathway to the development of liver toxicity and cancers in these animals. Vol.New York.. 2006).805:49-56. Mackay D. testicular atrophy. Corbett JT. reducing estrogen production. The Handbook of Environmental Chemistry. McKee et al. Population estimates of concentrations of specific phthalate metabolites may differ by age. 227-262. interactions with macromolecules and species differences in metabolism of DEHP. A biomarker approach to measuring human dietary exposure to certain phthalate diesters.. Peck and Albro. 2001)..cdc. Also. Available at URL: http://www.html. However.. Metabolism of di(2-ethylhexyl) phthalate. 2004.nih.gov/ reports/index. Environ Health Perspect 1997. and race/ethnicity (Silva et al.niehs.. 2007. Automated solid phase extraction and quantitative analysis of human milk for 13 phthalate metabolites. Sauer MJ. These differences may contribute to species-specific differences in toxicity (ATSDR. Castle L. ovarian abnormalities in the female animals (Jarfelt et al. Calafat AM. 2002. In animals. Available at URL: http://www. 1982.18(12):10681074. Hauser et al. Environ Health Perspect 1982. 2006).atsdr. The monoester metabolites are thought to mediate toxic effects for some of the phthalates. Schroeder JL. 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. Hauser et al. Evaluation of a recombinant yeast cell estrogen screening assay. phthalates have been shown to induce peroxisomal proliferation in rodents.html. 2005. Coldham NG. 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. 4/20/09 Albro PW. Information about external exposure (i. Needham LL. van der Broek PH.. Slakman AR. but there are known species-related differences in the hydrolysis of diester phthalates. 2004). Clark K. Food Addit Contam 2001. 2001. Determination of four metabolites of the plasticizer di (2-ethylhexyl) phthalate Fourth National Report on Human Exposure to Environmental Chemicals 259 . 2004. 1985..cdc. Silvapathasundaram S. Biomonitoring Information Urinary levels of phthalate metabolites reflect recent exposure to the parent phthalate diester. 2004. 2004. and benzylbutyl phthalate (BzBP) during the fetal period produced lowered testosterone levels. 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.21:13-34. effects that may be mediated by inhibiting testicular and ovarian steroidogenesis. Matthews HB. and Sertoli cell abnormalities in the male animals and. Massey RC. McDonnell DP. at very high levels. Pharmacokinetics. NTP-CERHR. Hoppin et al.. atsdr. Part Q: Phthalate Esters.gov/toxprofiles/ tp135.. pp.

Baird DD. Stringer WT. Urinary phthalate metabolites and biomarkers of reproductive function in young men. Occurrence and daily variation of phthalate metabolites in the urine of an adult population. Albro PW.112(17):1740]. Mechanisms of phthalate ester toxicity in the female reproductive system. Estimation of estrogenic and anti-estrogenic activities of some phthalate diesters and monoesters by MCF-7 cell proliferation assay in vitro. Available at URL: http://cerhr. Liss GM. 2000b [online]. Davis BJ. Csanády G. Int Arch Occup Environ Health 1993. Reprod Toxicol 2004. Anal Bioanal Chem 2005. et al. Hass U.nih. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. Milligan SR. Yokoyama Y. Calafat AM. Balasubramanian AV.html. Andersson A-M. Chen Z. Giwercman A. Hanaoka T. Relative potency of xenobiotic estrogens in an acute in vivo mammalian assay.nih. et al.25(2):293-302. Boehmer S. Am Ind Hyg Assoc J 1985. 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Phthalate ester exposure—air levels and health of workers processing polyvinylchloride.Phthalates in human urine samples. Environ Health Perspect 2002. Koch HM. Parker MG. Pan G. Jonsson BAG. NTP-CERHR. Reprod Toxicol 2005. 2000c [online]. Silva MJ. Singh NP.19(4):505-515. Chahoud I. Leffers H. Mortensen GK.nih.11(5):381-387. 6/2/09 NTP-CERHR. Suzuki T. Yoshimura M. Main KM. Hoppin JA. Sumpter JP.nih.110(5):515-518. J Androl 2004. Jacobsen H. Skerfving S. Environ Health Perspect 1998. Int J Hyg Environ Health 2007.64(8):555-560. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. et al. Research Triangle Park (NC). Fromme H. Determination of phthalate monoesters in human milk. Biol Pharm Bull 2003. Kalita JC. Environ Health Perspect 2004. Harris CA. Available at URL: http://cerhr. Kano I. Ryan L. Ryan L. A variety of environmentally persistent chemicals including some phthalate plasticizers are weakly estrogenic. Ladefoged O. 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Ostby JS. et al. Bratt H.36:459-479.58:339349.45:11-17. et al. Environ Health Perspect 2004. Modes of action and species-specific effects of di-(2-ethylhexyl)phthalate in the liver. Fielden MR.S. et al. The plasticizer diethylhexyl phthalate induces malformations by decreasing fetal testosterone synthesis during sexual differentiation in the male rat. Wu ZF. Caudill SP. Jackson SJ. Zacharewski TR. Rusyn I. Peck CC. Parks LG. Silva MJ.114(11):1643-1648. Pratt IA. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Toxicol Sci 1998. Examination of the in vitro and in vivo estrogenic activities of eight commercial phthalate esters. Barr DB. Clemons JH. Klinefelter GR. Toxic potential of the plasticizer di (2-ethylhexyl) phthalate in the context of its disposition and metabolism in primates and man. Rhodes C. Matthews JB. Abbott BD. Environ Health Perspect 2006. Comparative pharmacokinetics and subacute toxicity of di(2-ethylhexyl)phthalate (DEHP) in rats and marmosets: Extrapolation of effects in rodents to man. 112(5):A270]. Cunningham ML. Environ Health Perspect 1982.Phthalates phthalate (DEHP): a cross-sectional study in China.65:299-308. Environ Health Perspect 1986. Reidy JA. Lambright CR.46:282-293. Barlow NJ. Fourth National Report on Human Exposure to Environmental Chemicals 261 . Crit Rev Toxicol 2006. Meek MD. Toxicol Sci 2000. Batten PL.112(3):331-338. Urinary levels of seven phthalate metabolites in the U. Malek NA. Hodge CC. Albro PW. Peters JM. Orton TC.

4 (68.1) 31.4) 12.5-33.9-14.3-75.2) 14.4) 14.0-130) 101 (86. 2000).1-15.2-31.9 (11.9 (70. car care products.1) 14. vinyl tile.6 (13.9) 43.2-38.6) 24.5 (76.4 (32.6-38.0) 32.6) 13.7-82.1 (19.6) 15.2 (14.0 (12.4 (48.6) 13.8-121) 79.0 (20.8 (21.2 (19.5-94.3 (30.8 (10.9) 15.2-33.2) 14.4) 75th 35.0-106) 58.1 (10.9-28.0-55.6 (21.0) 23.4) 98.0) 90th 67.0 (11.8) 63.6-43.3-27.3) 54.9) 14.9 (28.5-25.5) 23.2-17.0 (30.6) 25.9-27.9 (22.4 (13.1) 32.3.5-18.8-16.6) 35. and to a lesser extent.0 (43.S.2-115) 113 (91.4 (32.4 (10. Food crops take up BzBP. and 0.7) 38.2-40.1 (13.4) 38.5-145) 138 (106-241) 143 (127-179) 120 (99.7-16.3) 13.7 (15.8 (30.3 (29.1-61.2-183) 101 (78.9 (39.9) 14.4 (53.3-88.8) 14.2) 33.8-13.7) 23.3 (33. population from the National Health and Nutrition Examination Survey.1-214) 166 (116-191) 145 (110-213) 88.1 (13.0 (33.1-90.7-35.4-15. and 2003-2004 were generally similar those reported in U.8-17. People exposed to BzBP will excrete mono-benzyl phthalate (MBzP) and small amounts of mono-n-butyl phthalate in their urine.6-29.7-14.0-26.8-76.7 (13. IARC considers BzBP not classifiable with respect to human carcinogenicity.6 (53.7 (12. respectively.3-74.6-92.9) 49.6) 95th 103 (94.8-14.1) 13.7-16.6) 14.8-133) 89.8 (80. particularly male animals (McKee et al.5 (67.8-72.2-16.6-132) 103 (84.8-18.1) 68.5) 55.5 (66.9-16.6 (13.2 (25.6) 67.7-170) 169 (134-198) 152 (99.3) 37.7 (70.6 (66.8 (38.1-39.5-41.2-39.7-25.1 (14.4 (10.3 (44.4 (31.4-127) 80.3 (54.6 (13.1-43.7-16.3 (12. in a small sample of pregnant women in New Urinary Mono-benzyl phthalate (MBzP) Metabolite of Benzylbutyl phthalate (BzBP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.6) 29.5-35.1-116) 122 (93.1) 67.9) 12.4) 81..8-64.4 (53.2-19.8-14.2) 12.7) 40.4) 33.5) 15.4 (29.0 (27.3-12.0) 33. and diet is the major source for general population exposure.0) 70.7-13. some personal care products.2 (11.9) 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 39.1 (20. and 03-04 are 0.9-47.9) 13.5 (61.0 (26.3 (12.9-62.1 (58. 2004.4-25.2-155) 91.1-18.0) 16.5 (27.7-15.4-24.2 (10.1-35.4) 129 (98.9 (16.2) 15. residents (Blount et al.3-21.3-18.6 (13.2-20.4 (59.7 (82.9) 18.8) 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 16.6-92. see Data Analysis section) for Survey years 99-00.1) 12.8) 33.3 (29.8.2) 13.2) 66.0) 34.4-92.8 (71.5-62.5-84.2 (47.5) 16.6 (32.5) 65.4) 65.3-34.5 (26. including MBzP.3-130) 122 (88.1) 29.3 (12.8 (14.4) 49.8) 28.8 (28.4) 35.0 (14.3) 13.6-18.9-87.4) 80.5-97. BzBP can be released into the environment during its production and.S.5) 15.0 (30.1-16.2) 69.1-16.8 (71.7 (11.9-49.8-41. sealants.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. interval) 15.4-62.5) 214 (108-399) 235 (183-330) 255 (146-365) 125 (93.8 (12. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.9 (12.9-30. 85-68-7 General Information Benzylbutyl phthalate (BzBP) is a solvent and additive used in products such as adhesives.7-119) 99.7 (51.0) 20.6-17.2 (19. 0.1-38.6-39.0 (15.1.5) 30.8-98.0 (23. High dose BzBP and its monoester metabolites.3) 23.5-14.7-172) 103 (74.6) 16.3) 94.6) 63.9 (13.6) 14.6 (41.5-36.8) 24.5) 27.5-40.2) 22.9 (21.2 (43.9 (12.2) 78. Biomonitoring Information The median levels of MBzP in NHANES subsamples from 1999-2000.8-48. 2001-2002.4) 71.1-120) 52.6-116) 122 (102-142) 101 (85.4 (63.1) 76.3-161) 99.4-16.6-79.6-72.1 (55.6) 50.1 (32.Phthalates Benzylbutyl Phthalate CAS No. 262 Fourth National Report on Human Exposure to Environmental Chemicals .7-58. because it is not bound to products in which it is incorporated.0 (15.3-18.0 (55. 01-02.3-91. 2000).0-85.1-15.1) Selected percentiles ( 95% confidence interval) 50th 17.5) 82.5 (47.4 (27.5-36.3) 15.8 (86.0) 24.3-82.3 (22. can produce developmental and reproductive toxicity in rodents.7 (80.8-17.5 (13.6 (12.6) 37.2) 32.1 (14.9-190) 86. it can be released into the ambient air during use or disposal of the products.3-125) Total 15.2-116) 122 (102-143) 101 (84.7-17.3-43.4) 35.3) 63.8 (53.4) 51.6) 35.5 (55.5 (57.4) 108 (96.8 (50.6-150) 94.8-16.9) 11.3 (13.2) 17.7 (53.2-16.0 (34..3-122) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.8-35. NTPCERHR.

3 (23.8 (64.0-53.6-47. Hauser et al.3) 13.7) Sample size 2541 2782 2605 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 40.8) 54.3) 12.3 (24.0 (49.3 (12.2-15.3 (39.4-18. 2003).0) 60.9-104) 62.8 (57..6-81..4-19.9-23. 2002).8-15. in men attending a Boston infertility clinic (Duty et al.8) 24.1) 39.6 (36.9) 12.7) 19.7 (38.2) 11.0 (13.0 (41.9) 11. A small study of African-American women in Washington.8-13.4) 90th 50.4 (13.4-142) 134 (116-176) 136 (85.6) 12.9-62.1) 35. adolescents compared with adults.1 (21.5 (42. Biomonitoring studies on levels of urinary MBzP provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of BzBP than are found in the general population.7 (21.8-16. 2005).9 (15.6) 53.2-49.8-85.1) 12.4 (26.6-86.5) 78.0 (33.4-27.1) 80.2-12.0) 49.4-79.5-26.6 (11.0) 15.6) 73.3) 16.7 (13.0 (62.4) 60.4 (46.3-11.1 (11.0-27.6 (11.5) 95th 77.7-56. 2004.6-40.7-20. In an annual sample of German university students.4 (21.8-60.8) 34.6-13.5) 20.1-79..0-15.5 (9.6-20.4) 50.3 (60.6) 38.4 (12.7-15.3) 67.7 (23.4-42.2-17.6 (15.3) 18.1-125) 86.3 (35.4-90. median urine levels of MBzP were about one-half the median levels in NHANES subsamples from 1999-2002 (Wittassek et al.8-14.1 (21.5 (10.7) 11.8 (11.8 (50.4) 44. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.. interval) 14.0 (12.7 (19.1 (34.2) 26.4 (74.5) 16. 2007).8-173) 195 (121-305) 229 (99..8-14.7-31.1) 24.9 (22.6 (14.8) 53.9) 64.9-83.1 (53.7 (14.8 (46.8-64.5-76.8-69.3-34.8-27.1 (21.6 (19.4) 21.1 (43.9-115) 57.9-13.8) 15.1 (23.0 (12.0) 24.4 (11.2 (56.5) 41.6) 25.6-26.2) 12.3) 29.8 (69.3) 90.8) 16.1) 142 (99.4 (60.9 (24.7 (11.6) 58.1 (25.0) 12.0-48.4-14.2-21.9) 12.2-117) 95.3 (15.6 (30.0-90.9) 11.4) 17.8 (30.3) 36.1) 23.4-99.1 (41.1-35.7 (18.1-29.8-34. 2002. and in a small sample of German residents (Koch et al.9 (29. 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.2) 11. 2007).4-14.4 (34.1-12.1 (9.4) 14.73-12.4) 13.3) 73.5) 17.2 (40.9 (39.5-29.5 (10.9 (10.5 (35.9 (12.9-69.9 (12.3) 13..9 (10.7 (13. Finding a measurable amount of MBzP in the urine does not mean that the levels of MBzP or the parent compound cause an adverse health effect.5) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Fourth National Report on Human Exposure to Environmental Chemicals 263 .6-116) 74.0 (38.9 (54.5-31.8-13.3 (38.2 (69.4-93.8 (10. In NHANES 1999-2000.6 (30.2-15.5-99. 2003).0) 24.9) 12.1 (13.8) 71.1) 27.2-13.4-116) 73.2) 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 12.5 (11.5) 13.5-79.5 (56. and females compared to males (Silva et al.7 (11.7-12.5 (48. 2004).9-16.7 (54.3-64.2-57.2) 67.S.5-16.3) 21.7-15.8-39.1 (21.5-13.8) 33.7-123) 77.5 (12.7-19. Weuve et al.4-15.4-23.4) 12.7-14.5-61.4 (33.8) 108 (75.3-16.7-69. in young Swedish men (Jonsson et al.1-27.0 (11.6) 30.9 (43.0 (67.4) 28.7-20.5) 46.8) 80.8) 33.8) 46.7-90. 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.7 (12.9) 52.9 (55.3) 37.2 (27.Phthalates York City (Adibi et al.9 (15.3 (13.8 (49.69-11.5 (49.6) 75th 25.2) 32.9) Total 14.7-61.8 (12.7 (59.2) 11.4) 25.5-58.0-109) 65.7) 25.4) 13.9-40.8-80.0) 13.1 (13.7) 46.6 (22.5-42.9-28.1-58.9) 24.1-120) 77. DC reported median urinary MBzP levels that were about twice the levels of adults and females reported in NHANES 1999-2002 (CDC.3-73.8-13.8-42.3) 13.2-78.3) 89.7 (11.9-14.7-397) 70.1) 17.7) 56.2) 15.2-51. Hoppin et al. 2005.6) 12.9-13.6-12.1 (18.5-38.5) 10..0) 11.4 (63.8) 53.4 (25.5-57.0 (10.4) 104 (89.0-51.8) 11.8) 13.9 (51.5-213) 49.4 (11. 2006).3) 14.9) 100 (80.6 (24.3-38.6 (57.8-48.1-12.1 (46.1 (14.8-15.3) 55.8) 26.6 (34.6-99.7-19.4 (11.4-102) 70. the adjusted geometric mean levels of urinary MBzP were significantly higher in several subgroups: children compared to adolescents and adults.4) 51.4 (69.4-17.3) 14.4) 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 12.8) 56.8 (13..7 (55.1-14.7-29.5-23.1 (19. population from the National Health and Nutrition Examination Survey.2 (41.4 (10.1) 24.4) 15.0) Selected percentiles ( 95% confidence interval) 50th 13.9) 42.2-13.7-14.5-26.6 (51.0-26.9 (9.4-60.. Survey years 99-00 01-02 03-04 Geometric mean (95% conf..9 (24.95-14.6) 13.5) 14.1 (15.5) 23.7) 38.2-26.6 (11.8) 68.5-58.6-15.0 (41.

Needham LL.nih. Ryan L.gov/ chemicals/phthalates/bb-phthalate/bbp-eval. Urinary phthalate metabolites and biomarkers of reproductive function in young men. Phthalate monoesters levels in the urine of young children. Silva MJ.Phthalates References Adibi JJ. Jonsson BAG. Sanchez GN. et al. Hagmar L. Gans G. Brock JW. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. Eckard R. Hilborn ED. Angerer J. Third National Report on Human Exposure to Environmental Chemicals. Environ Health Perspect 2004. Malek NA. Environ Health Perspect 2003. et al. Camann DE. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine.html.114(9):1424-1431. Available at URL: http://cerhr. Baird DD. Jedrychowski W. Reprod Toxicol 2004. Environ Health Perspect 2000. Int J Hyg Environ Health 2007. Butala JH. Blount BC. et al. Rylander L. Research Triangle Park (NC). Brock JW. Perera FP. Environ Res 2003. Duty S. Atlanta (GA). Meeker JD.S. Caudill SP. Chen Z. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Silva MJ. Jacek R. Koch HM. et al. Urinary levels of seven phthalate metabolites in the U. Reproducibility of urinary phthalate metabolites in first morning urine samples. Dobler L. Wittassek M.niehs. Singh NP. Richthoff J. Calafat AM. Sampson EJ. Weuve J. Exposure to phthalates in neonatal intensive care unit infants: urinary concentrations of monoesters and oxidative metabolites.22(3):688-695. Hauser R. Centers for Disease Control and Prevention (CDC). Drexler H.25(2):293-302. Caudill SP. 112(5):A270]. Rossbach B. Hum Reprod 2007. Wiesmuller GA. Hoppin JA. Schettler T.18(1):122.68:309-314.108(10):979-982. Barr D. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. et al. 2005. NTP-CERHR. 264 Fourth National Report on Human Exposure to Environmental Chemicals . McKee RH.210(3-4):319-333.111(14):1719-1722. Duty SM. Reidy JA. Giwercman A. Poland. Silva MJ. Monograph on the Potential Human Reproductive and Developmental Effects of Butyl Benzyl Phthalate (BBP). Bull Environ Contam Toxicol 2002. Koch HM. 4/20/09 Silva MJ. Environ Health Perspect 2006. Barr DB. Silva MJ. Environ Health Perspect 2002. Levels of seven urinary phthalate metabolites in a human reference population. Brock JW.110(5):515-518.93:177-185. Calafat AM. Helm D.112(3):331-338. et al. Internal phthalate exposure over the last two decades—a retrospective human biomonitoring study. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. Ryan L. Hu H. J Androl 2004. Pirkle JL. Hodge CC. Prenatal exposures to phthalates among women in New York City and Krakow. Caudill SP.16(4):487-493. Davis BJ. et al. 2000 [online]. Green RA. Epidemiol 2005. Needham LL. David RM.

55 (3.46 (3.2) 5..70 (2.30-6.4 (14.40-4.7 (16.7 (7.0 (13.56 (5.3-30.0) 24.5 (20.2 (8. CDC.00-6.50) 90th 12.40-3.5) 18. 2004.90 (6.9 (16.24-8.0-14.30) 5.30-3.60 (4. 2004.2-33.6) 17.9-23. and insecticides. NIOSH and ACGIH have established guidelines for workplace air exposure to di-n-butyl phthalate.20-12. exposure to benzylbutyl phthalate (BzBP) will also result in small amounts of mono-n-butyl phthalate appearing in the urine.70) 3.1) 16. in men attending a Boston infertility clinic (Duty et al.48 (2. 2003).3-20.. 2000.50 (6.5) 14.30) 10.0 (13.60 (2.10) 11.5-16.10 (4.50-6.00 (7.71 (2.46) 2.3 (16.7-31. 2001-2002 and 2003-2004 subsamples were similar to MBP levels reported in U.80 (5.6) 16.33 (2.7) 4.10-2.00) 6.00-6.20 (3.9-14.40-9.8) 40.5) 12.10 (3.30) 10.00 (5.4) 12.97) 4.7-18.5-16.10 (4. Koch et al.1 (13.5 (10..1-20.40-12.0-25.6 (14.10) 3.40-5.80 (3. and also in some printing inks.6) 26.44-2.40 (7.00-4.50-2.0) size 2782 2605 Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 03-04 50th 2. see Data Analysis section) for Survey years 01-02 and 03-04 are 1.2-22.6-34.7 (9.56) 3.0-18.90 (3.46-5. In addition.90-4.3) 33.00) 10.6-14.90-2.02) 4.1-12. Studies of children found age-related differences in urine MBP levels.6 (13. Neither IARC nor NTP has evaluated dibutyl phthalates with respect to human carcinogenicity.7 (17.3-43. and in a small sample of Japanese adults (Itoh et al..3 (11.30-11.0) 1371 1250 1411 1355 01-02 03-04 01-02 03-04 01-02 03-04 3.7) 14.7 (18.6 (9..5) 25.00-11.46 (2.80 (5.1 (8. 2001).5-29.6) 17.22 (3..0 (11.70-4.6 (14.7) 15.60) 3.40 (6.3 (19.6) 10. 2005).80-5.60 (8.97-7.00) 4.81 (3. referred to as DBP) are industrial solvents or additives used in many personal care products such as nail polish and cosmetics.3-19.40 (3.0 and 0.3 (18. Survey Geometric mean (95% conf.4) 5.Phthalates Di-n-butyl Phthalate CAS No.4-12.50 (3.0) 20. 2005).43) 6. Fourth National Report on Human Exposure to Environmental Chemicals 265 .5) 22.6 (29.00-9. pharmaceutical coatings.3 (13. residents (Blount et al.30-2.20 (7. Compared with the median for 6 to 11 year olds in NHANES 1999-2004 (CDC.80-5.4-27. population from the National Health and Nutrition Examination Survey.3.25) 01-02 03-04 01-02 03-04 01-02 03-04 4.2 (12.8) 21..0) 13.6) 16.30) 2.60-6.0) 9.91) 4.17) 4. 2003). 2007).10) 9.84) 4.6) 12.5-24.1-17.20) 7.6-18.4 (20.7 (17.10-9. Median MBP levels in two European studies were about two to six times higher than median levels in this Report (Jonsson et al.30) 6.7-31.56-4.0 (19.90-7. DBP can produce reproductive toxicity in male rodents (McKee et al.3) 18.5 (27.3 (13.50) 18.40-4. 2000).3-18.37) 6. 2005.5) 23. they have been referred to as monobutyl phthalate (MBP).59) 3.40-17.19-3.97) 2.00) 7.11-3.55) 2.80) 75th 5. Following oral administration of DBP to humans.5) 18.10) 8.5 (17.70-8.50) 8.90 (4.40 (2.30-6.8) 677 652 703 699 1216 1088 Limit of detection (LOD. Biomonitoring Information Median concentrations reported in the NHANES 19992000.40-3.1-25.70) 5. People exposed to dibutyl phthalates will excrete mono-n-butyl phthalate (MnBP) and mono-isobutyl phthalate (MiBP) in their urine.4) 22.67 (5.90 (4.7) 7. OSHA has established a workplace air standard for external exposure to DBP.26 (2.5) 19.50) 2.07 (3.50-10.20-2.50) 5. 2005). 84-74-2 Di-isobutyl Phthalate CAS No.22) 3.73-5.50) 7.3 (16.6-20.49-2.94) Selected percentiles ( 95% confidence interval) Sample 95th 17.30-7.10) 2.6 (10. in a small sample of pregnant women in New York City (Adibi et al.1) 25.30-13.66) 2.6-26. about 65% to 80% of a dose is eliminated in urine within 24 hours.20-12.7-20.2 (11.70 (5.20 (6.2-14.10-9.72-3. the median Urinary Mono-isobutyl phthalate (MiBP) Metabolite of Di-isobutyl phthalate (DBP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.6 (11.90-4.63) 3.85-6.1) 22.6 (13.3) 3. Small amounts of mono-3-carboxypropyl phthalate are also produced from di-n-butyl phthalate.20-6. 84-69-5 General Information Dibutyl phthalates (both di-n-butyl and di-isobutyl phthalates.90) 12.70-4.9) 15.20-9.0) 393 342 742 729 1647 1534 01-02 03-04 01-02 03-04 2.82-3. mostly as MnBP (Anderson et al.3-24.5 (11.7) 18.6 (10.30 (4.8 (9.80 (2.50-4.60 (5..30 (3. interval) 2. When total DBP metabolites have been measured.73 (2.68 (2.S.3-48.S..30 (1. Hauser et al.40 (2.0-38.56 (3.17 (2.20) 4.96) 3.28-5.9) 10.0) 12.00) 4. NTP-CERHR.9 (16.80 (2.40) 5.

10-5.64-10.85 (2.52-3.46) 3.69) 6.75 (4.03-11.65-11.39-3.80 (3.76-3.1) 10.0) 11.33 (2.related differences in the adjusted geometric mean levels of urinary MiBP and MnBP (CDC.79-8.56-15.8) 10.8-18.04-5.57 (3.74 (4. 2002.17) 90th 8.26 (2.18) 4.5) 13.76-15.81 (6.1-25.45) 3.15-4.32) 7.14 (4. Between 1998 and 2003.1 (10.53-3.84 (4.6 (9.1) 7.2 (10.93-6.3) 13..79 (4. Studies measuring urinary MnBP have reported variable median values compared to the NHANES 2001-2002 and 2003-2004 subsamples.47-12. samples from German university students had consistently higher median urine levels of MnBP and MiBP.74-3.9-16.7 (11. respectively.99-4.86) 6.1) 11. 2005). Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.80-3.1-24.78) 8.43) 3.0) 393 342 742 729 1647 1534 01-02 03-04 01-02 03-04 2.59 (4.95-3.8-18.6 (15.89-5.6) 11.69-7.42) 2.95) 2. ranging from more than one-tenth the NHANES median (Itoh et al.03 (5.08-2.68 (2.07 (2.55-6.47 (3.7) 19.96 (3.Phthalates for neonates was lower (by about half) and the median for toddlers was higher (by about sixfold) (Brock et al.21 (5.13-6.4-16.30) 2.66) 10.38 (6.0) 3.94) 6..69) 4.36-2.81 (3.4 (12.11 (5.11-2. Differences in urinary MBP population estimates by gender have also been shown (Silva et al.00-3.54) 2.9-26.36-7.6-19.52) 3.7 (9.31) 2.91-6. In an analysis of NHANES 1999-2000.29-8. 2007).43) 3.S.80) 7.6 (8.6) 13. up to four and 13 fold.7 (21.1-15.89) 6.1) 677 652 703 699 1216 1088 266 Fourth National Report on Human Exposure to Environmental Chemicals .8 (9.56-4.35) 3. 2004).19 (2.8-13.0-18.99) 7.3) 16.17-12.22 (2.43) 3.8-36.6 (12.01-2.00) 01-02 03-04 01-02 03-04 01-02 03-04 4.04) 3.7) 3.66 (8.2) 8.51) 15.54 (4.82) 4.00 (3.28 (4.34 (3.46-11.88 (2.33 (3.2) 24.20 (2.11) 5.32 (7.94 (5.05) 2.20-2.56) 5.03-7.9 (15.1 (11.81) 4.95) 10.86-4.37) 3.17 (2.53-5.7) 1371 1250 1411 1355 01-02 03-04 01-02 03-04 01-02 03-04 3.69 (2.9) 12.51) 5.33-9.83 (2.18 (4.2-15.6) 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 2.75 (6. to about two to fourfold higher (Fromme et al.64-7.78) 9.57-4.and gender.5-19. 2004).1) 15.8 (8.3 (17.58-3.00-3.61-3.33) 3.51) 2.27-12..5) 15.41 (2.2-13. population from the National Health and Nutrition Examination Survey.7-28. 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.3) 18.92 (7.20-3.57 (3.67-5.54 (2.25) 5.65-4.66) 2. Weuve et al.0) 7. 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.62 (6.02 (7.0 (12.76 (3.4) 15.64-7.72-7.31 (7. An analysis of NHANES 2001-2002 showed similar age.98 (2..62-12.00-7. Survey Geometric mean (95% conf.79-6.5 (9.15) 3.89 (3.9-40.04) 7.7) 10.73) Selected percentiles ( 95% confidence interval) Sample 95th 12.76-3.68) 5.73 (5.1) 13.20 (7. Over this time.72) 5.39) 5.78-8.6 (8.5 (11.0 (8.56) 2.18-4.0) 15.08) 75th 4.9 (11.7) 11. 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. interval) 2.4) 23.4) 7.18) 3.58-4. the students’ median values for MiBP levels remained relatively unchanged.68) 3. 2007).21) 10. Biomonitoring studies on levels of MnBP and MiBP provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of dibutyl phthalates than are found in the general population. 2005).52-20.31 (2.47-5.0 (10.02-10.6 (10.8 (10.29-3.46 (2.1) 4.28-13. while MnBP declined (Wittassek et al..24) 3.20-4.2 (11.7 (13.65 (4..30 (6.3 (13.31) 2.1-12.18-10.09-2.26-2.44 (3.84 (8.97-2.3) 28.32 (3.52 (2.53-4.82 (4.38-10.18 (1.3) 13..81) 9.2) 9.13 (2. 2006).9 (9.20 (2.07-5.94-12.6-19. than adults in NHANES subsamples during the same time period.66) 4.

8-42.1-92.5) 47.5) 31.6-44.5) 65.5) 21.7 (38.6-69.6-40.5-43.4 (72.1) 25.8-22.2-56.5) 78.9.7-24.2) 90th 98.7 (22.7 (18.8) 43.0 (25.1 (19.1 (19. *In the 1999-2000 survey period.0 (20.2 (20.2 (59.1) 20.1-24.0-73.0 (30.2 (21.0-24.6-20.4 (36.3-67.6-48. concentrations of mono-isobutyl phthalate and mono-n-butyl phthalate were measured together and expressed as a combined value.7-34.1-22.4) 52.2 (74.6-31.1 (31.9-92.0) 20.0) 21.6 (61.2-22.7) 124 (98.0) 117 (104-131) 112 (84.5) 17.8) 62.9) 21.3-96.0 (78.1 (19.4 (38.7) 42.0) 31.9-42.7 (43.2 (78.1) 23.4-44.2-24.3 (30.0-19.6 (55.6) 39.2 (58.1) 31.5) 20.4-42.1 (36.3) 36.9 (79.3) 40.9 (17.2) 26.3-21.7) 92.4-26.6-24.1-75.3 (30.4) 22.1-80.4 (35.0) 120 (98. 01-02.4) 20.5-27.4) 59.3) 21.2 (75.2-93.1 (21.5) 36.5 (29.2 (18.0 (72.5-121) 106 (94.6 (44.3-136) 137 (107-162) 119 (90.4.3) 23.4) Selected percentiles ( 95% confidence interval) Sample 95th 150 (121-169) 108 (94.9 (17.0 (31.8) 75th 51. Fourth National Report on Human Exposure to Environmental Chemicals 267 .4 (35.1) 36.9-33.9-79.0-51.0 (23. and 03-04 are 0.9) 71.1 (16.1 (58.0) 30.7 (64.2-23.8-25.0) 38.4-25.7-106) 69.4-60.7) 74.6) 21.0-19.2) 42.4-20.2 (19.6-29.5) 40.5 (59.9 (79.3 (36.3-85.5) 95.2) 38.9) 46.7-53.6) 20.1) 30.5-47.7) 28.4 (71.6-37.4 (35.6) 38.1) 47.4 (25.3 (42.7-42.5-117) 95.6) 35.8-29.9-28.5 (28.5-60.1 (51.5 (59. and 0.4 (23.0-24.8) 23.4 (84.2 (17.3-145) 85.4-159) 107 (84.3) 19.6 (48.2-159) 92.9-53.0-58.1 (41.6) 17.6 (16.3 (23.6-143) 127 (99. see Data Analysis section) for survey years 99-00.8) 19.7 (19.7 (28.0 (45.7-91.7-34.1.1) 23.9) 26.4 (35.9) 36. Survey Geometric mean (95% conf.1) 23.4-18.3) 26.2-32.3-79.9) 75.1 (18.2) 62.6-36.6-29.5) 19.0 (18.7 (24.7 (18.2-33.3-76.6-33.8) 58.4 (21.7-121) 97. referred to as monobutyl phthalate (MBP).6 (22.3 (17.3) 18.9-22.0-32.5) 36.8-123) 101 (90. respectively.9-114) 116 (97.6 (19.6) 71.6) 166 (127-279) 159 (110-290) 191 (150-243) 165 (121-227) 148 (106-185) 134 (110-158) 143 (117-161) 95.2-21.7-127) 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 22.3-60.5 (30.6) 46.2-49.0 (17.2 (25.7 (16.5) 24.9-87.1 (62.6 (65.9-22.6-49.7-116) 95.1 (28.3 (23.6 (26.0 (15.5-53.7-20.3) 24.1) 19.9) 18.1 (26.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. population from the National Health and Nutrition Examination Survey.3 (60.8 (57.5-42.S.7-111) 64.4) 64.3-24.8) 48.2) 32.6-113) 108 (90.8-165) 167 (143-197) 138 (110-184) 144 (115-168) 142 (111-161) 107 (89.1 (34.6 (90.1-20.8-119) 90.2-87.7-117) 118 (108-143) 93.1 (54.9-101) 77.5) Age group 6-11 years 99-00* 01-02 03-04 99-00* 01-02 03-04 41.2-114) 73.7-42.7-124) 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.5) 85.7 (51.5) 26.5 (74.5-44.1-122) 122 (104-137) size 2541 2782 2605 Total years 99-00* 01-02 03-04 50th 26.5-47.0 (36.0) 27.1-82.7-92.2-63.6 (32.2 (21.6) 80.2) 68.8 (19.5) 37.0-26.7) 52.7 (70.5) 34.7 (33.0-21.1-29.9 (20.1) 17.4-31.8-111) 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 23.1-51.8-132) 95.7-26.3 (51.1) 46.1 (19.1 (17.3-40.1-27. 1.0) 84. interval) 24.2) 20.9) 29.4 (19.3 (37.2 (79.3 (56.

8) 17.5-23.5 (18.2-73.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. Survey Geometric mean (95% conf.4 (23.6) 24.4) 16.6 (57.3 (60.8-23.2-22.0 (70.8-235) 137 (108-198) 88.6-22.0) 26.0) 25.0 (18.7) 20.1) 17.7 (43.2-18.5-41.9-56.3-23.3 (52.6 (19.9-84.4-135) 71.6-28.6) 37.4 (45.6-43.1) 20.5 (30.3-78.3 (17.5-70.3-49.5-30.8) 19.3 (21.1) 61.8 (65.2-48.9) 39.5) 17.3) 59.6-24.5-142) 89.0-92.7-26.3-21.9) 19.3) 18.8 (17.0 (69.1 (34.0 (20.7 (73.5) 84.8 (22.6 (29.4) 19.4 (16.2) 16.4-103) 117 (83.0) 29.3 (52.0-17.8) 35.7 (54.3) 52.3-26.7 (57.0 (61.3 (19.3 (16.3 (17.3-39.9) 30.0) 28.7-19.3-18.8-43.5-15.4 (18.1) 42.0) 94.8 (25.4 (13.5-76.9-49.9-68.3 (46.2 (19.0 (15.1) 50.8) 17.6-16.0-113) 104 (83.4) 51.4) 15.7) 19.1-115) size 2541 2782 2605 Total years 99-00* 01-02 03-04 50th 21.0-41.1-18.2) 74.3 (69.7 (19.1 (21.3) 33.6 (17.4 (56.6-19.8) 23.7) 36.8-32.8) 28.3 (42.6-92.0) 55.8) 22.6-53.3 (55.1-99.9 (30.4 (53.4-65. 268 Fourth National Report on Human Exposure to Environmental Chemicals .2-179) 84.6) 83.8 (18.6) 14.0 (26.7-19.5-21.3 (48.9) 20.4 (68.2 (19.1) 20.1 (56.2-61.8) 40.7-80.5) 60.6-44.3 (71.7 (60.9 (64.5) 134 (93.8 (18.4) 21.9 (30.9) 14.3-114) 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 17.5-22.8) 20.1) 22.2) Age group 6-11 years 99-00* 01-02 03-04 99-00* 01-02 03-04 41.9) 52.0 (19.7 (81.9-70.4 (19.6) 34.2-108) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites 99-00* 01-02 03-04 *In the 1999-2000 survey period.6-128) 96.8-24.7-28.2-16.4) 15.5 (15.3-71.1 (29.4 (20.6) 64.9-26.1-23.0) 59.6-23.4-61.3 (17.7-78.7 (14.7-21.2) 159 (102-263) 147 (93.4 (50.0) 70.6 (41.1-128) 97.1-99.8) 75th 38.2-22.6-42.8 (50.3 (24.6-74.0 (50.3) 35.4 (33.6-23. population from the National Health and Nutrition Examination Survey.1) 44.7-20.9-14.2) 21.1) 35.0 (52.6) 65.1) 21.1) 53.9 (35.6 (31.0 (71.9-68.2-27.9) 28.0) 35.0 (34.0-47.5 (81.7 (60.4 (31.9 (56.1-21.8) 30.8 (13.5-18.6) 24.4-24.5) 21.3) 19.6-26.5-16.3 (76.4 (31.0) 108 (71.2-85.3-20.3-32.8) 34.6) 18.4 (37.9) 91.4 (47.0) 19.0-38.7-37.2 (38.7 (12.1 (46.8 (18.6) 31.1 (15.7 (27.6) 25.6-50.9 (16.9) 62. concentrations of mono-isobutyl phthalate and mono-n-butyl phthalate were measured together and expressed as a combined value.3) 17.2-106) 64.6 (72.9 (20.4) 53.5 (18.9 (30.2-21.6-32.7-42.7 (16.7 (20.0 (18.0 (43.2) 31.7 (28.0-75.4-72.3-17.5) 39.6 (25.6) 38.0) 53.0-60.9-105) 85.2 (16.5-142) 81.9-100) 86.4) 20.4 (31.6) 39.0) 41.7-51.5) 90th 68.S.9 (21.8) 63.8) 20.0-90.5 (14.5-37.8 (16.2) 65.9 (39.6-44.1-83.0) 75.2 (83.5) 91.4-34.7-39.2-22.9 (37.1-62.2) 59.4-164) 96.4-47.3-40.6-24.0 (27.6-119) 63.6) 23.4 (16.0 (16.2 (35.5) 82.5-64.8 (33.4 (17.3) 67.9 (73.2-28.3) 33. interval) 22.6-139) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00* 01-02 03-04 99-00* 01-02 03-04 21.9) 24.6-155) 91.4-131) 81.6-27.6 (61.3-21.1 (61.7-23.8-24.1-32.0) 81.4 (17.4) Selected percentiles ( 95% confidence interval) Sample 95th 97.9 (35.9-36.1) 37.6 (27.9 (19.8) 13.6 (74.4 (50.2-86.4-76.3) 20.6 (25.3-81.5 (64.7) 42.8) 34.0-19.1 (32.3-38.9) 49.3) 21.9-34.4) 62.8) 17.3 (28.3) 19.3-106) 74.9-38.9 (58.

210(3-4):319-33.nih. Phthalate monoesters levels in the urine of young children.112(3):331-338. 2000 [online].25(2):293-302. Schettler T. Weuve J. 2005. Brock JW. Eckard R. et al. Duty SM. Dobler L. et al. Camann DE. Perera FP. McKee RH. Exposure to phthalates in neonatal intensive care unit infants: urinary concentrations of monoesters and oxidative metabolites. Bolte G. Hilborn ED.68:309-314. Barr D.S. Needham LL. Pirkle JL. Prenatal exposures to phthalates among women in New York City and Krakow. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. Singh NP. Ryan L.22(3):688-695. Jedrychowski W. Koch HM.18(1):122. Richthoff J. Gans G. Silva MJ. Sampson EJ. et al. Available at URL: http://cerhr. Brock JW. Monograph on the Potential Human Reproductive and Developmental Effects of Di-n-Butyl Phthalate (DBP). Bull Environ Contam Toxicol 2002. Green RA. Urinary phthalate metabolites and biomarkers of reproductive function in young men. Boehmer S. et al. Caudill SP. Silva MJ. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites.18(12):10681074. Masunaga S. Itoh H. Wiesmuller GA. Rylander L. Hu H. Evaluation of the effect ofa governmental control of human exposure to two phthalates in Japan using a urinary biomarker approach. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Barr DB. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine.html. Malek NA. Atlanta (GA). Chen Z. Fromme H.Phthalates References Adibi JJ. Int J Hyg Environ Health 2007. Angerer J. Scotter MJ. Caudill SP. Yoshida K. Environ Health Perspect 2004. Giwercman A. Levels of seven urinary phthalate metabolites in a human reference population. Hauser R. Wittassek M. Silva MJ. Fourth National Report on Human Exposure to Environmental Chemicals 269 . Duty S. Hagmar L. Environ Health Perspect 2006.208:237-245. Jonsson BAG. Urinary levels of seven phthalate metabolites in the U. Environ Health Perspect 2000. Int J Hyg Environ Health 2005. et al. Environ Res 2003. J Androl 2004. Helm D.gov/chemicals/ phthalates/dbp/dbp-eval. Drexler H. A biomarker approach to measuring human dietary exposure to certain phthalate diesters. Calafat AM. Internal phthalate exposure over the last two decades—a retrospective human biomonitoring study.108(10)979-982. Sanchez GN. Drexler H. NTP-CERHR. Springall C.16(4):487-493. Hodge CC.niehs.93:177-185. et al. Poland.114(9):1424-1431. Third National Report on Human Exposure to Environmental Chemicals. Rossbach B. Epidemiol 2005. Research Triangle Park (NC). Blount BC. Koch HM. et al. Jacek R. Hum Reprod 2007. Butala JH. Silva MJ. 4/20/09 Silva MJ.111(14):1719-1722. Castle L. Needham LL. David RM. Food Addit Contam 2001. 112(5):A270]. Angerer J. Ryan L. Calafat AM. Int J Hyg Environ Health 2007. Meeker JD. Centers for Disease Control and Prevention (CDC).210:21-33. et al. Reidy JA. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. Koch HM. Anderson WA. Caudill SP. Environ Health Perspect 2003. Reprod Toxicol 2004. Occurrence and daily variation of phthalate metabolites in the urine of an adult population. Massey RC. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction.

500) 1. respectively.400 (<LOD-.300 (.300 (.700) .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.00-3.400) size 2541 2782 2605 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .500) < LOD < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.3.600) .300 (<LOD-.10 (<LOD-1.500 (. 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.300-.600) .400-.300 (. 0.70) .500 (.500) 1. Neither IARC nor NTP has evaluated DCHP with respect to human carcinogenicity.400 (.300-.700) .200-.300-.300 (.10 (<LOD-1. 84-61-7 General Information Dicyclohexyl phthalate (DCHP) is used to stabilize some rubbers.Phthalates Dicyclohexyl Phthalate CAS No.80) .70 (1.400) 1.200-.500) < LOD < LOD .400) 1.70 (1.600) . 270 Fourth National Report on Human Exposure to Environmental Chemicals . < LOD means less than the limit of detection. including nitrocellulose.600 (.500) 1.00 (<LOD-1.200 (<LOD-.400 (<LOD-. polyvinyl acetate.400-.400 (<LOD-.400 (.300-. People exposed to DCHP will excrete mono-cyclohexyl phthalate (MCHP) in their urine.300-.400 (. population from the National Health and Nutrition Examination Survey.600) . and polyvinyl chloride.400-.400 (.500 (.300-.00-2.400) < LOD < LOD .200-.200-.300-.400-.500 (. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1. and 0.500-.400 (.2.400-.300-.00 (<LOD-1. and polymers.500 (.20) .S.50) .400) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (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.300 (.00 (<LOD-1.600) .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 1.200-.300-. resins.500 (.500) < LOD 1.10 (. which may vary for some chemicals by year and by individual sample.10) .70) .400 (.300) < LOD .400) < LOD 1. 01-02.00) . see Data Analysis section) for Survey years 99-00.500) . Survey Geometric mean (95% conf.300 (.90) .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 (<LOD-.500 (.500) .500 (.200-.9.500 (.300) < LOD .400 (. and 03-04 are 0. In this Report.10 (<LOD-2.500) .900-1. 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. only levels at or above the 90th percentile could be characterized.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 .50) .700) .300 (.300-.600) < LOD .

220 (<LOD-.74) .590) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .690) < LOD < LOD .17) .710) .610 (.630 (<LOD-.240-.370 (<LOD-.06) .560) 1.800-1.620) < LOD .880 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th 3.740) < LOD < LOD .82 (1.690) < LOD * * * Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1.06) .170-.670 (<LOD-.770-1.82) .770 (.390 (.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.530-.500 (.910 (.910 (.490) . Survey Geometric mean (95% conf.330 (.770) < LOD 2.53) .380-.690-1.480 (.310) < LOD .12-1.290-.630 (<LOD-.910 (. Fourth National Report on Human Exposure to Environmental Chemicals 271 .590 (<LOD-.450 (.260-.830) 1.790-1.410 (.14 (<LOD-3.510-.690 (.420-.54-6.53) .33) .34) .250 (.33 (<LOD-3.590 (.22 (<LOD-1.S.350-.44) .18) .310-.420-.530 (.00 (<LOD-3.270) < LOD .510 (.950 (.740) .11) .940 (.16 (<LOD-3.470 (.500) size 2541 2782 2605 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .54 (<LOD-2.910 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.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 .770-1.16) .10) .530-1.43 (1.500-.05) .530) 1.450 (.400-.400-.660) < LOD < LOD .360-.770-1.67 (1.00) .500) 3.330 (. population from the National Health and Nutrition Examination Survey.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.36-1.690) < LOD 2.670-1.380 (.660) .420-.54) .470) 3.

Phthalates Diethyl Phthalate CAS No.3-110) 211 (160-278) 197 (159-243) 225 (187-270) 190 (164-219) 191 (171-214) 205 (176-238) 75.4. 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 91.3-103) 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. shampoos. People exposed to DEP eliminate mono-ethyl phthalate (MEP) in their urine.9 (61.7 (70. and hand lotions. deodorants.9-92.3 (82.1-93. colognes. In contrast. Biomonitoring Information MEP levels in the NHANES 1999-2000. population from the National Health and Nutrition Examination Survey. 0. and 03-04 are 1. 84-66-2 General Information Diethyl phthalate (DEP) is a solvent used in many consumer products.4 (62.9.3 (74. particularly those containing fragrances. Neither IARC nor NTP has evaluated DEP with respect to human carcinogenicity. 2003) and African-American women in Washington.2-102) 95. DC (Hoppin et al. 272 Fourth National Report on Human Exposure to Environmental Chemicals . Workplace air guidelines for external exposure to DEP have been established by ACGIH and NIOSH. 2001-2002.S. and 0. A small study of children less than 2 years old reported mean urine MEP levels that were about twice as high as levels in children (aged 6-11 years) in NHANES 2001- Urinary Mono-ethyl phthalate (MEP) Metabolite of Diethyl phthalate (DEP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.1 (71.. respectively. see Data Analysis section) for Survey years 99-00... a sample of young Swedish males entering the military had median urinary MEP levels that were somewhat higher than males in the NHANES subsamples. 2007).2. 2002).8-111) 85. 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.5) 81.7) 71. 01-02. Products that may contain DEP include perfumes. soaps. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.

S. 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. 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. This age-related trend is opposite the direction seen for other phthalates.6 (65. 2005).5-114) 101 (87..9-110) 96. 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. Median MEP levels found in a small sample of German residents (Koch et al.0-117) 142 (119-169) 152 (126-184) 168 (141-201) 179 (161-199) 181 (164-200) 197 (174-223) 79. 2004). In an analysis of NHANES 1999-2000.2 (66.5-113) 122 (93. Other population estimates also differed by sex and race ethnicity (Silva et al. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 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. population from the National Health and Nutrition Examination Survey.0 (66. with adjusted geometric mean levels of urinary MEP that increased with age (CDC.6 (77...3-105) 87. Analysis of NHANES 2001-2002 showed similar findings.9 (82. 2003) were slightly lower than levels found in NHANES 2001-2002.7-110) 81. 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.0-156) 140 (111-180) 150 (123-184) 154 (136-177) 160 (146-182) 177 (147-202) 165 (127-208) 177 (135-224) 180 (145-203) 364 (275-495) 330 (249-409) 363 (292-485) 390 (336-452) 419 (363-486) 512 (423-632) 341 (219-554) 512 (290-802) 470 (310-596) 879 (676-1260) 808 (590-1100) 791 (589-1080) 1010 (803-1460) 1060 (884-1320) 1230 (989-1610) 625 (400-784) 843 (512-1320) 719 (470-1330) 1760 (1000-2000) 1330 (868-1840) 1470 (987-2220) 2170 (1790-3350) 2120 (1520-2790) 2290 (1770-3200) 328 393 342 752 742 729 1456 1647 1534 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 141 (124-159) 148 (130-168) 154 (139-171) 187 (165-211) 187 (166-210) 211 (180-248) 120 (107-134) 126 (110-147) 127 (108-150) 158 (142-179) 171 (148-188) 181 (148-217) 324 (249-415) 352 (282-425) 390 (341-465) 377 (307-495) 407 (355-473) 508 (379-634) 1000 (693-1480) 1100 (839-1480) 1070 (852-1360) 822 (697-1170) 860 (712-1100) 1120 (889-1400) 1950 (1460-2900) 2120 (1490-3030) 2000 (1610-2410) 1930 (1170-3410) 1430 (1190-2010) 2250 (1440-3330) 1214 1371 1250 1322 1411 1355 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 164 (142-190) 213 (182-249) 241 (213-271) 208 (183-236) 247 (226-271) 254 (225-287) 149 (135-165) 157 (142-173) 165 (144-189) 154 (136-174) 199 (164-242) 233 (202-270) 196 (166-228) 227 (185-270) 212 (188-246) 128 (111-142) 136 (124-150) 135 (120-158) 382 (314-472) 461 (396-572) 533 (417-665) 443 (390-505) 557 (478-618) 619 (476-791) 313 (239-387) 338 (288-402) 386 (338-485) 814 (673-974) 1080 (860-1650) 1230 (956-1610) 1030 (762-1700) 1240 (961-1480) 1530 (1200-1970) 856 (655-1390) 919 (712-1160) 989 (831-1330) 1330 (974-1920) 1940 (1410-2630) 2270 (1810-3140) 1920 (1230-2590) 2090 (1550-2800) 2590 (2160-3500) 1950 (1480-2740) 1590 (1320-2170) 1920 (1400-2780) 813 677 652 603 703 699 908 1216 1088 Non-Hispanic blacks Non-Hispanic whites Fourth National Report on Human Exposure to Environmental Chemicals 273 . 2002).

S. Brock JW. et al. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Bull Environ Contam Toxicol 2002.111(14):1719-1722. Poland.93:177-185. Davis BJ. et al. Caudill SP. Meeker JD. Barr D. Angerer J. Hauser R. Jedrychowski W. Silva MJ. Urinary levels of seven phthalate metabolites in the U. Singh NP. Camann DE. Atlanta (GA).Phthalates References Adibi JJ. Silva MJ. Koch HM. Hoppin JA. Hum Reprod 2007. Phthalate monoesters levels in the urine of young children. 274 Fourth National Report on Human Exposure to Environmental Chemicals . Hilborn ED. Hodge CC. Duty S. Caudill SP. Environ Res 2003. et al. Brock JW. Needham LL. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Environ Health Perspect 2002. Malek NA.112(3):331-338. Ryan L.22(3):688-695. Baird DD. Environ Health Perspect 2004. Environ Health Perspect 2003. Third National Report on Human Exposure to Environmental Chemicals. Reproducibility of urinary phthalate metabolites in first morning urine samples. Prenatal exposures to phthalates among women in New York City and Krakow. 2005.110(5):515-518. Drexler H. Jacek R. Centers for Disease Control and Prevention (CDC). Rossbach B. Barr DB. 112(5):A270]. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. Reidy JA.68:309-314. Silva MJ. Perera FP.

75-4.8 (19.2-35.4-27.98) 2.40) 75th 7.79) 2.5-27.8-36.50-6.0 (13.60-7.90) 4.30-6.20 (3.10 (4. and blood product storage and intravenous delivery systems.80-27. and 03-04 are 1.70 (8.0-19.6) 14.5-41.00 (7.10-5.00) 19.90-3.4) 23.50-2.89-3.10) 8.1 (10.80) 9.6 (10.20 (1.50-11.5 (24.90) 4.40) 2.3-64.10 (2.3 (19.39) 3.6-60.6) 39.67-4.9-29. Fourth National Report on Human Exposure to Environmental Chemicals 275 .9 (26. DEHP is metabolized to more than 30 metabolites which are rapidly eliminated in urine.14 (1.80-5.60) 90th 14.70 (1.0-84.40-9.7) 6.7) 27.70-6.10-2.7-18.50-2.10-3.90) 1.0) 39.9-19.00) 9.2-39.8) 15.0 (14.6) 5.96-5.70 (2.10-4.68 (3. 2002.4) 22.00) 5.30-8.30-13.9 (29. Four metabolites were measured in this Report: mono-(2-ethyl-5-hexyl) phthalate (MEHP).5 (12.40) 11.8 (19.16-3.80 (1.40) 8.1-17.50-3.42) 3.21 (2.37-4.70 (3. Peck and Albro.60 (5.35 (1.94-3.2) 29.8 (17.20 (4.54) 4.80-9.4 (21.10-3.60) 7.46) 3.1-48.1-29.10 (6. and 0.0 (19.50 (3.10-11. and in humans.70 (7.4) 5.34 (2.9 (17.70 (1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.50 (2.1) 19.0) Total 4.0) 31.0 (17.83) 2.10 (4.57-7.80 (2.7) 22.10) 3.4 (16.0) 35.50 (7.50-5.2-28.5) 40.50-20.9 (17.30) 2.62) 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 5.40 (4.3-25.0) 11.63-4.50 (7.43 (3.60-11.3) 28.20 (3. mono(2-ethyl-5-oxohexyl) phthalate (MEOHP).90) 4.80) 6.70-5.49 (3.0 (18.4-42.1 (8.90 (3.2) 4.7-58.5 (25.1) 22. 1982.0.7) 37.6) 14.40-9.9) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.4 (13.5) 19.5 (11.1) 25.27 (3.6 (12.80-8.51) 4.70-8.85) 4.30 (7.00) 11.9 (13.84-4.70-3.84 (2.40-8.85 (3.35) 4.9-48.10 (3. MEHP is primarily formed by the hydrolysis of DEHP in the gastrointestinal tract and then absorbed.70 (3.50-14.70) 2.61 (3.19-3.40 (6.9.00 (4.57 (3.3 (15.21 (2.5-28.32 (3.40) 4.70-4.1 (11.69) Selected percentiles ( 95% confidence interval) 50th 3.3-26.80 (8.2.9) 13.3-49.10-11. packaging film.2 (10.4) 13.82 (3.6 (16.6-38. Concentrations in plastic materials may reach 40% by weight.4-20.31-4. ATSDR.30 (3.8-50. which is used for many consumer products.84) 3.23) 3.7) 8.4) 33.90) 7.90-5.15 (1.4) 22.60) 9.9 (16.77 (2.56 (2.90) 3.00 (2.3) 13.40 (2.40 (4.75 (3.2) 23.12 (4.0 (19.70 (1.5) 23.50 (3.6-25.9 (15. respectively.80 (8.10-5.00-5.16 (2.96) 4.23 (2.00) 2.90-4.20 (1.0) 23.5-40.80-4.40-12.0-18.0) 23.80-3.4) 6.2-17.2 (7.6 (20.50-16.10 (5. see Data Analysis section) for Survey years 99-00.4-53.3 (11.41 (3.6) 95th 23.92) 4.5 (30.20 (3.27) 2. toys.9-57. interval) 3.1982).50) 9.10) 2.3 (10.70) 16.5 (12.50-3.7 (17.7-32.0 (21. 1.40-8.10) 4.86) 2.7) 18.7) 19. population from the National Healt