2009

Fourth National Report on Human Exposure to Environmental Chemicals

Fourth National Report on Human Exposure to Environmental Chemicals

2009

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

Contents

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

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

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

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

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

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

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

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Introduction

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

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

Fourth National Report on Human Exposure to Environmental Chemicals

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3.1.5.6'-Hexabromodiphenyl ether (BDE 154) 2.2-bis[4-Hydroxyphenyl] propane) 4-tert-Octyl phenol (4-[1.2-Dichloroethane (Ethylene dichloride) 1.4’.5'-Hexabromodiphenyl ether (BDE 153) 2.4'-Tetrabromodiphenyl ether (BDE 47) 2.2'.html. 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’.5.4.4.6.4'.3'.4.2-Dichloropropane 2.4’.3.2'.1.5'-Tetrachlorobiphenyl (PCB 49) 2.4.6-Heptabromodiphenyl ether (BDE 183) 2.5-Dimethylfuran Ethylbenzene Hexachloroethane Methyl-tert-butyl ether (MTBE) Nitrobenzene Styrene 1.5'.2'.and p-Xylene o-Xylene 2 Fourth National Report on Human Exposure to Environmental Chemicals .4.2'.3-Tetramethylbutyl] phenol) Triclosan (2. 75 new chemicals are added for the 2003-2004 survey period and are listed in Table 1.2'.4'.3’. 2009 Acrylamide Adducts Acrylamide Glycidamide Total and Speciated Arsenic Arsenic.2-Dichloroethene trans-1.2'.6-Pentabromodiphenyl ether (BDE 100) 2.4.3.4.5.6'-Decachlorobiphenyl (PCB 209) Perchlorate Perfluorinated Compounds Perfluorobutane sulfonic acid (PFBuS) Perfluorodecanoic acid (PFDeA) Perfluorododecanoic acid (PFDoA) Perfluoroheptanoic acid (PFHpA) Perfluorohexane sulfonic acid (PFHxS) Perfluorononanoic acid (PFNA) Perfluorooctane sulfonamide (PFOSA) Perfluorooctane sulfonic acid (PFOS) 2-(N-Ethyl-Perfluorooctane sulfonamido) acetic acid (Et-PFOSA-AcOH) 2-(N-Methyl-perfluorooctane sulfonamido) acetic acid (Me-PFOSA-AcOH) Perfluorooctanoic acid (PFOA) Perfluoroundecanoic acid (PFUA) Phthalate Metabolite Mono-(2-ethyl-5-carboxypentyl) phthalate (MECPP) Polybrominated Diphenyl Ethers (PBDE) and Polybrominated Biphenyl 2.4.4'-Tribromodiphenyl ether (BDE 28) 2.4'.5'-Tetrachlorobiphenyl (PCB 44) 2.cdc.1-Dichloroethane 1. Paradichlorobenzene) 1.2-Dibromo-3-chloropropane (DBCP) Dibromomethane 1.2.4-Tribromodiphenyl ether (BDE 17) 2.1.1-Trichloroethane (Methyl chloroform) 1.2'. The process for selection is described at http://www.2-Dichlorobenzene (o-Dichlorobenzene) 1.2'3. Chemicals reported for the first time in the Fourth National Report on Human Exposure to Environmental Chemicals.4.5'-Hexabromobiphenyl (BB 153) Volatile Organic Compounds (VOCs) Benzene Chlorobenzene (Monochlorobenzene) 1.2'. Table 1.4’-Trichloro-2’-hydroxyphenyl ether) Non-dioxin-like Polychlorinated Biphenyls 2.4'-Pentabromodiphenyl ether (BDE 85) 2.4-Dichlorobenzene (p-Dichlorobenzene.4.5-Pentabromodiphenyl ether (BDE 99) 2.What’s New in this Report What’s New in this Report In this Fourth Report.2-Dichloroethene Dichloromethane (Methylene chloride) 1.2-Tetrachloroethane Tetrachloroethene Tetrachloromethane (Carbon tetrachloride) Toluene 1.2'4.gov/exposurereport/chemical_selection.1.4'.4'-Tetrabromodiphenyl ether (BDE 66) 2.3.3-Dichlorobenzene (m-Dichlorobenzene) 1.2-Trichloroethane Trichloroethene (Trichloroethylene) m.5.4.2’.1-Dichloroethene (Vinylidene chloride) cis-1.4'.2'.

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

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

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

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

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

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

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

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

7 (55.6) 90th 141 (124-155) 03-04 03-04 03-04 03-04 03-04 03-04 03-04 59. acrylamide has produced upper airway irritation following inhalation of high levels.7) 96.7-60.5) 66. and in some cosmetics.6-66. are heated at temperatures used for frying and baking.8 (57. soil conditioners..5) 58. smoking.6 (51. environmental releases of acrylamide can enter aquatic systems and soils where it degrades within days and does not bioaccumulate (U.4 (51.7 (65. These estimated intakes are hundreds of times lower than occupational exposures. and from dermal contact with products that contain residual acrylamide.4-76. interval) 61.7-64. Smaller scale applications of polyacrylamides include additives to paperboard used for food packaging.8 (81.7 (63.8 (91.6-75. Animal studies indicate that acrylamide is well absorbed. People may be exposed to acrylamide from foods.1) 55. and in the synthesis or compounding of dye materials. drinking water. or to glutathione conjugates (Calleman et al.4-60. EPA reference dose of 0. and well below doses known to cause nerve damage or carcinogenicity in animals.7-64.5 (79.8-55.2 (75. see Data Analysis section) for Survey year 03-04 is 3. EPA.6) 71.0 (57. 1990.4 (53.6-104) 82. Elimination occurs mainly in the urine as mercapturic acid conjugates. 79-06-1 General Information Acrylamide is a small organic molecule existing as a white crystalline powder in its pure state.1) 53.0) 57.1) 101 (95. FAO/WHO.6 (81.2-93.3) 63.0 (53.S.2 (62. (NTP-CERHR.4-83.1 (52. it was discovered that acrylamide is formed when starch-rich foods.3 (55.9-105) 86.5-80.8 (52.2-67.6) 73.. as an absorbent in disposable diapers.1 (83.9 (60.3-71. Fourth National Report on Human Exposure to Environmental Chemicals 11 . Estimated intakes in children are about twice that of adults (DiNovi and Howard.1-64. but are generally above the U. but can covalently bind to form adducts with proteins.4) 57. Recently. and cosmetics (NTP-CERHR. 2005).6 (56.2-114) 163 (147-191) 96.9-52. in permanent press fabrics. and peripheral neuropathy following chronic Acrylamide Geometric mean and selected percentiles of hemoglobin adduct concentrations (in pmol/g hemoglobin) for the U.3) 86.0-49. mineral processing. Fennell et al.1-61.3 (53. In humans.2-70. 2005). 2006).0-58.9-61. Acrylamide is not thought to accumulate in the body at environmental doses.0-108) 152 (139-175) 126 (111-142) 108 (86.6) 90. Natural substances in the food are converted to acrylamide.4 (54.4 (59.2) 57.1 (47.1) 46.4 (54.0 (67.9) 75.2-59.S.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. 1994). Commercially. ocular and dermal irritation from direct contact with acrylamide containing materials.2-77.S.7 (58.9) 58. and is either metabolized to the reactive epoxide.Acrylamide Acrylamide CAS No. although additional exposures from cosmetic products could add a similar amount (NTP-CERHR. In the general population. pulp and paper production.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 54.5-85.5 (44. Since acrylamide has limited volatility and high water solubility.6-65.6-61. acrylamide is synthesized and used in the production of polyacrylamide polymer.9 (54.5 (74. Tareke et al.5 (52. 2004.S.1-64. 2002). Polyacrylamides are useful water-compatible polymers used in water treatment. Survey Geometric mean (95% conf.0-66.7) 75th 79.0 (69. 2006.2-91. such as potatoes and some grains.6) 50.1 (73. FDA.7) 73.4-89. glycidamide.0-115) 156 (120-203) 146 (129-163) 149 (125-179) 218 (172-271) 197 (172-223) 1792 1874 2994 Limit of detection (LOD.1 (88. EPA. the main source of exposure is from the diet. 2005). and an average daily intake is estimated as 0. 2004).4) 57.0) 85.2) 57. widely distributed in tissues.9 (69.S.7) 58. in some sealing grouts.0..4-60.9) 63. 2005). 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.7) 54. In 1997.1) 62.3) 70.2-118) 98.2 (58.3-2. and binding agents. population from the National Health and Nutrition Examination Survey. gels.1-57.6-108) 61. 217 million pounds of acrylamide were produced commercially in the U.8-57.0 μg/kg for adults (FAO/ WHO.4) 100 (89. 2005. 2005).2 μg/kg/day (U.9) 57.

1-70.0 (75.1 (70. fetal death. U. Survey Geometric mean (95% conf. 2005). and neuronal DNA reactivity (Doerge et al.7) 90. Biomonitoring Information Acrylamide and glycidamide hemoglobin adducts (AHA and GHA.5-94.4 (81. Schettgen et al.7-64.S.4 (56. 2005) and sperm DNA adducts (Xie et al. After exposure ceases.3-101) 95. 2006).5) 71.S.5) 90th 130 (120-141) 03-04 03-04 03-04 03-04 03-04 03-04 03-04 71.3) 59.2) 87.. and cancer (mammary. 2004). Several of these studies have shown that smokers have adduct levels that are three to fourfold higher than non-smokers. interval) 59.5-92.0 (80.9-78.int/ ipcs/food/jecfa/summaries/summary_report_64_final. U. 2006.6-62.. Schettgen et al.9-76.4) 53.8 (51. population from the National Health and Nutrition Examination Survey.0-62.0) 118 (103-126) 121 (112-134) 113 (94. AHA levels have been shown to increase with dietary intake (Hagmar et al.1) 56. Vesper 2005) and smoking (Bergmark. IARC classifies acrylamide as probably carcinogenic to humans. EPA.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. presynaptic nerve terminal binding (LoPachin.7 (61.4-98.5 (83.4 (90.who.5 (56..5-64. although different analytic methods can affect results. NTP-CERHR. Vesper et al. Glycidamide Geometric mean and selected percentiles of hemoglobin adduct concentrations (in pmol/g hemoglobin) for the U.1 (56. In addition. EPA at: http://www.5 (59. 2005..1) 60..4-103) 79.9 (58. 2008).9) 65.6-90. Axonal degeneration.4-65. Acrylamide is clastogenic and can produce dominant lethal mutations. glycidamide (NTP-CERHR. male germinal cell injury. 2005.. 2005.2 (56. 2005. 2005. altered gene expression in testicular tissues (Yang et al. Hagmar et al. Maniere et al.7-86..3) 59. uterine. 2005.4 (57.9-64.2) 55. 2005. 2009).6 (66. Animal studies have shown that acrylamide can cause nerve damage (neuropathy)..5 (42.2) 65. levels of AHA adducts decline but may remain detectable for several months (Hagmar et al.4 (61.7 (87..7) 61. Puppel et al.9-138) 143 (130-159) 96. 2003.0 (70.1 (57. 1997.4 (51. 12 Fourth National Report on Human Exposure to Environmental Chemicals .1 (66. 2006) have been demonstrated after acrylamide dosing.6 (90.5-66.9-62.. dominant lethality).5) 75th 85. Levels of AHA and GHA reported the NHANES 20032004 sample are generally similar to those seen in several previous studies of non-occupationally exposed subjects (Bergmark et al. 2005).2-90. reproductive effects (reduced litter size.8-61.7 (84. 1997.8-49.9) 75.2-68. 2005.2 (63.. 2006). Adducts are formed when either acrylamide or glycidamide react to form a permanent covalent bond with hemoglobin in the blood. probably through its epoxide metabolite..8) 45. scrotal.epa.4-59..S.5) 87..6-64.3) 85.Acrylamide occupational exposures. adrenal. Glycidamide has been shown to react with DNA (Doerge et al. 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.0-93. respectively) are markers of integrated acrylamide exposure over the preceding few months.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..2 (72.9 (57.7 (57. see Data Analysis section) for Survey year 03-04 is 4. most non-smokers had levels less than about 100 pmol/gram hemoglobin.1-62.7) 74.1-60.9 (81. Mucci et al.1) 62.8) 60.4) 83.8 (44.7-62. 2004.3 (56.0 (52. 2002. gov/iris/ and from the Food and Agriculture Organization of the United Nations and WHO at: http://www..3) 59.9-77. 2005). 2005) have been demonstrated in animals...S. 2002..4) 46. 2005).9) 59. 2005. 2005.. Younger children may have slightly higher levels possibly due to increased intake of acrylamide-containing foods relative to body size (Dybing et al.1-56.2-91. Puppel et al. 2008). and to increase DNA reactivity when glutathione availability is reduced (Klaunig et al.7) 60. Rice.8-48.0) 94. thyroid. and other sites) (FAO/WHO.3-78. Klaunig et al.9) 87. EPA. 2005.0. Additional information is available from U. to increase the unscheduled synthesis of DNA in tumor susceptible tissues (Klaunig et al.1 (82.5) 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.pdf. 2001).

Available at URL: http://cerhr. Bridson WE. Bruze M. Burgess J.580(1-2):131-141.10(1):78-84. Joint FAO/WHO Expert Committee on Food Additives. Duale N. [Epub ahead of print] Dybing E. Aprea P. Wirfalt E.gov/chemicals/ acrylamide/Acrylamide_Monograph. Simultaneous analysis of hemoglobin adducts of acrylamide and Fourth National Report on Human Exposure to Environmental Chemicals 13 . 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. Becher G. CFSAN/Office of Plant and Dairy Foods. Tornqvist M.int/ipcs/ food/jecfa/summaries/summary_report_64_final. Relationships between biomarkers of exposure and neurological effects in a group of workers exposed to acrylamide. Fennell TR. et al. Farmer PB. 2/3/09 Perez HL. Available at URL: http://www. Guffroy M.Toxicol Appl Pharmacol 1994. et al. Perez et al. Survey data on acrylamide in food: individual food products. Toxicol Sci. gov/~dms/acrydata. Food and Drug Administration (FDA). 2005. Determination of hemoglobin adducts in humans occupationally exposed to acrylamide. Italy. Scand J Work Environ Health 2001. Tian G. smoking habits and gender. Adv Exp Med Biol 2005..56. Bergmark E. Fennell TR.126(2):361-371.niehs. Food Chem. Doerge DR. Mechanisms of acrylamide induced rodent carcinogenesis.27(4):219-226. Laurentie M. Churchwell MI.85:447-459.html#u1004.Acrylamide In occupational settings. Bergmark E. Acrylamide neurotoxicity: neurological. Maniere I. Differences in hemoglobin adduct levels of acrylamide in the general population with respect to dietary intake. Toxicol Sci 2005.fda. Calleman CJ. February. Available at URL: http://www.cfsan. Alexander J. smokers and nonsmokers. Cheong HK. Mucci LA. The Updated Exposure Assessment for Acrylamide. Bergmark E. et al.. Bjellaas T. 054472. Costa LG. Chem Res Toxicol 1997 Jan. Center for the Evaluation of Risks to Human Reproduction (NTP-CERHR). 2/3/09 Hagmar L.561:21-37. 2004. Malmberg B. AHA levels were several fold to several hundredfold higher than levels in non-exposed non-smokers (Bergmark et al. and 39% of workers with levels above 1000 pmol/gram hemoglobin had these symptoms (Hagmar et al. 2001). DNA adducts derived from administration of acrylamide and glycidamide to mice and rats. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Monograph on the Potential Human Reproductive and Developmental Effects of Acrylamide. 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.nih. symptoms of numbness or tingling in the extremities did not occur in exposed workers whose AHA levels were below 510 pmol/gram hemoglobin.120(1):45-54. et al. References Bergmark E. Axmon A. DiNovi M and Howard D. Human exposure and internal dose assessments of acrylamide in food. Granath F.580(1-2):119-129. Wu Y. Doerge DR. 2/3/09 Klaunig JE.. 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. National Toxicology Program. 1999). NIH Publication No. Mutat Res 2005.pdf.43:365–410. Calleman CJ. Churchwell MI. Acrylamide intake through diet and human cancer risk. Acrylamide is metabolized to glycidamide in the rat: evidence from hemoglobin adduct formation. Chem Res Toxicol 1990. Calleman CJ. Mutat Res 2005. Hagmar L. Costa LG. Kamendulis LM. Chicago. 64th Meeting: Summary and Conclusions (FAO/WHO). Adv Exp Med Biol 2005. Rome.3:406-412. Haugen M. Godard T. da Costa GG. Yang JS. He F. 8-17 February 2005. Magnusson AL.who. Rosen I. Hemoglobin adducts of acrylamide and acrylonitrile in laboratory workers. Toxicol 2005. 1993. McDaniel LP. and Research Strategies. He F. LoPachin RM. Nordander C. Andersen M. Snyder RW. Spicer R. Toxicol Appl Pharmacol 1993. Paulsson B. Health effects of occupational exposure to acrylamide using hemoglobin adducts as biomarkers of internal dose.. Summer SCJ. 2001.pdf. 2006. July. Beland FA. Metabolism and hemoglobin adduct formation of acrylamide in humans. 2004 Acrylamide in Food Workshop: Update Scientific Issues. et al. In another study. Wilson KM. Illinois. 6013-6019. 1994). Uncertainties. J Agric Food Chem 2008. April 13-15. Hagmar et al. Kautiainen A. Paulsen JE. Mutat Res 2005. Zhang S. 2009 Jan 8.580(1-2):157-165. Osterman-Golkar S. Twaddle NC. Biomarkers of human exposure to acrylamide and relation to polymorphisms in metabolizing genes. Tornqvist M.561:49-62. morphological and molecular endpoints in animal models.. DNA damage and DNA adduct formation in rat tissues following oral administration of acrylamide.

Tornqvist M.S.274(1):59-68. Toxicological effects of acrylamide on rat testicular gene expression profile. Acrylamide. Cross-sectional study on acrylamide hemoglobin adducts in subpopulations from the European Prospective Investigation into Cancer and Nutrition (EPIC) Study. Analysis of acrylamide. Xie Q. Reprod Toxicol 2005. Office of Pollution Prevention and Toxics.epa. Myers GL. 2/3/09. EPA).56(15):6046-53. Fu D.Acrylamide glycidamide by gas chromatography-mass spectrometry. Int J Hyg Environ Health 2003.580(1-2):71-80. Mutat Res 2005. Tareke E. Chae C. Angerer J. Han CH. Karlsson P. Benetou V.gov/chemfact/s_acryla. Ospina M. Agudo A. J Agric Food Chem 2002. Licea-Perez H. Ospina M. Gray JG. Pilot study on the impact of potato chips consumption on biomarkers of acrylamide exposure.S. Drexler H. Angerer J. Toxicol Lett 2002. Lee SH. Hemoglobin adducts of ethylene oxide. Drexler H. DNA strand breaking capacity of acrylamide and glycidamide in mammalian cells. Drexler H. Rossbach B. et al. Ingham L. Liu Y. Int J Hyg Environ Health 2004. Eriksson S. Hallmans G. Broding HC.206(1):9-14. Vesper HW. et al.580(1-2):3-20. Washington (DC). EPA). Schettgen T. Toxicol Lett 2006.561:89-96. Jin Y. Choi JH. Han DU. Schettgen T. Angerer J. Ding X. Marko D. Available at URL: http://www. Weiss T. U. Puppel N.txt. Meyers T. Determination of haemoglobin adducts of acrylamide and glycidamide in smoking and non-smoking persons of the general population. Liu K. Letzel S. revised 1/3/06.S.20(6):959-64. Adv Exp Med Biol 2005. Chemical Summary for Acrylamide. Environmental Protection Agency (U. Integrated Risk Information System (IRIS). Tjaden Z. Lee MH. J Agric Food Chem 2008. A first approach to estimate the internal exposure to acrylamide in smoking and non-smoking adults from Germany. Environmental Protection Agency (U. Rapid Commun Mass Spectrom 2006. Smith A. Yang HJ. Rydberg P. The carcinogenicity of acrylamide.134(1-3):65-70. Kutting B.163(2):101-8. a carcinogen formed in heated foodstuffs. Anal Biochem 1999. September. U.19(4):527-34. 1994. 2/3/09 Vesper HW. Automated method for measuring globin adducts of acrylamide and glycidamide at optimized Edman reaction conditions.gov/iris/subst/0286. Available at URL: http://www. Rice JM. Tjønneland A. Vesper HW. Meyers T.S. 14 Fourth National Report on Human Exposure to Environmental Chemicals .207(6):531-9. acrylonitrile and acrylamide-biomarkers in occupational and environmental medicine. Schettgen T. Sun H.epa. Fueller F. Adduction of biomacromolecules with acrylamide (AA) in mice at environmental dose levels studied by accelerator mass spectrometry. Mutat Res 2005 Feb 7. Slimani N.htm.50(17):4998-5006. propylene oxide.

210 (.22) 2789 3152 2937 3210 3667 3383 Females Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 * .02) 1.216 (.153-.850 (.34 (1.05.S.950-1.370-.320) .100-.23 (2.150) .110-.164 (.62) 2.190-.505 (. 83% of measurements had an LOD of 0.068) .060-.570-1.060) .910-1.75) 1.21-1.30) * .040 (.310-1. Persons exposed to secondhand tobacco smoke (environmental tobacco smoke [ETS]) may have adverse health effects that include lung cancer and coronary heart disease.130) .110-.050 (<LOD-.68) .09-2.50-4.070) 75th .820) .17 (.175 (.197) .630 (.310-1.S. acute respiratory infections.840) 3.059-.080-.65 (1.160 (. The smoke produced by burning tobacco contains at least 250 chemicals that are toxic or carcinogenic.200) 1.S.120 (.190-.076-.580 (.20 (.428-.42-4. see Data Analysis section) for Survey years 99-00.167 (.93) .234) .23 (.053 (<LOD-.66 (1.625) .163) .110) .00) 1.040 (.260) 1.78) 2.139) * .30) 2.39) 3.49) 2241 1878 1707 1333 1602 1704 1950 2847 2500 Non-Hispanic blacks Non-Hispanic whites 99-00 01-02** 03-04 Limit of detection (LOD.350-.480-1.160 (.059-.770-1.18-3.630 (.540-. emphysema.40) .193) . DHHS.770) .470-. and various other disorders (U.054 (.28-1.150) .63-2. and 03-04 are 0. maternal exposure during pregnancy can result in lower birth weight.620-1.02 (.800 (.047-.020-.094) .76 (1.11) .15 (2.740-1. and 17% had an LOD of 0.110 (.300) . 2004).077) .106-. Cigarettes contain about 1.690 (.180) .50 (1.188) .080 (.09-3. Survey Geometric mean (95% conf. and more than 50 compounds present in ETS are known or reasonably anticipated to be human carcinogens (NTP.087 (.040-.108) * .063) .50) 3.360) .00) .570 (.070) .99) 2.600-1. Fourth National Report on Human Exposure to Environmental Chemicals 15 .16) .050 (<LOD-.77 (1.19-2.997-3.080-.198) * .160-.83-2.54 (1.66-3.53 (1.Cotinine Cotinine CAS No.28) .260-1.080) < LOD .071 (.22) 2.104-.015 ng/mL.53-4.077) .030-.131 (.061) < LOD . DHHS.920 (.14-1.137-. producing roughly 1–2 mg of bioavailable nicotine per cigarette (Benowitz and Jacob. < LOD means less than the limit of detection.30) 2.54 (1.990) .090-.154-.120 (.57) 2.580-1.145) .580) .111-.060 (.220) .79) 3.48-2. population from the National Health and Nutrition Examination Survey.120 (. Children exposed to ETS are at increased risk for sudden infant death syndrome.540 (.02) 1.110 (.040 (.860 (.280 (.19) .01) 3.073) < LOD .44 (2.140-.080-.740-1.430-1.42 (1.38-2.080) < LOD < LOD .080 (.04 (1.089) Age group 3-11 years 99-00 01-02** 03-04 .144 (.21 (. respectively.35 (2.960-1.410) .310) .110 (.187) .49) 1.240 (.060 (<LOD-.19) 1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.92) 1174 1415 1252 1773 1902 1783 3052 3502 3285 12-19 years 99-00 01-02** 03-04 99-00 01-02** 03-04 20 years and older Gender Males 99-00 01-02** 03-04 99-00 01-02** 03-04 .140 (.50-1.55 (1.20) 1.05) 1.163 (.060 (.68) 2.33-2.071) .44) 2.900-1.201) .60-2.050 (<LOD-.050 (.23-2.160) .990 (. The consequences of smoking and of using smokeless tobacco products are well known and include an increased risk for several types of cancer.052 (<LOD-.080-.350-.400-. stroke.060 (<LOD-.533-.180) .190-.066-.54) size 5999 6819 6320 Total years 99-00 01-02** 03-04 50th .120-.15) 2.087-.050 (<LOD-.92 (1.450-.180 (.84-3.110 (.070) .726) .310) 90th 1.21-1.66) 1.115-.48-3.050-.350 (.12 (1.090-.480-.32) 1.057-.040-.090-. 2004).084) .140 (.110-.930 (.85 (1.308 (.39 (1. 486-56-6 Metabolite of nicotine (a component of tobacco smoke) General Information Tobacco use is the most important preventable cause of premature morbidity and mortality in the United States. cardiovascular disease.70) 2.160 (.140-.180 (.96-4. 1998).126) .710 (..050) . acute respiratory illness.213) .96) 2.87-3.060-.060-.47-3.12 (2.180) .220) .068) .180) .14) .066) .730 (.520 (.88 (.130 (. 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.32-2.230) .148-.660) .54) 1. and 0.510 (.164 (.302) .137 (.030-.14) .88 (1.55-2.120-.26-1.075 (.20 (1.77 (1.670) .12) 1.070-.087) < LOD < LOD .5% nicotine by weight (Kozlowski et al.70-2.94) 1.81-2.120 (.124 (.96 (1.050-.43 (1.12-4.44 (1. and exacerbated asthma (U.950 (.070 (<LOD-.050) .052 (<LOD-.49) 1.110) .180) .066 (.45) 1.17 (1.68 (1.506 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.120) . ** In the 2001-2002 survey period.120 (.621-1.142-.015.030-.32-2.62 (2.047-.89) 1.086 (.05 ng/mL.23 (1.01 (1.63 (2.220-.630 (. ear problems.088-.44) 2.99) 2.20-2.058 (.620 (.030 (.062 (.770) .110 (.09-3.20) .500 (.95) 1. 2006).17) .230 (.043-.790) .160) .312) .77 (2. which may vary for some chemicals by year and by individual sample.

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

Brody DJ. et al. Available at URL: http:// cancercontrol.280:152-156. IARC Monogr Eval Carcinog Risks Hum. 4/13/09 National Cancer Institute (NCI). Environ Health Perspect 2006. Benowitz NL. Benowitz NL. Sosnoff CS. 4/13/09 Perez-Stable EJ.114(6):853-858. Caraballo R. June. Cotinine as a biomarker of environmental tobacco smoke exposure. Decrease in the prevalence of environmental tobacco smoke exposure in the home during the 1990s in families with children. Centers for Disease Control and Prevention. et al. Maurer KR. Am J Public Health 2004. Tobacco related exposures. Dollery CT. [online].iarc. 1988-1991. George CF.gov/eid/rmca/critdocs/ criteriadoc/33. Clin Pharmacol Ther 1994.surgeongeneral. Epidemiol Rev 1996. JAMA 1998. Perez-Stable EJ.63:139-43. Third National Report on Human Exposure to Environmental Chemicals. Schober SE. Herrera B. Benowitz NL. JAMA 1998. 4/13/09 International Agency for Research on Cancer. available at URL: http://mtn. Jarvis MJ. Giovino GA. Giovino G.S. U.niosh.291(3):1196-1203. National Institute for Occupational Safety and Hygiene (NIOSH). Mehta NY. Bernert JT. The Health Consequences of Involuntary Exposure to Tobacco Smoke: A Report of the Surgeon General — Executive Summary.S Department of Health and Human Services (U. DHHS).7:369-375.4:313-316. iarc. Office on Smoking and Health [online] 2006.pdf. Etzel RA. Benowitz NL.php. Trends in the exposure of nonsmokers in the U. Filter ventilation and nicotine content of tobacco in cigarettes from Canada. JAMA 1996.fr/ENG/Monographs/ allmonos90. Pollack HA. U. Warner K. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans.280:135-140. In Report on Carcinogens.nih. Tobacco Smoke and Involuntary Smoking. Available at URL: http://monographs. 1999. Biomonitoring data can also help scientists plan and conduct research about exposure to ETS and about its health effects. National Center for Fourth National Report on Human Exposure to Environmental Chemicals 17 .gov/ntp/roc/eleventh/profiles/ s176toba. Bernert JT. Kira S.S. Department of Heath and Human Services. Jacob P.cancer.S. population to secondhand smoke: 1988-2002.S Department of Health and Human Services (U.fr/ENG/Monographs/allmonos90. Available at URL: http://ntp. Soliman S. J Pharmacol Exp Ther 1999. References Armitage AK. Vol 38. Centers for Disease Control.pdf. Benowitz NL.56:483-493.niehs. Modin G.gov/tcrb/monographs/10/. The Health Consequences of Smoking: The Surgeon General’s Report—Executive Summary. Current Intelligence Bulletin 54: Environmental tobacco smoke in the workplace. Kozlowski LT. Schwartz SS.php. Metabolism of nicotine to cotinine studied by a dual stable isotope method. National Center for Chronic Disease Prevention and Health Promotion. IARC Monogr Eval Carcinog Risks Hum. Tob Control 2006. Summary of Data Reported and Evaluation [online] 2004. Pechacek TF. Metabolism and disposition kinetics of nicotine. Fong I. population to environmental tobacco smoke: the Third National Health and Nutrition Examination Survey. Vol 83. International Agency for Research on Cancer. Pickett MA. Pharmacol Rev 2005. Jacob P III. Flegal KM. cigarette smokers: the Third National Health and Nutrition Examination Survey.15:302-307. Caudill SP. Racial/ethnic differences in serum cotinine levels among adult U. 1988-1991. DHHS). Tob Control 1998. Available at URL: http://www. Respiratory nicotine absorption in non-smoking females during passive smoking. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans.57(1):79115.275:1233-1240.S. 4/13/09 Iwase A. Jacob III P. Houseman TH.S. Turner DM. BMJ 1975. 4/13/09 U. Summary of Data Reported and Evaluation [online] 1986. Pechacek TF. 2004. Strauss WJ. Centers for Disease Control and Prevention. Health Effects of Exposure to Environmental Tobacco Smoke: The Report of the California Environmental Protection Agency. Aiba M. National Toxicology Program (NTP).S. 1999-2002. 4/13/09 Centers for Disease Control and Prevention (CDC). Richter PA. Smoking and Tobacco Control Monograph 10 [online]. Ethnic differences in N-glucuronidation of nicotine and cotinine. Nicotine metabolism and intake in black and white smokers. Tobacco Smoke. Sweeney CT. Department of Heath and Human Services. Available at URL: http://monographs. Brody DJ. Vogler GP.cdc. Herrera B. Curtin LR. 1991. and the United States.94(2):314-320. Coordinating Center for Health Promotion. Mowery PD. Exposure of the U.Cotinine and public health officials determine whether people have been exposed to higher levels of ETS than are found in the general population. Int Arch Occup Environ Health 1991. Pirkle JL. 11th ed. Smoke-free laws and secondhand smoke exposure in US nonsmoking adults.gov/library/ secondhandsmoke/. Lewis PJ. Pirkle JL. U.18:188-204. Absorption and metabolism of nicotine from cigarettes. Coordinating Center for Health Promotion. Hukkanen J. the United Kingdom. Jacob P III.S. Atlanta (GA): 2005.

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

240) < LOD . < LOD means less than the limit of detection.gov/pesticides/. and it has not been rated by IARC or NTP with respect to human carcinogenicity. 2003). Exposure can also occur from consuming food contaminated by DEET on hands or that was sprayed nearby. (Kolpin et al.250) < LOD .210) 480 580 672 829 825 1126 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .130 (. 134-62-3 General Information N.100-.120-.1.140) < LOD .100-. 2002).S.140 (. DEET is also used in combination with dermal sun screens (U. Human health effects from DEET at low environmental doses or at biomonitored levels from low environmental exposures are unknown.110 (.170 (. but higher DEET concentrations and different formulations may result in greater absorption (Sudakin and Trevathan.110-.100-. Additional information is available from U.130 (. One survey detected DEET in 74% of sampled streams in the U. EPA. which may vary for some chemicals by year and by individual sample..270) 688 678 518 700 598 956 Limit of detection (LOD.210 (. After absorption.. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. have been reported as result of self-poisoning by ingestion or excessive dermal application. 1998).S.120-.130-.180) < LOD .N. population from the National Health and Nutrition Examination Survey. DEET is metabolized via hydroxylation and dealkylation pathways and eliminated in the urine within approximately 24 hours (Selim et al. Neurological effects in humans.S.160) < LOD . Its use is recommended for prevention of several vector-borne diseases.449 and 0. including seizures and encephalopathy.S. People in outdoor occupations may apply DEET more frequently or use higher concentration formulations resulting in higher levels of exposure.130) < LOD . interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD .180 (.220 (.140) < LOD .S.110 (. DEET has low acute toxicity.100-.epa. 2003).100-. 1995.180 (.130 (.130-.110 (. Sudakin and Trevathan. General population exposure to DEET occurs from skin application and from inhalation of aerosol formulations.N-diethyl-meta-toluamide (DEET) is an insect repellent that was first marketed in 1957.210) 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 .EPA at: http://www.100 (<LOD-. 2002).190) < LOD . There are over 225 insect repellents brands containing DEET.130-.EPA.N-Diethyl-meta-toluamide (DEET) CAS No.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 .170 (. DEET is not genotoxic.140-.110-.130) < LOD . Urinary N.EPA. Fourth National Report on Human Exposure to Environmental Chemicals 19 . DEET can be applied to clothing and the skin to repel biting insects.110 (<LOD-.140) < LOD .130-. 1998). * Not calculated: proportion of results below limit of detection was too high to provide a valid result.520) < LOD .S.110 (<LOD-. DEET is not registered for use on agricultural commodities.. and they range in concentration from 4% to 100%. Most reports of adverse effects from overexposure to DEET involve skin reactions (Bell et al.N-Diethyl-meta-toluamide (DEET) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.100-.180 (.560) < LOD . 2005). (U.150) < LOD . DEET is not a developmental or reproductive toxicant in animals (U.140) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .110 (. Survey Geometric mean (95% conf. About 3-8% of dermally applied DEET is absorbed.N-Diethyl-meta-toluamide (DEET) N.

330 (.S.550) 688 678 518 699 598 956 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. Urinary levels of DEET were characterized only at the 90th and 95th percentiles of the U.410-.270 (<LOD-. DEET was detected in 10% of 60 Latino children in eastern North Carolina farm worker households (Arcury et al.370-. Urinary N. the limit of detection was lower than for the NHANES 1999-2000 survey period (CDC.390-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 20 Fourth National Report on Human Exposure to Environmental Chemicals .330 (.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 . representative subsamples from NHANES 2001-2002.350-.410 (.150-.190 (. In this survey period. Finding a measurable amount of DEET in urine does not mean that the level of DEET causes an adverse health effect.300 (.350) < LOD ..490) < LOD .350) < LOD . 1992). Survey Geometric mean (95% conf.140-.320 (. Urinary DEET levels as high as 5.500) 480 580 672 828 825 1126 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .250) < LOD .640 (. 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.270) < LOD .240) < LOD .410 (.200 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD . population from the National Health and Nutrition Examination Survey.480 (.290-.150) < LOD .190 (<LOD-.240-.230-.250 (.370) < LOD .230-.N-Diethyl-meta-toluamide (DEET) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U..270 (. 2007).690 µg/L were measured in eight park employees who applied 71% DEET once a day (Smallwood et al.N.170-.130 (<LOD-.93) < LOD .N-Diethyl-meta-toluamide (DEET) Biomonitoring Information Urinary levels of DEET reflect recent exposure.270-.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 .190-.S.250-. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.190 (.280 (. 2005).280-1.580) 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 .230) < LOD .320) < LOD .440) < LOD .500 (.630) < LOD .

4/9/09 U. Furlong ET. Int J Toxicol 2002.41(6):831-839. Osimitz TG.pdf. Hartnagel RE Jr. Gabriel KL.N-diethyl-mtoluamide following dermal application to human volunteers. Barr DB. DeBord KE. Pesticide urinary metabolite levels of children in eastern North Carolina farmworker households.S. 1993-1997. Toxicity and Exposure Assessment in Children’s Health.EPA. Fundam Appl Toxicol 1995. EPA. Washington (DC): U. and excretion of N.36(6):1202-1211.S. pdf.16(1):10-13.S. 4/9/09 Fourth National Report on Human Exposure to Environmental Chemicals 21 . 2005.25:95-100. Selim S. Trevathan WR.N-diethyl-mtoluamide insect repellents reported to the American Association of Poison Control Centers. metabolism. Chemical Summary.EPA). Veltri JC. Tapia J. Environmental Protection Agency (U. Zaugg SD.S. Atlanta (GA). U. Barber LB. Grzywacz JG.EPA). N. Chen H. Absorption. et al. pp. Schoenig GP.gov/oppsrrd1/REDs/0002red. Lowry LK. Environ Health Perspect 2007. Meyer MT.N’-diethyl-mtoluamide (m-DET): analysis of an insect repellent in human urine and serum by high-performance liquid chromatography. J Toxicol Clin Toxicol 2003. Environmental Protection Agency (U.115(8):1254-1260.epa. Available at URL: http://www. Page BC. Pharmaceuticals. 1999-2000: a national reconnaissance. Smallwood AW.S. Bell JW. Third National Report on Human Exposure to Environmental Chemicals.gov/teach/chem_summ/ DEET_summary. 2005 Kolpin DW. Environ Sci Technol 2002. DEET: a review and update of safety and risk in the general population. Diethyltoluamide (DEET). Centers for Disease Control and Prevention (CDC). September 1998. Thurman EM.S. 1-118.N.2:341352. Available at URL: http://www.epa. Reregistration Eligibility Decision (RED): DEET. hormones. streams.S. J Anal Toxicol 1992. U. Sudakin DL. Human exposures to N. EPA 738-R98-010. and other organic wastewater contaminants in U.N-Diethyl-meta-toluamide (DEET) References Arcury TA. Quandt SA.

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

NTP-CERHR Panel Report on Reproductive and Developmental Toxicity of Bisphenol A. Kiguchi M. Haighton LA. Joskow R. and Hajszan.it/DOCUMENTS/ Existing-Chemicals/RISK_ASSESSMENT/SUMMARY/ bisphenolasum325.pdf. Ekong J.pdf . An evaluation of the possible carcinogenicity of bisphenol A to humans. Szigeti-Buck. Yoshinaga J.. Brine DR. Han SY.312(2):441-448. 4. McConnell EE. Exposure of the U. Keimowitz AR. Cohen JT. Life Sci 2001. National Toxicology Program Center for the Evaluation of Risks to Human Production (NTP-CERHR). Pharmaceuticals. Barton L. Shin HC. Ecotoxicity and the Environment (CSTEE). Timms BG. 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. Kim CS. Marr MC. J Chromatogr B Analyt Technol Biomed Life Sci 2002. Munro IC. Hum Ecol Risk Assess 2004. Twomey K. MacLusky. 2003. Endocrinology 2008. Joint Research Centre Institute of Health and Consumer Protection. Available at URL: http://ntp. Hanaoka T.niehs.S. Reidy JA. Available at URL: http://cerhr.nih.4’-Isopropylidenediphenol (Bisphenol-A) Summary Assessment Report. Meyer MT. K. Leranth. Measurement of bisphenol A in human urine using liquid chromatography with multi-channel coulometric electrochemical detection. Ye X.S. Ispra.Environmental Phenols References Akingbemi BT. August 2001. Harazono A. 2/4/09 Ouchi K. In vitro and in vivo interactions of bisphenol A and its metabolite. Furukawa M. Needham LL. Weight of the evidence evaluation of low-dose reproductive and developmental effects of bisphenol A. Three-generation reproductive toxicity study of dietary bisphenol A in CD Sprague-Dawley rats.102(19):7014-7019.149:988-994. et al.14(2):149-157. Regul Toxicol Pharmacol 2002. Exposure to bisphenol A from bis-glycidyl dimethacrylatebased dental sealants.S. Rat two-generation reproductive toxicity study of bisphenol A. Imai H. 32 Fourth National Report on Human Exposure to Environmental Chemicals . Serizawa S. 1999-2000: a national reconnaissance. J Am Dent Assoc 2006.59(9):625-628. niehs. Wong LY. Needham LL. Hughes C. NTP-CERHR Panel Report on Reproductive and Developmental Toxicity of Bisphenol A. et al. 2/4/09 National Toxicology Program’s Report of the Endocrine Disruptors Low-Dose Peer Review (NTP). Barber LB. C. September. et al. Biochem Biophys Res Commun 2003.pdf . Ema M.145:592-603.gov/ntp/htdocs/liason/ LowDosePeerFinalRpt. Needham LL. Pyo MY. Fujii S. NC. National Institute of Environmental Health Sciences. U. Richter CA. Lynch BS. and Hardy MP. Estimation of intake level of bisphenol A in Japanese pregnant women based on measurement of urinary excretion level of the metabolite. vom Saal FS. with estrogen receptors alpha and beta. Urinary bisphenol A and plasma hormone concentrations in male workers exposed to bisphenol A diglycidyl ether and mixed organic solvents. Belgium.jrc.59(4):403-408. Urinary concentrations of bisphenol A and 4-nonylphenol in a human reference population. Calafat AM. 2007. Brussels.nih.116(1):39-44.Scientific Committee on Toxicity. Tyl RW. Bisphenol A prevents the synaptogenic response to testosterone in the brain of adult male rats.gov/chemicals/bisphenol/bisphenol. Available at URL: http://cerhr. 2/4/09 Fujimaki K. European Commission. Reprod Toxicol 2001. Cha SW.gov/chemicals/bisphenol/BPAFinalEPVF112607. Kim YH.. 2008. hormones. Environ Health Perspect 2005. Furlong ET. T. National Institutes of Health. Zacharewski TR.113(4):391-395. 2/4/09 National Toxicology Program Center for the Evaluation of Risks to Human Production (NTP-CERHR). Park S. Rhomberg et al.68(1):121-146. Nippon Eiseigaku Zasshi 2004. niehs. population to bisphenol A and 4-tertiary-octylphenol: 2003-2004. Klinefelter GR. Kolpin DW. 5: 505-523.780(2):365-370. Howdeshell KL. Barr DB. Human Health. Kawamura N. bisphenol A glucuronide. Reidy JA. Gender differences in the levels of bisphenol A metabolites in urine.eu/ health/ph_risk/committees/sct/documents/out156_en. and other organic wastewater contaminants in U. Bradley S. 2002.137(3):353-362. Watanabe S. Available at URL: http://ecb. Myers CB. Italy. Endocrinology 2004. Research Triangle Park. 2/4/09 European Commission. Han SS.10:875-921.pdf.35(2 Pt 1):238-254. Koulova AI. Sottas CM. Calafat AM. Department of Health and Human Services. Doull J. Barr JR.36(6):1202-1211. Kim JC. Chung MK. Tsugane S. Caudill SP. Yang M. May 22. Thomas BF. Available at URL: http://ec. Koh WS. Kuklenyik Z.. Proc Natl Acad Sci USA 2005.nih. Bisphenol A. Toxicol Sci 2002.J. Occup Environ Med 2002. Zaugg SD. Rubin C. N. Chem Res Toxicol 2001. Hlywka JJ. Watanabe C. November 26. Gray GM. National Toxicology Program. Hara K. Evaluation of developmental toxicity in rats exposed to the environmental estrogen bisphenol A during pregnancy. Calafat AM.pdf. Estrogenic chemicals in plastic and oral contraceptives disrupt development of the fetal mouse prostate and urethra. streams.69(22):2611-2625. Cunha G. Environ Sci Technol 2002. Ikka T. DirectorateGeneral Health and Consumer Protection. Environ Health Perspect 2008. Matthews JB.europa. Kroes R. Thurman EM. Arakawa C.

Morgan MK. Hughes C. bisphenol-A. Dekant W. Chem Res Toxicol 2002.113(8):926-33. Witorsch RJ.Environmental Phenols Volkel W. Low-dose in utero effects of xenoestrogens in mice and their relevance to humans: an analytical review of the literature. An extensive new literature concerning low-dose effects of bisphenol A shows the need for a new risk assessment. Large effects from small exposures. Biological monitoring of bisphenol a in a Korean population. Food Chem Toxicol 2002. Wilson NK. Colnot T. Kim SY.15:12811287. Nagel SC. Environ Res 2007. An observational study of the potential exposures of preschool children to pentachlorophenol. Arch Environ Contam Toxicol 2003. Csanady GA. et al.40(7):905-12.103(1):9-20. Vom Saal FS. Endocrine mechanisms mediating effects of bisphenol A at levels of human exposure. Welshons WV. Chuang JC. Environ Health Perspect 2005. Fourth National Report on Human Exposure to Environmental Chemicals 33 . Lordo RA. and nonylphenol at home and daycare. Metabolism and kinetics of bisphenol A in humans at low doses following oral administration. Sheldon LS. Kawamoto T. III.44(4):546-51. Chang SS. Jang JY. Filser JG.147(6 Suppl):S56-69. vom Saal FS. Endocrinology 2006. Lee SM. Yang M.

Katsuda et al. which may vary for some chemicals by year and by individual sample. and from contact with some personal care products and detergents. and to alkylphenoxycarboxylates.20-2.500) . Disposition in humans has not been studied sufficiently.5% of 139 U. In the 1990s. 2006.00 (1.500) 75th .20) 2. altered estrus cycles and reproductive outcomes. Less frequently. impaired steroidogenesis.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 . and some personal care products..500 (.20) 1. and emulsifiers.10 (.1. did not bioaccumulate.S.. 34 Fourth National Report on Human Exposure to Environmental Chemicals . 2004).477) .30 (.60) . see Data Analysis section) for Survey year 03-04 is 0.300 (<LOD-.600-1.369 (. textiles.90) 2.40 (1.200-. Laws et al.60) 1.600-1.400 (. over 500.30) 1.60-3.40) 2.20-2.800-1.50) 1.400 (.90) 2. through sewage. 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.300 (<LOD-.900 (.60-3. and the polyethoxy chain may consist of up to 50 ethoxy units. Human exposure to alkylphenols and alkylphenol ethoxylates may occur through ingestion of contaminated foods (e.20-2.10 (1. Indoor and to a lesser extent. and impaired spermatogenesis (e.60-3.70 (1. < LOD means less than the limit of detection.20-2.900 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.10) 1. an alkylphenol.600-1. population from the National Health and Nutrition Examination Survey.50) . Several alkylphenols.20-2. 4-octylphenol monoethoxylate was detected in 43. Ying et al.000 tons of alkylphenol ethoxylates were produced annually worldwide.30-2.299-.500) .268-.Environmental Phenols 4-tert-Octylphenol CAS No..20) 314 715 1488 03-04 03-04 * * .300-.200-.80 (1. to shorter chain alkylphenol ethoxylates.497) * . Commercial formulations of alkylphenol ethoxylates usually contain a mixture of oligomers and isomers. Bian et al.g.30 (1. They are biodegraded to the corresponding alkylphenol (octylphenol or nonylphenol).500-1. have demonstrated estrogenic effects particularly when injected at high doses in animals.60) 613 652 1092 Limit of detection (LOD.20 (1. During the 1980s and 1990s.10) 2.900 (. and was quickly eliminated from the blood (Certa et al.300 (<LOD-.20-2.00) 1229 1288 03-04 03-04 03-04 * . Blake and Boockfor.00 (. testicular atrophy. 2003.. outdoor air may have detectable levels of 4-tert-octylphenol and 4-tert-octylphenol monoethoxylates.3-Tetramethylbutyl] phenol) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. several European nations banned the use of alkylphenol ethoxylates in domestic detergents and other uses.274-..60-3.900 (. including 4-tert-octylphenol..600) .80) 2.30 (1.. The alkylphenols can bioaccumulate in some fish.10-2.70 (1.g. Nonylphenol ethoxylates are more commonly used than octylphenol ethoxylates.60-3. 1995.600-1.3. the various alkylphenols have also been used as emulsifiers and modifiers in paints.600) 1.400 (.40) 1.50 (1.600-1.500-1. In 1999-2000. altered neonatal sexual development.50) 1.70 (1. 1997.30) 90th 1.40) 1.. and some of their degradation products are toxic to aquatic life.300 (<LOD-. pesticides.00 (.50) 1. 2002).400) 1. Saito et al.300-.70 (1. orally administered 4-tert-octylphenol was well absorbed. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.60-3. 2000.40) 2. industrial cleaners. The alkylphenol ethoxylates enter the environment through human use of products containing them. which are anionic surfactants used in detergents.S. In rats. leading to inhalation as another potential exposure route (Rudel et al.30) 2. 2000.700-1. These high dose parenteral effects of 4-tert-octylphenol have included altered sex hormone levels and hypothalamicpituitary suppression. 2002).300 (<LOD-. streams in 30 states (Kolpin et al.507) * < LOD .50-3. Octylphenols and nonylphenols can also enter the environment directly from manufacturing waste streams.900 (.80 (1. 140-66-9 General Information 4-tert-Octyphenol. fish) and drinking water. 1996).500) .30 (1.80 (1.600-1. is used to manufacture alkylphenol ethoxylates. and through manufacturing waste streams (Warhurst..600) ..30 (1. Urinary 4-tert-Octylphenol (4-[1. Alkylphenols also have been used as plasticizers and antioxidants in plastics and resins.2.389 (.600) .50) .50-2.357 (. Survey Geometric mean (95% conf.10 (.40) * 03-04 03-04 03-04 .

62 (1.300 (<LOD-.68-2.320 (<LOD-.400) ..43) 1.76 (2.435 (. Fourth National Report on Human Exposure to Environmental Chemicals 35 . representative subsample of NHANES 2003-2004.11-2.15) 1.78 (1.17 (.470-1.33 (2.450) .41) .25-2.460 (.337-.43-3.36-3.740 (.370 (<LOD-.20 (1.05-2.160-. 2000. the urinary concentrations of 4-tert-octyphenol were near or below the detection limit (Inoue et al.170-.. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.11) 2. 4-tert-Octylphenol is not considered directly genotoxic.24) 612 651 1091 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.S.530) .620-1.270 (. Kawaguchi et al.64 (. 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.59) 1.770 (.540-1.276 (.65-3.450) 1.25) 2.14) 314 713 1487 03-04 03-04 * * .85 (1. 2005.78) 3.630-1. 2004. Calafat et al. It is unclear if estrogenic or other effects occur in animals through oral dosing. Yoshida et al.25) 90th 1. 1999).850 (..199-.31 (1.620) .40 (1.40-4.43) 1.00) 1.62 (1.860 (.3-Tetramethylbutyl] phenol) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.71) 2.260 (<LOD-.00) 2.384) * .420) .610) . interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.1.3.640-1.68) 2.00) size 2514 Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th . Biomonitoring Information Urinary levels of 4-tert-octyphenol reflect recent exposure.10-2.11) 1. Nagao et al.470-1.730-1.S.410 (.81 (1.890-2. 2001. or their corresponding ethoxylates with respect to human carcinogenicity.62) ..570) ..470) 75th .207-.67-2.50 (2.03 (1.740 (.349) * < LOD . Urinary 4-tert-Octylphenol (4-[1..00 (.02-4.910 (.73) 2. 2001). IARC and NTP have not rated octylphenol.03-6. nonylphenol.270-.06 (2.78) 1228 1286 03-04 03-04 03-04 * .18-4.96-4.270 (.29) 2.00) 2. In a small number of adult Japanese volunteers. 2003. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.33) 3.59 (1.54) * 03-04 03-04 03-04 . Survey Geometric mean (95% conf.00 (.380 (<LOD-.500-1.08) 1.269 (.31-2. Finding measurable amounts of 4-tert-octylphenol in the urine does not mean that the levels of 4-tert-octylphenol cause an adverse health effect. population from the National Health and Nutrition Examination Survey. at lower or environmentally relevant doses (Blake et al.550-1. Sweeney et al. Tyl et al.280-.560) .60 (1.03 (1.22) .53-3. (2008) showed that urinary levels of 4-tertoctyphenol were detectable in slightly greater than half of the participants of the U. 2004).Environmental Phenols Myllymaki et al.

Seto H.folliclestimulating hormone. Kawaguchi M. et al. Marr MC. Indoor air pollution by alkylphenols in Tokyo. Cooper RL. Food Chem Toxicol 2006.S.28(3):215-226.30(2 Pt 1):81-95. Maternal exposure to octylphenol suppresses ovine fetal follicle-stimulating hormone secretion. testis size. 2/4/09 Ying GG.Environmental Phenols References Bian Q. Fail PA.799(1):119-125. Brooks AN.co. Zaugg SD. Carey SA. Ono H. Furlong ET. streams. Takenaka A.57(2):255-266. An environmental assessment of alkylphenol ethoxylates and alkylphenols. Toxicokinetics of p-tert-octylphenol in male Wistar rats. Maekawa A. Paranko J. Onuki A. Horie M. Katsuda S. Boockfor FR. Korn LR. Nair-Menon JU. 2003. Karjalainen M. hormones.foe. Xu L. Sakui N. Taya K. Needham LL. Okada F. Yoshida M. Reidy JA. Maekawa A. Makino T. Exposure of the U. Irreversible effects of neonatal exposure to p-tert-octylphenol on the reproductive tract in female rats. and other endocrine-disrupting compounds in indoor air and dust. 36 Fourth National Report on Human Exposure to Environmental Chemicals . Camann DE. Thurman EM. Kawaguchi M. Nakagomi M. Watanabe G. Endocrinology 2000. Blake CA. Ito R. Yoshimura S. Indoor Air 2004.uk/resource/reports/ethoxylates_alkylphenols. and sertoli cell number. Taya K. Myllymaki SA. J Chromatogr B Analyt Technol Biomed Life Sci 2004. Calafat AM. Kookana R. Izumi S. Millette CF. Muller AM. 1995. et al. Environmental fate of alkylphenols and alkylphenol ethoxylates--a review. Barber LB. Song L.15(6):683-692. Toxicol Appl Pharmacol 2000. Environ Sci Technol 2002.116(1):39-44.44(8):1355-1361.141(7):2667-2673. Laws SC. Saito I. Bodman GJ. Inoue K. Two-generation reproduction study with para-tert-octylphenol in rats. and testosterone. 1999-2000: a national reconnaissance. nonylphenol. Nicol L. Williams B. Rudel RA. Infantile 4-tert-octylphenol exposure transiently inhibits rat ovarian steroidogenesis and steroidogenic acute regulatory protein (StAR) expression. Myers CB.S. polybrominated diphenyl ethers.207(1):59-68.18(1):43-51. population to bisphenol A and 4-tertiary-octylphenol: 2003-2004. pesticides. Effects of neonatal exposure to a high-dose p-tertoctylphenol on the male reproductive tract in rats. Saito Y. Pharmaceuticals. Chen J. The toxic effects of 4-tert-octylphenol on the reproductive system of male rats.pdf. Environ Int 2002. 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. Phthalates. Boockfor FR. Kolpin DW.165(3):217-226. Toxicol Lett 2001. Toxicol Appl Pharmacol 2005.71(1-2):112-122. Wang X. Fedtke N. Estrogenic activity of octylphenol. Seely JC. Yoshida M. Brine DR. prolactin. Qian J. Regul Toxicol Pharmacol 1999. Ferrell JM. Brody JG. Sweeney T. Watanabe G.54(1):154-167. bisphenol A and methoxychlor in rats. Warhurst AM. et al. Environ Health Perspect 2008. et al. Blake CA. Ye X. and other organic wastewater contaminants in U. Meyer MT. Katsuda S. Tyl RW. Reproductive effects in male and female rats from neonatal exposure to p-octylphenol. Toxicol Sci 2000. Anal Chim Acta 486:41-50. Measurement of 4-nonylphenol and 4-tert-octylphenol in human urine by column-switching liquid chromatography-mass spectrometry. Arch Toxicol 1996. alkylphenols. Raychoudhury SS. Inoue K. Wiegand HJ.37(20):4543-53. Chronic administration of the environmental pollutant 4-tert-octylphenol to adult male rats interferes with the secretion of luteinizing hormone. Haavisto TE.36(6):1202-1211. Reprod Toxicol 2004. Available at URL: http:// www. Biol Reprod 1997. Roche JF. Reprod Toxicol 2001. Certa H. Yoshimura Y. Wong LY. Usumi K.121(1):21-33. Nagao T. McCoy GL. Bolt HM.14(5):325-332. Effects of 4-tert-octylphenol given in drinking water for 4 months on the male reproductive system of Fischer 344 rats. Takai N. Toppari J. Environ Sci Technol 2003. Spengler JD.

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

9 (8.90-10.4) 357 (225-456) 203 (87.0-19.8) 7.0 (26. interval) 13.8) 14.9) 7.6-111) 33.4.6) 31.10-9.0 (11.00 (4.86-12.3 (8.9) 8.8 (21.22-10.50-10.1) 50.6-14.45 (5. interval) 12.1 (45.0) 49.80 (5.2-46.6-14.18 (5.20 (7.7 (39.2 (27.0 (8.1) 14.8) 9.4 (11.8-85.9) 32.S.21 (6.6 (9.6-65.2-58.4) 25.9 (11.6-15.6-20.5) 20.89-11.4’-Trichloro-2’-hydroxyphenyl ether) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.4) 51.S.5-250) 574 (461-716) 380 (258-430) 1229 1288 03-04 03-04 03-04 14.48-10.0-73.3) 10.7 (14.6) 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 9.29-12.2) 9.82 (8.9) 75th 47.6 (30.50) 10.0-15.20-11.32-14.3-35. population from the National Health and Nutrition Examination Survey.5) 13.10) 84.40-17.45-13.8-63.7-318) 224 (186-272) 236 (115-336) 356 (169-580) 385 (308-506) 314 713 1487 03-04 03-04 13.4) 75th 43.1-39.3. population from the National Health and Nutrition Examination Survey.6) 90th 212 (172-241) 03-04 03-04 03-04 9.3-15.Environmental Phenols Urinary Triclosan (2.1) 13.9 (50.1 (15.1) 9.70-16.1) 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 9.4) 7.2) 13.2 (13.9 (33.3 (26.8) 116 (39.6-37.7) 123 (36.16 (6.6) 12.2 (10.0-15.20-10. see Data Analysis section) for Survey year 03-04 is 2.11-11.0 (34.6 (10.0) 9.38-18.6) 237 (175-294) 182 (138-217) 384 (294-506) 336 (225-480) 1228 1286 03-04 03-04 03-04 13.1) 11.4 (12. Survey Geometric mean (95% conf.1) 9.4’-Trichloro-2’-hydroxyphenyl ether) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.8-60.5) 66.8-112) 30.3-31.2 (37.3) 6. Urinary Triclosan (2.7) 10.1 (8.5-14.20-13.5) 11.93 (7.72-13.2 (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 .4-19.2) 12.6) 10.1) 9.4) 73.3) 47.3 (11.40-11.6) 39.4 (38.4) 90th 249 (188-304) 03-04 03-04 03-04 8.60 (8.3 (9.0) 65.7 (9.3-67.00-8.4.43-13.1) 7.45-10.4 (32.4) 317 (231-433) 144 (96.60 (6.92-12.5-86.1) 9.55 (4.7 (28.2-14.9-61.48 (8.20 (7.4-18.2-58. Survey Geometric mean (95% conf.6 (12.2 (25.9-236) 193 (90.5 (11.30-14.8-127) 37.7 (11.4-163) 304 (134-566) 261 (198-317) 157 (113-380) 655 (310-890) 472 (406-522) 314 715 1488 03-04 03-04 16.74 (5.5-341) 245 (163-334) 597 (372-992) 450 (254-750) 461 (383-527) 613 652 1092 Limit of detection (LOD.7) 292 (151-432) 132 (78.0 (36.94 (7.54 (8.

Food Chem Toxicol 2000. Mar Environ Res 2000.Environmental Phenols References Aiello AE. phthalates. Osachoff H. Barber LB.23(5):579-583. 4’-trichloro-2’-hydroxydiphenyl ether. Environ Health Perspect 2007.4’-trichloro-2’hydroxydiphenyl ether). Ye X. Wolff MS.69(20):1861-1873. Ebersole R. Sandborgh-Englund G. Shiratsuchi H. Ferrer I. Percutaneous penetration and dermal metabolism of triclosan (2. Am J Infect Control 1996. IMS Ind Med Surg 1969.66:1052-1056. Skirrow RC. Gunderson MP. Ishibashi H.50(1-5):153-156. Hirano M. et al. and other organic wastewater contaminants in U. and phenols in girls. Levy SB. Pilot study of urinary biomarkers of phytoestrogens. Furia T. Br J Clin Pharmacol 1987. Developmental evaluation of a potential non-steroidal estrogen: triclosan. Toxicology of 2. Wigmore H. et al. Biol Pharm Bull 2005..24(3):209-218. Environ Health Perspect 2008. Hong HC. Katsura E. Watanabe N. Effects of nonylphenol and triclosan on production of plasma vitellogenin and testosterone in male South African clawed frogs (Xenopus laevis). Clapson DJ. Wong LY. Reidy JA.17(5):637-644. Benson WH. Teitelbaum SL. Fourth National Report on Human Exposure to Environmental Chemicals 39 . Lyman FL.38(4):361370.7/2.8-dibenzodichloro-pdioxin as a photodegradation product of triclosan in water and wastewater samples.S. Bodey GP.67(4):532-537. Williams FM.36(6):1202-1211.4. Mezcua M. Ogawa H. Veldhoen N. Triclosan: applications and safety. Okui T. Kanetoshi A. Gomez MJ. Howes D. Windham G. Photolytic degradation of triclosan in freshwater and seawater. Chemosphere 2007.38(2):64-71. Aranami K. Kolpin DW.S. Aquat Toxicol 2006. 1999-2000: a national reconnaissance. Erratum in: Aquat Toxicol 2007. Bennett ER. Moss T. 4. Arch Environ Contam Toxicol 1988.115:116-121. Adolfsson-Erici M. The oral retention and antiplaque efficacy of triclosan in human volunteers. Fernandez-Alba AR. population: 2003-2004. Williams PE. The bactericidal agent triclosan modulates thyroid hormone-associated gene expression and disrupts postembryonic anuran development. Furlong ET. Pharmacokinetics of triclosan following oral ingestion in humans. Matsumura N. Gilbert RJ. Environ Sci Technol 2002. Britton JA. Hernando MD. Thurman EM. Readman JW. Ekstrand J. Bhargava HN.45 Suppl 2:S137-S147. Consumer antibacterial soaps: effective or just risky? Clin Infect Dis 2007. Calafat AM. Urinary concentrations of triclosan in the U. et al. hormones. Disposition and excretion of Irgasan DP300 and its chlorinated derivatives in mice. Zaugg SD. Meyer MT. J Toxicol Environ Health A 2006. Foran CM. Needham LL.524:241-247. Larson EL.116(3):303-307. J Invest Dermatol 1976. streams. Chelimo C. Evidence of 2. Nagao Y. Leonard PA.28(9):1748-1751. Pharmaceuticals. Pinney SM. Aguera A. et al. Anal Chim Acta 1004. Randomized trial of a hexachlorophene preparation and P-300 bacteriostatic soaps. Kaneshima H.80(3):217-227.83(1):84. Odham G.

mollusicide.350 (.65 (.18 (<LOD-1.00) 2. 1979).350 (.48-2.350-. has been restricted.g.650) 1.350-. PCP also may be eliminated in urine as a metabolite of hexachlorobenzene.70) 2.25 and 0. and animals. which may vary for some chemicals by year and by individual sample.350) < LOD .60) 1. and it is used primarily as a preservative for wood to be used outdoors (e.80) . 1976.350) < LOD .350 (.S.350-.860-2.350-. PCP is distributed to most tissues and is not extensively metabolized.680-1.350) < LOD .980 (..58-2.350-.09) .990-2.42) 973 1190 1021 1338 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * . 2002. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.350-.350) < LOD .10) 1. population from the National Health and Nutrition Examination Survey. Kohli et al. algaecide and insecticide.S. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. In the environment.480-2.350) < LOD .350-2.350) < LOD < LOD 75th .65 (.54-2. PCP use in the U.350-. along with small amounts of tetrachlorohydroquinone and conjugates.67) 1.78) 1.00 (. air.350-1.30 (.10 (<LOD-1.32 (. other polychlorinated benzenes.350-1.50) 1.47-5.30) .83 (2.890-1.500-2.350-.350 (. bactericide. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.10) 1.350 (.350-2.350 (.350-.350 (. herbicide.350) < LOD .350) < LOD . Since 1984..350) < LOD . 1997).350 (.64) 1.350-. 40 Fourth National Report on Human Exposure to Environmental Chemicals .390 (.91 (1.660 (.51) 1.30) 1.350-.350) < LOD .30) 1.350 (.350-.350) < LOD . 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.90) 2.62 (.350-..770 (.76) 1.350-2. the elimination half-life may be a week or more (Uhl et al.350-.90 (1. Effects including hyperthermia.350 (. Survey Geometric mean (95% conf. After a single dose.40 (.. PCP has been detected in soils.630 (.510-3.350) .350-1.30 (1. The parent compound and conjugates.53) 482 577 681 826 831 1125 99-00 01-02 99-00 01-02 * * * * . PCP is eliminated over a few days (Braun et al.350-. and possibly of lindane (IPCS. Human exposure to PCP has become less common.350 (.350 (.350) 90th .10 (1.350-.510-5.350-2.960) 1.890 (.350 (.70) .350 (.530) 1.60) 1.08-3.94 (1.01 (<LOD-1.350 (.350-. Human health effects from PCP at low environmental doses or at biomonitored levels from low environmental exposures are unknown.58-2. PCP is degraded by sunlight and metabolized rapidly by microorganisms.30 (.350-. 1986).10 (.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 .00) 1.33) .350 (.94 (1. General population exposure to PCP may occur by inhalation of contaminated air.350) < LOD .33-2.350) < LOD . and dermal contact with PCP-treated products.590-1.850-2.Fungicides Pentachlorophenol inhale it or absorb it through exposed skin.37 (. are eliminated in the urine. < LOD means less than the limit of detection. After absorption.76) .45-2.23 (.650 (.48 (. water and sediments because of the large amounts that were produced and used historically.350 (. with repeated or chronic exposure. PCP cannot be used on wood in residential or agricultural buildings.04) 1. so it is relatively non-persistent. ingestion of contaminated food or water.390 (. hypertension.350) < LOD .5. Acute.990 (<LOD-2.350-.47-3. 87-86-5 Also a Metabolite of Several Organochlorine Insecticides General Information Pentachlorophenol (PCP) and its sodium salt were once widely used as a fungicide.350) < LOD .75) 2.350-.90) 1.76) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .42) 696 680 521 696 603 951 Limit of detection (LOD.73 (1.350 (.350 (. To-Figueras et al. PCP is absorbed rapidly and well by all exposure routes.350) < LOD .350-2. plants.350) < LOD ..350 (.350 (.350-1.350-.00) 1.37) . and metabolic acidosis were observed in CAS No.98 (1.350-. utility poles and fence posts). high dose exposure to PCP can induce a hypermetabolic state and excessive heat production as a result of uncoupling mitochondrial oxidative phosphorylation.

40) 1.400 (. IARC has determined that pentachlorophenol is possibly carcinogenic to humans.67-2.40) 1.75) 1.610 (. Survey Geometric mean (95% conf.830) < LOD .40) 1.57 (1. 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. 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.94-3.710-1.06) 1.650) 90th 1.92) 1.11) 2.82) 1.6 and 14.780) < LOD .330-..700-2. 1991). 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.e.67 (1. carcinogenic.240-.S. respectively) (Becker et al.570 (.00) 1.40) 1. and the FDA has established a standard for bottled water.00-1.73 (1.290-. 1989).84) 1.epa.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 .280) < LOD .580-.56) 1.Fungicides adults and children severely exposed to PCP through ingestion.84-4.gov/ toxpro2. inhalation.19) 2.360-.440 (.320) < LOD .590) < LOD . chronically administered high doses of PCP were hepatotoxic.atsdr.910-1.310) < LOD . population from the National Health and Nutrition Examination Survey. 2000).350) < LOD .470 (.67 (1.EPA.25) 1.16 (.10-2. or skin absorption.67 (1.19 (1. Urinary Pentachlorophenol (creatinine corrected) Also a Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.560-.S.52) 1.800) < LOD 1.35) 1. environmental levels) and health effects is available from the U.94 (1.09-1.84 (1.26 (1.34 (.850 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.52 (1. 1995).320 (. children in the 1980’s..06 (.08 and 5. 1989).29-3.40-2.500-1. In NHANES 2001-2002 subsamples. The U... EPA at: http://www. 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.19) 2.320) < LOD .S. and adversely affected thyroid function (U.500 (. Fourth National Report on Human Exposure to Environmental Chemicals 41 .510-.75 (<LOD-2. Among adults in the NHANES 1999-2000 subsample. Death can result from seizures and cardiovascular collapse.780-1.260 (.590-1.30-2.69 (1.35-2.270-.67-3.950-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.900-1.52 (<LOD-1.78) 1.300 (..560) < LOD .920 (.gov/ pesticides/ and from ATSDR at: http://www.30) 1. respectively) (Seifert et al.83 (1.18) .S..290-.560) < LOD . More information about external exposure (i.25-1.html.21 (.950-1.380-.40) 1.09 (<LOD-2. OSHA has established an occupational standard.78) 1.300 (.500-. the median and 95th percentile urinary PCP levels were approximately three times lower than comparable values in German adults (2.250 (.48-2.990 (.99) 482 577 681 825 831 1125 99-00 01-02 99-00 01-02 * * * * .67 (1.36) . 2003).S.57 (.220-. 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. Pentachlorophenol is not mutagenic or teratogenic.510-.10 (1.35-2.08) 696 680 521 695 603 951 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.320) < LOD < LOD 75th .430) < LOD .760 (.16-1. 2004.94 (1.13 (.430-.9 mg/L.340-. 2003). In a small sample of U.360 (. van Raaij et al.25 (1.300 (.730) < LOD .30) 1.630 (.82 (1.55) 1.25-2.290) < LOD .490) < LOD .21-2. In animals.25-2.06-3.310-.cdc.800-1.67-3. EPA has developed standards for PCP in drinking water and the environment.52 (<LOD-1.19) 2.55) 973 1190 1021 1337 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .420) < LOD .650 (..79) 1.75) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .30 (.950-1.0 mg/L.26 (1.35) 1.650 (.370 (.00-1.95) 3.90) 1.250 (.18 (1.220-.67 (1.51) 1.270-..25 (1.

Int J Hyg Environ Health 2003. Kaus S. Chenoweth MB.4:289296.inchem. Needham LL.58:182-186. Schulz C. Santiago-Silva M. drinking water and indoor air. Shealy DB. Can J Biochem 1976. References Becker K. Available at URL: h t t p : / / w w w. Blau GE. To-Figueras J. Schlatter C. Krause C. The metabolism of higher chlorinated benzene isomers. Otero R. Arch Toxicol 1986. house dust. Barrot C. van den Berg KJ. Effects of hexachlorobenzene and its metabolites pentachlorophenol and tetrachlorohydroquinone on serum thyroid hormone levels in rats. htm. Bragt PC.org/documents/jmpr/jmpmono/2002pr08. Seiwert M. 42 Fourth National Report on Human Exposure to Environmental Chemicals . Arch Environ Contam Toxicol 1989. The German Environmental Survey 1990/1992 (GerES II): reference concentrations of selected environmental pollutants in blood. Pesticide residues in urine of adults living in the United States: reference range concentrations. Becker K. Smith SJ. Seifert B. 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. Head SL. et al. The metabolism/ pharmacokinetics of pentachlorophenol in man and a comparison with the rat and monkey.18:475-481. 4/21/09 van Raaij JA.18(4):469-474. Helm D. Schulz C. Arch Environ Contam Toxicol 1989. Uhl S. Biomonitoring data can also help scientists plan and conduct research about PCP exposure and health effects. 206:15-24. Dev Toxicol Environ Sci 1979. Safe A. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children. Braun WH. Bailey SL. Notten WR.S.105(1):78-83. Holler JS. Pentachlorophenol measurements in body fluids of people in log homes and workplaces.54(3):203-208. Seiwert M. U. g o v / f d m s p u b l i c / c o m p o n e n t / main?main=DocketDetail&d=EPA-HQ-OPP-2004-0402. Hill RH Jr. Needham LL. EPA). Engel R. Pesticide residues in food-2002-Joint FAO/WHO meeting on pesticide residues. PCP: Human Risk Characterization [online]. Metabolism of hexachlorobenzene in humans: association between serum levels and urinary metabolites in a highly exposed population. Schmid P. Hill RH Jr.Fungicides Finding a measurable amount of PCP in urine does not mean that the level of PCP causes an adverse health effect. r e g u l a t i o n s . available at URL: http://www.S. J Expo Anal Environ Epidemiol 2000.10:552-65. 2002.71:99108. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Hill RH. Environ Health Perspect 1997. et al. Cline RE. Rodamilans M. 4/21/09 Kohli J. Gregg M. Sala M. Baker S. Seifert B. Lindane. To T. Jones D. hair. urine. Environ Res 1995. Toxicology 1991: 67(1):107-16. et al. Environmental Protection Agency (U. International Programme on Chemical Safety (IPCS). Fast DM. Pharmacokinetics of pentachlorophenol in man. 11/30/2004. Phillips DL.

Cnubben et al.20-3.23) 480 577 681 827 830 1125 99-00 01-02 99-00 01-02 .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 .80 (2.450 (<LOD-.EPA.433-.90) 1.88) 1.50-4. 1998).80-3.50) 1.80) 1.28-3.930 (.690-1. whereas SOPP is not volatile and is more water soluble.880-2. Estimated human intakes have been below recommended intake limits (U.600) < LOD 75th . Workers who manufacture.10) 1.40-5.10) . leaving the chemical residue OPP.550-1.508 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.610 (.90) .00) . on ornamental plants and turfs. which may vary for some chemicals by year and by individual sample.670) 2.50) < LOD .00) < LOD . fungicides.60-3.20-2.570 (.Fungicides ortho-Phenylphenol CAS No.450 (<LOD-.624) * . sodium ortho-phenylphenate (SOPP).10) 1. or oral routes from residential use and by ingesting treated food or food that was in contact with treated surfaces or equipment.389-. OPP is still used as a disinfectant fungicide for industrial applications.760-2.696) * .420 (<LOD-. are antimicrobial agents used as bacteriostats.09) 2. inhalational.490 (<LOD-.690) < LOD .540-2. in paints. population from the National Health and Nutrition Examination Survey. Both have been used in agriculture to control fungal and bacterial growth on stored crops.636) * .S.370-. EPA. however.00) .40-5.800-3. In the past.3.60 (1.10) 2. interval) .10) .50-3.85) 2..20) 2.60 (1.50 (1.570-.770 (.386-.890 (.580-1.790) 2. and it is eliminated rapidly from the body as OPP glucuronide and sulfate conjugates (Bartels et al.490 (<LOD-.S. 2006). Timchalk et al.61) 2.90 (1.742) * .402-. Most agricultural food applications have been revoked.840-1.60-2.90) .610-1.30) < LOD 1.30-7.80) 1.00 (1.27 (.03) 1.710-2.22) 2.10 (1.33 (.632) Selected percentiles ( 95% confidence interval) Sample 95th 2.50 (1.20) < LOD 1.50-2.S. 2006). 1989).970 (.364-.498 (. < LOD means less than the limit of detection.750-2.496 (.950) < LOD .493 (. OPP is considered to be moderately toxic after acute oral doses in animal studies.740 (. formulate.349-.570-1.630) < LOD .470 (<LOD-.17 (.490 (<LOD-.480-1. 2006).00 (1. 1998. but OPP and SOPP are still used on pears and citrus (U.40-2.10-2.552 (.860) * 99-00 01-02 99-00 01-02 99-00 01-02 .350-1.640) < LOD .520 (. OPP is volatile.00 (1.90 (1.600-1.890) 1.76) 1. and as a wood preservative. such as fruits and vegetables. and sanitizers.3 and 0.00 (1. or apply these chemicals may be more highly exposed than the general population.600-1.780) < LOD . see Data Analysis section) for Survey years 99-00 and 01-02 are 0.50 (1.860 (.570 (.S.00-2.30 (1.30-2. and it has limited water solubility. 2006).50) .20 (. small amounts of OPP have been measured in human adipose tissue (Onstot and Stanley.389-.60 (1. 90-43-7 General Information Ortho-phenylphenol (OPP.30) < LOD .509 (.10 (1.836) * .710) 3.890 (.820 (.30) < LOD 90th 1.450 (<LOD-.30) 1.567 (. Both chemicals degrade within hours to weeks in the environment (U. Survey Geometric mean (95% conf.410-.590-2.28 (.. OPP was detected in 40 of 60 different canned beers at concentrations in the low parts per billion (Coelhan et al.370-.20 (1.40 (. 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.600) < LOD 1.370-. Fourth National Report on Human Exposure to Environmental Chemicals 43 .10) ..14 (<LOD-3.560-8.50) < LOD . General population exposure can occur via dermal.600) < LOD .645) * . OPP is efficiently absorbed from the gastrointestinal tract and through the skin. SOPP is applied topically to the crop and then rinsed off.830 (.638) * .02) 1.92 (.20 (1.600) < LOD .19 (. it was used in home sanitizers for surfaces.EPA.500-2.770 (.91) 973 1190 1018 1339 99-00 01-02 99-00 01-02 99-00 01-02 .50) < LOD .07 (. Human health effects from OPP at low environmental doses or at biomonitored levels from low environmental exposures are unknown.490 (<LOD-. Available evidence suggests that OPP does not accumulate in the body.570-2.22 (.621) * .23) 695 680 520 695 603 953 Limit of detection (LOD.34) 1.40-7.497 (.850 (.600-1.466 (.490 (<LOD-. or 2-phenylphenol) and its water-soluble salt.390-.90) 2. 2002.20) < LOD 2.

570) < LOD 1.670 (.360 (<LOD-.750-2.. 2005).508) * . Survey Geometric mean (95% conf.453 (.96 (1. 1992.43-2.510 (<LOD-. 44 Fourth National Report on Human Exposure to Environmental Chemicals . In high dose animal studies.791) * .S. These metabolites may induce carcinogenicity via nongenotoxic regenerative hyperplasia of the bladder (Appel.270-.980 (.09-6.970) 1.4 mg dermally had urinary levels of OPP that were several hundred times higher than median levels found in NHANES 1999-2000 and 2001-2002 (Bartels et al.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 .38) 1.91 (1.770-2.460-.990) < LOD .484) * .93 (1. U.61 (1.410 (<LOD-. 1984..S.11 (.444 (.670) < LOD . or.46) < LOD 1. 2000.40-13.38) 2.600-1. ortho-phenylhydroquinone and ortho-phenylbenzoquinone.96-4. reproductive.17) * 99-00 01-02 99-00 01-02 99-00 01-02 .21 (.320 (<LOD-.900) < LOD . 1997.28 (<LOD-4.343 (.291-.558) Selected percentiles ( 95% confidence interval) Sample 95th 2.568) * . Brusick.. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.12) < LOD 1. OPP or SOPP produced carcinomas of the bladder only after phase II detoxification pathways were saturated. Bomhard et al.580-1.88-4.510-. 1993.810-1.800-1. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.560-2.93) 1. by possible genotoxic mechanisms (Hagiwara et al.24-2.EPA 2006).910 (.07) 2. Murata et al. or developmental toxicity was observed (Bomhard et al. Detectable levels were seen in over half the U.S..31) < LOD .0) 1.64 (2.81) 1.00 (. leading to production of two metabolites.420 (<LOD-..311-.26) 1. less likely. CDC.473) * . population in the subsamples from NHANES 1999-2000 and 2001-2002 (CDC. U. population from the National Health and Nutrition Examination Survey.33) . 1998.810) < LOD .93) . 2002.353-. 2005).32) 3.480-.860 (.91) 695 680 520 694 603 953 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.666) * . and it has classified OPP as not classifiable with respect to human carcinogenicity. Nakagawa et al.29) 1.690 (.59) .44 (1. 1999.epa.96) 1.S.. 2002.560) < LOD 75th .43) 3. 1984.420 (<LOD-.EPA at: http:// www.. but no neurologic.43 (1. Biomonitoring Information Urinary OPP levels reflect recent exposure.385 (.02 (. 2005. Smith et al.500) < LOD .550-.S.74 (1.620-1.670 (.52 (.61 (.. 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.656) * .08-1.89 (1. Additional information is available from U.17) 2.11-1.640-1.650-1.09-3. Dermally applied OPP was not carcinogenic in a 2-year experimental study in animals (NTP. Ito et al.780-14.11) < LOD 90th 1.11 (.550 (. 1986).86 (1.84 (1.590) * .440 (.910 (<LOD-1.380 (.75 (1.13) 1.25-6.75 (1.750 (.900-1.53) 1.21-2.93) .12-2.329-. OPP was not found to be mutagenic..78 (2.33-2.514 (.980 (<LOD-1.880-1.610) < LOD 1. 1999.840 (.17 (.51-3.248-.940-2.410 (<LOD-.EPA 2006).470 (<LOD-. Urinary ortho-Phenylphenol (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. Zhao et al.30) 480 577 681 826 830 1125 99-00 01-02 99-00 01-02 .04-4.29) 1.21) 1.950) < LOD .Fungicides anemia.403-.620-1. Finding a measurable amount of OPP in urine does not mean that the level of OPP causes an adverse health effect.17 (.01) 1.20) < LOD 3.496 (.382 (.47) . Pathak and Roy.38) 973 1190 1018 1338 99-00 01-02 99-00 01-02 99-00 01-02 .301-.00 (1.580) < LOD . interval) .11) 4.38-3.28 (2.780 (.06-4. Volunteers exposed to 0.59) 1.27) < LOD .43-2.18) 2.08) 1.860 (.08-2.4) 3.06-5.62) .361-.05-2.750 (.24-2.96 (1.61 (2.550) < LOD .gov/pesticides/.32) 1.69 (1.470) < LOD .. 2002).910-1.09 (1. IARC has classified SOPP as a possible human carcinogen.06 (1.455-. Kwok et al.58) 2.97 (2.

Cnubben NH. 4/13/09 Onstot JD. Brusick D. EPA-560/5-89-003. J Agric Food Chem 2006. Hakkert BC. Third National Report on Human Exposure to Environmental Chemicals. Zhao S. Turteltaub KW. Narang A.nih. Hagiwara A. In vivo genotoxicity of sodium orthophenylphenol: phenylbenzoquinone is one of the DNA-binding metabolite(s) of sodium ortho-phenylphenol. Fukushima S. Selim S. NTP Technical report on the toxicology and carcinogenesis studies of ortho-phenylphenol (CAS No.703(12):97-104. National Toxicology Program (NTP). Reregistration Eligibility Decision (RED) for 2-phenylphenol and salts (Orthophenylphenol or OPP). Hum Exp Toxicol 1998. Mutat Res 1993. Long-term toxicity and carcinogenicity study of sodium o-phenylphenate in B6C3F1 mice. Brzak KA. 2006. July 28. U. Arch Toxicol 2000. Coelhan M. Moldeus P. J Chromatogr B Biomed Sci Appl 1997. Determination of orthophenylphenol in human urine by gas chromatography-mass spectrometry. Tayama S. 90-43-7) in Swiss CD-1 mice (dermal studies). Hirose M. Environ Mol Mutagen 2005. IARC Sci Publ 1984. Roberts AL. Regul Toxicol Pharmacol 2002. Atlanta (GA). 1989. Eadon G. Vogel JS. et al.32(6):551-625.S. Crit Rev Toxicol 2002.pdf. Arnold LL. van de Sandt JJ. Glas K. Shirai T. Mendrala AL. Timchalk C. Bartels MJ. Determination and levels of the biocide ortho-phenylphenol in canned beers from different countries. Identification of SARA compounds in adipose tissue. Herbold BA. U. Eastmond DA. Kawanishi S.epa. Available at URL: http://ntp.gov/ntp/htdocs/LT_ rpts/tr301.17(8):411-417. Detection and characterization of DNA adducts formed from metabolites of the fungicide ortho-phenylphenol. Bormett GA. Bomhard EM. Fukushima S. Timchalk C. Analysis of genotoxicity and the carcinogenic mode of action for ortho-phenylphenol. Bartels MJ.20(5):851-857. St John MK. Pathak DN. Environmental Protection Agency (U.pdf. 4/9/09. Toxicol Appl Pharmacol 1999. Sangha G.150(2):402-413. Bartels MJ. Christenson WR. Ito N. Inoue S.45(5):460-481. Office of Toxic Substances. Imaida K. Nakagawa Y. Drugs.S. et al.EPA).S. Sangha GK.35(2 Pt 1):198-208.S. Stanley JS.50(11):3351-3358. Richter M. Carcinogenesis 1999. Xenobiotica 1998. Meuling WJ.286(2):309-319. Cano M. rat and man. Fourth National Report on Human Exposure to Environmental Chemicals 45 . Available at URL: http://www. Smith RA. EPA).niehs. Hagiwara A. EPA 739 R-06004. McNett DA.43(7):14311437.74(2):61-71. Relationship between metabolism and cytotoxicity of ortho-phenylphenol in isolated rat hepatocytes. Kwok ES. Biochem Pharmacol 1992.159(1):18-24. Urinary physiologic and chemical metabolic effects on the urothelial cytotoxicity and potential DNA adducts of o-phenylphenol in male rats. Freyberger A. food additives and natural products as promoters in rat urinary bladder carcinogenesis. Gierthy J. Shibata M. Moore GA.(56):399-407. J Agric Food Chem 2002. 2005. Moriya K.gov/oppsrrd1/REDs/ phenylphenol_red.. Toxicol Appl Pharmacol 1998. O-phenylphenol and its sodium and potassium salts: a toxicological assessment. Buchholz BA. Ito N. Brendler-Schwaab SY. Christenson WR. Food Chem Toxicol 1984. Comparative in vitro-in vivo percutaneous penetration of the fungicide ortho-phenylphenol. Environmental Protection Agency (U. March 1986. The pharmacokinetics and metabolism of 14C/13C-labeled ortho-phenylphenol formation following dermal application to human volunteers. Murata M. Elliott GR. Dose-dependent binding of ortho-phenylphenol to protein but not DNA in the urinary bladder of male F344 rats.54(16):5731-5735. Bartels MJ.28(6):579594. Roy D. Oxidative damage to cellular and isolated DNA by metabolites of a fungicide orthophenylphenol. Bromig KH. Comparative metabolism of orthophenylphenol in mouse.Fungicides References Appel KE.22(10):809-814. Centers for Disease Control and Prevention (CDC). The carcinogenicity of the biocide ortho-phenylphenol. Leser KH.

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

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

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. population from the National Health and Nutrition Examination Survey. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.S. Urinary Acetochlor mercapturate (creatinine corrected) Metabolite of Acetochlor Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.S. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2500 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 576 819 1105 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1178 1322 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 678 672 952 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. Survey Geometric mean (95% conf. see Data Analysis section) for Survey year 01-02 is 0. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2501 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 576 820 1105 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1178 1323 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 678 673 952 Limit of detection (LOD.1.Herbicides Urinary Acetochlor mercapturate Metabolite of Acetochlor Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. 48 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. < LOD means less than the limit of detection.

reservoirs and ground water in the Midwestern United States.111(5):749-756. Evaluation of the potential carcinogenicity and genetic toxicity to humans of the herbicide acetochlor. Bravo R.S.edu/profiles/herbgrowthreg/24-d-butylate/acetochlor/acetochlor_pet_100. Hodgson E.108(12):1151-1157. Davison KL. Xenobiotica 1994. 2000.gov/oppsrrd1/reregistration/REDs/acetochlor_tred.S. Environmental Protection Agency (U. Deddens JA. Sci Total Environ 2000.24(10):1003-1012. Kolpin DW. et al. Atlanta (GA).Herbicides References Ashby J. J Expo Anal Environ Epidemiol 2005. Tinwell H. Whyatt RM. Available at URL(non U. Larsen GL. Available at URL: http://www. imidazolinone. 5/30/06 U.pdf. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. Peter CJ.17(6):559-566. Olsson AO. et al. Comparative metabolism and elimination of acetanilide compounds by rat. Rose RL. EPA). Federal Register: January 24. Casida JE. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. Curwin BD.39(17):6561-6574. Environ Health Perspect 2000. Coleman S. Identification of human urinary metabolites of acetochlor in exposed herbicide applicators by high performance liquid chromatography-tandem mass spectrometry. Barr JR. Linhart SM. and other herbicides in rivers. 5/30/06. Finding minimal herbicide concentrations in ground water? Try looking for their degradates.248(2-3):123-133. Comparative metabolism of chloroacetamide herbicides and selected metabolites in human and rat liver microsomes. Lefevre PA. Ward EM.html. and metolachlor herbicides in rats. Chem Res Toxicol 1998. epa. Feil VJ. Heederik D. Hsiao JJ.37(4):10881093. Hines CJ.S. sulfonamide.S.15(9):702-735. U. Jefferies PR. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. Barr DB. Sci Total Environ 2000. Thurman EM. 1998.11(4):353359. Barr DB.S.cornell. EPA). Linderman R. Dialkylquinonimines validated as in vivo metabolites of alachlor. acetochlor. Quistad GB. Hum Exp Toxicol 1996. Burkhardt MR. Wratten SJ. Wilson AG. Fourth National Report on Human Exposure to Environmental Chemicals 49 . Environ Health Perspect 2003.248(2-3):115-122. J Agri Food Chem 1989.cce. Hein MJ. Acetochlor (Harness) Pesticide Petition Filing 1/00. Roberts AL. Environ Sci Technol 2005. EPA 738-R-00-009. Kier L. Third National Report on Human Exposure to Environmental Chemicals. Feng PCC. Barr DB. J Expo Sci Environ Epidemiol 2007. Sanderson WT.15(6):500-508.EPA): http://pmep. Number 15. Green T. Furlong ET. Hladik ML. Camann DE. et al. Alavanja MC. Volume 65. 2005. Striley CA. Environmental Protection Agency (U. Report of the Food Quality Protection Act (FQPA) Tolerance Reassessment Progress and Risk Management Decision (TRED) for Acetochlor. Battaglin WA. Centers for Disease Control and Prevention (CDC). pages 3682-3690. Occurrence of sulfonylurea. Reynolds SJ. Andrews HF. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. Kinney PL. March 2006.

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

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

Background document for development of WHO Guidelines for Drinking-water Quality. U. acetochlor. Centers for Disease Control and Prevention (CDC). Feng PCC. Thelin GP.56(6):853-859. Supplemental Technical Information (available on-line only).gov/nawqa/pnsp/pubs/circ1291/ supporting_info. Kier LD.111(5):749-756. Hull RD. Driskell WJ. Available at URL: http:// www. Chem Res Toxicol 1998. Clark JM. World Health Organization (WHO). Xenobiotica 1994. Roberts AL.htm. Third National Report on Human Exposure to Environmental Chemicals. Jefferies PR. 86. 1997. Furlong ET. revised February 15.56(9):883-889. Ann Occup Hyg 2003. Linhart SM. Geological Survey (USGS). Dialkylquinoneimine metabolites of chloroacetanilide herbicides induce sister chromatid exchanges in cultured human lymphocytes. Martens MA. Environ Health Perspect 2003. 1992-2001. Available at URL: http://water. Atlanta (GA). Circular 1291. Shealy DB. Shoemaker DA. Wilson AG.S. Gilliom RJ). Biagini RE. March 2006. Andrews HF. reservoirs and ground water in the Midwestern United States.epa. Camann DE. Hines CJ. 1996. and other herbicides in rivers. Peter CJ. DNA adduct formation by alachlor metabolites. imidazolinone. California. 1999. Quistad GB. Sci Total Environ 2000.org/documents/pds/pds/pest86_e. Am Ind Hyg Assoc J 1995. Sanderson WT. J Agri Food Chem 1989. who. 2/27/09 U. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. World Health Organization. et al.18(6):363-391. EPA). MacKenzie B. Erratum in: Life Sci 1989. et al. Hladik ML. An evaluation of the carcinogenic potential of the herbicide alachlor to man. 1999. Alachlor in Drinking-water. Kimmel EC. The Quality of Our Nation’s Waters Pesticides in the Nation’s Streams and Ground Water. Life Sci 1988. Biagini R. International Programme on Chemical Safety (IPCS). Tolos W.11(4):353359. Water-Resources Investigations Report: Distribution of Major Herbicides in Ground Water of the United States Water Resource Investigations Report No. Striley CA. Mutat Res. Wratten SJ.usgs. 98-4245 (by Barbash JE. EPA 738R-98-020. ALACHLOR. Available at URL: http://www. Available at URL: http://www. Whyatt RM. Barr DB.pdf. No.S. sulfonamide. 2007. 2003. Finding minimal herbicide concentrations in ground water? Try looking for their degradates. Occurrence of sulfonylurea. Casida JE. 4/2/09 U. Comparative metabolism and elimination of acetanilide compounds by rat. Hum Exp Toxicol. Quantitative assessment of the mutagenic potential of environmental degradative products of alachlor. Brown KK.Herbicides References Battaglin WA. Hill RH Jr. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. Dialkylquinonimines validated as in vivo metabolites of alachlor.int/water_sanitation_health/dwq/chemicals/en/alachlor. 2/27/00 52 Fourth National Report on Human Exposure to Environmental Chemicals . Lau H. and metolachlor herbicides in rats. Geological Survey (USGS). Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. WHO/ FAO Data Sheets on Pesticides. Environ Sci Technol 2005. Environmental Protection Agency (U. Thake DC. Hines CJ. Heydens WF. 1998. Bull Environ Contam Toxicol 1996.gov/oppsrrd1/ REDs/0063. Sacramento.248(2-3):115-122. J Ag Food Chem 1995.43(25):2087-94.47(6):503-517. Barr JR. Biological monitoring of commercial pesticide applicators for urine metabolites of the herbicide alachlor. Quistad GB.39(17):6561-6574.44(18):1325. Henningsen G.inchem. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor.43(9):2504-2512. Hsiao JJ. Casida JE. Identification of a major human urinary metabolite of alachlor by LC-MS/MS. December 1998.395(2-3):159-171. Hill AB. Kolpin DW.S. Kinney PL.S. Reregistration Eligibility Decision (RED) Alachlor. Brown MA.php. 2/27/09 Jefferies PR. Burkhardt MR. Sci Total Environ 2000. Kolpin DW.248(2-3):123-133. Larsen GL.24(10):1003-1012. Tessier DM. 2005.pdf. Casida JE. Feil VJ. Deddens JA.37(4):10881093. Davison KL. Geneva. Thurman EM.

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

delayed onset of puberty. 2003b). the dealkylated atrazine metabolites and hydroxyatrazine can occur in the environment from the breakdown of the parent chemical. Stoker et al. myocardial muscle degeneration.. Sathiakumar and Delzell. 2005.. and U. Estimated human exposures are thousands of times lower than doses that caused effects in animals (Gammon et al.. 2000 and 2003. 1994.S.S. 1999). Some human ecologic and epidemiologic studies of reproductive and cancer outcomes have shown either positive or no associations. IARC considers atrazine not classifiable with respect to human carcinogenicity. developmental ossification defects.. 2003. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.atsdr. increased pituitary weight. Sanderson et al. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1878 2476 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 449 568 639 808 790 1100 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 919 1162 959 1314 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 667 676 498 683 550 918 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. atrazine is rated as having low acute toxicity.EPA considers atrazine unlikely to be a human carcinogen.. Survey Geometric mean (95% conf. Dealkylated metabolites from atrazine can also result from metabolism of other chlorotriazine pesticides. 1994 and 1999. Atrazine product formulations can be mild skin sensitizers and irritants. 1997). Eldridge et al.Herbicides particularly diaminochloroatrazine (the main dealkylated product).gov/pesticides/ and from ATSDR at: http://www. Urinary Atrazine mercapturate (creatinine corrected) Metabolite of Atrazine Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. Laws et al. EPA at: http://www. Stevens et al. and cyanazine.. population from the National Health and Nutrition Examination Survey. 2000 and 2002. 2002. prolactin. Atrazine and the dealkylated chlorinated metabolites did not have estrogen receptor activity. U.html.S. Atrazine is not considered genotoxic. Gammon et al.. and testosterone (Gillis et al.gov/toxpro2.. Chronic high dose toxicity observed in animals includes decreased body weight. and reduced levels of luteinizing hormone. Rayner et al. Human health effects of atrazine at environmental doses or at biomonitored levels from environmental exposure are unknown. 2004. Additional information is available from U. Thus.. propazine. 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. 2005. 2000. Gammon et al. including simazine. In addition to being human metabolites of atrazine... 54 Fourth National Report on Human Exposure to Environmental Chemicals . 2003). altered estrus cycles.epa.. In mammalian studies. may mediate some effects of atrazine (Laws et al. 2005).EPA. impaired fertility.S. liver toxicity. detection of these dealkylated metabolites in a person’s urine may also reflect exposure to these degradates in the environment. but the effects are difficult to attribute due to lack of exposure markers or due to mixed chemical or pesticide exposures (ATSDR.cdc.

58(2):366-376.115(8):1254-1260. ATRAZINE. In a small number of field workers. J Toxicol Environ Health 1994.109(6):583-590. J Expo Anal Environ Epidemiol 2005. demasculinized frogs after exposure to the herbicide atrazine at low ecologically relevant doses. Seiber JN.. the urinary geometric mean levels for herbicide applicators in Ohio and Wisconsin were about 6 μg/L (Hines et al. Lioy PJ. Blewett C. atrazine was detected in only four children (Arcury et al. Gillis JH. J Toxicol Environ Health 1994. Brown KK. Biological monitoring of human exposure to atrazine. et al. urinary concentrations ranged from 5-1756 μg/L (Lucas et al. J Agric Food Chem 1982. Eberly LE. International Programme on Chemical Safety (IPCS). Gillis JH. 2005).53(2):297-307. The effects of atrazine on female wistar rats: an evaluation of the protocol for assessing pubertal development and thyroid function. Sanderson WT. In the NHANES 2001-2002 subsample. Ferrell JM. Pubertal development in female Wistar rats following exposure to propazine and atrazine biotransformation by-products. Moseman RF. 3/11/09 Arcury TA. 2000). Toxicol Sci 2000. Barr DB. Barbieri F. The geometric mean of urinary atrazine mercapturate was 1. Stoker TE. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. Cooper RL. Freeman NC. Goodrow MH. 1999) and 83 Minnesota children with multiple urine collections during 1997 (Adgate et al.15(6):500-508. Short-term effects of chlorotriazines on estrus in female Sprague-Dawley and Fischer 344 rats. Vonk A. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Stuart AA. Toxicological profile for atrazine. Ferioli A. 2003. Through immunoassay atrazine equivalents (detected mostly as atrazine mercapturate). 1993). Jones AD. Atlanta (GA). Collins A. Determination of atrazine metabolites in human urine: Fourth National Report on Human Exposure to Environmental Chemicals 55 . Tapia J.64(9):672-678.. Eldridge JC. Proc Natl Acad Sci USA 2002. 2007). Available at URL: http:// www. Steroids 1999. Hermaphroditic. Quandt SA.cdc.. WHO/ FAO Data Sheets on Pesticides. 1996. Toxicol Lett 1993. The mammary tumor response in triazine-treated female rats: a thresholdmediated interaction with strain and species-specific reproductive senescence. References Adgate JL.. Pesticide urinary metabolite levels of children in eastern North Carolina farmworker households. 2001 [online]. Deddens JA.43(2):155-167.Herbicides Biomonitoring Information Urinary levels of atrazine mercapturate reflect recent exposure. Lucas AD. Breckenridge CB. Perry et al. Agency for Toxic Substances and Disease Registry (ATSDR). Determination of urinary residue levels of the N-dealkyl metabolites of triazine herbicides.atsdr.99(8):5476-5480. Environ Health Perspect 2007. Extrom PC. Schmid J. World Health Organization. Chen H. McElroy WK..61(4):331-355. Hayes TB. Carr WC Jr. et al.org/documents/pds/pds/pest82_e. No. Environ Health Perspect 2001. Third National Report on Human Exposure to Environmental Chemicals. Cooper RL. Hein MJ. Lee M. Hines CJ. Saiz SG. Goldman JM. et al. Barr DB. Barr DB. Grzywacz JG. et al. Mendoza M. Aldous CN. Cooper RL. Eldridge JC. Reynolds SJ.2 μg/L in 15 farmers studied several days after spraying the pesticide (Curwin et al.43(2):155-167. Pest Manag Sci 2005. 3/11/09 Laws SC. levels of atrazine mercapturate were generally not detectable (CDC. et al. 2005.. Wetzel LT.gov/toxprofiles/tp153. Ann Occup Hyg 2003. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample. Wetzel LT. Simpkins JW. Tyrey L.76(1):190-200. Sanborn JR. Toxicol Sci 2000. Toxicol Sci 2003. Laws SC. Heederik D.inchem. Curwin BD. In small studies of Maryland residents in 19951996 (MacIntosh et al. Short-term effects of chlorotriazines on estrus in female Sprague-Dawley and Fischer 344 rats. Pfeifer KF. 82.html. Noriega N. 2005). Finding measurable amounts of atrazine mercapturate in urine does not mean that the levels of atrazine mercapturate cause an adverse health effect. Maroni M.69(2):217-222. Cottica D. Geneva. In a study of 60 farm worker children. Centers for Disease Control and Prevention (CDC). Catenacci G. A risk assessment of atrazine use in California: human health and ecological aspects. et al. Bersani M. Striley CA. Stoker TE. Clayton CA. Shoemaker DA. 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.. Stoker TE.30(2):244-247.htm. Available at URL: http://www. Gammon DW. Biagini RE.47(6):503-517. Bradway DE. Fleenor-Heyser DG. Stevens JT. 2001). atrazine mercapturate was infrequently detected at the detection limit of < 1 μg/L. Ferrell JM. Atrazine disrupts the hypothalamic control of pituitary-ovarian function. diamino-S-chlorotriazine and hydroxyatrazine.

A longitudinal investigation of selected pesticide metabolites in urine.S. Pesticides and Toxic Substances. 2003b.58(1):50-59.9(5):494-501. Geological Survey (USGS). Stoker TE.pdf.gov/scipoly/sap/meetings/2003/june/ finaljune2002telconfreport. 0062.67(2):198-206.27(6):599612. Exposure parameters necessary for delayed puberty and mammary gland development in LongEvans rats exposed in utero to atrazine.S.pdf. Stevens JT.S. Crit Rev Toxicol 1997. Toxicology 1990. Needham LL.S. Perry M. Laws SC. Circular 1291. Guidici DL. J Expo Anal Environ Epidemiol 1999. Environmental Fate and Effects Division. Environmental Protection Agency (U.gov/nawqa/pnsp/pubs/ circ1291/supporting_info.56(2):69-109. Case No. Rayner JL. The Quality of Our Nation’s Waters. Available at URL: http://water. 6/1/09 U. Stoker TE.S. Toxicol Appl Pharmacol 2002.6(1):107-116. Christiani D. Supplemental Technical Information (available on-line only). Available at URL: http://www. EPA). Sathiakumar N. Fenton SE. Determination of the effect of tridiphane on the pharmacokinetics of [14C]-atrazine following oral administration to male Fischer 344 rats. Ann Epidemiol 2000. revised February 15. A review of epidemiologic studies of triazine herbicides and cancer. Breckenridge CB. 3/11/09 U. A risk characterization for atrazine: oncogenicity profile. Timchalk C. EPA Office of Pesticide Programs. Laws SC. Toxicol Sci 2000. Washington (DC).php. 1992-2001. Interim Reregistration Eligibility Decision For Atrazine. Dryzga MD. Osborne DW.61(1):27-40. Boerma J. Induction and inhibition of aromatase (CYP19) activity by various classes of pesticides in H295R human adrenocortical carcinoma cells.10(7):479.182(1):44-54. van den Berg M. Delzell E. Langvardt PW. Kastl PE. Environmental Protection Agency (U. Available at URL: http://www. Singzoni B.epa. March 2006. Hammerstrom KA. Chem Res Toxicol 1993. Tortorelli J. Wetzel L.Herbicides development of a biomarker of exposure. Cooper RL. White paper on potential developmental effects of atrazine on amphibians. Dagenhart D. Sanderson JT. Toxicol Appl Pharmacol 2004. Cooper RL. MacIntosh DL. Wood C. Lansbergen GW. The effects of atrazine metabolites on puberty and thyroid function in the male Wistar rat. J Toxicol Environ Health A 1999. 2007. Pesticides in the Nation’s Streams and Ground Water. EPA). Urinary biomarkers of atrazine exposure among farm pesticide applicators. Guidici DL.epa. 4/2/09 56 Fourth National Report on Human Exposure to Environmental Chemicals .usgs. Toxicol Sci 2002.gov/oppsrrd1/REDs/ atrazine_ired. U. The effect of atrazine on puberty in male Wistar rats: an evaluation in the protocol for the assessment of pubertal development and thyroid function.195(1):23-34. May 2003a. Ryan PB. Office of Prevention.

4-Dichlorophenoxyacetic Acid CAS No.230-.00-2.22) 962 1135 1015 1278 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .Herbicides 2. 4-D.490) < LOD < LOD < LOD .400) < LOD .48) < LOD 1.S.S. population from the National Health and Nutrition Examination Survey. 2.810-1. It was first registered with U.27 (1.210-. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. and delayed Urinary 2.320) 90th . the chlorophenoxy herbicide 2. dizziness. 2005). renal and hepatic injury.13) < LOD .690-1. although dermal exposure may be significant for herbicide manufacturing plant workers exposed to high concentrations of 2.960-1.440-1.60) 1.4-D is eliminated mostly unchanged in the urine with an elimination half-life ranging from 10 to 33 hours (Arnold et al.610 (. and mecoprop). nausea. Survey Geometric mean (95% conf. 2.230 (<LOD-.350) < LOD < LOD < LOD .EPA in 1948.730 (.310 (.910) 1. < LOD means less than the limit of detection. agricultural. headache.210 (<LOD-.690 (. 1974.02-1.80) 1.21) 1. Recent estimates of chronic intakes of 2. 1977).08) < LOD . it acts as a plant growth hormone. and it is often mixed with other chlorophenoxy acid herbicides (such as dicamba. It is not well absorbed through the skin.32 (1.10) < LOD 1.670-1.660) 1..4-D may occur during residential applications.490 (.690 (. At low levels.420-. It is poorly bound in soils.66) < LOD 1.37) 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 .16) < LOD .51 (1. Once absorbed.. which may vary for some chemicals by year and by individual sample.S.40) 1. Kohli et al.4-D can be applied either as an aqueous salt or as oil-soluble esters. 2. abdominal pain. Human health effects from 2. hypotension.540-.680-1.250 (<LOD-.930 (.20 (<LOD-1.370-.260 (<LOD-.43) 1.310) < LOD .690 (.250 (<LOD-.890 (.22) < LOD .4-D has low acute toxicity. As much as 62 million pounds of 2. in 2001 (U. 2. Fourth National Report on Human Exposure to Environmental Chemicals 57 .24 (.EPA.07 (. myotonia.550-1. Similar to other chlorophenoxy herbicides.55 (1. 2004).S. MCPA.4-D at low environmental doses or at biomonitored levels from low environmental exposures are unknown.20 (. General population exposure to 2. with a half-life of several days to several weeks.952 and 0.2.4-D is rapidly absorbed via oral and inhalation routes.890) < LOD .4-D) controls broadleaf weeds in residential. and by consuming food or drinking water contaminated with 2.S.740 (.420) < LOD .910) < LOD . It is rarely detected in ground waters (USGS.4-D have been below recommended intake limits (U.560-1.330 (.930-1. 1989.EPA.4-D were used in the U.4-dichlorophenoxyacetic acid (2. Sauerhoff et al.70) 1.49) 477 546 677 797 823 1070 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD .610-. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 1. Intentional overdoses and unintentional high dose exposures to chlorophenoxy acid herbicides have resulted in weakness. these herbicides can enhance plant growth.760 (.10 (<LOD-1.410) < LOD . 94-75-7 General Information Widely used throughout the United States. and aquatic environments.4-Dichlorophenoxyacetic acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. Acid and salt forms are much less toxic to fish and aquatic invertebrates than the ester forms.30 (<LOD-2. by direct contact with agricultural and residential areas after applications.03) 695 659 520 668 589 892 Limit of detection (LOD. but at higher levels they are herbicidal.910) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .10 (<LOD-1.560-.05-2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 2007)..27-2.27 (.4-D or exposed for prolonged periods.

8-tetrachlorodibenzo-pdioxin) (Garabrant and Philbert. 2000).08 (.350 (<LOD-.56) . eyes. U..380-. It is unclear whether these associations are related to the chlorophenoxy herbicides.670 (<LOD-1. IOM.980) < LOD 1.08 (.S.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. 2.340-. Kutz et al.4-D had urinary levels several hundred to several thousand times higher than the 95th percentiles of the NHANES subsamples (CDC. 2006.13 (.EPA 2005). 1994). The acid and salt forms of 2.920) < LOD 1. 1995. 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.660 (. in small samples of children (Hill et al.17 (..660) < LOD . 2.810-1. 58 Fourth National Report on Human Exposure to Environmental Chemicals ..790) 1.7.820-1.. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 1. or teratogenic effects in chronic rodent studies (Charles et al. IPCS.850) < LOD .410) 90th . 2002.S.480 (.gov/pesticides/. 2005).39) < LOD 1.. IPCS.570) < LOD .700 (. liver.670 (.680) < LOD . Knopp et al.620-.4-D does not have significant reproductive.4-Dichlorophenoxyacetic acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.29) 477 546 677 796 823 1070 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD . 1992).470) < LOD .73) .580-.. thyroid.. 2002.. 2003. Additional information is available from U..S. population from the National Health and Nutrition Examination Survey. Survey Geometric mean (95% conf.epa.41 (1.780 (.590 (<LOD-1.790) < LOD .380 (<LOD-. 2005.610-.390) < LOD < LOD < LOD .670 (. 2001.560-.40) 695 659 520 667 589 892 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. adrenals and gonads (NTP.24) 1.550-. Acute high doses administered to laboratory animals produced ataxia. Post-application levels in farmers and home gardeners were dependent on Urinary 2.990-1.S. 1995). 1980.720 (. Pearce and McLean.380) < LOD .440 (. 2005. Average post-application urinary levels of 2.780-1.560-.32 (<LOD-2.640 (.780) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.4-D levels were detectable in less than a quarter of the individuals studied.740 (..810-1.05) .27-1. Frank et al.26) 962 1135 1015 1277 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .16) 1.19) .410) < LOD 1.26) 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 . IPCS. In previous samples of the U. 1996.EPA.14 (.380 (<LOD-.4-D was not found to be genotoxic or carcinogenic in animal studies (Garabrant and Philbert. 2005). or to contaminants in the herbicide formulations (specifically 2.08 (. and of adults and children (Baker et al. with the exposure to chlorophenoxy herbicides as defoliants or contaminated herbicides. 2005.610-.4-D are eye irritants.590 (<LOD-1. 2004).930-1. myotonia. Epidemiological studies have reported associations of several types of cancer.270 (<LOD-. U.S.S. U. developmental.340 (. 1989). 1996.Herbicides neuropathy (Bradberry et al. Kolmodin-Hedman and Erne. 2005).890) < LOD 1. 2. Hill et al.520-. IARC considers the chlorophenoxyacetic acids group of chemicals as possibly carcinogenic to humans.410 (<LOD-.13 (. other exposures. U.270-.490 (.35) < LOD . 2005. population (Hill et al.410) < LOD < LOD < LOD .330-.780) .EPA.4-D production plant workers and a few forestry workers spraying 2. 2005). 1985.EPA at: http://www. such as soft tissue sarcoma and non-Hodgkin’s lymphoma. Biomonitoring Information Urinary levels of 2.S.4-D reflect recent exposure. CDC. and evidence of histological injury to the kidneys. urinary 2.3.890-1.EPA. 1996.

Quantification of selected pesticide metabolites in human urine using isotope dilution high-performance liquid chromatography/ tandem mass spectrometry.nap. Absorption and excretion of 2. Campbell RA. Available at URL: http://ntp. Gupta BN. Scand J Work Environ Health 2005.gov/index. Arch Environ Contam Toxicol 1985. Kutz FW.4:318-321. Khanna RN. Wilson RD.. Murphy RS. Heederik D. Biomonitoring of herbicides in Ontario farm applicators. Occup Environ Med 1994. Sircar KP.4-D in urine does not mean that the level of the 2. Dichlorophenoxyacetic acid. Baker S. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. J Environ Sci Health B 1992.4-dichlorophenoxyacetic acid in man. Exposure of homeowners and bystanders to 2.4-D than levels found in the general population. Atlanta (GA). Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Cook BT. Reynolds SJ. Centers for Disease Control and Prevention (CDC). Bus JS. Stephenson GR.4-D).htm. Arnold EK. 3/17/09 Knopp D. Shealy DB. Carter-Pokras OD.37(2):277-291. Needham LL.31(2):121-125. Sirons G J. Mandel et al. Estimation of occupational exposure to phenoxy acids (2. Developmental toxicity studies in rats and rabbits on 2. Biomonitoring studies of 2. Pesticide residues in urine of adults living in the United States: reference range concentrations. Cole DC. 2005).4:97-100. Brody D. 2005 Charles JM. Kolmodin-Hedman B. 2005.php?record_id=10603.4-D. Harris SA.10(6 Pt 2):789-798.4:427-435.15(6):500-508. National Toxicology Program (NTP).71(2):99-108.60(1):121-131. Veterans and Agent Orange: update 2002. Frank R. Needham LL. Third National Report on Human Exposure to Environmental Chemicals. the number of acres to which it was applied (Curwin et al. Alexander BH. Holler JS. Toxicol Sci 2001. Hein MJ.32(4):233-257.51(3):152-159. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children.nih. Philbert MA. 2006. 2005). In farm families. Harris et al.niehs. Baker BA. Biomonitoring for farm families in the farm family exposure study. Updated March 7.4. Environ Res 1995. Finding a measurable amount of 2. Curwin BD. Kohli JD. Chapman P. Sanderson WT.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. References Arbuckle TE. Garabrant DH.4 dichlorophenoxyacetic acid (2. the amount of pesticide applied.inchem. Fast DM. 2003. Pesticides residues in food: 1996 evaluations Part II Toxicology. van Ravenzwaay B. Assessment of exposure to 2. Solomon KR. Board on Health Promotion and Disease Prevention. International Programme on Chemical Safety-INCHEM (IPCS).4-. Crit Rev Toxicol 2002. Bailey SL. 1992). Arch Environ Contam Toxicol 1989. The pharmacokinetics of chlorinated phenoxy acid herbicides: a literature. Ritter L. Arch Toxicol Suppl 1980. Available at URL: http:// www. Hill RH Jr. Washington (DC): National Academies Press.edu/catalog... 2005. Xenobiotica 1974.4-D and 2. 3/17/09 Institute of Medicine (IOM).4-dichlorophenoxyacetic acid and its forms. Review of 2. Driskell WJ.27(1):23-38. Scand J Work Environ Health 2005. Head SL.18(4):469-474. Tandon JS.4-dichlorophenoxyacetic acid in the chemical industry: results of a five year biological monitoring study. Honeycutt R. et al. 914.4-dichlorophenoxyacetic acid (2. Beeson MD..4-dichlorophenoxyacetic acid (2. Ripley BD. Beasley VR. Available at URL: http:// www.4-D): exposure and urinary excretion. cfm?objectid=06FF8DA6-E5A1-90CD-3F26562CEC5CDDE5.4-D were highest in the farmers who applied the 2. J Toxicol Environ Health 1992. et al. Committee to Review the Health Effects in Vietnam Veterans of Exposure to Herbicides (Fourth Biennial Update. Mandel JS. geometric mean urinary levels of 2. Smith SJ. Dhar MM. Gregg M. Forestry workers involved in aerial application of 2. general population. and the use of protective clothing or equipment (Arbuckle et al.S. J Expo Anal Environ Epidemiol 2000. Erne K.4-D will result in an adverse health effect.4-D) epidemiology and toxicology. To T.Herbicides the time since application. Survival and Growth Curves from NTP Toxicity Studies. Tables. other family members had levels ranging only slightly higher than the 95th percentile levels in NHANES 1999-2000 and 2001-2002 subsamples (CDC.org/documents/jmpr/jmpmono/v96pr04.4-Dichlorophenoxyacetic Acid). Barr DB. TOX-63 Peroxisone Project (2. Hanley TR Jr. Hill RH Jr. Baker SE. Selected pesticide residues and metabolites in urine from a survey of the U. Barr DB. et al.31 Suppl 1:90-97. 3/17/09 Fourth National Report on Human Exposure to Environmental Chemicals 59 . TOX-63: TOXICITY REPORT CURVES.31 Suppl 1:98-104. Vet Hum Toxicol 1989.5-T). 2. J Expo Anal Environ Epidemiol 2005 Nov. Acquavella JF.

Available at URL: http://water.4-D) following oral administration to man. Available at URL: http://www.gov/oppsrrd1/ REDs/factsheets/24d_fs. Toxicology 1977. 60 Fourth National Report on Human Exposure to Environmental Chemicals .S.pdf.S. 2007.EPA). 2. 3/17/09. Washington (DC): U. The fate of 2. Environmental Protection Agency (U. 1992-2001. Braun WH. 3/17/09 U. 4/2/09 U.S. The Quality of Our Nation’s Waters.epa. Environmental Protection Agency (U. gov/oppbead1/pestsales/01pestsales/market_estimates2001.Herbicides Sauerhoff MW.S. May. Gehring PJ.php. Available at URL: http://www. Pesticides in the Nation’s Streams and Ground Water. Office of Prevention Pesticides and Toxic Substances. revised February 15.usgs.4-dichlorophenoxyacetic acid (2.8:3-1U.epa. Pesticide industry sales and usage .gov/nawqa/pnsp/pubs/ circ1291/supporting_info.EPA).4-D RED Facts.htm. Circular 1291. Geological Survey (USGS). March 2006.EPA.S. S. EPA 738 F-05-002. 2004. Blau GE. June 2005. Supplemental Technical Information (available on-line only).2000 and 2001 market estimates.

2005). The geometric mean metolachlor mercapturate was 4. 2003). Metolachlor did not show developmental or reproductive toxicity in chronic animal studies. formulators..S. but another metabolic pathway can produce 2-methyl-6-ethylaniline and its reactive metabolite which may account for observed effects (Coleman et al. Kolpin et al.Herbicides Metolachlor available from U. Additional information is Urinary levels of metolachlor mercapturate reflect recent exposure. Metolachlor is well absorbed dermally. whereas 60% of applicators had detectable amounts. Human health effects from metolachlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown.S.. Metolachlor has low potential for acute toxicity (U. 2003). and eliminated in urine and feces over two to three days (WHO. 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.S. 2003). WHO. sorghum and other crops. Estimated human intakes have been below recommended limits (U. This metabolite is not a marker of exposure to either plant metabolites or environmental degradates of metolachlor which can be present in the environment.EPA. 2000. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Davison et al. 2005. 1995). and field workers may have significant exposures via this route.. Occasionally in the past. 2007.. Urinary levels of metolachlor mercapturate were generally not detectable in the NHANES 2001-2002 subsample.gov/pesticides/.S.. People exposed to metolachlor will excrete metolachlor mercapturate in their urine. mercapturate conjugates were the predominant metabolites.200 μg/L (CDC. Finding measurable amounts of metolachlor mercapturate in the urine does not mean that the levels of metolachlor mercapturate cause an adverse health effect. (2003) showed that 2. Fourth National Report on Human Exposure to Environmental Chemicals 61 . 1995. Metolachlor shows little potential to bioaccumulate but is moderately toxic to fish. Hladik et al. USGS. so applicators. WHO. EPA at: http://www. 1995). 1994. It is absorbed by plants and inhibits plant protein synthesis.2% of a small reference population had detectable metolachlor equivalents by immunoassay in their urine.S. in both ground and surface waters (Battaglin et al. Biomonitoring Information CAS No. 1998). soybeans. metolachlor was quickly absorbed after dermal or oral doses.S. 1999. and it was not mutagenic in mammalian cells (U. EPA. Jefferies et al. including corn. 2000. and on non-crop land for general weed control. though the 95th percentile for males was 0. NTP and IARC do not have ratings regarding human carcinogenicity. Hines et al. Gilliom. 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. lacrimation. In animals. metolachlor levels in water have exceeded lifetime human health advisory levels (U.epa. 1989. U.. Salivation. 1995). and convulsions were observed at lethal doses in animal studies.EPA. Metolachlor or its degradates can leach from soils and have been detected in watersheds of agricultural land.EPA considers metolachlor to be a possible human carcinogen. 2007.7 μg/L in the urine of farmers after they had sprayed metolachlor (Curwin et al..EPA. In animal studies. 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. 2005). General population exposure may occur through the consumption of contaminated food or drinking water. Feng and Wratten.

S.740) 679 700 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.220) < LOD 1192 1346 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.200 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Urinary Metolachlor mercapturate (creatinine corrected) Metabolite of Metolachlor Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. 62 Fourth National Report on Human Exposure to Environmental Chemicals . 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 . < LOD means less than the limit of detection.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. which may vary for some chemicals by year and by individual sample.240) 679 701 957 Limit of detection (LOD.200 (<LOD-.S. 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.Herbicides Urinary Metolachlor mercapturate Metabolite of Metolachlor Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. Survey Geometric mean (95% conf.440 (<LOD-. Survey Geometric mean (95% conf.670 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.2.

Curwin BD.gov/nawqa/ pnsp/pubs/wrir984245/text.usgs. Comparative metabolism of chloroacetamide herbicides and selected metabolites in human and rat liver microsomes.37(4):10881093. Sacramento. Atlanta (GA). Environ Health Perspect 2000. Burkhardt MR.html. Environ Sci Technol 2007. Barr DB.who. Gillion. Feil VJ. acetochlor. World Health Organization (WHO). 4/2/09 U. Shoemaker DA. The Quality of Our Nation’s Waters Pesticides in the Nation’s Streams and Ground Water. Roberts AL.gov/nawqa/pnsp/pubs/circ1291/ supporting_info.Herbicides References Battaglin WA. Brown KK.41:3409-3414. Larsen GL. Furlong ET.usgs. Available at URL: http://water. Thurman EM. Reynolds SJ. Wratten SJ. Centers for Disease Control and Prevention (CDC). In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor.pdf.248(2-3):123-133. Linderman R.pdf 3/30/09 Hines CJ. Available at URL: http://www. U. Sci Total Environ 2000. et al. 3/26/09 U. Environmental Protection Agency (U. Geological Survey (USGS).15(6):500-508. et al. Hladik ML. Biagini RE. Barr JR. R.11(4):353359. Comparative metabolism and elimination of acetanilide compounds by rat. April 1995. Reregistration Eligibility Decision (RED) Metolachlor. J Agri Food Chem 1989. Supplemental Technical Information (available on-line only). Alavanja MC. Barr DB. Camann DE. Striley CA.24(10):1003-1012. Finding minimal herbicide concentrations in ground water? Try looking for their degradates. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. Geological Survey (USGS).S.S. Sci Total Environ 2000. Available at URL: http://water.epa. imidazolinone. 2007.gov/oppsrrd1/ REDs/0001. Environ Health Perspect 2003. Kolpin DW.int/water_sanitation_health/dwq/chemicals/ metolachlor. 1992-2001. Quistad GB. and metolachlor herbicides in rats.gov/nawqa/pnsp/pubs/files/051507. 2003.S. 1999. Third National Report on Human Exposure to Environmental Chemicals. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. Occurrence of sulfonylurea. Heederik D.108(12):1151-1157. sulfonamide. Hodgson E.php. usgs.47(6):503-517. Davison KL. Water-Resources Investigations Report: Distribution of Major Herbicides in Ground Water of the United States Water Resource Investigations Report No. Gilliom RJ). Xenobiotica 1994. Kinney PL. Kolpin DW. Ann Occup Hyg 2003. California. Environ Sci Technol 2005.248(2-3):115-122. 3/27/09 Fourth National Report on Human Exposure to Environmental Chemicals 63 .S. 6/1/09 Whyatt RM. EPA). Linhart SM. 98-4245 (by Barbash JE. Hsiao JJ. Sanderson WT. reservoirs and ground water in the Midwestern United States. revised February 15. Background document for development of WHO Guidelines for Drinking-water Quality. Available at URL: http://water. Deddens JA. J Expo Anal Environ Epidemiol 2005. Feng PCC. March 2006. 2005. Hein MJ. Casida JE. Available at URL: http://www. and other herbicides in rivers. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. Peter CJ. Circular 1291. Pesticides in U. Rose RL.111(5):749-756. streams and groundwater. Andrews HF.ESTfeature_gilliom. Thelin GP. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. Coleman S. Dialkylquinonimines validated as in vivo metabolites of alachlor. Chem Res Toxicol 1998. Jefferies PR.S.pdf. Metolachlor in Drinkingwater. EPA 738R-95-006.39(17):6561-6574. 1998. Ward EM.

renal and hepatic injury. dizziness. Given the commercial unavailability of 2. Survey Geometric mean (95% conf. Although 2.2 and 0. Agent Orange).5-T was once applied as either an aqueous salt or as an oil-soluble ester. 1992.4.5T is rapidly absorbed via oral and inhalation routes. Once absorbed into the body. with an elimination half-life of approximately 19 hours (Arnold et al.4.5-T) is a chlorophenoxy acid herbicide that is no longer registered for use in the United States..4. 1974).4.g. 93-76-5 General Information 2. and concern about contamination with 2.. 1989.5-Trichlorophenoxyacetic acid (2. with the exposure to chlorophenoxy herbicides as defoliants Urinary 2.1. Teratogenic and developmental effects have been reported in studies of multiple rodent strains treated with high doses of technical grade 2..5-trichlorophenol and other degradates. 64 Fourth National Report on Human Exposure to Environmental Chemicals .4. population from the National Health and Nutrition Examination Survey. 2. Kohli et al. ranging from several weeks to many months. 1986.4. Chlorophenoxy herbicides act as plant growth hormones.5-T and 2.5-T degrades to 2. Nelson et al. The half-life of 2. 1992).4.7. see Data Analysis section) for Survey years 99-00 and 01-02 are 1. it is not well absorbed through the skin.5-T (Holson et al.4. which may vary for some chemicals by year and by individual sample. nausea.5-T has been rarely detected in ground waters (USGS.4.5-T.4.5-T is eliminated mostly unchanged in the urine. 2. abdominal pain. but higher levels are herbicidal. the general population is unlikely to be exposed to it.. these herbicides can enhance plant growth.4. < LOD means less than the limit of detection.5-Trichlorophenoxyacetic acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. 2004).4. Epidemiological studies have reported associations of several types of cancer. 2. myotonia. Human health effects from 2. Omer.4. hypotension. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 2.5-Trichlorophenoxyacetic Acid CAS No. Mohammad and St.3..4. such as soft tissue sarcoma and non-Hodgkin’s lymphoma. 2007)..4. Intentional overdoses and unintentional high dose occupational exposures to chlorophenoxy acid herbicides have resulted in weakness.5-T in soil varies with conditions.4-D were used as defoliants in the Vietnam War (e. and delayed neuropathy (Bradberry et al.4. headache. 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. At low levels.5-T at low environmental doses or at biomonitored levels from low environmental exposures are unknown.8-tetrachlorodibenzo-p-dioxin (TCDD) led to the discontinuation of 2.S. Ester forms of 2.5-T use as a herbicide in 1985.Herbicides 2.

3. 2003.5-T does not mean that the level will result in an adverse health effect. Biomonitoring Information Urinary levels of 2.5-T than levels found in the general population.4. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.4.5-T were generally below the limit of detection. or to contaminants in the herbicide formulations (specifically 2. IPCS. IOM.4.5-T also were below the limit of detection (Kutz et al. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1814 2537 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 430 580 618 830 766 1127 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 891 1192 923 1345 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 652 679 483 700 531 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.epa. 2005). Mean urinary levels of 2.4. in which urinary levels of 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.4.5-Trichlorophenoxyacetic acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. Pearce and McLean.4. Survey Geometric mean (95% conf. urinary levels of 2.7.4.4.S.5-T itself is not mutagenic. Urinary 2. 2005.5-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 2.5-T reflect recent exposure. population from the National Health and Nutrition Examination Survey. similar to results of NHANES II (19761980). 2002. It is unclear whether these associations are related to the chlorophenoxy herbicides. In the NHANES 1999-2000 and 2001-2002 subsamples (CDC.8-tetrachlorodibenzop-dioxin) (Garabrant and Philbert. other exposures. Fourth National Report on Human Exposure to Environmental Chemicals 65 .S.EPA. Biomonitoring studies on 2. 1992).4. Finding a measurable amount of 2. IARC considers the chlorophenoxyacetic acids group of chemicals as possibly carcinogenic to humans.000 times higher than the detection limit for the NHANES 2001-2002 data (Kolmodin-Hedman and Erne.S. U. 1996. 2. Additional information is available from U. 1980). 2004).Herbicides or contaminated herbicides..5-T measured after a day of exposure in a few asymptomatic herbicide applicators were 35.gov/pesticides/.EPA at: http://www.

Vet Hum Toxicol 1989.19(2):298-306.4:318-21. et al. Agricultural exposures and non-Hodgkin’s lymphoma.EPA. McLean D. Wolff GL.S. Available at URL: http://www. Fundam Appl Toxicol 1992. discussion 5-7. Veterans and Agent Orange: update 2002. Multireplicated dose-response studies in four inbred strains and one outbred stock of mice.5-trichlorophenoxyacetic acid (2. Developmental toxicity of 2. Khanna RN.23(2):65-73.EPA). Available at URL: http:// www.4-D/2. II.4-.5-T in four-way outcross mice.4-D) epidemiology and toxicology. et al. Dhar MM.5-trichlorophenoxy acetic acid in man. Scand J Work Environ Health 2005. May. Dichlorophenoxyacetic acid. Environmental Protection Agency (U. Arch Int Pharmacodyn Ther 1974.epa. Murphy RS. Gaylor DW. 3/17/09 Institute of Medicine (IOM). Nelson CJ. Absorption and excretion of 2.5-T). St Omer VE. 210:250-255. International Programme on Chemical Safety-INCHEM (IPCS).5-trichlorophenoxyacetic acid (2. Review of 2. Vale JA. Nelson CJ.4. 2004. Gaines TB. Centers for Disease Control and Prevention (CDC). S. Sircar KP. Erne K.S. LaBorde JB. Mohammad FK. Washington (DC): National Academies Press. The pharmacokinetics of chlorinated phenoxy acid herbicides: a literature. Beasley VR.4. Garabrant DH.5-T). Atlanta (GA). Board on Health Promotion and Disease Prevention. Fundam Appl Toxicol 1992. Proudfoot AT. Committee to Review the Health Effects in Vietnam Veterans of Exposure to Herbicides (Fourth Biennial Update.4. Philbert MA. Pesticides residues in food: 1996 evaluations Part II Toxicology.nap. Washington (DC): U.4.org/documents/jmpr/jmpmono/v96pr04. Poisoning due to chlorophenoxy herbicides. Estimation of occupational exposure to phenoxy acids (2. Cook BT. Behavioral and developmental effects in rats following in utero exposure to 2. Crit Rev Toxicol 2002. Pesticide industry sales and usage . Third National Report on Human Exposure to Environmental Chemicals.37(2):277-91. Neurobehav Toxicol Teratol 1986. 914. Multireplicated dose-response studies with technical and analytical grades of 2.S. general population.edu/catalog.5-T).4. Gaines TB. 3/17/09 Kohli JD. I.32(4):233-257.31 Suppl 1:1825. Kutz FW.Herbicides References Arnold EK. Arch Toxicol Suppl 1980.8(5):551-60.pdf.4-dichlorophenoxyacetic acid (2.php?record_id=10603. Gupta BN. 3/17/09 66 Fourth National Report on Human Exposure to Environmental Chemicals .4. Office of Prevention Pesticides and Toxic Substances. Holson JF.4-D and 2. Bradberry SM. LaBorde JB.19(2):286-297. Developmental toxicity of 2. Brody D.5-t mixture. gov/oppbead1/pestsales/01pestsales/market_estimates2001. Selected pesticide residues and metabolites in urine from a survey of the U. Kolmodin-Hedman B. Tandon JS. McCallum WF. J Toxicol Environ Health 1992. 2.4.31(2):121-125.htm. Available at URL: http:// www. Toxicol Rev 2004.2000 and 2001 market estimates. Carter-Pokras OD. Pearce N. 2003.4. U.inchem. 2005. Sheehan DM. Holson JF.

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

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

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

7 (14.3 (19.5 (16.5-15.202) 539 456 484 487 980 885 < LOD means less than the limit of detection for the lipid adjusted serum level.80 (<LOD-10.7-19.4) 21.060) .1-18. Survey years 01-02 03-04 Geometric mean (95% conf.170) .093) .130-.4) 14.110 (.9 (13.096-.077-.180) .5-17.117) < LOD .110) .090 (<LOD-.089 (.190) .112-.109-.139 (.138) .100-.140) .7 (15.4 (12.054-.100-.103 (.090 (.080) .8-19.090-.120 (.4-18.113 (.4-17.1) 15. < LOD means less than the limit of detection.140-.064 (.180) .2-15.4) 539 456 484 487 980 885 Limits of detection (LOD.130-.150 (.4) 20.130) .109-.8) 15.9-23.110 (.9 (13.8 (9.177) Sample size 2159 1952 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD .140 (.138 (.0 (11.90) 90th 15.055 (.30 (8.120 (.110) .60-10.160 (.70 (7.8 (18.3 (13.086-.120) .112) 95th .7) 15.102 (.070-.0 (10.100) .9 (12.120-.120 (.064) 90th .3 (14.048 (<LOD-.S.1) < LOD 9.6-24.5) 15.30 (8.8) 14.6-33.7) 716 587 1443 1365 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD 9.7 (<LOD-15.4) 95th 20.4) < LOD < LOD 16.9 (14.8-17.6 (14.9-38.8) < LOD 8.00 (8.3-21.049-.8-24.1) 14.059 (.182) 716 587 1443 1365 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD . see Data Analysis section) for survey years 01-02 and 03-04 are 10.062-.073-.100) .4) 19.1) 20.0) < LOD 9. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.8-17.090-.1-19.2) 12.80-9.1-24.0) 19.7-22.075) < LOD .0 (15. * 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.0 (10.108-.147 (. population from the National Health and Nutrition Examination Survey.6 (15.80-10.139 (.50) 15.070 (<LOD-.190) .160) .069) < LOD < LOD .062 (.083-.50 (8.130-.5) 21.9 (12.8.098 (.0-25.5 (<LOD-11.124) .130 (.1 (18.6) 9.080 (.8 (11.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-. Fourth National Report on Human Exposure to Environmental Chemicals 79 .0-21.4 (12.084-. Survey years 01-02 03-04 Geometric mean (95% conf.5) 19.158) .110 (.100-.149) .088-.100 (.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 .2) 11.3 (18. which may vary for some chemicals by year and by individual sample.1-16.2) Sample size 2159 1952 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD 10.109 (.063-.103 (.080-.40-10.40-9.090-.242) .2) 14.0) 21.8-25.058) < LOD .6-24.6 (15.1 (13.160 (. population from the National Health and Nutrition Examination Survey.054-.6) 16.00-14.062 (.10 (<LOD-16.4) 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. 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 9.101) . 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 .9-22.3 (18.1) 13.150 (.5-17.130) . Serum Dieldrin (whole weight) Also a Metabolite of Aldrin Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U.054-.2) 15.1) 15.130) .077 (.6) 19.070) .S.053 (<LOD-.1) 10.5 and 7.056-.116) .

Jorgensen T. Roy ML. Part A 2000. Aldrin and dieldrin: A review of research on their production environmental deposition and fate. Brock JW. Chapin RE.66(4):229-234. Kitzazwa M. PA. Ginsburg KS. Cancer Epidemiol Biomarkers Prev 2000. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.47:1059-1087.91(1):122-126. Sonnenschein C. Environ Health Perspect 1995. 1989. Psychopharmacology (Berl) 1987. Jr. Effect of occupational exposure to aldrin on urinary D-glucaric acid. 2 Classes of Pesticides.html. Pesticides in the Nation’s Stream and Ground Water. Evaluation of epidemiologic and animal data associating pesticides with Parkinson’s disease. 6/1/09 Ward EM. Six high-priority organochlorine pesticides. J Occup Environ Med 2005. pp. Turner W. Olea N.cfsan. J Toxicol Environ Health 1989. Corrigan FM.fda. Wienburg CL. 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. Narahashi T. Priestly BG. Patterson DG Jr.14:95-102. McIntosh LJ.org/documents/ehc/ ehc/ehc91.gov/toxprofiles/ tp1. Needham LL. Exp Neurol 1998. Buckland SJ. 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. Garrett N. Available at URL: http://www.gov/ circ/2005/1291/. Sodium and GABA-activated channels as the targets of pyrethroids and cyclodienes. August 2008. Grajewski B. Reprod Toxicol 2000. Chung KL. Mann D. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. 15. J Toxicol Environ Health. are nonestrogenic in transfected HeLa cells. Ellis H. Lancet 1998. either singly or in combination.54:1431-1443. plasma dieldrin. and lymphocyte sister chromatid exchange. Sanchez-Ramos J. 2007 [online]. Stehr-Green. Environmental Health Criteria 91. David VL. Cox. The E-SCREEN assay as a tool to identify estrogens: an update on estrogenic environmental pollutants. et al. New York. References Agency for Toxic Substances and Disease Registry (ATSDR). Shore RF. bioaccumulation. Anantharam V. Toxicological profile for aldrin/dieldrin [online]. Facca A. Dieldrin-induced neurotoxicity: relevance to Parkinson’s disease pathogenesis.64-65 Spec. Smith AG. Eds. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. Schulte P. Mink PJ. Daniel SE.Organochlorine Pesticides in the NHANES 2001-2002 and 2003-2004 subsamples (Edwards and Priestly 1994).htm. International Programme on Chemical Safety (IPCS). In Hayes WJ. 4/21/09 Hoyer AP. Basit A.html. 4/21/09 Jorgenson JL. No:429-436. Kanthasamy A. et al. Organochlorine exposure and risk of breast cancer. Teta MJ. Fernandez MG.352:1816-1820. Carlson JN. Serrano FO. Toxicol Lett 1992. Serum organochlorine levels and breast cancer: a nested case-control study of Norwegian women. Chlorinated Hydrocarbon Insecticides. Mumtaz MM.gov/~dms/ pesrpts.150:263-271. Food and Drug Administration (FDA). Toxicity of dieldrin for dopaminergic neurons in mesencephalic cultures.9:1357-1367. Vol. Aldrin and Dieldrin [online]. 4/21/09 Bates MN. Rosellini RA.109(Supp1):113-139. Soto AM. 1992-2001. and epidemiology in the United States. Andersen A. Frey JM. Chemosphere 2004. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods.usgs. Available at URL: http://www. VT. Environ Health Perspect 2001.59:229-234. United States Geological Survey (USGS).cdc. 1991. Demographic and seasonal influences on human serum pesticide residue levels. Available at URL: http://pubs. Revised Feb. Int Arch Occup Environ Health 1994. Hartvig HB. Song S. Exposure to low doses of the environmental chemical dieldrin causes behavioral deficits in animals prevented from coping with stress.26:701-719. Kanthasamy AG. Finley B. toxicology. 731-915. Academic Press. Li AA.103(Suppl 7):113-122. Neurotoxicol 2005.inchem.atsdr. September 2002. Jr and Laws ER. 80 Fourth National Report on Human Exposure to Environmental Chemicals .27:405-421. Available at URL: http://www. Organochlorine insecticides in substantia nigra in Parkinson’s disease. Tully DB. Patterson DG Jr. Inc. Edwards JW. Handbook of Pesticide Toxicology. Grandjean P.

4) 18.5) 10.2) 22. 2007).9 (26.5-42.2 (21.7) 42.8-61.S.6) 9.9) 11.9) 39.2-26.9-21.1 (<LOD-12.1 (44.9-42.8) 27.8-33.0 (26.0) 31.0) 75th 20. 57-74-9 Heptachlor CAS No.2) 33.2) 36. which may vary for some chemicals by year and by individual sample.5) < LOD < LOD < LOD < LOD 13.3-45.5) 628 557 462 350 501 493 559 1031 898 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.7 (17.4 (10.8) size 1661 2249 1978 Total years 99-00 01-02 03-04 50th < LOD 11.2 (41.8-43.1-19.9) 11.4) 39.8) 53.1-15.8) 18.4 (31.2 (9.0-12.0 (16. chlordane was used to kill termites and other insects on agricultural crops.8 (10.7-56.5) 38.3) 37.6-24. 2007).4 (35. population from the National Health and Nutrition Examination Survey.9) 36.7) 9. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.2 (10.5 (34.6 (43.4) 22.2-49.1) * 11.20-10.8.1 (40.6 (25.7 (10.5 (33.2) 46.7-12.1-65.0-18.1 (27. Until 1988.8-73.37 (8.3) 10.5-65.9) 13.0 (37.6) 9.5) 21.5-44.2) < LOD 11. 1994.3-43.0 (20.1 (<LOD-12.6) < LOD 11.5) 44.1 (25.9 (21. and in soil.4) 29.10 (8.7 (<LOD-13. from the early 1950’s until the mid-1980’s.7 (32.6-24.9 (18.9 (31.8 (40.6 (16. As a result of the manufacturing process.3-24.1-25.8-32.1 (17.7 (43.0 (32.8 (17.5 (31. 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.7 (34.8) 663 752 595 998 1497 1383 20 years and older Gender Males 99-00 01-02 03-04 * 11.5-41.7 (<LOD-32.3-45.0-13. lawns.10-18.6 (9.6) 8.6) 23.S.5-47.0) 21. and dairy products are the usual sources of exposure to these chemicals in the general population.1) 22.6 (9.9-21. Heptachlor and chlordane and their metabolites bioaccumulate in fatty animal tissues.9 (11.9 (36.0-25. Technical grade chlordane had contained 7% trans-nonachlor.4 (<LOD-12.3-49.1 (20. Chlordane is not currently produced or used in the U. the technical grade product of each chemical contains 10%-20% of the other chemical. see Data Analysis section) for Survey years 99-00.4 (30.6) 48.74 (<LOD-10.82-11.0) 41. 01-02.30-11.3) 10.9) 31.1) 90th 34.0-33.7-14.36-11.1) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * 12.9 (11.4-40.8 (18.4) 37.20-11.1) 30. Both of these chemicals and their metabolites can cross the placenta and are excreted into breast milk.8 (42.6) 36.2 (37. in addition to trace amounts of numerous other related compounds (ATSDR.1 (16.6-53.8-33.10-11.89-10.8-20.5) 37.1-51.3 (11. fish.8) 44.6) 20.4-21. and 7.5) 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 * * * * 11.9 (15.3 (20.0-67.7) 31. 1994).20 (<LOD-11.1-50.70 (<LOD-10.2-21.1) 30.3 (26.7 (19.8-23.2 (36.6) 49.5 (8.6) 11.8) 52.7) 19.6) 39.5.7-70.3) 18.0) 20.1-25.4-51.9-38.1) 16.9 (15.3) 41.9) 23.2) * 12.2) 34.6-45.5-40.5 (41.9) 47. Survey Geometric mean (95% conf.8 (17.9 (29.2-28.69-10.5) < LOD < LOD 9.9) 23.9) 17.0) 27.6-12.S.5-38.7) 19. 76-44-8 General Information Chlordane and heptachlor are structurally related organochlorine pesticides and were used in the U.6) 48.5-32.5) 9.8 (10. heptachlor use has been limited to treatment of fire ants near power transformers. foods high in fat such as meat.8) 52.7) 28.Organochlorine Pesticides Chlordane CAS No.9) 37.1 (15.. buildings.9-40. < LOD means less than the limit of detection.4-14.7 (34.1) * 11.2 (39.8-42.1 (11. interval) Selected percentiles ( 95% confidence interval) Sample 95th 44.3 (27.7) 35.90 (8.1) < LOD < LOD < LOD < LOD < LOD 8.3-32.0-61.4) 12.5.2-49.6-18.2) < LOD 11. Since 1992.0 (<LOD-12.5 (<LOD-12.4-45.9) 10. and 03-04 are 14.3 (28.63 (8. 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. Fourth National Report on Human Exposure to Environmental Chemicals 81 .2-56.4 (22.3) 18.3 (<LOD-19.4) < LOD < LOD < LOD 23.2) 37.5-43.3 (9. Consequently.7-39.7-25.0) 37.3 (21.5) 56. respectively. Heptachlor was used as a soil and seed treatment and for termite control in and around buildings until 1988. 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.3 (25.4) < LOD 11.9 (26.4 (30.9 (17.7 (42. 10.8-31.2 (28.1 (<LOD-12.5-13.

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 * * * * .227) < LOD . 82 Fourth National Report on Human Exposure to Environmental Chemicals .130-.170-.070-.410) .220-.092) . and alterations in immune function of offspring.070-.320) .080 (.207) .070 (<LOD-.240-. and inhalation exposure. 1986).320 (.200-. 2006).133) 90th . The U.310) .280) .066 (.280-.140 (.055-.160) .Organochlorine Pesticides (Dallaire et al.168-.290) .200 (. which may vary for some chemicals by year and by individual sample. and heptachlor epoxide in foods and bottled water.115-.204 (.280-.320 (.290-.250 (. chronic doses of heptachlor have produced liver enlargement and injury. Rogan.074-.200-.330 (.300-. 1977a.130 (. Takahashi et al. Acute.230) .150 (.S.450) .140) .106-.062) < LOD .210-.286 (.207 (.140 (.302) .250 (.370 (. Chronic feeding studies with either chlordane or heptachlor have demonstrated reduced fertility.271 (.066 (<LOD-.080) . Elimination of all these chemicals from the body occurs over months to years.100-.200-. high doses of either chlordane or heptachlor block inhibitory neurotransmitters and result in central nervous system toxicity.063) .286 (.120-.130) .063) * .050 (<LOD-.340) .350 (.068) . dermal.130-. IARC.108-.260 (.225 (.430) . 2002.150 (.400) .062) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * .208 (.270 (.083 (.370 (.280-.190-. Epidemiologic studies have not demonstrated teratogenic or developmental effects (Baker et al.220-.065-.063 (.090-.077) .270 (.057) * .300 (.130 (.063-.058-. heptachlor.280 (.300) .560) .100 (.160) .269 (...070 (<LOD-.230 (. both chlordane and heptachlor induced hepatic cytochrome P450 enzymes and increased the incidence of liver tumors (NTP.064) < LOD .140-.110-. to heptachlor.128 (.070-.203-.199-.150 (.180-. 1991.082 (. 2001. Survey Geometric mean (95% conf.290-.400) .170) .136) .077) .104-.070 (<LOD-.310) .063 (.220 (.130 (.069 (<LOD-. neonatal mortality. interval) Selected percentiles ( 95% confidence interval) Sample 95th .070 (.057-.130-.053-.360) .083) .370 (.250-.190-.260 (.126) .070) .160) . Shindell and Ulrich.047 (<LOD-.104) .310) .320) .060 (<LOD-.068-.130-.380) .240-.300) .258 (.240) .126 (.110 (<LOD-.087-. 1986).058-.112 (.150) .450) . Chlordane and heptachlor are absorbed after oral.067 (. 1981).290) . No clear evidence of excessive cancer rates was demonstrated in human epidemiologic studies (ATSDR.291) size 1661 2249 1978 Total years 99-00 01-02 03-04 50th < LOD .300) .300) . and the U.270 (. 1977b.230 (.048-. Smith.120-.148-. and breast milk is a major excretion route in lactating women.315 (.231) .223) .148) .071 (.290-.130-.053-.091) ..320) 663 752 595 998 1497 1383 20 years and older Gender Males 99-00 01-02 03-04 * .150-.149 (.160 (. 1996.350) .050-. EPA has established environmental criteria for chlordane and heptachlor.260 (.210 (. Le Marchand et al.216-.146) < LOD < LOD .180) .230-.189 (.165-.100 (<LOD-.S.130) .320 (.510) . In laboratory animal studies. IARC considers chlordane and heptachlor as possibly carcinogenic to humans.120-.068) 75th . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.246-.079) < LOD < LOD < LOD .140 (.180) . OSHA has established occupational exposure criteria.077) . 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.440) .170) .058 (.280 (.287) .320 (.430) .213) * .080) .075 (.070 (<LOD-.140-.140 (.080) .258-.090) . The major metabolite of heptachlor is heptachlor epoxide.S.146) .230-.170) .230-.120 (.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.080 (. characterized by seizures and paralysis. Subtle neurodevelopmental effects have been observed rodents after prenatal exposure to heptachlor (IPCS.180-.310 (.073) < LOD < LOD < LOD < LOD .170) .063 (.190-.210 (. and NIOSH and ACGIH have recommended workplace exposure levels for each pesticide.245-.057 (.348) .073 (.079) .373) .350 (. 2007).077) .076) < LOD . Chlordane is metabolized primarily to oxychlordane and to a lesser extent.170) . 1991).056 (.049 (<LOD-.340) .310-.115 (. which is also persistent in the body (ATSDR.063 (.066-. FDA established allowable residues of chlordane.066-.189-.100-. Human health effects from either chlordane or heptachlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown.290 (. population from the National Health and Nutrition Examination Survey..240 (.260-.119 (.253-.070) < LOD < LOD < LOD < LOD < LOD . 2007.090) .242-.061-.

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

5) < LOD 14.20 (<LOD-9.3) 18.9-29. respectively.2-27.3) 10.3 (13. population from the National Health and Nutrition Examination Survey.1 (16.8 (15.8-24. and 7.0-16.6) 14. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.1-38.2 (18.9-25.6 (16.5 (18.1) 23.2 (<LOD-62.4) 18. 84 Fourth National Report on Human Exposure to Environmental Chemicals .6-21.2-16.2) 15.8 (13.5 (<LOD-32. interval) Selected percentiles ( 95% confidence interval) Sample 95th 24.6-17.9) * * * 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 8.2 (<LOD-25.5 (10.6 (16. 10.4 (<LOD-54.6 (12.9) 15.S. see Data Analysis section) for Survey years 99-00.8) 19.8-24.8.4 (11.8 (18.9 (15.5) 760 1047 956 829 1212 1007 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 7.3-18.5) 598 553 460 336 503 490 539 1041 888 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.4 (11.6.6) 22.1-29. < LOD means less than the limit of detection.3) 23.9-23.8) 13.0-19.0) 638 741 592 951 1518 1371 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 13.40) 15.7 (10.9-16.6 (8.7-25.8) 16.90 (<LOD-9.0) 13. Survey Geometric mean (95% conf.0) size 1589 2259 1963 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th 90th 15.2 (<LOD-16.8) 14.3) 27.2-17.2) 13.8) 20.6 (14.8 (13.5.7-18.6 (13.3) 18.8 (18.3) 16.2) 26.0 (11.6 (11.1 (19.0-17.4) 21.8-23.Organochlorine Pesticides Serum Heptachlor epoxide (lipid adjusted) Metabolite of Heptachlor Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U.9-29.10-13.7 (13.50) < LOD < LOD < LOD 17.1) 20.5 (11.9 (12.8-24. 01-02.8 (<LOD-23.6) < LOD < LOD < LOD 27.7-19.3 (<LOD-25.1-16.5) 19.0-54. and 03-04 are 14.0 (15.6) 13.8) 15. which may vary for some chemicals by year and by individual sample.7 (16.2-27.4 (<LOD-19.8) 19.5 (<LOD-21.1) 13.1-15.8) 13.8-46.0-17.4 (15.8) 14.8) 21.3) 22.2) 20.6 (<LOD-27.3) 18.5 (11.

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

8 (26.3-86.86-13.1) 17.5) 48.0) 75th 31.7-77.7-35.8 (16.1) 14.0-68.8-19. population from the National Health and Nutrition Examination Survey.1-55. Survey Geometric mean (95% conf.6 (56.5-20.2 (15.8-129) 74.2 (19.1 (65.2) 17.8 (19.0 (48.5 (44. and 03-04 are 14.7-20.8 (30.6-19.8 (45.6 (12.8 (11.8 (13.0) 33.8.9-69.5) 14.0 (16.8 (13.0-93.3) 15.3) 32.9-65.1-22.6 (56.3) 30.9) 922 1062 955 1011 1224 1000 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 * 11.7-29.5) 9.2 (27.8) 19.7-22.2) 34.2) 39.3-58.7 (59.9) 14.9 (19.4) 59.5-17.4-36.9-45. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.0 (16.1-34.2) 59.7 (30.9-40.9 (15.4-52.6 (32.4 (30.1 (47.7-34. see Data Analysis section) for Survey years 99-00.7 (18.7 (16.5 (15.6-88.3-57.7-32. respectively.8 (26.6) 34.1) 17.0) Selected percentiles ( 95% confidence interval) Sample 95th 79.2 (25.9-89.0) < LOD < LOD 8.5-19.4 (28.3 (14.0) 40.3-74.5 (25.6 (52.7-160) 86.2-18.9 (36.8 (28. interval) 18.S.3) 25.6) 10.2-37.2-21.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.3) 30.9 (51. 86 Fourth National Report on Human Exposure to Environmental Chemicals .5) 36.0 (19.1) 18.5 (45.0-38.9-22.5-95.7 (13.0) 13.1-126) 67.1 (41.3 (14.4) 16.1) 32.4) 107 (84.6) 25.2-18.5-69.3-50.9-65.8 (15.0-23.6-20.4-22.1) 78.0-20.1-16.9) 14.5 (15.3 (49.4) 55.0 (15.1) 17.8-21.7) 73.2-23.3) 36.1) 17.0 (13.2 (14.5) 77.2-88.8 (42.7) 35.0 (42.6-82.9) 51.3) 19.4-23.5) 22.8 (28.1-51.4 (67.9 (66.9 (<LOD-14.9-58. and 7.9 (51.0 (29.7) 78.6 (50.6 (16.8-79.5 (13.7-17.1) 62.7) 78.6 (<LOD-14.4 (45.2) 19.9 (28.6-54.0-37.9 (16.6) 82.8) 80.8 (17.2 (64.1 (22.9-64.1) 31.3-39.1) 30.0-93.6) 56.0-113) 68.3) 16.4 (16.6-66.10 (<LOD-11.6) 13.2 (7.3) 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.5-111) 68.7-18.2 (59.2 (60.7-23.1) 18.1-20.7) 56.5) 78. 10.8 (26.5) 19.5-87.5) 26.7 (35.3-32.3-30.2) < LOD 10.8-90.6-22.1-16.6) 54.2-17.8 (12.8 (71.8 (49.6) 60.9) < LOD < LOD < LOD 20.1 (17.0) 18.2 (14.3 (58.5-36.2-16.5) 90th 55.8-19.8) 51.4-35.8-16.4) 20.3) 32.9-36.3) 18.4-62.9 (15.8 (<LOD-20.7) 28.2) 30.7-38.9 (47.1 (48.5.1) 17.7) 14.1) 78.0) 664 758 589 1269 1528 1366 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 17.0-143) 112 (68.7 (74.4) 48.0 (60.8-16.1) 16.70 (<LOD-12. which may vary for some chemicals by year and by individual sample.6 (57.8-67. 01-02.7-21.4-18.0 (13.2) 20.8-90.5) 35.5) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * 20.8-41.3 (17.0 (15.8) 47.7 (11.7) 17.7 (28.2 (36.7) 15.5.1) 17.1-18.7) 52.6) 84.3) 18.0-24.7-113) 68. < LOD means less than the limit of detection.0 (42.1-34.2 (26.6 (15.8-77.4) 19.7 (59.4 (12.4-67.1 (10.8-110) 59.1) 17.0 (62.3-21.9) 51.9 (29.9-20.5) 30.5) 14.0-22.5) 20.8 (28.0-23.0 (14.1-28.0-123) 74.4 (11.3 (45.0-59.6) 56.0) 49.9-35.7) 59.3 (16.3 (56.3) size 1933 2286 1955 Total years 99-00 01-02 03-04 50th 17.0) 19.

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

Mortality of workers employed in the manufacture of chlordane: an update.org/documents/iarc/ vol79/79-12. Toxicological profile for heptachlor and heptachlor epoxide [online]. 1993. 4/21/09 Dallaire F. Tartter P. Trends in birth defects for a Hawaiian population exposed to heptachlor and for the United States. Granath F.gov/toxprofiles/tp31.nih. Sci Tot Environ 2006. Arch Environ Health. Bioassay of heptachlor for possible carcinogenicity.110:617-624. Organochlorine exposures and breast cancer risk in New York City women. Gilman A. Inc. Stehr-Green P. Dewailly E.8:1-123. Environ Health Perspect 2002. Chlordane and heptachlor [online]. organochlorine pesticides and polybrominated diphenyl ethers in human umbilical cord serum. 79. Evaluation of human exposure to the heptachlor epoxide contamination of milk in Hawaii. Eds. Available at URL: http://www. et al. Poland. et al. Organochloride pesticide residues in human milk in Hawaii. Circumpolar maternal blood contaminant survey. Bleiweiss IJ. Pollutants in breast milk. 88 Fourth National Report on Human Exposure to Environmental Chemicals . Takei G. Available at URL: http://ntp. Bioassay of chlordane for possible carcinogenicity. et al. Dewailly E. Environ Health Perspect 2002. 4/21/09 Baker DB.28:497501. Chlorinated Hydrocarbon Insecticides. Handbook of Pesticide Toxicology. 4/21/09 James RA. Barker J.nih. Wong L. Covaci A.org/site/foundation/ research/projects2. Glynn AW.html. 1986.pdf. Charles MJ. 6/1/09 National Toxicology Program (NTP).atsdr. Hansen JC.84:151-161. Natl Cancer Inst Carcinog Tech Rep Ser 1977b. et al. Willman E.110(8):835-838. Aune M.Summaries & Evaluations. Vol. August 2007. Senie R. Keller JA. JAMA 1988. Brower S. Available at URL: http://ntp. Siegel BZ.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR).htm. 4/21/09 Agency for Toxic Substances and Disease Registry (ATSDR). Distribution of polychlorinated biphenyls.pdf.gov/ntp/ htdocs/LT_rpts/tr008. Jaraczewska K. 1979-1980. LeMarchand L. An evaluation of serum pesticide residue levels and liver function in persons exposed to dairy products contaminated with heptachlor. Atuma S. Odland JO. Temporal trends of organochlorine concentrations in umbilical cord blood of newborns from the lower north shore of the St. Dendle WH. 2006. Jr. May 1994. Available at URL: http://www. Head SL. Determinants of serum polychlorinated biphenyls and organochlorine pesticides measured in women from the child health and development study cohort. Saidein D. Smith AG. Organochlorines in Swedish women: determinants of serum concentrations. Kolonel LN.cdc.cdc. Natl Cancer Inst Carcinog Tech Rep Ser 1977a. Chashchin V. New York.atsdr.htm.372:20-31. Bull Environ Contam Toxicol 1981:27:506-511.259(3):374-377. Vol.111:349355.inchem. Takahashi W. Baker DB. Academic Press. Berkowitz GS. Van Oostdam JC.inchem. Toxicological profile for chlordane [online]. Drews K.gov/ntp/ htdocs/LT_rpts/tr009. Muckle G. Lulek J. maternal serum and milk from Wielkopolska region.org/ documents/cicads/cicads/cicad70.50(3):108-118.niehs.150:981-990. KalubaSkotarczak A.330:55-70. 1994-1997 organochlorine compounds. Voorspoels S.heptachlor. Jr and Laws ER. Estimation of Human Exposure to Heptachlor Epoxide and Related Pesticides in Hawaii. Ayotte P. 9/25/07 International Programme in Chemical Safety (IPCS). J Occup Med 1986. 6/1/09 Rogan WJ. Available at URL: http://www. 2001. Available at URL: http://www. gov/toxprofiles/tp12. In Hayes WJ. Shindell S and Ulrich S.html. International Agency for Research on Cancer (IARC). Bjerselius R.9:1-109. A Report to the Hawaii Heptachlor Research and Education Foundation. 1991 pp. Hertz-Picciotto I. Available at URL: http://www. Royce W. National Toxicology Program (NTP). Sci Total Environ 2004. Hawaii Med J 1991.niehs. 731-915.41:145–148. Arch Pediatr Adolesc Med 1996. International Agency for Research on Cancer (IARC) . Laliberte C. Wohlleb JC. Lawrence River (Quebec. 1963-1967. Environ Health Perspect 2003. Canada). Loo S. Darnerud PO.html. Concise International Chemical Assessment Document 70 Heptachlor [online]. Environ Res 2000. Wolff MS. 2 Classes of Pesticides.

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 8.2-dichloroethenylidene)-bis[4-chlorobenzene] (DDE) and 1.0 (18. interval) Selected percentiles ( 95% confidence interval) Sample 95th 28.9 (<LOD-20.5) < LOD < LOD 9.6 (31.0-15.S. population.4. DDT usually refers to the technical product.6 (25. air.S.6 (9. 2008.0-155) 83.7) 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 (<LOD-40. DDT and DDE can cross the placenta.9 (21.8-17.0) 19. DDT is converted to DDE and several other metabolites. and 03-04 are 20. although DDT and DDE intakes have decreased over time (FDA.1-27. 1991). food.3 (<LOD-21. fish. and 7.10 (<LOD-12.1) 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. or dermal exposure.0 (18.7) < LOD 18.9) 14. Survey Geometric mean (95% conf. < LOD means less than the limit of detection.1 (23. including 1.00 (<LOD-10.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. 1991).9 (10. and trace amounts of several related compounds. In the body. depending on conditions. In the general U. 2002. and water.90 (<LOD-12. 01-02. DDT and DDE are distributed to all body tissues with the highest concentrations found in adipose tissues (ATSDR.3) 28. Fourth National Report on Human Exposure to Environmental Chemicals 89 .8) 15. DDT was used at one time as a treatment for head and body lice.1’-(2.3-590) 293 (104-541) 48.5-54.9-34.2 (11.0-37.9 (10. 17.4) < LOD < LOD < LOD 61. Only a small proportion of DDT is metabolized and excreted (Smith.50-11. inhalation.1) 31.9) 29. continues to be the primary source of DDT exposure. resulting in fetal exposure. Food imported from countries that still use DDT may contain the chemical or its residues.0-53.0-27.10-13.p’-DDD (4% or less). 1988). particularly for endemic vector and malaria control.70 (8.8-23.6) 635 566 461 356 514 490 564 1061 890 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. 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.8) 36.0) 26.5 (14. particularly meat.0) 20.9-28.5 (23.0 (10.7-16. when virtually all use of it was banned.5) 23.5) 25. which is a mixture containing p.3-236) 24. and dairy products.4) < LOD 17.5 (23.3) 21.7 (19. o.8.3) 22.8) 30.2) 30. as well as in plant and animal tissues.p’-DDT (15%-21%).4 (23.3-16. respectively.p’-DDT (65%-80%).1 (<LOD-39.2) 155 (59. These chemicals are highly persistent in soil.1-71. It was produced and used in the U. see Data Analysis section) for Survey years 99-00.6 (22.9 (10. The biodegradation half-life of DDT in soil varies from 2 to 15 years.1 (33. It is still used in some countries.S.7.5) size 1679 2305 1965 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * * 11.2-bis(p-chlorophenyl) ethane (DDD). DDT can be absorbed after ingestion.9) 17. sediments.0 (21. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.5-36.6 (<LOD-25. after World War II until 1972.0-35.7 (15.0) 40.9) < LOD < LOD 9. DDT is converted in the environment to other more stable chemical forms.7) 12.2-95. Smith.2-65.1’-dichloro-(2.8-26. p. Gunderson.8-39.2) < LOD < LOD 9. population from the National Health and Nutrition Examination Survey.3 (<LOD-31. which may vary for some chemicals by year and by individual sample.3) 21.3 (27.5 (15. Both Serum p.6-33.Organochlorine Pesticides Dichlorodiphenyltrichloroethane (DDT) CAS No.

250-1.250 (. 1956). Epidemiologic studies of children with environmental exposure to DDT and DDE have not demonstrated neurologic or developmental abnormalities (Gladen et al. Snedeker. which may vary for some chemicals by year and by individual sample.. Mariussen and Fonnum. both DDT and DDE may induce specific cytochrome P450 isozymes (Nims et al.180 (.069) .150-.140-.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 .170 (.106-.051 (<LOD-. 2002.064 (.530) .343) < LOD .240 (.190 (.054-. polychlorinated biphenyls.180) . DDT may bind to estrogen receptors (Chen et al.098-.230) .170) .146 (..34) . 2002.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.143) < LOD < LOD .080-.061) < LOD < LOD < LOD .130-. and leukemia have also been inconclusive (ADSDR.01) .078 (.105-..203) . and duration of lactation.071 (.095) < LOD .170-.180) .330-4.132-..p’-DDD and p. overt signs of acute human toxicity include vomiting.180 (. Several reviews of cancer epidemiologic studies have concluded that a link between DDT and breast cancer is inconclusive (Beard. 2000.140) .130 (<LOD-. premature delivery. Studies of DDT exposure and pancreatic cancer..627) . 2004.097) 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 ..130 (<LOD-. interval) Selected percentiles ( 95% confidence interval) Sample 95th .167) size 1679 2305 1965 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * * . and o.. population from the National Health and Nutrition Examination Survey.62 (.065-. 1998).106) . 1996).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.079) < LOD < LOD .570-4. fertility.074-. Hayes et al.190 (.260) .048 (<LOD-. It is difficult to attribute outcomes in human studies solely to DDT because of potential co-exposure to other persistent organohalogen chemicals (e.230) .g... tremor.130 (<LOD-.114-.26) 1. Animal studies reported reduced fertility. accidental exposures.106) < LOD < LOD .150-.. 2001).128 (. 90 Fourth National Report on Human Exposure to Environmental Chemicals .160-.290) .190-1. 1997). Jusko et al. dioxins and furans).086 (.00) .420) .00 (. 2001).220) . have not been consistently demonstrated (Beard.400 (. and seizures. 1995. lung cancer.S.400) . 2001). 2002. Human health effects from DDT at low environmental doses or at biomonitored levels from low environmental exposures are unknown. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.084 (.071-. 2006. resulting in exposure to nursing infants (Rogan.075) 1. 2002. Survey Geometric mean (95% conf.120-. although the risk for preterm delivery may be related to maternal DDE levels (Longnecker et al. Calle et al. 2006. 2006.142 (.150) . and altered behavior after neonatal exposure (Eriksson and Talts. In high dose.313 (.108 (.200 (.Organochlorine Pesticides chemicals are excreted in breast milk.240) .112 (. Gladen and Rogan. reproductive organ abnormalities.150 (<LOD-.120 (<LOD-. In laboratory animals. 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. 2006). A workplace standard for DDT has been established by Serum p.150 (<LOD-. Longnecker et al..220) .063 (<LOD-..078-. other organochlorines.059-.087 (.068-.p’-DDE can produce anti-androgenic effects (Gray et al. Beard. 2001).530 (.189-.201 (. Reproductive effects in humans affecting birth weight.180-. Jusko et al.146 (. 2006).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 . Gray et al. 2006).

1989). Survey Geometric mean (95% conf. Biomonitoring Information DDE persists in the body longer than DDT. mean serum levels of DDT and DDE in the U.. compared to levels observed in this Report (Anderson et al.e.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.. and the most recent median levels for German adults and children are similar to levels in this Report (Becker et al. 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. 2002. mean DDE levels were about fivefold higher among women of southern Spain exposed by virtue of Serum p. 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. population from the National Health and Nutrition Examination Survey. Smith. levels of DDT and DDE increase as a person ages as a result of cumulative exposure (ATSDR. In general. Declining DDE levels over time have also been observed in the German population.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. 2003). 2005). 2002.gov/ toxpro2.7-119) 113 (100-140) 93.p’-DDT) as a possible human carcinogen. In a population-based sample of men and women from eastern Slovakia.S. EPA at: http://www.S. so serum DDE levels may be an indicator of historic exposure and may be higher than DDT levels in the same person. 1998.6 (81.7-129) 297 (256-344) 338 (303-376) 268 (217-332) 108 (97. environmental levels) and health effects is available from the U. and 03-04 are 18. IARC classifies DDT (p.cdc.S. Fourth National Report on Human Exposure to Environmental Chemicals 91 . respectively.gov/ pestcides/ and from ATSDR at: http://www. Link et al. 2004)..epa. respectively.8... 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. 2003..Organochlorine Pesticides OSHA and a guidance established by ACGIH. Compared to females in the NHANES 1999-2000 subsample. 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.atsdr.3. 2004). NTP considers DDT as being reasonably anticipated to be a human carcinogen. Heudorf et al. 01-02. see Data Analysis section) for Survey years 99-00. Since the 1970’s. More information about external exposure (i.html. for males and females in the NHANES 19992000 subsample (Pavuk et al..6.. 1991). population declined by about fivefold to tenfold. and 7. Stehr-Green.

78 (4. 2004).63 (1.14) 2.65 (1.49 (1.51-15.26 (1.32-9.69) 4.13-2.12 (.30 (1.50 (2.69 (1.5) 7.488-.430-.48 (6.5) 5.2 (19. 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.51-49.4-19.77 (1.79) Selected percentiles ( 95% confidence interval) Sample 95th 11.10-1.82 (1. 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.91-3.81 (7.72) 1.7) 13.84-3.49 (1.9) 5.66-17. 1971). Consumers of Great Lakes sport fish had mean serum DDE levels that were only slightly higher than nonconsumers.66) 4.90) 22.646) .71) 32.p’-DDT.87 (5.01) 1.84 (3.75) 1.1) 7.39-2.04-1.66) 3.58) 1.91 (6.9-38.1 (9.01-11.2 (9.385-.3) 937 1069 955 1027 1229 1001 Females 99-00 01-02 03-04 Race/ethnicity Mexican Americans 99-00 01-02 03-04 3.18-3.4) 13.77 (1.30-1.7-48.9 (26.6) 11.39) 1.32 (1.2) 19.76-3.47 (1.91) 3.5) 16.520 (.7-20.22-1.27) 3.11-1.57-13.41-12.36 (3.6 (8.18) 1.03-4.54-7.96) 1.09-1.870 (.590 (.80) 1. 1989).40-4.92 (3.06) 1.963-1.56-6.62-6.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..6) 9.29 (1.02-8.76) 1..34 (7.75) 2.64) 3.46 (1.82) 1.680-1.25) 8.79) 4. which is similar to the overall geometric mean of 260 ng/g lipid in the NHANES 1999-2000 subsample (Bloom et al.5) 22.Organochlorine Pesticides nearby agriculture (Botella et al.36-11.14 (1.31 (1. Workers involved in production or application of DDT developed neurologic abnormalities associated with blood levels around 100-300 mg/L.820-1.14-9.68 (2.49 (6.61-2.01-11.8 (13.76) 1.01-1.6 (7.7 (8.59) 3.12 (6.15-4.33-1. 2005).03-1.48-4.81) 11.00 (6.39 (3.4 (8.1) 12.76 (2.p’-DDE in serum does not mean that the level of the chemical causes an adverse health effect.11 (2.611-1.4 (12.43-4.9) 7.38 (1.8 (13.24-17.p’-DDT.23 (7.01) 1.p’-DDT were below the limits of detection.9-17.88-35.8 (14.37 (1.25-14.43-4.30-1.45 (1.69 (2.90-8.75 (4.2 (6.600) .18-4.79) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 .72) 1.04 (6.19) 4.8) 15.726) .31-12.50-17.34-11.490 ng/L) were found many years ago in a study of pesticide workers in Argentina (Radomski et al.37-10.18 (6.91-2.3) 13.6 (17.635) 1.24) 1.32 (1.65) 1..3 (8. or p.51 (1.965-1.46-2.85-10.53) 7.64-2.32) 1.623 (.59) 6. Finding a measurable amount of p.7) 9.25 (.37-4.1) 40.6) 9.00) 7.8 (9.31-2.4) 14.66) 1.96) .36-2.7) 16.55-9.730) . o.6) 13.419-.14) 2.80) 1.890-1.58) 1. High mean levels of whole blood DDT (about 3.41 (1.36) 3.63 (6.994-2.87-16.34) 2.75 (8.01-1.80 (2.S.56-2.80) 3.55 (2. Serum p. 309 versus 268 ng/g lipid.37-1. less than one percent had detectable serum levels of o.4) 9.44) 1. population from the National Health and Nutrition Examination Survey. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.53) 1.17 (3.06) 3.02) 1.57 (1.07 (5.57-2.796 (. 2001-2002 and 2003-2004 subsamples.83 (1.51) 3.99) 1.92 (3.6 (9.34) 6.57 (3.36-1.02 (2.30 (1.66-2.81-5.19-14.60-13.0 (12.81-18.54 (1.5) 10.05 (3. considerably higher than levels in this Report (Smith.43 (5.16 (2.8) 686 758 588 1278 1540 1368 20 years and older Gender Males 99-00 01-02 03-04 1.68) 2.0 (9.52-6.26-2. 2004).20 (.6) 12.25-16.58) 75th 3.07) 1.46 (1.68-4.69) 8.88 (2.3) 16.27-1.16-1.561 (.97 (3.75) 6.05) 1.13 (1.25 (1.22) .21) 90th 7.24 (1.63 (1.35) 1. Survey Geometric mean (95% conf. 1991).10) .2) 26.8-90.93 (7. interval) 1.14-1.57-3.71 (6.0) size 1964 2298 1956 Total years 99-00 01-02 03-04 50th 1.557) 1.81 (1.10-5.97-4.6) 9.53-15.69 (.52 (1.456 (.26-10. serum levels of o.10) 2.66) 1.57 (1.13) 4.32-1.47) 3.53 (2.71 (5.2-32.00-1.51-8.59 (1.85-4.26) 3.63-15.6) 8.59 (4.12-1.28) 1.25) 1.01-15.56-3.52 (3.54) 8.07) 1.92) 1.59 (1.3-43.. In a subsample of NHANES II (19761980) participants.32-1.39-1.0) 2.61 (1.70-3.18-1.17-3.49) 8.37-16.66-4.40-4.21) 3.51) 1.43-8.40-8.7-19.3) 10.1 (8.516 (.40 (3.534-.56) 2.70) 1.6) 9.00 (.71) 12.01-5.860 ng/L) and DDE (about 14.9 (15.0) 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 .85 (1.p’-DDT (Stehr-Green. In the NHANES 1999-2000.45 (1.57) 2.2 (9.18-1.34-3.500-.22 (7.3 (9.38 (1.

respectively. Fourth National Report on Human Exposure to Environmental Chemicals 93 . and 7. and 03-04 are 20.4. < LOD means less than the limit of detection. population from the National Health and Nutrition Examination Survey. 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 Limit of detection (LOD. 17. 01-02. which may vary for some chemicals by year and by individual sample.p'-Dichlorodiphenyltrichloroethane (lipid adjusted) Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.7.Organochlorine Pesticides Serum o. see Data Analysis section) for Survey years 99-00.S.8.

94 Fourth National Report on Human Exposure to Environmental Chemicals .S.p'-Dichlorodiphenyltrichloroethane (whole weight) Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U. Survey Geometric mean (95% conf. population from the National Health and Nutrition Examination Survey. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD < LOD size 1669 2279 1946 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD < LOD 90th * * * Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 667 756 588 1002 1523 1358 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 796 1059 949 873 1220 997 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 632 565 458 354 507 486 560 1045 880 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the lipid adjusted serum level. * 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.Organochlorine Pesticides Serum o.

Bates MN. Parks L.7(3):248-264. Epidemiology 2006. Jr. Int J Hyg Environ Health 2003. Maternal DDT exposures in relation to fetal and 5-year growth. Neurotoxicol 2000. Patterson DG Jr. Heudorf U. September 2002. Brock JW. Davis MD. Effects of environmental antiandrogens on reproductive development in experimental animals. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. Jr. HCH. Olea-Serrano MF.111:349355. lindane (g-HCH). Katz SH. Moysich KB. Herrman T.atsdr. Gunderson EL. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. India. Klebanoff MA. Environ Res 2004. Saiyed HN.106(5):279-289. Hurd C. Glynn AW. Profiles of ortho-polychlorinated biphenyl congeners. Talts U. Environ Res 2005. Chemosphere 2004. Chemosphere 2005. hypospadias. Calle EE.72:261265.54:1431-1443. Am J Public Health 1995. Wolf CJ. Furr J. Drexler H. Krause C. April 1982 to 1984.html. et al. Vorojeikina DP. Maternal serum level of 1. Levels of DDT. Kashyap R. Neonatal exposure to neurotoxic pesticides increases adult susceptibility: a review of current findings. Barr DB.71(6):1200-1209. Gray KA. Lambright C. Biomonitoring of persistent organochlorine pesticides. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Environ Health Perspect 2004.1-dichloro2. Bhatnagar VK. Sci Tot Environ 2006. Frumkin H. Zhou H. et al. Rivas A. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. and HCB residues in human blood in Ahmedabad. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. Ostby J. hexachlorobenzene.cdc. Association between maternal serum concentration of the DDT metabolite DDE and preterm and small-for-gestational-age babies at birth. CA Cancer J Clin 2002. Botella B. Bjerselius R. Lancet 2001. Available at URL: http://www. Hanrahan L. a biostable metabolite of dichloro(diphenyl)trichloroethane (DDT). Organochlorines in Swedish women: determinants of serum concentrations. Granath F. Environ Health Perspect 2003.17(6):692-700. Burse VW. Garrett N. Longnecker MP. Piechotowski I. Zhou H. August 2008. Bull Environ Contam Toxicol 2004. Hayes WJ. Darnerud PO. Available at URL: http://www.97(2):178192. The effect of known repeated oral doses of chlorophenothane (DDT) in man.gov/ toxprofiles/tp35.85:504508. Swanson MK.cfsan. Ellis H. et al. Olea N. Rogan WJ. Klebanoff MA. et al. et al.21(1-2)37-48. DDE. Savitz DA. Needham LL. Kulkarni PK. Hum Reprod Updat 2001. The Great Lakes Consortium. Atuma S. Bloom MS. Lepom P. Gray LE Jr. DDE and shortened duration of lactation in a northern Mexican town. Charles MJ.52:301-309.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Notides AC. selected elements. Thun MJ. Organochlorines and breast cancer risk. dietary intakes of pesticides. and dichloro(diphenyl)ethylene (DDE). Gladen BC. Gabrio T. Arnold SF.gov/~dms/ pesrpts. Olson J. dichlorodiphenyldichloroethylene. Cueto C. J Assoc Off Anal Chem 1988. Beard J. Willman EJ. Environ Health Perspect 1998. Prenatal DDT exposure in relation to anthropometric and pubertal measures in adolescent males. Hediger ML. Food and Drug Administration (FDA).155(4):313-322. Brock JW. Needham LL. Klebanoff MA. Chen CW. DDT and human health. Transcriptional activation of the human estrogen receptor by DDT isomers and metabolites in yeast and MCF-7 cells. Fourth National Report on Human Exposure to Environmental Chemicals 95 . Link B.96:34-40. et al.. Buckland SJ. et al. Greenfield TA. Int J Hyg Environ Health 2002. and polythelia among male offspring. et al. Baker RJ. Seiwert M.358:110-114. Kaus S. Olson JR. and other chemicals.355:7889.html.2-bi(p-chlorophenyl)ethylene and risk of cryptorchidism.53(8):1161-1172.206:485-491. JAMA 1956. Jusko TA. 4/21/09 Gladen BC. Am J Epidemiol 2002.58:1185-1201. Biochem Pharmacol 1997. Zaidi SS. Toxicological profile for DDT. and Mirex among male Lake Ontario sportfish consumers: the New York State Angler cohort study. Eriksson P. Henley SJ. Exposure of women to organochlorine pesticides in Southern Spain. Cerrillo I.162:890-897. Aune M. Schulz C. Crespo J. Needham LL. Becker K. Paepke O. Vena JE.fda. Falk C.205:297-308. Angerer J. Durham WF. et al. 4/21/09 Anderson HA. Koepsell TD. and DDD [online]. Longnecker MP. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. Current internal exposure to pesticides in children and adolescents in Germany: blood plasma levels of pentachlorophenol (PCP). FDA total diet study. Zoellner I.112(17):1761-1767.

Chemosphere 2004. Lynch CF. In Hayes WJ. et al. and dieldrin. Environ Health Perspect 2001. Fonnum F.Organochlorine Pesticides Mariussen E. Pavuk M. J Toxicol Environ Health 1989. Jr. Toxicol Appl Pharmacol 1971. PA. Environmental exposure to PCBs and cancer incidence in eastern Slovakia. Rey AA. Crit Rev Toxicol 2006. Snedeker SM. Chovancova J. Pollutants in breast milk. DDE.20(2):186-193. and DDD in male rat liver and cultured rat hepatocytes. Astolfi E. DDE. Schecter A.27:405-421.109:35-47. Eds. Radomski JL. et al. Inc. Fox S. Arch Pediatr Adolesc Med 1996.54:1509-520. Handbook of Pesticide Toxicology. Vol. Cerhan JR. Stehr-Green. children and newborn infants. 96 Fourth National Report on Human Exposure to Environmental Chemicals . Jr and Laws ER. Smith AG.36:253-589. Deichmann WB. Rogan WJ. Lubet R. New York. 731-915. 1991 pp.150:981-990. Petrik J. Jones CR. Blood levels of organochlorine pesticides in Argentina: occupationally and nonoccupationally exposed adults. Demographic and seasonal influences on human serum pesticide residue levels.53:455-477. 2 Classes of Pesticides. Academic Press. J Toxicol Environ Health Part A 1998. Comparative pharmacodynamics of CYP2B induction by DDT. Neurochemical targets and behavioral effects of organohalogen compounds: an update. Thomas PE. Pesticides and breast cancer risk: a review of DDT. Reddy AB. Nims R. Chlorinated Hydrocarbon Insecticides.

72-20-8 General Information Endrin. Hepatic effects of endrin exposure have included necrosis. 1996.S. Endrin is absorbed rapidly after ingestion. 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. High doses produced renal tubular necrosis and diffuse kidney degeneration in animals. 1991).40) < LOD < LOD < LOD 1022 885 1165 940 01-02 03-04 01-02 03-04 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 5. 1992).09 and 7. and occasionally at low levels in sediment and surface waters.40 (<LOD-6. 1979...70) < LOD < LOD < LOD 730 539 1457 1286 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 5. Endrin has been detected in soils.20 (<LOD-5. Endrin was not widely used as a termiticide. endrin has been detected with declining frequency in U. At high doses.. In the body. Endrin was used as an insecticide.40-5. 1992). which may vary for some chemicals by year and by individual sample. population from the National Health and Nutrition Examination Survey.S. Smith.50) < LOD 5. Fourth National Report on Human Exposure to Environmental Chemicals 97 . endrin can persist for years. largely the result of historical agricultural application or run off from contaminated soils (ATSDR. Human health effects from endrin at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 1992). < LOD means less than the limit of detection. fatty infiltration.8. and inflammation (Smith. a stereoisomer of dieldrin. endrin is converted rapidly to its major metabolite..S. interval) Selected percentiles ( 95% confidence interval) Sample 95th 5. or discarded. unless the dose is high and the exposure is very recent. unlike aldrin and dieldrin. Kavlock et al. 1991). Serum Endrin (lipid adjusted) Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U. total diet surveys (FDA. have been cancelled by the U. 1981). 1992. is no longer manufactured in the U. 1987). Further conversion occurs to 12-ketoendrin and various conjugated metabolites which are excreted in urine and feces. General population exposure can occur after ingestion of endrin residues on food items imported from countries where endrin is still used. endrin blocks inhibitory neurotransmitters in the central nervous system resulting in excitation and seizures (Narahashi et al. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Because it is metabolized so rapidly.30) < LOD 5.50) < LOD < LOD < LOD 5.10 (<LOD-5. endrin usually is not detected in serum of exposed individuals. All uses of the pesticide in the U. 2008). Depending on soil conditions. Ketoendrin is a major photodegradation product (IPCS. characterized by generalized seizures in previously healthy persons occurred in Pakistan when sugar contaminated with endrin was ingested (Rowley et al.S. inhalation or dermal exposure routes.10 (<LOD-5.Organochlorine Pesticides Endrin CAS No. Survey Geometric mean (95% conf. EPA. see Data Analysis section) for Survey years 01-02 and 03-04 are 5. anti-12hydroxyendrin. rodenticide and avicide.S. Endrin does not accumulate in body tissues (IPCS. manufactured.60 (5. Over time.30 (<LOD-6.20 (<LOD-5. IPCS. or from contact with contaminated soils and sediments in areas where endrin was applied.40) < LOD 547 433 487 446 1000 831 Limit of detection (LOD. Skeletal abnormalities and cleft palate in the offspring were associated with endrin when it was fed to pregnant laboratory rodents (Chernoff et al.

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

I. Inc. Gray JA. Cancer Epidemiol Biomarkers Prev 2000. Rab MA. Smith AG. Crespo J. In Hayes WJ.96:34-40. II. Perinatal toxicity of endrin in rodents. Roy ML. Perinatal toxicity of endrin in rodents. Needham LL.79(6):928-934. Chernoff N. Fourth National Report on Human Exposure to Environmental Chemicals 99 . Frey JM. Patterson DG Jr. 1991. 4/21/09 Bates MN.atsdr. Rogers E.gov/toxprofiles/tp89.org/documents/ehc/ehc/ ehc130. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Available at URL: http://www. Cerrillo I. Liddle J. Available at URL: http://www. Hanisch RC. Olea N. Schulte P. Sodium and GABA-activated channels as the targets of pyrethroids and cyclodienes. 1992.cdc. Gray LE. Academic Press. Whitehouse DA. Available at URL: http://www. Fetotoxic effects of prenatal exposure in rats and mice. August 2008. Grajewski B. Ginsburg KS. Buckland SJ. Vol. Endrin [online]. New York. Exposure of women to organochlorine pesticides in Southern Spain. et al.fda. 4/21/09 Kavlock RJ. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Andersen A. No:429-436. Food and Drug Administration (FDA). Saleem M. Convulsions caused by endrin poisoning in Pakistan. Jr and Laws ER. Gray J.inchem. Chemosphere 2004.9:1357-136.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR).64-65 Spec. Eds.13:155-165. 4/21/09 International Programme on Chemical Safety (IPCS). Rowley DL. Ward EM. Botella B. Patterson DG Jr. Toxicology 1979. Ellis H. Fetotoxic effects of prenatal exposure in hamsters. Turner W.html. Olea-Serrano MF. Toxicological profile for endrin [online]. August 1996.21:141-150. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population.gov/~dms/ pesrpts. Garrett N. et al.54:1431-1443. Burse VW. Toxicology 1981. Rivas A.html.htm. 2 Classes of Pesticides. Hanisch RC.cfsan. Kavlock RJ. et al. Environmental Health Criteria 130. Toxicol Lett 1992. Sokal D. Chlorinated Hydrocarbon Insecticides. Environ Res 2004. Handbook of Pesticide Toxicology. 731-915. Serum organochlorine levels and breast cancer: a nested case-control study of Norwegian women. Gray LE. pp. Pediatrics 1987. et al. Narahashi T. Chernoff H. Hardjotanojo W. Jr.

and sediment (Barber et al.6-TCP) (To-Figueras et al. Gunderson.9-15.5-33.9) < LOD < LOD 20.2-15.0 (18..7-15.5-15. 118-74-1 General Information Hexachlorobenzene (HCB) was used from the 1930’s to the 1970’s in the U.1 (13.5-14.9) < LOD < LOD 19.6-26.S.2-15.0-28.4.2 (13.9-32.5 (13.8.3 (12. 31.9) < LOD < LOD 15..3 (22.7-29.4 (22. breast milk is an additional route of elimination in nursing women.3) 24.4) < LOD < LOD 19. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.3) < LOD < LOD 29.9) < LOD < LOD 28. 100 Fourth National Report on Human Exposure to Environmental Chemicals .3 (20.6 (21. < LOD means less than the limit of detection.7) 807 1058 957 895 1219 1004 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * 16.4.5-15. primarily as a fungicide and seed treatment until the U. see Data Analysis section) for Survey years 99-00. The FDA dietary surveys have shown that over time. Urinary metabolites include pentachlorophenol (PCP).6) < LOD < LOD 26.6-33.6-32.7-26.S.4 (18.0-25.2) < LOD < LOD 13.2 (17.2 (14.7-16. particularly by consuming fish.0) < LOD < LOD 24.Organochlorine Pesticides Hexachlorobenzene CAS No. 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. 2002).9 (25.5 (14.2 (14.6) < LOD < LOD 26.8) 583 554 460 350 511 488 636 1052 888 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.1 (17.3-20.9-17. wildfowl.9 (23.0 (14.9) < LOD < LOD 20.3 (14.5-14.1-16.3 (22. 1997). 1988).7 (27.7-22.5-18.5 (13.6) < LOD < LOD 24.7 (15.6) < LOD < LOD 14. HCB has been detected in fewer foods since the 1980s (FDA.8) < LOD < LOD 27. 01-02. and elimination occurs by renal and fecal routes. Survey Geometric mean (95% conf. HCB is slowly metabolized.4 (18. which may vary for some chemicals by year and by individual sample.8) size 1702 2277 1961 Total years 99-00 01-02 03-04 50th < LOD < LOD 14.4-16.6-44.0) * * 15.3) * * 15.6) < LOD < LOD 25. and foods with a high fat content.1) < LOD < LOD 15.4) < LOD < LOD 14.9) 19. or game taken from areas with HCB contamination.9-24.9) < LOD < LOD 16.4.8 (26.0-16. air.4.3-26..6-19.0. 2005).2 (24.7) < LOD < LOD 75th < LOD < LOD 90th * * 15.7) * * 14. Workers in chemical manufacturing industries may be exposed to HCB via inhalation or dermal pathways.0-19.3 (16. Although it is not manufactured as an end-product in the U.4) < LOD < LOD 23. and 03-04 are 118.8-15.6 (23.2-31. water.7 (15. HCB is well absorbed after oral administration.0) < LOD < LOD 15.5-trichlorophenol (2.0 (18.4) < LOD < LOD 22. and has been detected in soil. The general population may be exposed to HCB through diet.0) < LOD < LOD 15. and accumulates in fatty tissues where it persists for years.1) * * 15.9-20.8 (15. 2.7) < LOD < LOD 24.0 (25.1 (14.7-16.1 (14. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD 28.5) < LOD < LOD 18.5-TCP) and 2.9 (25. It is a persistent chemical and bioaccumulates in both aquatic and terrestrial food chains (ATSDR.S. respectively.3-22.3) < LOD < LOD 20.7 (19.7-21.6) 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. EPA cancelled its use in 1984. Hexachlorobenzene has entered the environment as a result of industrial activities and pesticide applications.7-30.. and 7. distributes widely throughout the body. Therefore.6 (24. population from the National Health and Nutrition Examination Survey.6-trichlorophenol (2. these metabolites can also be produced after exposure to other chlorinated compounds (Kohli et al.4) < LOD < LOD 18.1-20.2) < LOD < LOD 29.4 (11.8 (22. 2008.4.4-15.S. HCB may be created as either a byproduct or an impurity in the manufacturing process for certain chemicals and pesticides. 1976).4) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * 13.9 (14.4) < LOD < LOD 33.9-30.

082-.083) < LOD < LOD .094 (.epa. EPA has established a drinking water standard.148-.120 (.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 * * .174-. and many died before 2 years of age (Peters et al.073-. 1982.090 (. environmental levels) and health effects is available from the U. HCB interferes with normal heme synthesis.S.095) < LOD < LOD 75th < LOD < LOD 90th * * .129) < LOD < LOD . immunologic abnormalities.125 (.212) size 1702 2277 1961 Total years 99-00 01-02 03-04 50th < LOD < LOD .. Survey Geometric mean (95% conf.173) < LOD < LOD .069) * * .132) < LOD < LOD .121 (.095) * * .092-. Infants were exposed transplacentally and through breast milk. arthritis.081-.182 (.102 (.145-.163-. Schmid.099) < LOD < LOD . More information about external exposure (i.143-.167 (. Chronic feeding studies in animals have demonstrated kidney injury.cdc.130) < LOD < LOD . With chronic exposure.097) .118) < LOD < LOD . 1960).088-.. which is manifested by increased deltaaminolevulinic acid synthase activity and decreased uroporphyrinogen decarboxylase activity.094) < LOD < LOD .gov/pesticides/ and from ATSDR at: http://www.135-. ACGIH has developed workplace exposure limits 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.095 (.122) < LOD < LOD .099) < LOD < LOD .203) < LOD < LOD .092 (.099) < LOD < LOD .127-.167) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * .085) * * .147 (.111-.156 (. reproductive and developmental toxicities.e.114-.069) < LOD < LOD .087 (.169-.100) < LOD < LOD .091-.092 (.176) < LOD < LOD . a consequence of these heme abnormalities is a condition known as acquired porphyria cutanea tarda.225 (. Fourth National Report on Human Exposure to Environmental Chemicals 101 . This condition.118-.078 (.097 (.085-.072-.203) < LOD < LOD .147-.088-.092 (.191 (. 2002).088-.160 (.089-. and NTP classifies hexachlorobenzene as reasonably anticipated to be a human carcinogen. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD .114-.118-.157 (. 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.175) < LOD < LOD .079 (.086) < LOD < LOD . anorexia.218) 583 554 460 350 511 488 636 1052 888 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the lipid adjusted serum level.179 (.113-.107) < LOD < LOD .171 (. The U.098 (.077-.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 * * .157-.109) * * .062-.gov/toxpro2.090-.152) < LOD < LOD .097) < LOD < LOD .163 (.123 (. and the FDA has established a bottled water standard for HCB. EPA at: http://www.095 (.190 (.141) < LOD < LOD .159-. thyromegaly.090 (.html.081 (. as well as hypertrichosis.123 (.140 (. 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. acute doses produce central nervous system depression and seizures.196) < LOD < LOD .178-. very high. Biomonitoring Information Serum concentrations reflect the body burden of HCB.089-. IARC classifies hexachlorobenzene as possibly carcinogenic to humans.065 (. and weakness.atsdr. Human health effects from HCB at low environmental doses or at biomonitored levels from low environmental exposures are unknown.095-.S.111) < LOD < LOD .S.258) < LOD < LOD .060-.145-. and liver and thyroid cancers (ATSDR.115 (.Organochlorine Pesticides chemical.102) < LOD < LOD .104 (.126) .163) < LOD < LOD .064 (.086-.186 (.086-. In humans.155) < LOD < LOD . population from the National Health and Nutrition Examination Survey.123 (.176-.090 (.107-.

54(3):203-208. Safe A. Laliberte C. Ozalla D. Glynn et al. Paepke O. Factors predicting organochlorine pesticide levels in pregnant Latina women living in a United States agricultural area. Lepom P. 4/21/09 Glynn AW. Aune M. References Agency for Toxic Substances and Disease Registry (ATSDR).77:173182. Lackmann GM. Biomonitoring of persistent organochlorine pesticides.135(4):400404.. Peters HA. Darnerud PO.44 mg/L.17:388–399. Organochlorines in Swedish women: determinants of serum concentrations. Jones D. 1986. Muller C. Ayotte P. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Gunderson EL. Muckle G. In Spain.205:297-308.111:349355. 2002. 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. however. Can J Biochem 1976.. Gabrio T. August 2008. Bradman A. van Wijk D. 2002).9% of participants had quantifiable levels (Stehr-Green. Becker K.. Link et al. 2002. Available at URL: http://www.. Gocmen A. J Assoc Off Anal Chem 1988. 2002.gov/~dms/ pesrpts... Toxicological profile for hexachlorobenzene update [online]. 2005). Link B. April 1982 to 1984. Atuma S. than the limits of detection (on a whole weight basis) in NHANES 19992000 and 2001-2002 (Herrero et al. Herrman T. Bryan GT.. Arch Dermatol 1999. et al. Reference values updated.cdc. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. respectively. Lackman. September 2002. IARC Sci Publ 1986. Dogramaci I. FDA total diet study. Lackmann. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. factory workers chronically exposed to HCB and residents near the factory had serum HCB levels that were 150 to 50 times higher. Residency near industrial or agricultural areas has been associated with higher serum HCB levels (Barber et al.fda. Krause C.58:1185-1201. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Environ Health Perspect 2003. Bertram HP. Schwartz JM. but overall.cfsan. Chemosphere 2005.110(8):835-838. In the 1976-1980 NHANES subsample. Bjerselius R. Arch Neurol 1982. Epidemiology of hexachlorobenzene-induced porphyria in Turkey: clinical and laboratory follow-up after 25 years. 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. Canada). dietary intakes of pesticides. Bertram et al. Polychlorinated biphenyls and hexachlorobenzene in full-term neonates. Agerelated increases of HCB in body fat and serum have been consistently noted in general population studies (Becker et al. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003.39(12):744-749.atsdr.. Jones KC. Kaus S. Herrero C.. Urinary porphyrin excretion in a human population highly exposed to hexachlorobenzene. selected elements.349:144. Barr DB. Otero R. Sweetman AJ. and other chemicals. Over the past two decades. and the geometric mean concentration of HCB in whole blood was 0. Hexachlorobenzene content in human whole blood and adipose tissue: experiences in environmental specimen banking. Food and Drug Administration (FDA). HCB levels were directly related to age. Santiago-Silva M.Organochlorine Pesticides in the NHANES 1999-2000 and 2001-2002 subsamples. et al. 1989). HCB detection in serum also was proportional to age. Holland NT. Cripps DJ. only 4. et al. 4/21/09 Barber JL. J Exp Sci Environ Epidemiol 2007. more HCB levels were quantified. Schulz C. Lawrence River (Quebec. 2005. As a result of the lower limit of detection in NHANES 2003-2004. but approximately five times higher than the overall geometric mean level in 2003-2004 (Becker et al. Kohli J. Sci Tot Environ 2005. Bradman et al. 2006). Finding a measurable amount of hexachlorobenzene in serum does not mean that the level of the hexachlorobenzene causes an adverse health effect. Dallaire F. Biol Neonate 2002. In a representative sample of the 1998 German adult population. 102 Fourth National Report on Human Exposure to Environmental Chemicals ..71(6):1200-1209. 2002) and among children (Link et al. The metabolism of higher chlorinated benzene isomers. Environ Health Perspect 2002. Granath F.html. Piechotowski I. declines in background HCB levels ranging from around 50%90% have been documented in studies using cord blood (Dallaire et al. Hexachlorobenzene in the global environment: emissions. Kemper FH.. et al. Sala M. 2003).81(2):82-85. 1999). Zoellner I.gov/ toxprofiles/tp90. Dewailly E. Eskenazi B. lower than the limit of detection (on a lipid adjusted basis) in NHANES 1999-2000 and 20012002. Seiwert M. 2002. trends and processes.html. distribution. Lecha M. levels. Available at URL: http://www. 2005). Int J Hyg Environ Health 2002. Temporal trends of organochlorine concentrations in umbilical cord blood of newborns from the lower north shore of the St. Fenster L.

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

4) 27.7-69.5 (11.2 (18.8-68. water.7 (<LOD-16.7 (29.8) 27.4-111) 84.80 (<LOD-14.4 (12.0 (37.2 (31.6) 47.0-34.1 (30.7-166) 70.7) 27.5 (43. HCH isomers.8) * * * * * * 15.0 (35.9 (40. 58-89-9 General Information Hexachlorocyclohexane (HCH). each result has been multiplied by 1.6 (17.1-36.3 (13.1) 71.3-85. respectively. particularly alpha and gamma have been detected widely in air.20-16. It is no longer produced or sold in the U.6) 36.9-178) 48.30-11.8 (64.9-14.8) 95th 68.2) 13.3 (42. Lindane has a half-life of about two weeks in soils and water.0 (8.7 (62.1-32.3) 34.0-20.7) 18.2-55.7 (25.3) 25. HCH isomers are lipophilic. 319-85-7 gamma-Hexachlorocyclohexane CAS No.5) 29.3) 37.2-42.9 (62.76.4) 901 1067 952 992 1224 1007 Females 11.4) < LOD 9.1) 31.9 (30.9 (9.66-12.8 (9. 608-73-1 beta-Hexachlorocyclohexane CAS No. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.90-8.8-199) 134 (85.2-46.9) 17.1-27.8 (17.9) 15.0) 7. soil.6-14.1) 12.09) < LOD Gender Males 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD 14.2) 62. and have been used either as fungicides or to synthesize other chemicals.7-26.4) 51.1-15.6) 18.6) 653 758 589 1240 1533 1370 20 years and older 10.3 (26.2 (29.1-16. see Data Analysis section) for survey years 99-00. can be used as an insecticide and has been used to kill soil-dwelling and plant-eating insects. 104 Fourth National Report on Human Exposure to Environmental Chemicals .7) 73. so they can accumulate in fatty tissues of animals.1 (11.36.7) 56.8-87.5) 67.7) 23.7) < LOD < LOD < LOD < LOD < LOD < LOD 37.7-96.5 (14. population from the National Health and Nutrition Examination Survey.5528.8-19.2) 36.6) 16.6-62. 01-02.6-37.7) 10.7-20.0-70. As pesticide applications of HCH were increasingly restricted or eliminated.9) Selected percentiles ( 95% confidence interval) Total * * 50th < LOD < LOD < LOD 75th 19.4 (50.70-19.6-89.7) 32.4-73.50) 8.1 (16. HCH does not bioaccumulate to an appreciable extent in plants (ATSDR.45) < LOD Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 99-00 01-02** 03-04 16.3-56.2-22.1 (18. interval) 9. Survey years 99-00 01-02** 03-04 Geometric mean (95% conf.5) 90th 42.6 (33.2-20.6 (22. 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.7 (35.5) 14.5 (37.8 (10.60-13.0) 8.6 (10.2-98.8) 39.5) 22.6 (16.8) 7.4 (8.6) 35.43 (<LOD-9. EPA cancelled agricultural uses of lindane (ATSDR. which may vary for some chemicals by year and by individual sample.0-23. and sediment as a result of historic production and use. See the section “What’s New” at the beginning of this Report for details.0 (19.8 (21.70 (6.68 (<LOD-10.3) 51.1 (9.9 (11.0-111) 70.9-81.9 (50.1-49.0) 41.5 (16.2 (34.89 (<LOD-9.8 (23.4) 21.7) 10.0 (33.3 (62. **In survey period 2001-2002.2) 142 (99.3-38. The gamma isomer.6-18.5 (24.70 (8.56-12.80 (6.1-37.0) 17.S.6-135) 69.5-123) 49.1) 13.6-20. gamma.4-45.S.0-21. The other isomers can be formed during the synthesis of lindane.9 (32.2-67. the U.4) < LOD < LOD < LOD 46.61-12. environmental levels declined.2-17.7-69.9-51. 6.0) 71.6-47.8) 52.1-32.9-56. and delta.6) 50.8-54.4 (52.4 (16. 2005).9) 45.4) 11. and 03-04 are 9.87 (9.4) 44. In 2006.7 (30.7 (53. Lindane (1%) lotion and shampoo are available by prescription for singleuse application to treat human scabies and head lice.8 (32. and 7.1 (21.6 (40.S.9 (26.2 (9.5 (8.5) 16. including alpha. < LOD means less than the limit of detection.0) 35.0 (<LOD-12.2 (48.70-12.46-11.2) 9. beta.8. commonly known as lindane.8) < LOD 10. 2005).2-87.1 (27.7-96.3 (42. Technical grade HCH is a mixture of all four isomers.7) 97.9) 81.9-24.1 (9.4) Sample size 1893 2291 1959 Age group 12-19 years 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD 21.1 (12. However.04-10.Organochlorine Pesticides Hexachlorocyclohexane CAS No.0-70.8) 12.7 (13.90-8.9-21.5) 40.6-42.8-16.3) 14.90) 7.4) 10.4-50.8 (33. exists in several isomeric forms. containing about 64% alpha and 10%-15% gamma isomers. formerly referred to as benzene hexachloride.4 (11.5) 11.5-29.2-52.0 (14.1) 12.5) 632 563 460 403 513 487 702 1051 887 Non-Hispanic blacks Non-Hispanic whites Limits of detection (LOD.2 (50.

Workers who directly handled HCH have complained of headache.191-.281 (..064) .050 (<LOD-.620) .290) .840) . and FDA has established a bottled water standard and food residue tolerances for lindane.410) .Organochlorine Pesticides exposure to HCH is through the diet.560) ..057 (<LOD-.290) .103-. ingestion.090 (. population from the National Health and Nutrition Examination Survey.32) .270 (. Distribution is mainly to fatty tissues.103 (. respectively.167 (.580 (.305) .372 (.372) 632 563 460 403 513 487 702 1051 887 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the lipid adjusted serum level. After dermal application of lindane 1% lotion.521 (.190) . HCH isomers are metabolized to chlorophenol metabolites that are excreted in the urine (Angerer et al.058) < LOD Gender Males 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD .620-1. enlarged livers.442) Sample size 1893 2291 1959 Age group 12-19 years 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD .103) 90th .100-. probably by blocking inhibitory neurotransmitters in the central nervous system. ataxia. Gunderson 1988).360-. Pesticide applicators or agricultural workers could be exposed to HCH by inhalation and dermal pathways.067) .580-1.360) . Acute high dose toxicity in rodents affects the central nervous system producing decreased activity.244-. interval) .077) < LOD .180-.570 (. hepatic enzyme induction.220-.100-.480) .083) . from 6% of samples in 1982-1984 to 2% in 1994 (FDA.090 (. 1996.125) < LOD < LOD < LOD .S.140) .S..100 (.290 (.140) .600) . the serum half-life was about 20 hours among children (Ginsburg et al.098 (.680) .210 (.390 (.058 (<LOD-.260-.060) .051 (<LOD-.057-.470 (.260) .120) . The U. and nephropathy developed (IPCS.130-. HCH isomers are absorbed after inhalation. FDA pesticide monitoring program has shown a temporal decline in the detection of lindane.090 (. Fourth National Report on Human Exposure to Environmental Chemicals 105 .380 (.170-. 1986).287 (.130 (.040-.064 (.081-.073-. **In survey period 2001-2002. The beta isomer accumulates in fatty tissues and is metabolized more slowly.400) .5528.360 (.140 (.814) . Acute high doses of lindane after ingestion or excessive skin application of the 1% lotion have produced seizures in humans.420-.080-.560 (. 1983).910 (.056-.175 (.120 (.070-.S.01 (.100) .300-. resulting in a half-life of about seven years..118-.210) .050) .100 (.092 (.080) .254) 95th .120 (.190-.410) .450) . 1977).200-.047-.340) .048 (<LOD-.450-.370-. or dermal exposure.057-.065 (.450 (.191-.150 (.090-.065 (.150) . and memory loss (Nigam et al.080 (.250-.340-.280-.100) .250) .070 (. tremors.066) Selected percentiles ( 95% confidence interval) Total * * 50th < LOD < LOD < LOD 75th . each result has been multiplied by 1.050 (.110) .174) .139 (.510) .294-.216 (.089-.230-.096) .410 (.250 (. which may vary for some chemicals by year and by individual sample.050 (.214) .290 (.078 (.110) .190-1.124-.140) .131-.200 (.690) .05) .050-. and seizures.404) .442 (.480 (.331 (.290 (.250 (.310) .320 (.350 (.330 (.319) .091) .480 (.050-.150) . 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.068-.200-.120-. 1981).310 (.080) * * * * * * . OSHA and ACGIH have established workplace standards and guidelines.070-.710) .120-.470) .501) .308-.220 (.144 (. 2008.080-.120-.062 (.250-.400) .150-.062 (.160-.170-. paresthesias.220-.661) 901 1067 952 992 1224 1007 Females ..057) < LOD Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 99-00 01-02** 03-04 .050 (<LOD-. Human health effects from HCH isomers at low environmental doses or at biomonitored levels from low environmental exposures are unknown.056-.173-.350) .072 (. When animals were chronically fed lindane at high doses.070) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.160 (.070 (.110) .051-.120) .110-.210-.080-.120 (.083 (. Rogan.050-. 1971. U.460) . for lindane.234 (.410-.130) .190) .700) .221-. Saxena et al.310) .280-.260) .160) . HCH crosses the placenta and is also excreted in breast milk (Radomski et al. 2002).146-.330-.100-.070-.119) .297-.382-.059-. See the section “What’s New” at the beginning of this Report for details.210 (.118 (.460 (.222 (.240-.220) .067 (. EPA has established a drinking water standard.240 (.086) < LOD < LOD < LOD < LOD < LOD < LOD .080 (.050-.089) . Survey years 99-00 01-02** 03-04 Geometric mean (95% conf.412 (.250 (.587) 653 758 589 1240 1533 1370 20 years and older .077) < LOD .069) .37) 1.390-.

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

In a small study of adults who consumed sport fish from the Great Lakes. 1986. 1998). 2005).. respectively... * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 2003). 1971). interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD < LOD size 1799 2280 1960 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD < LOD 90th * * * Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 660 758 593 1139 1522 1367 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 863 1060 952 936 1220 1008 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 631 563 461 380 509 490 646 1045 884 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the lipid adjusted serum level. A study of Swedish women aged 54 years and older reported a median beta-HCH level that was slightly higher than the geometric mean for women reported in the NHANES 1999-2000 survey period (Glynn et al. the median beta-HCH levels were similar or slightly higher than the 95th percentile in this Report (Anderson et al. 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. Survey Geometric mean (95% conf.Organochlorine Pesticides 2001-2002 survey period (Link et al.. in this Report (Nigam et al.S. Finding a measurable amount of HCH isomers in serum does not mean that the level of HCH isomers causes an adverse health effect. Fourth National Report on Human Exposure to Environmental Chemicals 107 . Radomski et al. 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. which may vary for some chemicals by year and by individual sample.. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 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).

et al. 4/21/09 Anderson HA. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. Piechotowski I. Int Arch Occup Environ Health 1983. Rothman N.27:405-421. et al. et al. PA. Needham LL. Bhatnagar VK. Organochlorine pesticides and polychlorinated biphenyls in human adipose tissue. Astolfi E. Demographic and seasonal influences on human serum pesticide residue levels. Falk C. J Assoc Off Anal Chem 1988. Karnik AB.96:34-4Food and Drug Administration (FDA). Environ Health Perspect 1998. Angerer J. Stehr-Green. Potischman N.48:127-134. Wood PH. Granath F. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. Krishna Murti CR. 108 Fourth National Report on Human Exposure to Environmental Chemicals .120:1-82. Environ Res 2004. Seiwert M. August 2005. Saxena MC. J Toxicol Environ Health 1989. et al. available at URL: http://www. Siddiqui MKJ. Rey AA. Kashyap R. Zaidi SS.fda.71(6):1200-1209. Olson J. Brinton LA. Cerrillo I. Botella B.atsdr. Toxicol Appl Pharmacol 1971. Link B. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. Bjerselius R.205:297-308.html. Aune M. org/documents/jmpr/jmpmono/2002pr08. Olea-Serrano MF.111:349355. The Great Lakes Consortium. Gabrio T. Sturgeon SR.150:981-990. International Programme on Chemical Safety (IPCS).gov/~dms/pesrpts. Radomski JL. Bhargava AK. VI.57(4):315-320. Kutty D.54:1431-1443. Blood levels of organochlorine pesticides in Argentina: occupationally and nonoccupationally exposed adults. and HCB residues in human blood in Ahmedabad. Patterson DG Jr. and other chemicals. Kaus S. Levels of DDT. Garrett N. Gunderson EL. Environ Health Perspect 2003. 2002. Occupational exposure to hexachlorocyclohexane. Darnerud PO. Cancer Causes and Control 1998. Bull Environ Contam Toxicol 2004. Chemosphere 2005. Biomonitoring of persistent organochlorine pesticides. Lepom P. Serum concentrations of organochlorine compounds and endometrial cancer risk (United States). Deichmann WB. Absorption of lindane (g benzene hexachloride) in infants and children. Saiyed HN.cdc. Burse VW. Glynn AW. Raju GS. Nigam SK. Metabolism of gammahexachlorocyclohexane in man. et al. Ellis H. Herrman T. Needham LL.9(4):417-424. Visweswariah K. Lowry W. Crespo J. India. et al. dietary intakes of pesticides. Exposure of women to organochlorine pesticides in Southern Spain. Zoellner I.html. Reisch JS. Brock JW. 4/21/09 Ginsburg CM. Arch Toxicol 1981. Olea N.72:261265. FDA total diet study. Rogan WJ. Paepke O. et al. Pesticide residues in food-2002-Joint FAO/WHO meeting on pesticide residues.91:998-1000. Bai KM.cfsan. Toxicological profile for hexachlorocyclohexanes update [online]. Krause C. Needham LL. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Available at URL: http://www. Lindane. Schulz C. Heinrich R.inchem. Hanrahan L. Int Arch Occup Environ Health 1986.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Serum hexachlorocyclohexane residues in workers engaged at a HCH manufacturing plant. Available at URL: http://www. August 2008. Arch Pediatr Adolesc Med 1996. Kulkarni PK. Chemosphere 2004. J Pediatr 1977. 4/21/09 Kutz FW.52(1):59-67.20(2):186-193. selected elements. gov/toxprofiles/tp43. Majumder SK.htm. Int J Hyg Environ Health 2002.58:1185-1201. Bates MN. Atuma S. Bottimore DP. HCH. Organochlorines in Swedish women: determinants of serum concentrations. Becker K. children and newborn infants. Buckland SJ. Rev Environ Contam Toxicol 1991. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Pollutants in breast milk. FDA Pesticide Program Residue Monitoring 1993-2006 [online].106(5):279-289. Maass R. Placental transfer of pesticides in humans. Rivas A. April 1982 to 1984.

and 03-04 are 14. disposal.5-82.Organochlorine Pesticides Mirex CAS No.7) < LOD 66. which may vary for some chemicals by year and by individual sample. and 7. sediments. 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.8) < LOD 15.2) 51. 1995).70 (<LOD-15.70-40. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 57. see Data Analysis section) for Survey years 99-00.5 (<LOD-115) 153 (30. Mirex binds strongly to soil. soil. Fourth National Report on Human Exposure to Environmental Chemicals 109 .7) 8.1) 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 16.0-374) 11.8 (<LOD-73.6 (<LOD-108) 9.4) 617 548 459 398 500 484 688 1049 884 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.70-24.1 (13. Some states and the U. it is a highly persistent chemical in the environment.S. respectively.6) 9.5..7 (12.10-37. resulting in exposure to newborns and nursing infants. aquatic organisms. mirex was detected in human adipose samples. 10. Mirex is not metabolized in the body. In studies conducted in the 1970’s and 1980’s. Mirex is absorbed through the skin and from the gastrointestinal tract.1 (<LOD-65.0 (14. Survey Geometric mean (95% conf. population from the National Health and Nutrition Examination Survey. or pesticide application.5 (9.3 (15.8 (12.0 (12.90-29. after which it is widely distributed in the body and stored in fat. where it was applied directly to soil and by aerial spraying.3 (15. Mirex has been detected in air.40 (<LOD-13. especially those from persons living in the southeastern U.5 (<LOD-42. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.8. animals. 2385-85-5 General Information Mirex has not been produced or used in the U. Ingested mirex that is not absorbed is eliminated in the feces within about 48 hours.4) < LOD 63. 1985.7 (<LOD-47.3-225) 15. 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. EPA have issued public health advisories or warnings that fish from contaminated lakes and rivers may contain mirex. < LOD means less than the limit of detection.4 (8.3) 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. its major uses were as a flame retardant additive and as a pesticide to kill fire ants and yellow jackets in the southeastern U.2 (7. where it has a half-life of 12 years. Occupational exposure is limited to workers at sites where mirex contamination is present. Formerly. (Kutz et al. Mirex can cross the placenta and be excreted in breast milk.6.4) < LOD 15.2-230) 13.1 (8.0) * * * Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 19.1 (<LOD-104) < LOD < LOD < LOD < LOD 39.5-291) 11.6 (<LOD-31.6 (<LOD-23.S..4-230) 18. Mirex contamination of Lake Ontario and adjacent waterways has been well documented (ATSDR. water.6) size 1853 2257 1951 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th 15.S.5-425) 40.10 (<LOD-15.0 (<LOD-108) < LOD < LOD 50. and foods.S. 01-02. since 1977.S.6-305) 15.6) < LOD < LOD < LOD < LOD 71.3) < LOD < LOD < LOD < LOD < LOD < LOD < LOD 15. 1991).

102) < LOD < LOD < LOD < LOD .220) . environmental levels) and health effects is available from the ATSDR at: http://www.79) .110 (<LOD-.html.470) .140 (<LOD-. developmental abnormalities including cataracts and edema in the offspring have been reported (ATSDR..690) .090 (<LOD-.089-. The geometric mean mirex levels of the Inuit mothers were 8. The U.240) < LOD < LOD < LOD < LOD < LOD < LOD < LOD . serum mirex levels were generally below the limits of detection (Stehr-Green.220 (<LOD-.053-. population from the National Health and Nutrition Examination Survey. and NTP classifies mirex as reasonably anticipated to be a human carcinogen.310 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD .059 (<LOD-.atsdr.215) 659 728 592 1194 1529 1359 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .450 (.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 .079 (<LOD-. which is approximately twofold to threefold lower than the 90th percentile for females in the NHANES 20012002 subsample but similar to 95th percentile for females in the NHANES 2003-2004 subsample (Van Oostdam et al.052-. 110 Fourth National Report on Human Exposure to Environmental Chemicals .090-1.268) < LOD .093 (.170) size 1853 2257 1951 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .108 (. Survey Geometric mean (95% conf.090-1. which may vary for some chemicals by year and by individual sample.e. as well as in a subsample of NHANES II (1976-1980) participants. 2001-2002.635) < LOD .100 (<LOD-. and the FDA monitors foods for pesticide residue and has established an action level for mirex in fish tissue.92) . Biomonitoring Information In the NHANES 1999-2000.410 (.112 (.055-.077 (<LOD-.170-3.37) .7 ng/g of lipid.090 (<LOD-. reproductive toxicity included decreased fertility and testicular damage.8.41) .070-1.450) 1. and 2003-2004 subsamples.73) .064 (<LOD-.090-1.Organochlorine Pesticides exposures are unknown.090 (<LOD-. Fishermen in New York who consumed Great Lakes sport fish had median levels of lipid-adjusted serum mirex that were lower than the 95th percentile value among males the NHANES 2001-2002 subsample (Bloom et al. 7.100 (<LOD-.gov/toxpro2.610) < LOD < LOD < LOD < LOD . 1991).170) < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.470) .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. Smith.062-. IARC classifies mirex as possibly carcinogenic to humans.79) . In samples obtained between 1994 and 1997. and 4.430 (. 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) 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 . 1989)..02) .080-1.106 (. More information about external exposure (i.510) < LOD < LOD .08 (. EPA has established environmental standards for mirex. Laboratory animals fed high doses developed liver enlargement and liver tumors. 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. 1995.256 (.470 (. In addition..370 (.cdc. 2004).054 (<LOD-.080-1. 2005).S.106) < LOD .S.

Inc. J Toxicol Environ Health 1989. New York. August 1995. Vena JE. Fourth National Report on Human Exposure to Environmental Chemicals 111 . Academic Press. Strassman SC. Gilman A. et al. 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. 731-915. Bottimore DP. 2 Classes of Pesticides. Demographic and seasonal influences on human serum pesticide residue levels. 1994-1997 organochlorine compounds. Chashchin V. Kutz FW. Smith AG. Available at URL: http://www. Carra JS.cdc. Leininger CC.120:1-82.97(2):178192. Handbook of Pesticide Toxicology. Odland JO. Moysich KB.Organochlorine Pesticides effect. Jr. hexachlorobenzene. et al.atsdr. Wood PH. Stroup CR.330:55-70. Jr and Laws ER. 4/21/09 Bloom MS. Environ Res 2005. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Sci Total Environ 2004. Vol. Toxicological profile for mirex and chlordecone [online]. In Hayes WJ. Van Oostdam JC. Chlorinated Hydrocarbon Insecticides. Dewailly E. dichlorodiphenyldichloroethylene. Watts DL. References Agency for Toxic Substances and Disease Registry (ATSDR). Stehr-Green.27:405-421. Organochlorine pesticides and polychlorinated biphenyls in human adipose tissue.html. The human body burden of mirex in the southeastern United States.gov/toxprofiles/ tp66. Profiles of ortho-polychlorinated biphenyl congeners.15:385-394. Swanson MK. J Toxicol Environ Health 1985. Olson JR. and Mirex among male Lake Ontario sportfish consumers: the New York State Angler cohort study. PA. Hansen JC. Circumpolar maternal blood contaminant survey. Kutz FW. 1991 pp. Rev Environ Contam Toxicol 1991. Eds.

2.6-TCP were used as intermediates in the production of certain pesticides. which may vary for some chemicals by year and by individual sample.60 (. General population exposure may occur by ingesting contaminated food or water and by inhaling contaminated air.950 (<LOD-1.30-40. Exposure to trichlorophenols also may result from metabolism of lindane. 1976).40 (1.5-Trichlorophenol Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.40) < LOD 1.4. EPA.40) < LOD 4. soils.0) < LOD 5.980-3.50-16.0 (5. Formation of 2.8-tetrachlorodibenzo-p-dioxin occurs during the synthesis of 2. and polychlorinated benzenes (Kohil et al.4.60-8.00-3.72) < LOD 1.7. surface water.80 (2.4. 95-95-4 2.4.6-Trichlorophenol CAS No.4. 2.80) < LOD 1.0) 2.0 (3.0) 2. 2.3.20 (4.5-trichlorophenol.71 (<LOD-8.0 (4. are metabolites of several organochlorine chemicals.30-27.0 (8.0) 2.40-18.20) < LOD 90th 5. Environmental sources of these compounds include industrial discharges or run off from pesticide facilities or disposal sites.30-3.30-11. Trichlorophenols have been detected in fish taken from waters near waste water treatment and industrial discharges (ATSDR.0) < LOD 973 1178 1021 1319 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.20) < LOD 5.30-27. 1999).5-Trichlorophenol CAS No.40 (1. including hexachlorobenzene and hexachlorocyclohexanes.20-36.4.S.31 (<LOD-9.40 (2.40 (2.10-3.6-TCP).63) 18.60 (4.5-TCP) and 2.00-3.00 (2.40 (2. Such workers would probably Urinary 2.80 (1.0) 5.30) < LOD < LOD < LOD < LOD < LOD 1.60 (2.27) 482 570 681 815 831 1112 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD 1.50 (1.60) < LOD 8.7) 24. interval) Selected percentiles ( 95% confidence interval) Sample 95th 16.9 (<LOD-121) 9.4.4.42 (<LOD-8.9 and 0.40 (.0 (4.60-18.6-TCP in any of the samples (U. Occupational exposures.00-8.00 (3.57 (<LOD-15.0) < LOD 5.50) < LOD 1.0) < LOD 5. recent sampling of U.5-trichlorophenol (2. however.0) 2.19 (<LOD-6.0) 2.30-44.0) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 1.5TCP and 2. usually at herbicide production or waste incineration facilities. population from the National Health and Nutrition Examination Survey. public drinking water systems did not detect 2.8) 21. may occur by inhalation or dermal routes.Organochlorine Pesticides 2.S. Historically.50 (2.4. and sediments.S. < LOD means less than the limit of detection. hexachlorobenzene.0) 2. Trichlorophenols are no longer manufactured commercially.4.40) < LOD 6.0 (4.980-3.0) 14.4. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.27) 696 661 521 696 603 939 Limit of detection (LOD.0 (3.50 (.4. 1999).20-71..0) < LOD 11.50-63. Survey Geometric mean (95% conf.30 (.42 (<LOD-12.30) < LOD 4.40-11.9.940-3.920-3. but they may be produced as by-products during manufacturing of other chlorinated aromatic compounds.40 (2. Small amounts of trichlorophenols also can be produced during combustion of natural materials and the chlorination of drinking water or waste water that contains phenols.900-2.03) 9. 88-06-2 Metabolites of Organochlorine Pesticides and Other Environmental Chemicals General Information The chlorophenols. 2006). Both chemicals have been detected in air. other organochlorines.6-TCP was also used as a wood preservative and may still be used in production of some fungicides (ATSDR.71 (<LOD-8.27) 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. 112 Fourth National Report on Human Exposure to Environmental Chemicals .90-33.20) < LOD 1.40 (.80-41.0) < LOD 21.30-27.6-trichlorophenol (2.50-25.0) < LOD 11.

57 (3.55 (4. and other chlorinated compounds. In the same 2-6 year old children. Biomonitoring Information In the NHANES 1999-2000 and 2001-2002 subsamples.78 (3.32) < LOD 4.6-TCP at low environmental doses or at biomonitored levels from low environmental exposures are unknown.. Radon et al.820-2.24-11.68 (<LOD-8.8 (5.4.20-6. furans.2) < LOD 5.57 (<LOD-7. 1989).67 (1.31) < LOD 2. 2003.13-13.44 (1.68-4. Among 6-11 year old children in NHANES 1999-2000.Organochlorine Pesticides be exposed to mixtures of chlorophenols.16 (.4. Laboratory animals chronically fed high doses of 2.980 (<LOD-1.95 (3.02-3.4. IARC classifies combined exposures to polychlorophenols.33) < LOD < LOD < LOD < LOD < LOD 2.67 (1.4.4) < LOD 3.05-17..82 (<LOD-32.4.75 (<LOD-6.00) < LOD 4.6-TCP levels at the 95th percentile were up to eight times higher than 3. 1995) were similar.3 mg/L in a nonrandom subsample from NHANES III (Hill et al. Urinary 2.64 (4. environmental levels) and health effects is available from ATSDR at: http://www.19-4.37-11. as being possibly carcinogenic to humans.49 (1. population from the National Health and Nutrition Examination Survey.11) 482 570 681 814 831 1112 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD 1.02) < LOD 7.37) 696 661 521 695 603 939 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.78-19.920-2. Survey Geometric mean (95% conf.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.05-8.4.4. was similar to the corresponding percentile for 6-11 year olds in NHANES 1999-2000 (Hill et al.5) 11. More information about external exposure (i.0 mg/L. IARC considers the experimental evidence for animal carcinogenicity inadequate for 2.2) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 2. 1989).6) 4.4.5-TCP and limited for 2.69 (2. Neither 2. recent small studies have not demonstrated increased exposure to trichlorophenols in workers who dredged contaminated soils or incinerated waste materials (Agramunt et al.53-3.4 (6.5-TCP among adults in this Report and in a nonrandom subsample from NHANES III (Hill et al. interval) Selected percentiles ( 95% confidence interval) Sample 95th 11.90 (4. the 95th percentile urinary 2.4. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.S.6-TCP were developmental or reproductive toxicants in animals (ATSDR 1999).gov/toxpro2.78) < LOD 1.43) < LOD 12.. 7.5-TCP.5) < LOD 12.43 (2. The 95th percentiles for 2. leukemias.html.81 (<LOD-9. urinary 2.46 (1. which includes trichlorophenols.17) 9.4) 5.6-TCP. NTP classifies 2. Human health effects from 2.69-18.6-TCP as reasonably anticipated to be a human carcinogen. 2003).24) < LOD 5.74) 11.8) < LOD 9.47-8.24 (3.60-3. Fourth National Report on Human Exposure to Environmental Chemicals 113 .80 (1.24) < LOD 1.44 (.0) 7.57 (<LOD-7.1 (<LOD-58.9 (5.79-4.36 (1.4.62-20.3 (5.00-19.6-TCP had increased rates of hepatic tumors. However. At lower doses.8) 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.53-3.5-TCP or 2.6) 4.cdc. but almost twenty times higher than 95th percentile values reported in German adults aged 18-69 years (Becker et al.86 (3.15) < LOD 2.4..93-11. animals showed hepatocellular abnormalities.9) 12. 2003).4.1) 2. the 95th percentile urinary 2.73 (<LOD-8.27-17. 2004).28-25.7 (4..atsdr.5-TCP nor 2.4...6) 4.4) < LOD 3.24) < LOD 6.3 mg/L reported in German adults aged 18-69 years (Becker et al.88-16.11) 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 2.50) < LOD 2.e.16) < LOD 90th 5. 1995) and up to 19 times higher than the 95th percentile value of 1.2 (2. in addition to dioxins.19-12..2) 2.00-29. and lymphomas.75 (3.83-12.37) 16.29 (1..3) < LOD 973 1178 1021 1318 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .

0-44.2) 25. Biomonitoring data will also help scientists plan and conduct research about 2.20 (3.40) 4.8) 32.S.9 (11.70-6.0 (15.70-3..98-11.48-26.0 (20.0 (14.10 (5.85) * 3.4.58 (1. Sawmill workers exposed to chlorophenol wood preservatives had urinary 2.3 (11.0 (8.70-6.30) 4.80 (3.70) 5.3) 23.4.30-2.63) 90th 15.0) 17.40) 2.23) 3.5-TCP or 2.91-4. Finding a measurable amount of 2.6-TCP in urine does not mean that the level of 2.50 (2.95-6.5-TCP (0.0 (6.65) 15. respectively.60-37.35-3.45) < LOD 11.0) 6.4.10) 6.6-TCP provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of 2.70) 3.0 (6.20-3.0) 9.10-2.0 (15.90 (3.2) 12.7) 33.67) 4.0) 7.0) 19.0-18.8 (9.23) 2.95) 3.1 (10.46-3.7 (9.50-5.6-Trichlorophenol Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.Organochlorine Pesticides A small study of adults who ate Great Lakes sport fish reported a mean urine 2.6 mg/g creatinine) and 2.00-21.5-TCP and 2.92 (2.52-3.0) 14.0) 15.18-3.45 (2.4.31 (3..0 (11. population from the National Health and Nutrition Examination Survey.6) 26.0) 13.44) 75th 4.0 (20.5-46.4-17. see Data Analysis section) for Survey years 99-00 and 01-02 are 1. Mean values of 2.4. 1991).4.40) 3.79 (5.52 (2.3) 20.31) * 2.80-20.09-7.07 (<LOD-3.5-TCP level of 0.0-43.59-6. for males in NHANES 19992002 (Agramunt et al.10-3.4. which may vary for some chemicals by year and by individual sample.5-TCP or 2.24 (2.98-7.20 (3.4. Urinary 2.8-24.57 (<LOD-2.4.80-6.0) 10.30-11.00 (2.49 (6.0-54.8-15.7 mg/L.0) 12.2 (14.69 (3.4.0 (4.40-14.70) 1.4.74-3.90) 2.0-37.70 (2.0 (7. Urinary 2.99) 6. 1998).36-5.0) 13.4.20-23.0) 13.26 (2.10) 2.6) 970 1178 1019 1325 99-00 01-02 99-00 01-02 99-00 01-02 2.6-TCP level.45-9.7) * 99-00 01-02 99-00 01-02 99-00 01-02 4.4.4.40-7.5 mg/g creatinine) were similar to the limit of detection for 2.33-4.78 (2.65 (5.40-32.0 (16.68 (<LOD-2.30-33.56 (3.8) 18.74 (2.0 (12.6 (12.60 (2.58-3.32) 3.4 (9.6-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.53) 4.28) 24.54) 6.4.0-38.14 (2.40-2.0 (9.51-12.23-2. Survey Geometric mean (95% conf.0 (13.84) 2. interval) 2.32) * 3.59) 4.0 (6.20) 4.00-4.0) 9..00 (1.28) * 2.73-9.47 (3.60 (3.6) 21.6-TCP (0.7 (13.6TCP values. 114 Fourth National Report on Human Exposure to Environmental Chemicals .3-17.3 (11.06) * 2.87-14.90-8.6-17.10-3.18) Selected percentiles ( 95% confidence interval) Sample 95th 25.7) 21.01-6.0) 11.80 (2.80 (2.25-11.80-7.40 (2.53) 2.85 (2.0 (8.45 (5.12) 2.04) 2.0) 13.1-25.02) 2.66 (8.95 (4.80-25.08 (2.0-38.9) 694 677 519 696 602 931 Limit of detection (LOD.4.0) 7. 2003).2-0.60-3. Biomonitoring studies on levels of 2.00 (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 2.8-13.9 (13.4.4 (17.6-TCP were monitored in a group of hazardous waste incinerator workers from 19992002.32-4.5-TCP and to the median 2.6TCP causes an adverse health effect.36 mg/g creatinine.0 (14.89-6.4.4 (10.67-12.3.60-21.0) 17.90 (4.0) 14.0-50.70) 5.5-TCP or 2.4.6-TCP than are found in the general population.40-2.7-16.75 (8.0 and 1.70 (2.76) 3.4.6-TCP exposure and health effects.0 (14.5-TCP or 2.7-3.5-TCP and 2. was about six times lower than the median urinary levels for males in this Report (Radon et al.1 (8. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.1) 16.6 (11.0) 11.40-4.60 (3.0) 19.6-19.2) 481 574 678 820 830 1109 99-00 01-02 99-00 01-02 2.0-68.0) 10.3) 37.0-41.6-22.30-2. < LOD means less than the limit of detection. 0.60) 6. the median urinary 2.3-26.9) 13.78 (2.80) 1.72-10. similar to the limit of detection for this Report (Anderson et al. In harbor workers exposed to chlorophenol-contaminated river silt..40) 2.40 (2.09) 15.55-3.60) < LOD 5.4 (8.20-6.89 (3.36 (1. 2004).

05 (6.6) 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 2.89-2.52) 2.15 (6.42) 2.22-9.90) 2.4) 9.88-7.4 (12.14-13.88) 4.3) 8.38) 22.17) 13.73-22.87) * 2.8 (8.23) 4.51 (2.52 (3.02) 3.54 (2.4) 8.75) 75th 4.87 (3.05 (3.95-2.8) 11.56-5.49-3.90 (1.68) 2.2) 19.83-6.76) 1.9-64.38 (4.9) 481 574 678 819 830 1109 99-00 01-02 99-00 01-02 2.6-Trichlorophenol (creatinine corrected) Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.29 (6.66-4.9 (9.88 (2.72-16.79-17.Organochlorine Pesticides Urinary 2.7-36.6) 8.06) 4.88) 5.56 (7.1-21.5) 11.30-2.26 (6.88) * 2.43 (2.33 (7.02 (1.77-4.1) 14.76-8.9 (9.5) 8.16-10.91-2.53-11.11) 10.06-2.09-3.60-2.13-6.35 (3.1) 694 677 519 695 602 931 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.1 (8.40 (7.83-5.6 (10.2 (8. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.18-4.14-2.32 (2.71 (3.33) * 2.94-13.5 (10.51) 18.63 (<LOD-2.2 (7.38-5.63) * 4. interval) 2.41-6.06) 11.33 (1.87-6.4.50-8.6 (5.98 (1.4) 4.29-4.13 (1.52 (5.6 (6.55-2.6) 970 1178 1019 1324 99-00 01-02 99-00 01-02 99-00 01-02 2.73) 5.0) 10.82 (8.51-21.78) 90th 12.01 (3.22 (<LOD-2.53 (3.8) 19.1 (13.21-11.25-2.70-9.1) 11.23 (1.20-2.6-31.78 (2.1-32.63) 4.63-13.17-4.04-16.25 (3.3-23.40 (2.7 (14.S.53) 4.82-2.9-29.46-14.3 (9.04-2.78) 2.9) 8.10-9. Survey Geometric mean (95% conf.33-2.9) 7.63 (2.58 (4.10) 4.5) 11.87-7.18-2.32-19.22 (3.4 (11. population from the National Health and Nutrition Examination Survey.2 (12.44 (3.9-34.9-32.88) 1.5-28.52) 2.41 (3.0 (6.65) 2.2 (13.82 (3.6) 13.3-37.22 (1.6 (9.91 (7.8 (7.59 (2.7) 6.49) 4.65) 18.77) 2.53) * 2.81) Selected percentiles ( 95% confidence interval) Sample 95th 21.0 (9.60 (4.00) 4.27-9.5) 9.62-15.83-6.38 (2.5) 12.22-2.6 (22.43-7.25-17.6 (12.83 (3.76) 2.25 (3.81) 2.9) 19.15 (1.0) 8.26-13.82) 2. Fourth National Report on Human Exposure to Environmental Chemicals 115 .7) 25.26) * 99-00 01-02 99-00 01-02 99-00 01-02 4.25-15.68) 2.00 (2.96) < LOD 4.08-2.5 (8.50 (2.17) 2.6 (9.91 (3.0 (11.28-4.19-5.9) 8.29-4.99-2.87) 2.43 (<LOD-2.81-9.88) 4.76) 4.63-15.42 (2.10 (6.48-2.00) 4.92) 4.6) 12.56) < LOD 11.8) 21.47-5.72) 32.8) 12.98) 10.24 (1.5 (7.00 (3.65-2.65-21.67-17.89) 10.

U. Jarvisalo J. Int Arch Occup Environ Health 1991. Hill RH Jr. 4/21/09 Agramunt MC. Urinary excretion of chlorinated phenols in saw-mill workers. Aitio A. Hanrahan L.45:440-445. Int J Hyg Environ Health 2003. Bailey SL. Can J Biochem 1976.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Corbella J. Holler JS. S.epa. Falk C. Wegner R. Domingo A. Kohli J. Environ Health Perspect 1998. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children. Pekari K. To T. Fast DM.71:99108. Lindroos L. et al. Available at URL: http://www. Olson J. Environ Res 1995. et al. December 2006 Draft. The metabolism of higher chlorinated benzene isomers.gov/safewater/ccl/pdfs/reg_determine2/report_ ccl2-reg2_ucmr1_occurrencereport.S. Monitoring internal exposure to metals and organic substances in workers at a hazardous waste incinerator after 3 years of operation. Baur X. Anderson HA. Seiwert M.pdf. Environmental Protection Agency (U. Baker S. Schulz C. Safe A.106(5):279-289.EPA). Needham LL. 5/19/09 116 Fourth National Report on Human Exposure to Environmental Chemicals . Hill RH Jr. Head SL. Heinrich-Ramm R. Gregg M. 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]. Arch Environ Contam Toxicol 1989. Seifert B. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine.63:57-62. Chlorophenol exposure in harbor workers exposed to river silt aerosols. Needham LL. Am J Ind Med 2004. Jones D.18(4):469-474. Kaus S. Domingo JL. Szadkowski D. Pesticide residues in urine of adults living in the United States: reference range concentrations. Becker K. Toxicol Lett 2003. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. html. July 1999.146:83-91. Burse VW.gov/toxprofiles/tp107. Radon K. Available at URL: http://www. et al. Luotamo M. 206:15-24. Toxicological profile for chlorophenols [online]. Poschadel B. The Great Lakes Consortium. Shealy DB.54(3):203-208. Smith SJ.atsdr.cdc.

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

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

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

981 (.02-5.82) 10.20 (.10) < LOD .50 (.6) 7.37 (3.80) 4.0) 6.26-8.970-2.76 (2.98-12.08-15.83 (5.34-3.60-25.0) 10.490-2.0 (6.22 (.1.07-10.08-2.2 (14.700-1.96-3.52) * * 1.954 (.20-4.80) .0) 10.39 (3.00 (4.48-7.2) 16.46) 10.0) 5.10 (2.0) 6.90 (1.2) 14.66) * * 1.7 (14.21) 9.860-2.51) 2.45 (2.90-5.44 (2.54 (3.56 (1.00 (1.80) 2.599-1.20 (.52-11.1-17.0) 10.13 (2.56 (4.63) 1.58 (5.1 (10.89) 9.14) * * .2.81) 11.0 (12.82-12.290 (<LOD-1.56 (6.10 (.2 (7.99 (5.9 (8.00-27.8) 7.757-2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.47) 5.8) 7.0 (8.10-7.79 (5.97) 90th 7.00 (5. < LOD means less than the limit of detection.32) 1.38-5.810-1.20-7.13-2.2 (7.2) 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 1.80) 3.42) .4) 18.70) .73) * * .40-16.70-23.23-5.60 (1.39 (8.34-7.80) 11. 01-02.2 (9.750-1.0) 5.43-12.1) 13.81) 11.98-5.290 (<LOD-.35-12.17-3.2 (14.55-6.53) 4.26 (5.8 (12.2) 672 678 473 509 696 578 595 948 752 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.81) 1.4 (7.70) < LOD < LOD 1.26-6.94) * * .40-19.80) .8 (14.90) 3.7) 11.0) 7.4) 20.00-12.61) 4.58) Selected percentiles ( 95% confidence interval) Total * * 50th 1.3) 16.20 (.4 (9.30 (4.623-1.5-17.27-3.00-19.830 (<LOD-3.5-16.0) 5.03 (.8) 11.600 (<LOD-1.30-4.40-1.52) 6.33 (5.70-14. 120 Fourth National Report on Human Exposure to Environmental Chemicals .30 (2.40-11.12) 4.04) < LOD 1.57-7.0) 12.840-1.70 (4.4 (9.8-32.0 (9.2 (11.717-1.91) 4.27-15.3) 14.1) 95th 13.55-8.85 (3.44-38.70) < LOD < LOD 75th 3.740-2.10 (.32 (.579-1.50) 2.0-28.40-14.5 (11.9) 8.60) < LOD < LOD 4.44-3.42-3.60-18.4) 17.1 (9.2 (9.0 (8.9) 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 1.8) 19.74 (8.60 (5.00) 3.780) < LOD 3.56-13.30 (2.50-5. respectively.36-4. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. population from the National Health and Nutrition Examination Survey.9-18.2 (7.97) 8.0 (5.0) 11.95) 5.80-22. which may vary for some chemicals by year and by individual sample.70-11.58 (3.50 (4.00-12.60) .29) * * 1.61 (3.60-11.0) 11.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Diethylphosphate (DEP) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.80 (4.93 (4.0) 15.74 (8. and 0.0) 20.35-11.0 (4.70-19.58 (2. 0.10 (2.0-27.530 (<LOD-2.40-5. interval) 1.70 (2. see Data Analysis section) for Survey years 99-00.0) 9.01) * * 1.28) 1.890 (<LOD-2.1-23.0 (7.0) 11.50 (2.30-6.0 (7.2.758-1.9) 14.13 (2.1) 10.4 (7.0) 10.50-36.08 (<LOD-2.2) 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 1.620-1.00) 3.05-7.16) 4.21 (.80-24.86 (1. and 03-04 are 0.10) < LOD < LOD 4.S.20 (.80) 2.20-30.0) 10.0 (9.20 (2.11 (.93-24.15-12.5) 20.19) 9.80 (2.8 (8.0 (7.33-18.2) 16.35-16.47) * * 1.02) 4.0) 6.80) 2.15) 14.5 (8.7 (12.0) 11.16 (2.71-9.670-1.5) 15.67) 3.71 (2.3) 17.80-4.00-27.955 (.00-7.0 (6.6) 18.72) 5.2-20.0 (8.3-15.94) 3.79-7.90) 2.90-4.0 (7.40 (.12-19.68-7.86-15.8 (9.

5-32.830-1.960 (.43 (3.6 (10.40-12. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.79-3.29) * * .60) * * .66-15.98-22.6) 8.8) 6.37-5.98) .40 (3.4 (4.85 (6.890 (<LOD-1.6 (9.00-13.8) 8.80 (6.66-34.61 (1.2) 95th 12.77 (6.8) 7.3) 5.54-11.40-3.46-5.960 (<LOD-2.30) 2.860 (.34 (6.6) 11.04-6.34) * * .54-15.9 (5.57-10.82-6.76) < LOD .83 (7.87-5.31-14.9) 12.9-28.9 (9.30 (1. population from the National Health and Nutrition Examination Survey.430-1.7 (10.45-5.56) 4.820 (.7 (8.9) 16.52) 4.79-9.88 (5.75-7.69) 4.61 (1.25) < LOD .60) 2.34 (6.62) .5) 8.2 (10.41-12.6) 9.93-5.09-11.57 (4.40-14.01-2.0) 7.8 (10.88) 2.02-2.37) 9.35 (1.633-1.900 (.1 (9.570-1.39 (2.3) 952 1187 927 997 1332 1001 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.15-10.45-11.94 (4.9 (9.2) 9.883 (.540-1.78 (2.4) 4.83) 8.88-10.35) < LOD < LOD 3.92-5.56) .47) 2. Fourth National Report on Human Exposure to Environmental Chemicals 121 .42) 12.32-12.74) 4.68-4.7) 12.31 (3.00-19.72) 11.8) 12.43) 2.87 (1.510-1.56-13.23) 4.44 (2.24-3.02 (2.855 (.62-5.76-4.03 (2.66 (2.05 (1.440 (<LOD-2.02-14.10-13.28-9.93) 9.82-14.560-1.28 (4.1-15.85) 2.1) 4.03 (7.45-5.608-1.5) 12.37 (5.26) * * .82-14.37 (4.750 (<LOD-1.00-17.61-29.98 (3.40-28.66 (5.21-23.773-1.1) 4.25) 6.60-9.58) * * 1.9) 11.2) 8.19 (4.51-5.500-1. interval) .1 (7.574-1.2) 7.0 (8.8) 16.40) < LOD < LOD 75th 2.13) 4.5) 7.54-2.07 (.03) 2.56) 7.75) 2.0) 6.920 (.47 (3.47 (1.650-1.81 (1.1 (8.50) 7.69) 2.46) 2.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Diethylphosphate (DEP) (creatinine corrected) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.780 (<LOD-1.7) 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.94-9.7 (9.54-4.57 (6.20-8.75 (3.27) < LOD 2.71) 10. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.28 (2.95) 2.40) 4.870-2.620-1.57) 4.09 (.61-13.03-6.69 (4.47 (3.5 (4.95 (3.1 (10.1) 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 1.38) .89) * * 1.98-5.05) .18 (.2) 5.90-8.890 (<LOD-1.3) 12.2 (8.43 (.69-10.7) 5.5-20.4) 4.11-6.41) Selected percentiles ( 95% confidence interval) Total * * 50th .93-9.90-5.54) .53) 9.80 (7.89-3.2 (6.932 (.94-10.53 (6.37-3.81-5.75) 14.924 (.87 (3.88-15.98) 9.818 (.5) 11.98) .04 (1.92-2.5-13.3) 16.710 (<LOD-1.533-1.34) < LOD < LOD .00) 8.14 (3.41) .549-1.36) * * 1.75 (7.2) 5.S.67) 1.7) 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 .28) 10.4) 13.74) 90th 7.84) 7.71-2.4 (9.82-26.566-1.02 (7.67) 4.53-11.29 (2.790 (.996 (.7) 18.06-2.68) < LOD < LOD 3.05 (.40-5.94-22.38 (1.67-19.66 (1.42 (3.64-5.09) 2.80) 9.6) 13.2) 13.00 (4.84 (5.3) 15.23 (4.5) 7.94-23.5-16.1 (6.28 (5.00 (4.10 (3.73 (1.55-20.94 (2.1 (11.47) * * .80 (2.03) 2.

80) .1 (10.3) 10.80-6.27) .8-17.9-14.5 (8.90 (6.86-10.24-5.40) < LOD < LOD 75th 2.16-1.0-24.0) 13. population from the National Health and Nutrition Examination Survey.00-18.0) 12. and 0.7 (11.0) 11.9 (7. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.50-5.20-4.0) 7.60 (5.6) 14.3 (9.6-19.10-15.42 (1.60 (2.8) 8.70) 2.9) 95th 14.61-32.9-17.4) 7.0 (9.0 (15.98-9.22) 8.80-4.0) 14.80-3.11-6.14 (6.34 (6.910 (<LOD-2.0) 18.74) * * * * * 1.00-16.740 (<LOD-1.40 (2.80-14.70 (1.70 (8.88) 3.0) 12.58.4 (14.35-3.29) < LOD < LOD < LOD < LOD 3.92) 9.95 (2.3) 20.8-21.50) .00) 3.S.1) 11.5-26.66-13.0) 9.00-4.20) 3.39-13.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.5.75 (3.34-5.30) < LOD < LOD 4.67-10.00-18.01 (2.00) < LOD .34-3.04 (3.72) 2.70-5.0-29.33-11.59-3.29-4.10-4.0 (5.6) 18.27) 4.90 (5.5 (9.6-41.27) 9.7) 15.9) 16.10 (.35) 4.7) 14.5 (8.82) 8.63-14.90 (2.22-12.81-6.18 (3.0) 19.5.00-4.50-4.3) 22.34-10.64) 10.80-12.90 (6.0 (10.970 (<LOD-2.4 (10.49-4.0 (7.9-15.95 (5.90) 4.80 (2.35 (6.2) 14.0) 23.90-9.0 (14.89) 2.58 (1. see Data Analysis section) for Survey years 99-00.7) 22.7) 16.580-2.3 (12.77-14.7-21.9 (12.4) 672 678 498 509 695 579 595 948 757 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.92-17.8 (12.73) 7.90-15.53 (3.3 (7.5) 21.80-8.4-17.27 (7.20-8.22 (6.9) 9.7 (10.90 (2.650-1.5) 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 * * * * * * .8-20.80) .80 (2. 0.00) 3. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th .88) 10.31-12.8) 9.0 (8.3) 8.790 (<LOD-1.99 (3.62-17.10-10.670 (<LOD-1. which may vary for some chemicals by year and by individual sample.8-20.20) .2 (9.00) 7.90) 8.50) 3.31-7.27 (3.30) < LOD < LOD .97-4.3) 14.80) 5.66) 4.3 (6.77-3.22 (6.12 (4.50) 5.41-5.0) 14.30) 8.0 (13.1-23.75 (2.17 (7.96) 3.3 (11.60) < LOD < LOD 2.61 (3.70-9.6) 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) 12.680 (<LOD-1.90 (6.6) 11.4) 11.80 (5.51) < LOD 1.00) 8.46-28.28 (7.7-19.6 (10.25 (2.10 (<LOD-1.15-6.0-24.89 (2. and 03-04 are 0.96) 90th 7.41) 3.9) 10.18) * * * * * * * * 1.90 (1.10) 6.90-15.37) 2.67) 4.0 (10.0-19.24 (2.52 (6.70-9.80-21.0) 6. 01-02. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.78) 5.8 (12.31) 1.70-8.0) 11.37 (3.84-4.20-18.95-9.8) 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 1.90 (6.670 (<LOD-1.06 (2.45 (3.670 (<LOD-1.20) 3.0) 9.60 (6.90-31. respectively. 122 Fourth National Report on Human Exposure to Environmental Chemicals .670 (<LOD-1.1 (10.6) 14.67) 3.30) 3.3 (9.46-4.40 (2.20 (<LOD-2.39 (5.4 (10.7) 10.6 (10.00 (.15-2.2 (7.47-6.90 (2.00-9.0-33.0) 13.30) 3.0 (9. < LOD means less than the limit of detection.

7 (8.28 (1.973 (.5) 10.70-35.29 (5.4) 6.780-1.11 (5.7) 14.4) 7.23-3.75-3.7) 14.78-10.25 (4.8) 11.77) 3.68-19.51-10.6 (10.5) 22.3) 9.4-16.86-3.77 (2.95 (2.2) 12.48 (2.27) * * * * * * * * 1.760 (<LOD-1.72-4.1) 10.30-5.6 (12.54-5.89-13.3) 8.920 (<LOD-1.4) 16.88 (1.6) Sample size 1949 2518 1962 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.64-11.4) 7.00 (<LOD-1.4) 9. population from the National Health and Nutrition Examination Survey.1 (13.74-4.29) 3.00 (2.83 (6.27) 1.86 (3.3) 6.54 (7.9) 19.19) 3.6) 7.91-9.9-17.3 (7.95) 3.93 (2.71 (1.15) < LOD < LOD 75th 2.5 (10.37-5.14 (2.940) < LOD < LOD 1.8 (8.78) 4.8) 14.12 (7.4-15.00) 2.890-2.0 (13.06 (<LOD-1.34-18.20-3.09-11.82-8.2-30.78 (6.0) 14.86) 9.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.75-3.15 (1.2) 10.5 (15.3-21.25-9.58 (4.79-6.33-10.3-17.7-23.2) 12.05-3.78 (4.7 (10.7 (11.63 (2.7) 12.910 (<LOD-1.42) 7.6) 14.38 (2.94-14.850 (<LOD-1.1) 13.79-9.16 (3.03) 3.93 (<LOD-2.530-1.6) 12.69-11.9 (9.50 (6.89-3.68-4. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.28) 6.06) .30) 8.2) 16.9) 16.6) 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 * * * .810 (<LOD-1.52-3.2) 8.38-13.51-7.28-12.6-19.92 (5.18) 2.44-6.3-34.2-15.6 (11.12) < LOD < LOD 4.45) 3.6 (11.8) 16.620 (<LOD-.2) 19.42) 8.39-17.21-21.38) 1.6) 471 576 310 664 821 715 814 1121 937 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * .29-2.04) 9.6) 13.89-10.55 (2.43 (2.09-11.97) < LOD .27) 5.2 (9.4-16.32) 2.32-8.85-17.99 (4.50-17.89 (3.6) 95th 16.55) .6 (13.00 (7.41 (7.96-11.36 (2.80) 3.2) 672 678 497 509 694 578 595 948 756 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.3-17.93-10.38 (1.71) < LOD < LOD 2.1 (8.55) 16.89) 5.S.4) 15.950) .67 (7.2 (9.16-14.97-4.87 (3.6 (13.00 (3.27-13.73 (5.96-10.37) 3.0 (8.7) 9.5 (11.1 (19.5-17.0-21.77 (2.91) 3.3) 12.33) 3.68-10.30) 2.07 (5.45) 6.9-25.2) 15.6) 6.8 (10.34) < LOD < LOD < LOD < LOD 3.5) 13.21) * * * * * 1.42-19.74-19.30) 7.82-11. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th .0 (10.690 (.11-3.00 (5.1) 20.4) 7.07) 2.7 (10.07) 2.53-8.47-9.89 (2.9 (9.03 (6.00 (<LOD-1.54) 9.92) 3.02-4.94 (5.07-3.38 (.5 (9.590 (<LOD-. Fourth National Report on Human Exposure to Environmental Chemicals 123 .2) 12.29 (2.68) .95) 90th 8.5 (8.81 (7.0 (11.89-3.5) 8.72) 4.67 (1.7) 15.70-2.01-5.3-15.83 (7.85-8.61 (2.59-3.9 (9.63 (6.00) 8.03 (2.93 (6.0-19.27) < LOD .4 (11.4-18.99) 2.7-19.88-7.

45 (1.440-. and 0.50 (1.04) 1.39) 2.30) 2.45 (1.34) 2.14-1.584) .618) * .54-2.80) 2.700) .00) 2.750) 1. and 03-04 are 0.350-.89) 1.57 (2. which may vary for some chemicals by year and by individual sample.20-3.96-3.86 (1.880) < LOD 75th .780 (.30 (.63 (1.550 (.89) .840 (.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 * .760 (.95 (2. see Data Analysis section) for Survey years 99-00.450 (<LOD-.950) 90th 1.720-1.00) 1.500 (<LOD-.73 (2.940) < LOD .54 (2.48 (1.700) .749 (.35) 1.16) 1.77 (1.17) 1.91) 2.710) .690) .820 (.26) .22-2.17-4.570-1.570 (<LOD-.380) .680-1.41 (2.15) 2.37-2.690 (.83) 1.382-.83 (2. respectively.460-.36-4.80) 3.13) .20) 1.990-1.27 (3.00-4.790 (.240 (<LOD-.690-1.50) 1.390-.31) 2.570) * .820 (.70-2.22-8.380-. < LOD means less than the limit of detection.09.94 (3.11-3.46 (2.54) .10) 3.78) 952 1187 907 997 1332 998 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * .800 (.23-3.960-1.585) * * .750-1.388-.930-1.20-1.930) 1.76 (1.390-.60) 3.75 (2.18 (.11-3.970) 1.20) 2.74-5.949) .960) .83) .160 (<LOD-.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 * .20 (2.910) 1.01-3.14 (1.453 (.600-1.592) * .57 (1.30-3.710 (.09 (.510 (<LOD-.457 (.455 (.79) .930) < LOD .68-5.30 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.80) 3.79) .08 (2.740 (.600 (<LOD-.22-3.31-3.850) < LOD .60) 2.19-1.1.41-5.16-3.590-. population from the National Health and Nutrition Examination Survey.04) .620-1.S.00 (1.860) < LOD < LOD .10-1.549 (.60 (2.77-2.20 (1.75-2.2.425 (.30 (1.70 (1.50-2.600-.96-5.34) 2.97 (2.30-1.880 (.580-1. 124 Fourth National Report on Human Exposure to Environmental Chemicals .960) .587) * * .98 (2.10-1.80) 5. interval) Selected percentiles ( 95% confidence interval) Total * .20-2.29) 1.398-.65 (2.05-3.17) 1.40 (1.592) * 50th .87-3.98-3.730) .20 (1. 01-02.58 (1.74) 3.61 (1.76-6.29-2.90-4.40 (1.459 (.70-7.86) 3.90) 2.94 (2.27 (2.95) 2.570 (<LOD-.780 (.26 (2.46) 1.690-.32-1.15) 2.31-3.01-1.89) 672 678 478 509 695 553 595 948 745 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.90) 3.94) .20) 2.80 (1.780) .359-.59-2.03) 1.50 (1.930 (.21) 3. 0.592-.657) * * .960) 1.89-6.08 (2.30-3.30) 4.597) * .33-2.83) 2.22 (1.336-.25-1.449 (.570 (.980) 1.55 (3.20) 3.00-2.60-4.64 (1.18 (1.10) 1.740 (.20-2.47 (1.59-6.340-.30 (.20) 3.69-4.570 (.740-1.73-5.46 (1.46-3.210 (<LOD-.80 (2.73 (1.830 (.400) .303-.10) 1.960 (.38) 1.95-5.31) 95th 2.670) .70 (1.05-2.90) 2.50 (1.810) .48 (2.650-.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.47) 2.759) * .45 (2.83 (2.720-1.350-.13) 2.910-1.80) 2.560-.78) .32) 3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.343 (.720 (.80) 3.353-.30) 4.380-.20) 1.30) 1.01) .201-.280-.580-.22-3.970) .20 (1.50-2.16) 2.550 (.680-1.540 (.98) .490 (<LOD-.45-4.467 (.49) .32 (1.505 (.510 (.710 (.49) 2.740-.88) 1.50 (1.70 (1.10) 1.260 (<LOD-.910 (.880) < LOD .42-2.50 (1.90 (1.

62 (1.16-1.66) .99) 2.840) .45 (1.72 (2.380-.440-1.23 (.84-6.67 (1.08-3.07) 1.510-.04) 95th 2.136-.30-2.97) 1.50) 1.64 (2.630) * .830) 90th 1.97) 2.500-.900) 1.97 (1.07) 1.77-4.680 (.67-3.61-3.910) < LOD .08-2.24) 4.32) 5.22) 1.760) < LOD 75th .22-3.720-1.310 (<LOD-.560 (.980-1.820) 1.380) .700 (.510 (.790 (. Fourth National Report on Human Exposure to Environmental Chemicals 125 .33 (1.300-.57 (3.640 (.22-3.52) 3.57-2.740) < LOD 1.688) * .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 * .67 (1.377-.60) .71) 2.285-.393 (.99) 1.490 (.590-1.47 (1.89-3.444-.06) 4.17) 2.250 (<LOD-.61 (3.17) 2.57-4.270-.640 (.58 (1.840) 1.07-2.380-1.08-2.800) < LOD .460) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.42-8.23) 2.08 (2.710 (.70 (3.S.31-1.07-3.460-1.07) 1.740) .39 (1.80) 2.22) 4.11-2.00 (3.97) 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.850) 1.560-.820) .09) .19 (1.535 (.08-3.73-3.700 (.89 (1.390) .230 (<LOD-.710 (.28 (1.11 (.830 (.69 (3.61-3.350) .470) .08) 1.23) 1. interval) Selected percentiles ( 95% confidence interval) Total * .510 (.04-1.43) 1.720 (.30) 3.552 (.739) * .32) 2.62 (2.43 (1.550) .02-3.760) .92-8.92 (1.47-4.550-1.460 (.52 (1. population from the National Health and Nutrition Examination Survey.348-.400-1.310-.75 (1.335-.270-.04-5.03-2.90) 2.16) 1.20-7.670 (.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 * .520 (.65) 2.08) 2.05) < LOD .45 (2.660-.870 (.22 (2.88 (1.07) 5.480) .60 (1.645) .79 (1.250 (<LOD-.06-2.08-3.41 (.58-6.47 (1.23) 3.42-6.14 (2.580-.590) * 50th .08 (.64 (2.640 (.318-.77 (3.305 (.38 (1.71) .234 (.55 (1.412-.78) 3.88) .33) .330 (<LOD-.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.509 (.471-.97 (1.447 (.920) .49 (1.690) < LOD < LOD .55-3.13 (1.403) .08-3.92) 3.50 (1.00-1.270 (<LOD-.470 (<LOD-.320-.930-1.330-.540-.39) 2.16-2.60 (2.81) 2.390-1.23) 2.82) 2.11) 1.20) 1.370-.36) 3.32) 1.480-1.72) 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 * .29-4.34 (1.448 (.71 (1.05-2.03-1.742) * * .453 (.57 (1.485) * * .310 (<LOD-.95) 1.17-2.597) * .22) .940-1.75 (2.300 (<LOD-.180 (<LOD-.75) 6. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.72) 1.320-.76) 1.75-3.710 (.800-1.750 (.87 (2.580 (.790) .02-6.79) 1.63 (1.91 (1.94) .730) .520-.560-.82 (2.550-.67) .43) 2.98) 1.400) .550-.44) 2.870) .950-2.72-4.38-3.590 (.07 (.990-1.61) 2.00-3.591 (.02-3.530 (.08-2.67) 1.368) * .84 (2.750 (.42) .580) .05) 1.53) .20-2.43) 2.22-2.32-1.58) 3.44-2.77-3.18-2.372 (.515) * * .60) 1.880) 1.280 (<LOD-.25-3.05-4.42 (.05 (1.70 (2.10) 2.49-4.69 (1.38 (2.840) 1.73 (2.700 (.72 (1.253-.66 (2.32 (.

50-20.13 (1.83 (1.0) 20.0-53.9) 17.48-2.0 (38.9) 48.54 (1.16) * 1.0-39.4) 38.81-2.8 (26.5-45.5-27.19-2.41-4.18) 6.70-6.74-2.27-6.0 (38.83 (3.43-7.40) < LOD 2.06) * 2.2-33.1) 18.0) 28.04-8.2 (19.11) 2.1) 38.70 (1.1) 140 (46.10-13.9 (10.35-6.0) 17.07-5.53) * 2.0) 17.3) 28.85) * 2.23) 9.71-2.26 (.23-2.93-3.1 (10.44-7.91 (4.80) < LOD 1.3 (23.40-4.88) 1.48) 5.0) Sample size 1948 2518 1965 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 2.52 (4.46-2.12) 1.41) 1.04 (<LOD-2.20) 1.8 (12.21 (1.0 (8.0) 32.60 (2.53 (1.21 (4.0-69.11 (4.1-40.82 (1.77 (1.5) 30.83-2.86-3.2-39.49-2.4-22. interval) 1.2 (12.0 (8.29-9.10 (7. 01-02.0 (6. 0.95 (5.80-2.77) 38.90 (1.830-3.0 (20.75-14.2-62.17-2.30) 11.80-18.0 (37.2) 31.54 (3.9 (23.31-6.06 (1.9 (27.10) .21 (3.9 (19.7 (28.0 (38. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.70) 1.0) 42.660-2.4) 19.5) 69.0) 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. respectively.59 (1.S.30 (.16) 2.2-26.1-25.10 (1.90) 11.42) 1.1-19.610 (<LOD-1.00-24.8) 39.0-58.58-2.8 (12.40) 50th 2.0-52. 126 Fourth National Report on Human Exposure to Environmental Chemicals .41) 1.0) 15.76 (2.04) 3.90-8.9) 38.0) 45.5-74.6-45.99 (2.2-80.20 (2.1) 38.0 (7.4 (10.4 (19.0-50.8-21.7) 47.1 (25. which may vary for some chemicals by year and by individual sample.71 (4.29-4.2-27.0) 5.0) 18.44) 3.0 (38.0) 4.57-2.6 (9. population from the National Health and Nutrition Examination Survey.1 (26.05) * 2.7-41.0 (38.0) 3.2-27.14) 5.6 (11.79-2.8) 62.0) 8.40) < LOD 1.48-2.0-39.96) 5.0 (19.0) 20.1-46.50-7.87-7.0) 6.92) * 2.76 (2.0 (32.90 (1.59 (1.9-51.46 (.98 (1.4 (15.29) 2.50-17.26) 75th 11.0 (8.1) 95th 48.10 (1.80) 1.71) 5.98) * 2.53) 40.7 (12.0-41.0) 15.0) 16.10 (1.05-3.0 (11.0 (33.64-3.41 (1.41) 5.09 (4.72 (1.0-62.0-110) 42.0-53.70-17.0 (40. and 0.46-6.6 (26.70 (1.3 (12.0) 31.6-27.5 (24.9 (19.45) 2.3 (10.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.8-24.70) 1.50 (2.2-47.63-6.65 (4.13) 12.0-49.85 (1.0 (21.69) 2.57-2.2) 16. see Data Analysis section) for Survey years 99-00.60) < LOD 1.61 (1.12 (3.50-2.3 (24.44) Selected percentiles ( 95% confidence interval) Total * 2.0-92.18) 14.53) 1.8) 41.3) 33.830-4. and 03-04 are 0.50-5.0-47.4-76.0) 4.97) 6.70 (.18) 20.80) .58) 16.0-31.0) 13.10) 39.0-58.470 (<LOD-1.0 (25.1 (11. < 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.1 (25.0 (24.13 (1.0-260) 34.0 (26.23-2.92-5.0 (20.8) 32.70) 5.78) 9.7 (12.10 (1.0-41.05) 1.3) 31.0) 4.3 (12.5-20.0) 3.0) 3.66-5.6 (15.530-4.0) 33.10-4.33 (5.7-22.40-16.8) 952 1187 946 996 1331 1019 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.0-110) 34.7) 20.0) 16.3) 26.18.0) 19.00 (.8 (22.32 (2.600-2.79 (2.6-22.0) 28.25-3.0-29.44) 2.0-43.5-40.80) 90th 38.78 (1.0) 3.3) 38.8) 671 678 498 509 695 579 595 947 757 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.9-21.36-2.20-4.83-2.1-20.1-47.00 (.94 (1.02 (2.30) 4.9) 18.4.690-3.0-230) 35.67 (1.1 (22.6) 52.0 (38.6-54.0 (38.0 (13.88) 3.70 (7.81-3.5.30-14.0-41.3 (14.45) 2.86 (1.0) 30.61-2.64-8.0 (17.19) 2.79 (1.0-62.

5 (41.56 (2.9 (13.71-2.8 (7.75 (1.09 (5.51) < LOD 1.02 (.70-4.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) 24.9 (26.46-6.84-13.18-1.50-5.43) * 2.69-18.670-1.40 (5.3-19.4 (25.2-47.3 (10.7) 66.93) 5.68) 47.0 (17.27) 50th 2.5) 27.1 (33.5-190) 30.1-22.88 (1.2) Sample size 1948 2517 1962 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 2.94) 19.23-1.0) 47.7) 23.7 (10.79-17.1-63.28) 1.24 (1.82) 1.90 (.25-3.1) 25.3 (9.6-49.57 (6.88 (1.2 (16.5-97.36-13.5 (13. population from the National Health and Nutrition Examination Survey.26-4.4) 12.5) 70.36) 10.7) 95th 51.8) 31.8-43.4) 12.18) * 2.80-8.11) < LOD 1.40-7.95 (2.75) * 1.9-95.2-38.6) 7.0 (25.9 (10.45-1.27 (6.6 (27.28 (1.34) * 1.6 (11.01 (.02) * 1.03) 1.7) 26.54-15.8) 11.2) 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 1.0-118) 29.66) 8.3-42.4-39.19-14.7-109) 22.1 (34.38-5.18) 3.9 (39.33) 2.86) * 2.58-17.66 (1.6) 11.06) 75th 9.3-22.32 (3.4 (9.22-2.4 (12.02) 1.5-43.35) .7 (11.79 (2.14 (.870-3.64 (1.7 (24.0) 13.67-3.62) 4.2 (9.38 (3.6 (7.38-1.0) 30.35) 1.8-37.48 (4.4-34.57) 4.00-16.5-36.2) 41.1) 13.1 (39.0-71.55 (2.3) 28.20) Selected percentiles ( 95% confidence interval) Total * 1.29-5.8) 15.61-22.9) 12.7) 30.2 (22.8-26.52 (1.0 (32.69-5.33) 1.2 (8.16 (1.19) 5.5 (34.19-6.2) 4.97 (1.67 (1.46) 1.23) < LOD 2.6-38.4) 14. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.870-3.890-4.60) 4.3 (10.0) 10.5 (17.6) 3.96) 2.59-2.22 (.1 (12.6-32.6) 19.48) 1.52-4.1) 27.4 (11.1) 25.08 (1.94-20.70 (1.9) 3.9) 54.58-2.4-71.23) 37.2) 13.30) 28.00) 6.0) 48. interval) 1.95) 90th 32.0) 25.21 (4.2) 13.1) 52.67-16.2-34.1) 17.31) 2.51) .2-28.1) 13.0) 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 1.33) < LOD 1.68 (1.3-27.36 (4.43-12.2 (15.03-2.4-67.1) 27.9-52.6-51.71) 8.71 (1.8) 3.2) 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.14-8.7-20.61-2.37-2.72) 2.86) * 3.9) 24.8) 32.83 (.99-4.22 (2.6) 3.44) 9.0 (14.33-5.4 (21.53) 1.680-4.38) 5.60 (.0 (39.5 (8.9-37.61 (1.39 (1.07-2.88 (4.43-2.4 (5.07-2.0-40.35 (2.96-16.19 (1.00) 1.80 (1.6) 112 (40.91-2.930 (<LOD-1.5 (6.50 (2.47 (3.1) 15.66 (1.4) 3.94) 1.56) 1.59-15.3) 13.4 (25.27-3.0 (23.83) .S.46-22.88 (4. Fourth National Report on Human Exposure to Environmental Chemicals 127 .3 (20.40 (2.1) 36.0) 3.41 (2.9-18.59-2.0 (19.888-1.20-5.40-4.0-70.67 (1.17-3.16 (1.8) 23. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.5 (15.06) 1.7-37.7 (18.7-19.27) 10.9) 3.5 (15.46-5.2 (21.12) 3.37 (1.12 (1.32-3.06-1.899-2.3 (8.9-36.750 (<LOD-1.0 (23.08) 1.8-34.7) 61.16 (1.45 (1.22-3.870-3.95-16.7-43.7-38.0 (6.2-70.2) 36.63-5.7 (18.00 (4.54-2.62 (2.91 (6.1 (50.7) 15.8-45.7) 34.6 (24.860 (<LOD-1.17) 2.47 (1.75 (1.9-41.47-17.16-2.4-21.95-16.15 (.06) 1.26-2.4 (19.1 (25.07) 9.6) 23.11-2.76-2.75-6.9 (7.19) 5.9 (19.82 (2.7-47.2) 33.1-60.

740) < LOD .450 (.820 (.780) < LOD 1.650) .100 (.150) .05.830) < LOD .42) .450 (.930 (. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th 75th .830 (. see Data Analysis section) for Survey years 99-00.310) < LOD < LOD < LOD < LOD .140) .610-1.610 (.650) .240 (<LOD-.10) .230) .470-1.730-.310-.310 (.10) . 128 Fourth National Report on Human Exposure to Environmental Chemicals .410-.720 (.099-.200) < LOD < LOD .150 (<LOD-.380-.640) .58) .210 (.084-.15) .870) < LOD .220 (.490 (.210 (.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.990 (.110-.370-.13) .690-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.380-.60) 1.860) .S.640-1.720) .620 (.300-1.870 (.460-.990) .420-.860-1. respectively.940 (.260 (.360-.080 (<LOD-.280) < LOD < LOD < LOD < LOD .540 (<LOD-.30) .900 (.320 (.650-1.350) .410-.640 (.410-1. population from the National Health and Nutrition Examination Survey.870 (.160-.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 .510-1.640) .680) . < LOD means less than the limit of detection.290) < LOD < LOD < LOD < LOD 90th .130-.350) < LOD < LOD < LOD < LOD .680-1.870 (.090 (<LOD-.700-1.700-1.830) .630 (. and 0.40) .160) .720-1.650-1.300-.160) .310) < LOD < LOD < LOD < LOD .220 (<LOD-.090 (<LOD-.120 (<LOD-.190 (.450 (.30) .310 (.870 (.700-1.650 (.090 (<LOD-.760) < LOD .530-.990) .12 (.540) .140-.290) < LOD < LOD < LOD < LOD Non-Hispanic whites Limit of detection (LOD.820 (. 0.700-1.390 (.850 (.090 (<LOD-.10) .410) < LOD < LOD < LOD < LOD .680 (.330-.130-.560 (.540) .610 (.42) .840) .120-.130-.03) .380-.830 (.32) .770 (.840) .170-.770) < LOD 95th .120-.430 (.30) .600 (.190 (.550) .140-.470 (.190 (.610-.171) * * .1.560 (.270 (.130) .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 * * * * * * * * * . and 03-04 are 0.20) .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 * * * * * * .440-1.430-.460 (.290) < LOD < LOD < LOD < LOD .00) . which may vary for some chemicals by year and by individual sample.870 (.360-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.130) .370-.570) . 01-02.630 (.850) < LOD .390) < LOD < LOD .090 (<LOD-.180) .540) 672 678 498 509 694 579 595 947 757 Non-Hispanic blacks .680-1.1.290 (<LOD-.850 (.050-.730) .140-.162) * * * * * .320-.230-.400-.080 (<LOD-.36) .10 (.130 (.117 (.090 (<LOD-.660 (.

03 (.66) 1.490-1.100 (<LOD-.03) .78) .580 (.116 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.720 (.500 (<LOD-.080 (.43) .860 (.380-.24 (.700 (.570-.02) .330 (.520-.730) .410-.170 (.180-.270 (.440-1.500-1.610-1.67) .600-1.12) < LOD .260) .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 * * * * * * * * * .090 (<LOD-.140-.700 (.660-1.03 (.070 (<LOD-.140-.110) .080) .270) < LOD < LOD < LOD < LOD .110) .990) .300-.38) 1.760) .86) .Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Diethyldithiophosphate (DEDTP) (creatinine corrected) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.640) 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 .161) * * .400 (<LOD-.750) < LOD 95th .380-.084-.860 (.510-.300 (.140-.360-.140-.450 (.29 (.220) < LOD < LOD < LOD < LOD .09) .100-.330-.450) .320 (<LOD-.60) .210 (.19 (.050 (<LOD-.230) < LOD < LOD < LOD < LOD .14) 1.140) .870) .700) .410 (.460 (.360 (.230 (<LOD-.380 (.300-.03 (.02-1.120) .120) .340-.520) 672 678 497 509 693 578 595 947 756 Non-Hispanic blacks .220 (.290) < LOD < LOD < LOD < LOD 90th .060-.310) < LOD < LOD < LOD < LOD Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.240-.110-.850 (.390-.780) < LOD 1.650) < LOD .330-.070 (<LOD-.730) . population from the National Health and Nutrition Examination Survey.470 (<LOD-.080 (<LOD-.670 (.150-.057-.740 (.370 (<LOD-.670 (.880 (.200 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.990) .230-.070 (<LOD-.700-1.880-1.410) < LOD < LOD .670-1.570 (.190 (.940) .330-.740) < LOD 1.500) .360) < LOD < LOD < LOD < LOD .600) .580 (.170) < LOD < LOD .780 (.550 (.540 (.410) .190 (.970) .580) < LOD .720 (.58) 1.110) .580) .580-1.410-.01 (.250-.360-.070 (<LOD-.890 (.00) < LOD .62) 1.540 (.190-.800-1.20) 1.110) .410 (.540) .380-.960) .170 (.140-.280) < LOD < LOD < LOD < LOD .560 (.36 (1.390-.730 (.650-1.400) .640-1.24) .260-.440 (.200 (.550 (. Fourth National Report on Human Exposure to Environmental Chemicals 129 .330 (.310) < LOD < LOD < LOD < LOD .940) .86) .S.380-1.810 (.090 (.710-1.860-2.540) 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 * * * * * * .730) .570-1.111) * * * * * . interval) Selected percentiles ( 95% confidence interval) Total * * * 50th 75th .

70-17.330 (<LOD-1.31) .770 (<LOD-1.740 (.40) 2.90 (2.68) 2.0-40. and 0.30-3.610 (. 01-02.14) 2.05-3.10 (3.20 (1.800) 17.31-10.10-3.640 (.750-2.0 (5.840-3.70-3.0) 4.40) 1.0) 2.28) .86) 4.110 (<LOD-. see Data Analysis section) for Survey years 99-00.60) .36-3.66) 4.35) 5.63) 32.96 (1. < LOD means less than the limit of detection.63 (3.30 (1.40-8.40-4.0 (5.360-1. 130 Fourth National Report on Human Exposure to Environmental Chemicals .07 (3.90-28.37) .0 (4.14-5.46 (1.36-3.30-7.20-4.94-3.32-9.52 (1.00 (.1.11 (1.65) 1.07 (3.691 (.80) < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 4.080-1.0 (7.49 (1.18) 1.99) 19.370-.0 (13.83) 2.620-1.0) 2.0) 5.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Dimethyldithiophosphate (DMDTP) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.0 (5.580 (.00) .30 (1.870) < LOD < LOD .12) * * * * * * * * .52 (1.30) .900 (.87) 12.840 (.800-4.0 (5.0) 2.170-1.20) < LOD < LOD < LOD < LOD < LOD 1.800) 90th 13.47 (3.67 (2.21) 3.62-8. which may vary for some chemicals by year and by individual sample.53) 20.70-7.74) 5.720) 2.61 (1.07-3.39 (2.510-.960 (.40 (1.60) 1.45 (2.35-10.94 (1.10 (. and 03-04 are 0.05 (2.250 (<LOD-.07-3.90) .53 (2.21-3.40-20.00) .70-30.15) 14.99 (1.85-3.23-6.0) 5.97) 20.83-3.52) 5.99) 11.49) 17.50) 2.0) 2.210-1.690 (.260-.0 (17.20 (1.0-39.0) 2.640 (.28) 1.42) 2.90-9.0) 4.07 (1.48) 13.0 (17.0) 5.400-1.0 (17.11) .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 .6) 5.32 (1.43-4.30-6.750-1.00 (1.0) 5.42) .67) .610) < LOD < LOD < LOD < LOD < LOD 2. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th 2.0-40.425-1.S.30) 95th 19.0 (3.53-7.590 (.350-.55-4.890 (.28-9.40-7.82-4.480-.49 (1.850) 16.960 (<LOD-1.11) 13.83-3. 0.0) 4.33 (4.70) 2.94-8.70-50.07) 1.29-10.15) 19.26 (2.24-7.62) 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 * * * * * * .01) 5.05 (3.3) 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 * * * * * * * * * .0 (4.50) .90-20.40 (1.97) 20.0 (17.10-9.880) 5.12-1.10-3.0) 3.48 (2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.51 (2.0 (17.20-17.88-3.80 (4.38-3. 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.600 (. respectively.00-17.380-.0-44.51-8.0) 4.59-5.55-8.20-4.730 (.90) .10 (3.0 (16.90-37.90 (1.0) 7.30 (2.770) 2.190-1.30 (1.03 (.350-.00-17.14) .39) .0 (5.1.0-38.74 (3.840 (<LOD-1.35) 11.00) 1.76 (1.13 (3.0 (6.0-38.830 (.0-38.910) 2.30 (.67 (1.87) 5.0) 2.90) .08.6) 672 678 498 509 695 552 595 947 752 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.0) 2.

88-3.9) 6.4 (4.80 (.580 (.800-2.59 (1.430) 1.25-38.53) 27.64) 30.620-3.01 (1.310-.80) 3.91-4.1 (5.5) 7.55 (3.30 (4.474-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.50) 11.66-47.540-1.92 (2.17) 5.50) .43) . population from the National Health and Nutrition Examination Survey.22) 2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.10-3.4-34.33 (1.820 (.820) .40-12.60) < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 4.38 (2.13 (2.31-7.7 (6.67) 1.270-.14-6.650) 90th 10.88) 17.69) 2.710 (<LOD-1.9 (11.31-18.12-4.18) 1.8) 7.07-21.74 (2.370-1.00) .67 (2.40 (.33-3.48-7.02-4.67-6.86 (3.12 (4.11) .740-1.2-38.790) 11.08) .17 (1.48-42.00-19.48 (4.84) 9.8) 1.18) 95th 21.10) 2.650 (.96) 2.830-3.630-1.940-4.24) 3.0) 4.370 (.2 (8.47) 5.25-9.40-2.79 (.8-33.7 (12.75) 5.90-6.83 (4.500 (.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 * * * * * * .29-4.7) 4.64-4.36 (.85 (1.91) 2.7) 3.540 (.47) .04-16.29 (4.340-.600 (<LOD-1.890 (.770) .4) 2.260-.5 (8. Fourth National Report on Human Exposure to Environmental Chemicals 131 .86) .340-.60 (1.320-1.15) 9.580) 1.14 (1.03) 16.370) < LOD < LOD < LOD < LOD < LOD 1.960 (.82-11.02) .44) .390-.03) 2.32-6.47-10.1) 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.67) 2.45 (1.96-25.56) .40) 1.9) 5.430 (<LOD-.27 (2.41) 18.71 (.8) 7.5-40.35 (.5) 2.88 (2.50 (4.32) 9.57) 8.11-5.700) 6.97) .580-1.790 (.8) 2.470 (.02 (1.23-7.05) .1) 2.31) .62 (1.33-4.09-3.7) 6.37) 4.73 (4.41 (4.57 (.02 (.28-6.47-10.850-3.65 (2.52 (.330-1.930) .56 (1.780-4.260-.360 (.31) .7) 5.8 (20.49-2.53) .748 (.04 (1.55) 21.18) * * * * * * * * .S.860-2.5 (9.670 (.06 (.240-.77 (.51-4.590) 2.51-44.450 (.0 (4.1 (7.89 (2.07 (2.55) 21.33-5.560 (.190-1.730-3.21-3.8) 2.22-27.57) 1.700) < LOD < LOD < LOD < LOD < LOD 1.71 (2.250 (<LOD-.340-.69-7.56) 2.660) < LOD < LOD .830 (.340 (.580) 16.33 (3.5) 2.3) 2.61) Sample size 1949 2517 1927 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .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 * * * * * * * * * .85-3.0 (9.96-8.840-3.88 (.8) 4.81-17.57-40.3) 3.98 (4.150 (<LOD-.39) 20.44-11.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.970-3.5 (11.83-11.62-17.10 (2. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th 1.50 (2.270 (<LOD-.25 (1.690-5.

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Environmental and biological monitoring of exposure to organophosphorus pesticides: application to occupationally and non-occupationally exposed adult populations. 2005. Metabolites of organophosphorous insecticides in urine specimens from inhabitants of a residential area. Fenske RA. Hawk R. Robinson LR.110(8):829-833. Barr DB. Engel LS. The effects of occupational exposure to chlorpyrifos on the neurologic examination of central nervous system function: a prospective cohort study. Third National Report on Human Exposure to Environmental Chemicals. et al. Daniell W.46(4):367-378. Gillham RA. Young AD.113(12):1802-1807.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites References Albers JW.15(2):164-171. Environ Health Perspect 2000. Farahat TM. Amr MM. Kipen H. Checkoway H.7(5):715-731. Kelly-McNeil K. McKone TE. Neuropsychological performance among agricultural pesticide applicators. Astroff AB. 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epa. Rodnitzky RL.12(2):134-141. Pilkington A. Levy LS. Variation in organophosphate pesticide metabolites in urine of children living in agricultural communities.52(2):190-195.338(8761):223-227. vibration sense and tremor among South African farm workers.68(3):209-227 Maizlish N. Hansen S. U. and cholinesterase status of date dusters and harvesters in California. Calvert IA. Dinoff TM.332(1-3):71-80. Buccafusco JJ. Kidd M. Arch Environ Health 1975. Environ Health Perspect 2005. Wickremasinghe AR. Weisskopf C. Effects of chronic. Ruberu DK. Neurotoxicology 2005. Available at URL: http://www.26(2):199-209. et al. Caltabiano LM. Eskenazi B. Effects of occupational exposure to organophosphate pesticides on nerve and neuromuscular function. Association between in utero organophosphate pesticide exposure and abnormal reflexes in neonates. Savage EP. van der Hoek W. 1/12/09 Peiris-John RJ. Irish RM. Masala G. McCauley L. 1993 [online]. Arch Environ Health 1988. Pesticides in the Diets of Infants and Children.24(1):18-29. McConnell R.pdf. Steenland K. The presence of dialkylphosphates in fresh fruit juices: implication for organophosphorus pesticide exposure and risk assessments. Pesticide industry sales and usage . London L. O’Malley M.S. Prendergast MA. Bradman A. Spurgeon A. Muniz J. Heaton RK. Bull Environ Contam Toxicol 1994. Rothlein J. Occup Environ Med 2001. Stephens R. Rohlman D.20(2):115-22. Gillham R. Biological monitoring of organophosphate pesticides in preschool children in an agricultural community in Thailand.113(4):504-508. Neurotoxicity among pesticide applicators exposed to organophosphates. Nell V. Berry H. Organophosphate pesticide exposure and neurobehavioral performance in agricultural and non-agricultural Hispanic workers. J Occup Environ Med 2002.S. Samuels S. Muniz J. National Research Council (NRC). et al. 2004. Arch Environ Contam Toxicol 2000.12(2):153-172. Washington (DC): U. EPA). Chronic central nervous system effects of acute organophosphate pesticide intoxication.43(1):38-45. Buchanan D. low-level exposure to the organophosphate diazinon. et al.52(10):648-653. Chrislip D. Lancet 1995. Fourth National Report on Human Exposure to Environmental Chemicals 133 . Sci Total Environ 2004. Lambert WE. Lu C. Seiber J.2000 and 2001 market estimates. Hore P. Am J Public Health 1994. Int J Occup Environ Health 2006. Smit LA. low-level organophosphate exposure on delayed recall.345(8958):11351139. Am J Ind Med 1987. Beach J.58(11):702710. et al. S. Johnson C. and spatial learning in monkeys and rats. discrimination. et al. Twenty-four-hour urinary excretion of ten pesticide metabolites in healthy adults in two different areas of Italy (Florence and Ragusa). Keefe TJ. Marshall E. Neuropsychological effects of long-term exposure to organophosphates in sheep dip. Chronic neurological sequelae to organophosphate pesticide poisoning. Lasarev M. Tumino R. The Pesticide Health Effects Study Group. Chronic neurological sequelae of acute organophosphate pesticide poisoning. May. Jamal GA. Claypoole K. 1991. Salvini S. Available at URL: http://books. Santana J. Lasarev M. Lewis JA. A behavioral evaluation of pest control workers with short-term. EPA.44(4):352-357.php?record_id=2126&page=1. Aprea C. Russo J. Occup Environ Med 1995.84(5):731-736. Neurotoxicol Teratol 1998. Rosenstock L.nap. Gladstone EA. Schenker M. Daniell WE. metabolite clearance. Saieva C. Burcar PJ. Malathion deposition. Takamiya K. gov/oppbead1/pestsales/01pestsales/market_estimates2001. 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. Mounce LM. Phillips J. Frasca G. Office of Prevention Pesticides and Toxic Substances. Jenkins B. Pedersen L. Scherer J. 4/7/09 Young JG. Environ Health Perspect 2006.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Krieger RI. Stokes L. Terry AV Jr. Vitayavirasak B. Narang A. Scand J Work Environ Health 1998. J Toxicol Environ Health A 2005. Bravo R. Barr DB. Stark A. Petchuay C. Thompson ML. Robson MG. Lancet. National Academy of Sciences.114(5):691-696. Occupational exposure to organophosphate pesticides: a neurobehavioral study.38(4):546-563. Monitoring of urinary alkyl phosphates in pestcontrol operators exposed to various organophosphorus insecticides. Weerasekera G. Rothlein J. Myers JE. Washington (DC). Environmental Protection Agency (U.edu/ openbook. Keifer M. Ames RG. Effects of long-term organophosphate exposures on neurological symptoms.30(2):98-103. Visuthismajarn P.

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

16) 2. dermal.80) 12..36 (4.89-2.09 (2.0) 12.72) 2.9 (7. Chlorpyrifos is not well absorbed through the skin but dermal exposure can be significant when other routes of exposure are low.05-5.0) 12.1) 5.74-9. 5598-13-0 General Information The chemical 3.0) 14.30-1.80) 4. staying bound to soil particles.40 (5.95) 7.3 (10.0 (9.30) 5.61 (1.52-2.03) 1.28) 2.60-2.37 (1.15 (1.9) 11.67 (2.and post-construction structural applications for termite control were to be phased out by 2005 (U.70) 1.70-11. but can be detected in streams receiving runoff from application sites.02 (7.50-8.99-4.30) 4.30-9. Exposure can also result from contact with contaminated surfaces.68 (7.10) 2.80-8.31-2.50-4.37) 5.40-13.20 (2.3 (8.63 (1. It also has been applied directly on animals to kill mites.70-16.9) 697 660 521 701 602 947 Limit of detection (LOD.81-2.4 (9.74 (1. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.52-12. and on plants for days to several weeks.98-15.32-1.50 (2.71 (1.S.72-4. Chlorpyrifos-methyl is an organophosphorus insecticide also used in agriculture and not registered for residential use.70-15.20) 10.30 (4.47) 1.30-12. chlorpyrifos was no longer registered for indoor residential uses in the United States.40-10.0) 8.5) 7.20) 2.91) 16. Approximately 21-24 million pounds per year were used domestically from 1987-1998.00) 2.44 (3.0) 10.88 (1.50-14.10 (1.0) 12.0 (7. population from the National Health and Nutrition Examination Survey.44-2.Organophosphorus Insecticides: Specific Metabolites Chlorpyrifos CAS No.57 (2.17 (1.30-5.0) 8.8) 10. and is infrequently detected in ground water (IPCS.51-2.76 (1.04-10.50-2.77 (1. 2002).0) 18.90 (1. chlorpyrifos and TCPy were detected in all indoor air and dust samples (Morgan et al.20-16.19-3.51) 1.97-7.84) 1.0) 6.40) 2.7) 9.37 (4.95 (4. and sprayed to kill mosquitoes.6) 7. 2005).7) 13.22 (1.51 (1. in 142 urban homes and preschools in North Carolina. USGS.20-2.61) 75th 3.38 (3.60-3.63 (2.4) 481 573 681 823 832 1113 99-00 01-02 99-00 01-02 1.50 (2. Chlorpyrifos is very toxic to fish and aquatic invertebrates and shows modest degrees of bioconcentration.64) 3.78 (7.S.03) 99-00 01-02 99-00 01-02 99-00 01-02 2.32) 2. Approximately 80.25) 3.10 (4.28-3.EPA.24-3.90) 3. Chlorpyrifos is degraded in agricultural soils with a half-life of several months.80 (7.10 (3.86) 4.5-24.97) 2.70 (1.9 (10.40-26.66-15.20-4.77) 1.29-1. pre.04-10.20) 2.80 (1.000 pounds are used per year.97) 4.39) 4.71 (2.50 (1.50-4.13-3.4 and 0.0 (10.6-trichloro-2-pyridinol (TCPy) is a metabolite of chlorpyrifos and chlorpyrifos-methyl.0) 9.47-13.3) size 1994 2509 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th 1.35) 1.45 (1. and inhalation routes.0 (7.EPA.00-24.13 (1.47-9.4 (10.00-8.79-2.59) 2.60 (4.27 (7.46-2.62-2.5 (8. 2002).30) 4.77-6.63 (8.53 (1. air.91 (1.0) 12.25) 1. It has low leachability.05) 1.43-2.47 (4.0 (7.43-2.4-15.1-16.55-5. Fourth National Report on Human Exposure to Environmental Chemicals 135 .4.S.35) 2.61-7.19 (1.30-11.68-2. and dust.50 (2.30 (2.2 (10.47-11.59-2.67 (2.92 (1.80) 2.60 (2.0 (13.83) 1. Chlorpyrifos is a broad spectrum organophosphorus insecticide that has been widely used to control insects on food crops such as corn. After 2001.70-5.44-5.67 (1.9 (9.97) 2.5.02 (1.40 (5.22) 2.20-14.90-4.94 (4. interval) 1.7) 8.60-4.0) 12.50 (1. 1999. The general population may be exposed to chlorpyrifos via oral.00) 1.2) 972 1183 1022 1326 99-00 01-02 99-00 01-02 99-00 01-02 1.01) 1.24-1.09 (3.80-10.0 (7.40 (6.60) 5.20) 4.8-15. 2007).0) 15.77-15.29) 90th 7.0-28.40-2. 2921-88-2 Chlorpyrifos-methyl CAS No.80) 1.96) 3.6-Trichloro-2-pyridinol Metabolite of Chlorpyrifos and Chlorpyrifos-methyl Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.20 (4.02) 1.90 (6.90 (1.90-7.20-11. Survey Geometric mean (95% conf.4 (8.70-17. For instance.9-18.40) 9.30-2. although some tolerances for specific food crops have been reduced in the past to avoid exceeding recommended intake limits for total dietary intake in special groups (U.10 (5.87-6.76 (1.50-5.00) 3.7-23.0) 7.90 (3.50-2.20-3.10-17.60-3. Inhalational and dermal routes of exposure are important in pesticide formulators and applicators.66-4.34) 1.14) Selected percentiles ( 95% confidence interval) Sample 95th 10.26) 7.3) 8. Chlorpyrifos is Urinary 3.90-2.3 (11.0) 10.0) 10.70 (1.5.0) 11.90 (2. Estimated intakes from diet and water have not exceeded recommended intake limits.8) 9.30 (2.10) 6.97) 7.31-2.39-2.89 (2.90-8. applied to structures to kill termites.60 (5.21) 3.0 (7.71 (6.90) 7.

cholinergic effects.39) 6.75) 6.3) 8.99-8. population from the National Health and Nutrition Examination Survey.93 (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.02 (5.85-4.0) 10.88 (1.03) 1.91) 1. vomiting.47 (1. In addition to being a metabolite of chlorpyrifos and chlorpyrifos-methyl in the body. Howard et al.0) 12.58-5.44-6.83) 1.17-4.1-21.49-2.91-4.57) 9. 2002)..09-3.00-13. 2006b).0) 481 573 681 822 832 1113 99-00 01-02 99-00 01-02 1.64-2.45-1.85 (3.16 (4.Organophosphorus Insecticides: Specific Metabolites rapidly absorbed following ingestion.33 (1. 2006a.47-2.22 (4. Once absorbed.42 (6.34-1.30-1.25-12.26-14.88-8.53-5.29 (3.56 (1. 2005.72) 2. Based on animal data and human cholinesterase monitoring during occupational exposure.14-8.22) 1. and seizures.21-1.24-4. weakness.43-10.42-2.6) 10.94-14..93 (4.40) 1.78 (1.83-2. Slotkin et al.58 (1.0) 16. Survey Geometric mean (95% conf.. 1984).63 (5.71 (1. paralysis.21-6.80-11.58 (1.12) 1.6-Trichloro-2-pyridinol (creatinine corrected) Metabolite of Chlorpyrifos and Chlorpyrifos-methyl Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.82) 8.S. 2005.56) 5.62) 1.35-1. Chlorpyrifos and chlorpyrifos-methyl both demonstrate moderate acute toxicity in animal studies.55 (1.07) 1.5) 5.09-1.45 (1.71) 3.37 (1.EPA.58 (4.27-7.60-3.80-4.20 (2.25-11.31-1.44 (5.4) 4.62) 90th 5.2) 6.80) 3.47 (1.95 (3.11 (2. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”).07) 5.68) 6.30-4.64-7.91) 2.7) 7.66) 1.72-2.82 (3.93 (1.47 (5.06 (1.84-6.98 (7. Chlorpyrifos is eliminated from the body primarily in the urine with a half-life of approximately 27 hours (Nolan et al.85) 4. phosphorothioates such as chlorpyrifos are metabolically activated to the “oxon” form which has greater toxicity than the parent insecticide.940-1.49 (1.90-9.15 (4.43 (4.69 (1.00 (7.25-1.52 (5.93) 2.16) 6.58) 1.65-11.57-2.56-2.28) 2.63 (4.24 (1.44 (1.42 (5.8) 9.66-11.01) 99-00 01-02 99-00 01-02 99-00 01-02 3.81 (3.97) 3.19) 3.08) 6. resulting in excess acetylcholine at nerve terminals.39 (4. Roy et al.39-1.86 (3.91 (3.88) 6.33-7.7) 697 660 521 700 602 947 136 Fourth National Report on Human Exposure to Environmental Chemicals .64 (1.57) 2.02) 7.50 (4.94-12.75 (1.44 (5.33 (. chronic exposure to chlorpyrifos may be associated with slight alterations in some components of neurophysiologic testing (Steenland et al.86 (1.93) 5.91) 10.00) 1.60 (1.85 (2.17-4.82 (2.58) 5.70-4.62-7.00-8. and other metabolites..19) 6.77) 1. neurotransmission.57-2. the detection of TCPy in a person’s urine may reflect exposure to the environmental degradates.55) 1. Ricceri et al.91) 1.72) 1.06-4.23-1.3) 9. 2006.24-24.9 (12.12-1.81) 2.09-2. The metabolite TCPy does not inhibit acetylcholinesterase enzymes.46 (2..35) 2.79-13.1 (7.86 (1.88 (1.36) 1.80-6.63-2.05-1.97) 3.96) 3.09 (1. and producing acute symptoms such as nausea.76 (2.88-10.48 (1.24) 5.31) 1.28) 2.44 (1. Betancourt et al.59) 3.6) 9.88-9.85) Selected percentiles ( 95% confidence interval) Sample 95th 8. Urinary 3. 2000).97 (2.82-4.53 (2.19-2.24-5.1-38.05-4.1 (10. Thus.14) 1.92 (1.38) 3.46 (1.88-8.32) 1.24) 75th 2.05-3.24-1.05-8.3) size 1994 2508 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th 1.39 (2.54 (2.3) 8. Overt cholinergic toxicity from chlorpyrifos has been described following suicidal ingestion and unintentional high level occupational exposure.54) 5. These organophosphorus insecticides share a mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system.92) 3.12-3..01) 1.. 2005.31-4.99) 1.73 (1.41 (1.S.44 (6..83-11.35) 1.87-3.8) 972 1183 1022 1325 99-00 01-02 99-00 01-02 99-00 01-02 1.0) 6.19-1.05) 3.85) 1.76 (3.49-2.55 (4.68) 1..89) 4. interval) 1.56) 2.01) 3. TCPy can also occur in the environment from the breakdown of the parent compounds.22 (6. ubiquitous lowlevel environmental exposures in humans would not be expected to result in inhibition of cholinesterase activity.48 (2.92-2.11) 7.22-6.5 (6. Recent in vitro and in vivo animal studies suggest that effects on neuronal morphogenesis.66 (1.65-15.95 (1. In pesticide applicators.91 (4.74) 1.06 (5.51 (1.97 (3.11-9.01) 3.27-1.56 (4.20-1.3 (7.23) 14. TCPy is more persistent in the environment than chlorpyrifos itself (U.59-2. Metabolic hydrolysis leads to the formation of TCPy.97-3.49-2.33 (5.5.91-13.2 (7.98 (6. 2006.11 (2. Human health effects from chlorpyrifos or chlorpyrifosmethyl at low environmental doses or at biomonitored levels from low environmental exposures are unknown.33) 2. and behavior may occur at systemically nontoxic doses or at doses of chlorpyrifos that do not result in cholinergic signs (Aldridge et al.

Koch et al. 76% had detectable levels of TCPy and levels were similar to those reported for NHANES 1999-2000 (Eskenazi et al. 1995) and were similar to levels reported in studies of healthy adults in Germany (Koch et al.html and from U.cdc.. 2000).92(2):500-506.S. 2005).. et al. 2005). Catenacci G.82(2):305-312.e. Levels of TCPy in the U. Other small studies of environmentally-exposed persons have shown a high frequency of detecting low levels of TCPy. but not chlorpyrifos. Additional information about external exposure (i.. Some reproductive and teratogenic effects in animal testing were only observed at high doses of chlorpyrifos that caused overt maternal toxicity. 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. Betancourt AM. Environ Health Perspect 2005. Whyatt et al. Toxicol Sci 2006.S. 2001) than the corresponding values reported for the group aged 6-11 years from the NHANES 1999-2000 subsample (CDC. 2001). Clayton CA. the geometric mean urinary TCPy levels were similar in parents and children. Replacing conventional diets with organic diets in 23 children led to about a fourfold decrease in urinary levels of chlorpyrifos. Measurements of urinary TCPy in single spot urine collections show variability over time in environmentally exposed individuals and are poorly correlated between collections. Occup Environ Med 2006. 2005) appear roughly similar to values reported for a nonrandom subsample of NHANES III (1988-1994) participants (Hill et al. Giordani B. Aldridge JE. References Adgate JL.. Chlorpyrifos exposure and biological monitoring among manufacturing workers. Haidar S. U. but levels were roughly four to six times higher than the geometric means in the U. Biomonitoring Information Urinary TCPy levels reflect recent exposure.S.EPA.. Betta A.109(6):583-590. 2005). Lioy PJ. CDC..epa. Freeman NC.. Finding a measurable amount of TCPy in urine does not mean that the level will result in an adverse health effect.Reference values of urinary 3. 2003. 2005. Burns CJ.. Aprea C. subsamples of NHANES 1999-2000 and 2001-2002 (CDC. In a probability-based sample of 102 Minnesota children aged 3-13 years. Barr DB.. Garabrant D..S.. Effect of developmental exposure to chlorpyrifos on the expression of neurotrophin growth factors and cell-specific markers in neonatal rat brain.Organophosphorus Insecticides: Specific Metabolites 2004. MacIntosh et al. 2005. Perera et al. Alterations in central nervous system serotonergic and dopaminergic synaptic activity in adulthood after prenatal or neonatal chlorpyrifos exposure. EPA at: http://www.gov/toxpro2. 2004). Albers JW. Eberly LE. Estimation of dose or intake based on the urinary excretion of TCPy indicates that environmental doses are generally below recommended limits (Hore et al. Slotkin TA. J AOAC Int 1999.6-trichloro-2-pyridinol in the Italian population—validation of analytical method and preliminary results (multicentric study). Burgess SC.. the weighted population mean of TCPy measurements was approximately three times higher (Adgate. Chlorpyrifos levels in house dust and hand rinses did not correlate with levels of TCPy in urine (Lioy et al. Urinary levels of TCPy have been found to be hundredsfold higher for chlorpyrifos manufacturing workers (Burns et al. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. suggesting changing low-level exposure and variance in collection timing with respect to exposure (Meeker et al.. Magnaghi S. 2005). 2005). population (CDC. Meyer A. 1992.113(8):1027-1031. 2002). Curwin et al. et al. urinary TCPy levels averaged about sixfold higher than those in the NHANES 1999-2000 subsample (Mandel et al. 2005. Seidler FJ. Following crack-and-crevice application of chlorpyrifos in their homes. 2004).. Barisano A. 2006) and episodically many times higher for pesticide applicators than median levels from NHANES 1999-2000 (CDC. 2005). urinary TCPy levels in children were reported not to have increased (Hore et al. Carr RL. Berent S. 2007). Of 482 pregnant women living in an agricultural community. 1999). 2001) and Italy (Aprea et al. Chlorpyrifos is not considered to be mutagenic or carcinogenic (NTP. median urinary levels on the conventional diet were several fold higher than those in the NHANES 1999-2000 subsample (Lu et al..S. 2006). In Minnesota and South Carolina farmers who used chlorpyrifos. representative subsample of NHANES 19992000 (CDC.63(3):218220. environmental levels) and health effects is available from ATSDR at: http://www.atsdr. In Iowa farm families using several different pesticides. Lotti A.gov/pesticides/. et al.5.. (1999) reported mean urinary TCPy levels in a sample of Maryland adults that were about three times higher than adults in the U. Fourth National Report on Human Exposure to Environmental Chemicals 137 . Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample. Environ Health Perspect 2001.

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Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides.9(5):494-501.Organophosphorus Insecticides: Specific Metabolites Centers for Disease Control and Prevention (CDC). chlorpyrifos. Environ Health Perspect 2006b. Angerer J. Bravo R. Temporal variability of urinary levels of nonpersistent insecticides in adult men. et al.114(5):746-751.113(2):211-219. Environ Health Perspect 2006a. Slotkin TA. Fortuna S. Environ Health Perspect 2006.114(10):1542-1546.15(4):297-309. Curwin BD. Seidler FJ. Comparative developmental neurotoxicity of organophosphate insecticides: effects on brain development are separable from systemic toxicity. Biomonitoring for farm families in the farm family exposure study. Brain Res Dev Brain Res 2005. Weltzien E. et al. Biological monitoring of exposure of the general population to the organophosphorus pesticides chlorpyrifos and chlorpyrifos-methyl by determination of their specific metabolite 3. Interim registration eligibility decision for chlorpyrifos. Lu C. Steenland K. Available at URL: http://ntp. Bradman A.112(10):1116-1124. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population. 2005. Edwards RD. Freshour NL. 4/7/09 Perera FP. Reid TM. Hore P. Bennett DH. Urinary pesticide concentrations among children. Scand J Work Environ Health 2005. Robertson GL. Irish R. Lioy PJ. Quantitative morphological assessment reveals neuronal and glial deficits in hippocampus after a brief subtoxic exposure to chlorpyrifos in neonatal rats.S. 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. Seidler FJ. et al. Environ Health Perspect 2000. Chapman P. Bravo R. Roy TS. Toxicol Appl Pharmacol 2005.155(1):71-80. J Expo Anal Environ Epidemiol 2005. Acquavella JF. Dick RB. 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National Toxicology Program (NTP). Ozkaynak H. Venerosi A. Alexander BH. Croghan CW. 4/7/09 Koch HM.niehs. Yang D. et al. Robson M.cfm?objectid=6F5E95EB-F1F6-975E7C20F4211536F46F. Eskenazi B. Levin ED. Barr DB. Ryan L. Camann D. House dust levels of selected insecticides and a herbicide measured by the EL and LWW samplers and comparisons to hand rinses and urine metabolites.15(3):271-281. Hardt J. gov/ntpweb/index. Ann Occup Hyg 2007. Ryan PB.5. Kinney P. Bucelli R.5. Harley K. Chrislip DW. International Programme on Chemical Safety-INCHEM (IPCS). Baker BA.114(2):260-263. et al. Zhang J. Neurologic function among termiticide applicators exposed to chlorpyrifos. Third National Report on Human Exposure to Environmental Chemicals. Hammerstrom KA. A longitudinal investigation of selected pesticide metabolites in urine. Honeycutt R. Howell RJ. Executive summary of safety and toxicity information. et al. et al. Chuang JC. Head SL. Atlanta (GA). Nolan RJ. Lorenzini P.207(2):112-124. Jewell NP. Bruun D. Heederik D. Capone F. Effects of transplacental exposure to environmental pollution on birth outcomes in a multiethnic population. Int J Hyg Environ Health 2001. Hill RH Jr. Herrick RF. Meeker JD. Sheldon LS. Saunders JH. Pesticide residues in urine of adults living in the United States: reference range concentrations. Environ Res 1995.

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

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

see Data Analysis section) for Survey year 01-02 is 0. Survey Geometric mean (95% conf. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.200 (<LOD-. Fourth National Report on Human Exposure to Environmental Chemicals 141 . < LOD means less than the limit of detection.380 (<LOD-.S.200 (<LOD-.Organophosphorus Insecticides: Specific Metabolites Urinary 3-Chloro-7-hydroxy-4-methyl-2H-chromen-2-one/ol Metabolite of Coumaphos Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. 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.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 .2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.S.670 (<LOD-1. 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 .210) < LOD < LOD 567 815 1099 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1169 1312 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 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 . 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.270) < LOD 659 701 920 Limit of detection (LOD. which may vary for some chemicals by year and by individual sample. Survey Geometric mean (95% conf.

September 2000.epa. Sadowski MA. Available at URL: http://www. Reprod Toxicol 1998.gov/oppsrrd1/ REDs/0018tred.S.376(6):808-815.12(6):619-645. Environmental Protection Agency (U. Atlanta (GA). 2005. Anal Bioanal Chem 2003. EPA 738-R-00-010.S. Reregistration eligibility decision (RED) addendum and FPQA tolerance reassessment progress report: Coumaphos. Freshwater KJ. EPA). U. Nguyen JV.pdf. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine. Third National Report on Human Exposure to Environmental Chemicals. 1/14/09 142 Fourth National Report on Human Exposure to Environmental Chemicals . Olsson AO. Comparative organophosphate-induced effects observed in adult and neonatal Sprague-Dawley rats during the conduct of multigeneration toxicity studies. Centers for Disease Control and Prevention (CDC).Organophosphorus Insecticides: Specific Metabolites References Astroff AB. Barr DB. Eigenberg DA.

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

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

Banister EW. Centers for Disease Control and Prevention (CDC). Available at URL: http://www. 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. Noisel N.gov/ oppsrrd1/REDs/diazinon_ired. The Quality of Our Nation’s Waters. Semen quality in relation to biomarkers of pesticide exposure.S. Irish R.50(5):505-515. Brunet RC.usgs. Bravo R.S. 1998. Barr DB. March 2006. 4/7/09 Lu C. Garfitt SJ. Available at URL: http://pubs. Olsson AO. Sadowski MA. 2006). Diazinon. References Anthony J. Ann Occup Hyg 2006.111(12):1478-1484.. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine. Swan et al. Environ Health Perspect 2003. Toepel K. Toxicol Lett 2002. 2005.gov/circ/2005/1291/.114(2):260-263. U. Cocker J. urinary 2-isopropyl-4-methyl-6-hydroxypyrimidine levels were below the limit of detection (Bouchard et al. May 2004. et al. Jones K. Bull Environ Contam Toxicol 1986. Beeson MD.epa. Alteration of mice L-tryptophan metabolism by the organophosphorous acid triester diazinon. 6/1/09 Fourth National Report on Human Exposure to Environmental Chemicals 145 .htm. Liu F. Barr DB. Swan SH. Redmon JB. Exposure to the organophosphate diazinon: data from a human volunteer study with oral and dermal doses. 1/14/09 U. Driskell WJ.org/documents/ehc/ehc/ehc198. Available at URL: http://www.134(1-3):105-113. Study for Future Families Research Group. Baker SE. In a small number of men visiting fertility clinics in Missouri and Minnesota. Dumas P. EPA 738-R-04-006. Banister E.37(4):501-507. 1992-2001.pdf.10(6 Pt 2):789-798.9(2):117-131. (2003) found that 2-isopropyl4-methyl-6-hydroxypyrimidine was detectable in 96% and 58% of the subjects. Biochem Pharmacol 1992.44(11):2243-2250. Biological monitoring of exposure to organophosphorus insecticides in a group of horticultural greenhouse workers. Effect of sublethal levels of diazinon: histopathology of liver. Barr DB.S. Oloffs PC.Organophosphorus Insecticides: Specific Metabolites 2005).inchem. Atlanta (GA). International Programme on Chemical Safety-INCHEM (IPCS). Nguyen JV. Oloffs PC. Needham LL. In 54 Canadian greenhouse workers. Pewnim T. 2007 [online].376(6):808-815. Seifert J. 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. Carrier G. In 23 children. Diazinon. Bouchard M.. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. Environmental Health Criteria 198. Rajendra W. Effects of chronic intake of diazinon on blood and brain monoamines and amino acids. Anal Bioanal Chem 2003. revised February 15. J Expo Anal Environ Epidemiol 2000. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Mason HJ. Interim reregistration eligibility decision (IRED. Barr DB. Drug Chem Toxicol 1986. Fenske RA. Kruse RL. 2006). urinary 2-isopropyl-4-methyl-6hydroxypyrimidine was detected in less than 14% of multiple samples collected during varied diets (Lu et al. Environ Health Perspect 2006. Geological Survey (USGS). Drobnis EZ. EPA). Quantification of selected pesticide metabolites in human urine using isotope dilution high-performance liquid chromatography/ tandem mass spectrometry. Third National Report on Human Exposure to Environmental Chemicals. Environmental Protection Agency (U. Pesticides in the Nation’s Streams and Ground Water.

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

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

Lioy PJ. Geological Survey (USGS). MacIntosh DL.38(4):546-553. Eberly LE. Available at URL: http://pubs. A longitudinal investigation of selected pesticide metabolites in urine. In vitro studies on the genotoxicity of the organophosphorus insecticide malathion and its two analogues. Rappaport E. Eskenazi B. A toxicokinetic model of malathion and its metabolites as a tool to assess human exposure and risk through measurements of urinary biomarkers. Ryan PB. Harley K. Kizer KW: Exposure to aerial malathion application and the occurrence of congenital anomalies and low birthweight. Clayton CA. Barr DB. Szyfter K. Atlanta (GA). metabolite clearance. Genotoxic effects of malathion: an organophosphorus insecticide using three mammalian bioassays in vivo. Krieger RI. Bradman A. Goldhaber M. International Programme on Chemical Safety-INCHEM (IPCS).org/documents/jmpr/jmpmono/v2003pr06. Albertini RJ. Pesticides residues in food: 2003 FAO/WHO Meeting on Pesticide Residues. 4/7/09 Kissel JC.gov/oppsrrd1/REDs/ malathion_red.22(1):7-17. Toepel K. Bouchard M. Environ Health Perspect 2004. Fenske RA. Quintana PJ. Lu C. Malathion deposition.S. Giri A. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population. Needham LL. Harris JA.56(10):2393-2399. Am J Epidemiol 1990. Centers for Disease Control and Prevention (CDC). Dinoff TM.73(1):182-94. Cancer Res 1996. Dumoulin MJ. and cholinesterase status of date dusters and harvesters in California. U. Neutra R. J Expo Anal Environ Epidemiol 1999. Barr DB. Environ Health Perspect 2001. Barr DB. Hertz-Picciotto I.pdf. Environ Mol Mutagen 1993. EPA). 2007 [online]. Mutat Res 2002. Jaloszynski P. htm. Mutat Res 1999. Increased frequency of specific genomic deletions resulting from in vitro malathion exposure. Environ Health Perspect 2006. Sharma GD. Blasiak J. 6/1/09 U. Flessel P. J Expo Anal Environ Epidemiol 2005. Bravo R. Nicklas JA. Swan SH.S. Comparison of organophosphorus pesticide metabolite levels in single and multiple daily urine samples collected from preschool children in Washington State. et al. 6/1/09 148 Fourth National Report on Human Exposure to Environmental Chemicals . Genetic toxicity of malathion: a review. July 2006. Petitti D. Grether JK. Erratum in: Toxicol Sci 2003 Aug. O’Neill JP. revised February 15. Arch Environ Contam Toxicol 2000. Hammerstrom KA. The Quality of Our Nation’s Waters. Lu C. Environmental Protection Agency (U. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample.epa. Trzeciak A. Toxicol Sci 2003 May. Hooper K. Carrier G. Pluth JM. Giri S. Available at URL: http://www.445(2):275-283. Am J Public Health 1987.74(2):following table of contents. Gosselin NH. Brunet RC. Freeman NC.112(10):1116-1124. 1992-2001.77:1009-1010. Irish R. Prasad SB.S.usgs. Reregistration eligibility decision (RED) Malathion.109(6):583-590.Organophosphorus Insecticides: Specific Metabolites References Adgate JL.114(2):260-263.132(4):794-795. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. Weltzien E. March 2006. 2005. Kedan G.inchem. EPA 738-R06-030. Curl CL. et al.9(5):494-501. Griffith W. Barr DB. Jewell NP.514(1-2):223231. Malathion (addendum). Thomas D.gov/circ/2005/1291/. Samuel O. et al. Reproductive outcome in women exposed to malathion. Available at URL: http://www. Pesticides in the Nation’s Streams and Ground Water.15(2):164-171. Third National Report on Human Exposure to Environmental Chemicals.

< LOD means less than the limit of detection.28-4.10) 4.02-6.37) 2.32 (1.80) 2. and Nitrobenzene Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.02) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .300-.00 (2.26 (1. Methyl parathion has low water solubility.01) 695 660 518 679 603 941 Limit of detection (LOD. and aquatic invertebrates.Organophosphorus Insecticides: Specific Metabolites Methyl Parathion CAS No. In animal studies.860 (<LOD-1.85 (2.10) 22.32-1.70 (3.80 (2.40-3. Estimated intakes from diet and drinking water have been below recommended limits. In the 1990s. and of the chemical nitrobenzene. all registered uses were voluntarily cancelled (U.10 (3.62 (1.60-5.50 (2.40-4. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.44) 2.90-11.50 (1.37-4.40) 4. Increased risk of exposure via dermal.0) 4. and oral routes can occur in pesticide and agricultural workers (Muttray et al.13-1.0) 3. the potential for human exposure to either ethyl or methyl parathion through the diet or drinking water is low. O-ethyl-O-(4-nitrophenyl) phenylphosphonothioate.21-1.45) 5.71 (2.0) 3.770 (.28 (1.10 (<LOD-6.41-4.10 (3.60-36. phosphorothioates such as methyl and ethyl parathion are metabolically activated to the “oxon” forms which have greater toxicity than the parent insecticides.990-1.50) 2.33 (1.70 (<LOD-3.60-19.70-3.30-5. and eliminated rapidly from the body after absorption (Kramer et al. pulmonary.21 (2.30 (2.70-6.60-24.80 (1.74) 5.0) 2. Ethyl parathion.32-1.1.49 (1. ethyl parathion.S.05) 4.11) 2.20 (<LOD-2.00) 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 1.50 (1. on cereal grains.S. methyl parathion was rapidly absorbed after ingestion.70 (2. 2007).0) 3.790 (<LOD-.33) 2.700 (<LOD-. It had been applied to cotton.20) 5.40-4..89 (2.19 (. peak domestic use was as high as 5-6 million pounds per year.50-14. with limited applications in agriculture.69) 4.50 (1.92) 5.10-11.50) 1..90 (1.40 (1.27) 2.EPA.0 (3.57-4. Both are toxic to birds.37-2.70 (2.EPA.60 (4. and has a short half-life in soils and on plants.61) < LOD 1.8 and 0.71) 971 1164 1018 1313 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD . binds tightly to soils resulting in low leachability.850) < LOD .40) 1. Many previous registered agricultural uses of methyl parathion have been cancelled (U. 2000).60) 1.57) 1. 1977). Given its limited use.0) 3.92-2.70) 2.36-1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 5.70-6.47) 2. population from the National Health and Nutrition Examination Survey. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.22-3.00 (2. Fourth National Report on Human Exposure to Environmental Chemicals 149 .50 (2. was once a restricted-use insecticide with limited applications on certain agricultural crops.01) 4. and to a lesser extent.50-9. Methyl parathion is not registered for residential use in the United States.50) 3.72 (3. 2006).70) 2.298-00-0 Ethyl Parathion CAS No..45 (1.730 (<LOD-.910) < LOD .67 (1. but by 2003. Morgan et al.37-4. Methyl parathion use is highly restricted.30 (1. 2002.40) 2.34 (3.S.50 (1.28 (1.11-4. which may vary for some chemicals by year and by individual sample.15-3.09-1.58) 3.66 (2.48) 90th 2. Methyl Parathion.16) < LOD 1.0) 3.00) 3.71 (3.91-3.90-9.30-16.46 (3.24) 479 565 680 813 830 1099 99-00 01-02 99-00 01-02 * * * * < LOD . 56-38-2 General Information Para-nitrophenol is a metabolite of the insecticides methyl parathion.70 (2.79) 4. Ethyl and methyl parathion are infrequently detected in groundwater sampling (USGS.01-4. Metabolism of ethyl or methyl parathion leads to the formation of paranitrophenol.910) < LOD < LOD < LOD 1. Survey Geometric mean (95% conf. more slowly absorbed through the skin.12) < LOD < LOD 1.70) 2.20 (2. first registered in 1948. fish.20-5.940 (<LOD-2.30-3. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Urinary para-Nitrophenol Metabolite of Ethyl Parathion.50) 3.80 (2.69 (2.10-1.70-3.67) < LOD 1.61) < LOD 1.18-3. 2003). Once absorbed.70-6.910) < LOD < LOD .32-3.

15-10. 1978.26 (1.790-.540) < LOD .430 (. Overt cholinergic toxicity and death from methyl and ethyl parathion have been described following suicidal ingestion.59 (1.78-2.79) 1.720 (<LOD-.29) 2.33-3. or generally to have reproductive toxicity at doses below those causing acetylcholinesterase inhibition in most animal studies (IPCS.01-3.04 (2. does not inhibit acetylcholinesterase enzymes.850-1. teratogenic. Slotkin et al.44-3. Survey Geometric mean (95% conf.31-3. 2006. and unintentional acute or chronic high-level occupational exposure (Hill et al. In large doses.97-10.370 (<LOD-.96 (1.08) < LOD . 2006. weakness.93 (2.56-2.05) 4.23) 1.EPA considers methyl parathion unlikely to be carcinogenic to humans.73 (1.25) 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.37-1.33) 479 565 680 812 830 1099 99-00 01-02 99-00 01-02 * * * * < LOD . 1995.S.26) 17. Orsorio et al.. 2004).16-4. WHO..31) < LOD .930 (.11-4.38-3.880 (.44-3. At high animal doses of methyl parathion. and seizures.7) 3.21) 1.940 (<LOD-1.70) 3.67-2.89 (2.57-7.84) 3.80 (1. vomiting. Jaga and Dharmani. Lores et al. EPA at: http://www.640) < LOD < LOD 1.13) 4.08 (1.17-4.91 (1.00 (1. and other organophosphorus insecticides share a common mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system.970 (.96 (1.20) 3. gov/pesticides/.78-2.e.33-3.10 (1.14-3.94-4.91) 1.67 (3.06) 971 1164 1018 1312 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD . Methyl Parathion.Organophosphorus Insecticides: Specific Metabolites Metabolites”).html and from U.29 (2.. methyl parathion.970 (.00) 2.17) .77-7. In addition to being a metabolite of methyl and ethyl parathion.35-3. Zurich et al. and other metabolites.01 (2.45) 695 660 518 678 603 941 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.9) 1. and Nitrobenzene Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.80 (1.57-2. ethyl parathion.89 (2.13-12. 2005. paranitrophenol.79 (1. 1995).530) < LOD < LOD < LOD .30-1.S.78) 2.55) 2. and producing acute symptoms such as nausea.690-1.07 (1.atsdr.20 (3.87 (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 .94-47.07) 2.790-1.60 (1. Parathion and methyl parathion have high acute toxicity in animal testing.78 (2.950) < LOD . Thus.20) .29) 1.82) < LOD . gov/toxpro2. 1990.39 (1. population from the National Health and Nutrition Examination Survey.1) 2.21-21.01 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th 4. The metabolite. environmental levels) and health effects is available from ATSDR at: http://www.310-.97 (2. Additional information about external exposure (i.10) 90th 2.930 (.4 (3.55 (<LOD-3. Karanth and Pope et al. 150 Fourth National Report on Human Exposure to Environmental Chemicals .98-7. but lists ethyl parathion as a possible human carcinogen. 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. U.870) < LOD .800-1. retinal atrophy and sciatic nerve degeneration have also been observed (IPCS.88) 1.90 (1.03) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD . 1991).60) 2.71) 1.3) 2.57) 6.25 (2.92 (2.680 (<LOD-1.04) 1.48-4.83 (1.72-2.. paralysis. resulting in excess acetylcholine at nerve terminals.43) 4.S.11) 1..980 (.33-6.840 (. 2003.830-1.cdc.61) 4.30) 3.86 (2.08-3. the detection of para-nitrophenol in a person’s urine may also reflect exposure to the environmental degradate.39) 1.09) 2. accidental exposure..2) 2..730-1.35-3.440 (<LOD-.720-1.82 (2. Urinary para-Nitrophenol (creatinine corrected) Metabolite of Ethyl Parathion.15) 3.95) 1.41-2.400 (<LOD-.2) 2..71 (1.88 (1. para-nitrophenol can also occur in the environment from the breakdown of the parent these organophosphorus pesticides and from nitrobenzene.97 (<LOD-4. cholinergic effects.76-14.epa.00 (1. IARC does not consider ethyl parathion and methyl parathion classifiable as human carcinogens. Methyl parathion is not considered genotoxic. 2004).500) < LOD < LOD . Human health effects from parathion or ethyl parathion at low environmental doses or at biomonitored levels from low environmental exposures are unknown.60-2.

56(7):449553. Toxicology 2005. 2002). Needham LL. Lewalter J. Kissel JC. Measurement of p-nitrophenol in the urine of residents whose homes were contaminated with methyl parathion. McCann KG. J Expo Anal Environ Epidemiol 2005. Barr DB. McClure PC. Moseman RF. 2003) and in 482 pregnant females from an agricultural region of California (Eskenazi et al. Age-related effects of chlorpyrifos and parathion on acetylcholine synthesis in rat striatum. Barr DB. Rubin et al. general population (CDC.. Jewell NP. ACGIH recommends a BEI of 0. Curl CL. Hill RH Jr.inchem. 2005. Runkle KD. et al. Bradman A. 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. end-of-shift urinary para-nitrophenol levels ranged from 190 to 410 µg/ gram of creatinine (Leng and Lewalter. 1999). Giordano G. Alley CC. Lin LI. McCann et al. Parathion-Methyl (addendum). Role of individual susceptibility in risk assessment of pesticides. In a study of workers who handle parathion. Arch Environ Contam Toxicol 1977. Kramer RE. Bailey SL. Effect of organophosphorus insecticides and their metabolites on astroglial cell proliferation. et al. J Anal Toxicol 1990.5 mg (500 µg)/g creatinine for workers at the end of shift. Lores EM.15(2):164-171. Hetzler HL. et al. Slach EF. et al. 2004). 1995). Hill et al. population (Olsson et al. Lu C. Karanth S. oral or dermal administration. Pope C. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Baker SE. DiPietro E.Organophosphorus Insecticides: Specific Metabolites Biomonitoring Information Urinary levels of para-nitrophenol reflect recent exposure. and many residents were symptomatic (Barr et al. Pharmacokinetics of methyl parathion: a comparison following single intravenous.9:311-320. Costa LG. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population. 1995. Guizzetti M.6(2-3):159-173.. 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.org/documents/jmpr/jmpmono/v95pr14. Barr JR. 2002. 2005. Organophosphorus pesticide poisonings in humans: determination of residues and metabolites in tissues and urine. Chicago area methyl parathion response.S. Weltzien E. Hryhorczuk DO..71:99108. 2005).110 Suppl 6:1085-1091. Head SL.25(5):599-606. Occup Environ Med 1999. Rockhold RW. CDC. Finding a measurable amount of para-nitrophenol in urine does not mean that the level will result in an adverse health effect. Barr DB. J Biomed Sci 2002.112(10):1116-1124. Environ Health Perspect 2004. Arch Environ Health 1978. Dharmani C. 2005). Laboratory investigation of a poisoning epidemic in Sierra Leone.33(5):270-276. et al. Pesticide workers may have much higher levels following pesticide applications. Bradway DE. Clark JM. Comparison of organophosphorus pesticide metabolite levels in single and multiple daily urine samples collected from preschool children in Washington State.S. Environ Health Perspect 2002. References Barr DB. 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. 2005. Environ Res 1995.. Shealy DB. Gregg M. Morgan DP.21(1):5767. Rev Environ Health 2006. Hill RH Jr. and levels were similar or slightly lower that those in a small convenience sample of the U.14(4):213-216. Atlanta (GA). Harley K. Fourth National Report on Human Exposure to Environmental Chemicals 151 . 2002..215(3):182-190. Moomey CM. Kedan G. International Programme on Chemical Safety-INCHEM (IPCS). a range of values several hundred times higher than levels found in the U. Centers for Disease Control and Prevention (CDC). Urinary excretion of paranitrophenol and alkyl phosphates following ingestion of methyl or ethyl parathion by human subjects. Leng G. Methyl parathion: an organophosphate insecticide not quite forgotten. Eskenazi B.110 Suppl 6:1075-1078. Baker S. Turner WE. Available at URL: http:// www. Griffith W. Environ Health Perspect 2002. Ashley DL. 4/7/09 Jaga K. Neurotoxicol Teratol 2003. Pesticide residues in urine of adults living in the United States: reference range concentrations. Head SL...htm. Third National Report on Human Exposure to Environmental Chemicals. Levels of para-nitrophenol in the NHANES 1999-2000 and 2001-2002 subsamples were similar or slightly lower than those in a nonrandom subsample of NHANES III (19881994) participants (CDC. Baker RC. Wellman SE. Cline RE. Pathak S.

Geological Survey (USGS).gov/circ/2005/1291/.201(2):97-104. Esteban E. Tate CA. 152 Fourth National Report on Human Exposure to Environmental Chemicals . EPA-738-FOO-009. Case No. 2007 [online]. Slotkin TA.376(6):808-815. Involvement of glial cells in the neurotoxicity of parathion and chlorpyrifos. et al.S. Rubin C. 1992-2001. 1/14/09 U. Kieszak S. Ethyl parathion.162(2-3):219-224. pdf. Nguyen JV. Levin ED. Monnet-Tschudi F. Environ Health Perspect 2002.114(10):1542-1546. Seidler FJ. revised February 15. U. Assessment of human exposure and human health effects after indoor application of methyl parathion in Lorain County. Toxicol Lett 2006. Olsson AO.epa.Organophosphorus Insecticides: Specific Metabolites Muttray A. Environ Health Perspect 2006. Ohio. September 2000.pdf. Mengle DC.gov/oppsrrd1/REDs/factsheets/0155fct. EPA). Backer G. 1/12/07 U. Schilter B. Hill G. The Quality of Our Nation’s Waters. 2004.usgs. Am J Ind Med 1991. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine. Available at URL: http://www. WHO/SDE/WSH/03.04/106. Jung D.int/water_sanitation_health/dwq/chemicals/ methylparathion. 6/1/09 World Health Organization (WHO).S. Environmental Protection Agency (U. Sadowski MA. 1995-1996. Costa LG. EPA). Available at URL: http://www. Facts.D. Investigation of a fatality among parathion applicators in California. Anal Bioanal Chem 2003.S. R. March 2006. Available at URL: http://www. Osorio AM.pdf. May 2003. Organophosphate insecticides target the serotonergic system in developing rat brain regions: disparate effects of diazinon and parathion at doses spanning the threshold for cholinesterase inhibition. gov/oppsrrd1/REDs/methylparathion_ired.20(4):533-546.who. Yacovac R. Environmental Protection Agency (U. Pesticides in the Nation’s Streams and Ground Water.S. Hill RH Jr.110 Suppl 6:1047-1051. Ames RG.epa. Letzel S.E. Toxicol Appl Pharmacol 2004. Interim reregistration eligibility decision (IRED) for Methyl Parathion. Barr DB. Methyl parathion in drinking water. 0153. 5/19/09 Zurich MG. Available at URL: http://pubs. Rosenberg J. Ryde IT. Honegger P. External and internal exposure of wine growers spraying methyl parathion. Dunlop B.S.

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

760 (<LOD-.700-.460) 1165 1316 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .430 (<LOD-. < 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.740 (.670) 567 810 1104 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD . Survey Geometric mean (95% conf.08) 1165 1316 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . Survey Geometric mean (95% conf.300-1. which may vary for some chemicals by year and by individual sample.850 (.55) . population from the National Health and Nutrition Examination Survey. interval) Selected percentiles ( 95% confidence interval) Sample 95th .27) .250 (<LOD-.21) < LOD .840 (.680 (<LOD-.580-1.470 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.500 (.94) .210-1.770) 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 .210-.700-1.950) < LOD < LOD 1.780 (<LOD-1. population from the National Health and Nutrition Examination Survey.64) . interval) Selected percentiles ( 95% confidence interval) Sample 95th .00) 669 687 929 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.820) < LOD < LOD .410 (<LOD-1.670 (<LOD-1. 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.780 (<LOD-1.210 (<LOD-.780 (.780 (. see Data Analysis section) for Survey year 01-02 is 0.200-.840) 669 687 929 Limit of detection (LOD.880) 567 810 1104 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD .15) < LOD .S. 154 Fourth National Report on Human Exposure to Environmental Chemicals .31) .740-1.S.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 .07) .Organophosphorus Insecticides: Specific Metabolites Urinary 2-(Diethylamino)-6-methylpyrimidin-4-ol/one Metabolite of Pirimiphos-methyl Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.17 (.2.610 (<LOD-1.

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

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

. Estrogenicity of pyrethroid insecticide metabolites. Go V. Richardson JR.. Assessing estrogenic activity of pyrethroid insecticides using in vitro combination assays. Shin JH. Leng G. McCarthy et al. Lewalter J. WHO. Environ Health Perspect 1999. Toxicol Appl Pharmacol 2006. Lazarini CA. Neurotoxic effects of two different pyrethroids.. Florio JC. 1991. 2002). Toxicol Appl Pharmacol 1991. Toxicokinetics of pyrethroids in humans: consequences for biological monitoring. Neurotoxicol Teratol 2005. and seizures (ATSDR. 2006. Leng G. Idel H. Garey and Wolff. and catecholaminergic pathways and behavioral changes have been demonstrated at subacute and subchronic doses for some pyrethroid pesticides (Aziz et al. Okuno Y.. Concomitant exposure to organophosphorus insecticides may increase pyrethroid toxicity by slowing metabolic clearance of the pyrethroid. Biochem Biophys Res Commun 1998. 2004.50(2):245-255.. Bernardi MM.. Thomson BM. 2003. Seth PK.62:101-108. paresthesias) reported in agricultural workers from 1996 to 2002 (Spencer and O’Malley. Garey J. Available from URL: http://www.gov/toxpro2. Kamita Y. and permethrin) in the Hershberger and uterotrophic assays. McCarthy AR. choreoathetosis. Yang J. Generally. Hu JY. Hu et al.27(12):1273-1283. Berger-Preiss E. Estrogenic potential of certain pyrethroid compounds in the MCF-7 human breast carcinoma cell line. Guillot TS. Neurodevelopmental consequences of gestational exposure (GD14-GD20) to low dose deltamethrin in rats. Moniz AC. Yamada T. salivation. Abell AD. 2003. Adhami VM.1/15/09 Aziz MH. Fredriksson A. Shukla Y.Pyrethroid Pesticides and other ion channels may also explain some pyrethroid effects. Human cases of systemic poisoning are rare and usually result from accidental exposure or intentional ingestion of pyrethroid insecticides. Regul Toxicol Pharmacol 2002. Zhao RC. Soderlund et al.cdc. Indoor pyrethroid exposure in homes with woollen textile floor coverings. Kim TS. on immature and adult mice: changes in behavioral and muscarinic receptor variables. Shafer. [Effects of fenvalerate on reproductive and endocrine systems of male rats] Zhonghua Nan Ke Xue 2002.. hypersensitivity.. Miller GW. Ranft U. 1998. Pyrethroid pesticide-induced alterations in dopamine transporter function. Levsen K. Bernardi MM. Wieseler B. Pauluhn J. Kim IY. Ray et al. et al. Kim HS. 2006. 2006). Shaw IC.. Signs and symptoms of acute pyrethroid poisoning after massive ingestions include agitation. Bull Environ Contam Toxicol 1999. epa. In California. 2002). 2005). cdc. Spinosa HS. 2003. 2001. Idel H. Wang SL. 2002. Chen JH. Lemonica IP. Effects of prenatal exposure to deltamethrin on forced swimming behavior.. Lazarini et al.. Sunami O.251(3):855-859. Leng G. Xenobiotica 1997. Kunimatsu T. J Environ Monit 2006. though a few pyrethroid pesticides and some metabolites have shown weak or inconsistent estrogenic effects on standardized assays (ATSDR. Human doseexcretion studies with the pyrethroid insecticide cyfluthrin: urinary metabolite profile following inhalation. EPA at: http://www. Eriksson and Fredriksson. cyfluthrin was the most frequent pyrethroid associated with symptomatic effects (irritant respiratory and dermal effects. Pogo BG. 2000. In developing rodents. Lack of (anti-) androgenic or estrogenic effects of three pyrethroids (esfenvalerate. Agrawal AK.107(3):173-177. Wolff MS. the pyrethroids are not considered genotoxic in in vitro testing or carcinogenic in animal testing (WHO. Int J Hyg Environ Health 2002.108(1):78-85.8(1):18-21.23(6):665-673. Go et al. 2003.atsdr. Leng A.8(1):197-202.gov/pesticides/ and from ATSDR at: http://www. Cruz-Casallas PE. 2005). Neurosci Lett 2001. Estrogenic and antiprogestagenic activities of pyrethroid insecticides.27(4):609-614. Kim et al. Kuhn K. Sugiri D. Kuhn KH. Lee SJ. References Agency for Toxic Substances and Disease Registry (ATSDR). Wolff MS. Kunimatsu et al. et al. Moniz et al..S. 1999. Elwan et al. No relationship of indoor air or housedust concentrations of permethrin and irritant symptoms was found in a study of urban residents in 80 private homes (Berger-Preiss et al. Elwan MA.. neurochemical changes in cholinergic. tremor. Song L. dopaminergic. Neurotoxicol Teratol 2001. et al.atsdr. September 2003. J Reprod Dev 2004. motor activity.html. Toxicological profile for pyrethrins and pyrethroids. Behavioral and endocrine changes induced by perinatal fenvalerate exposure in female rats. 2005). et al.html.300(3):161-165. and striatal dopamine levels in male and female rats. Eriksson P. Ose K. 2001. Garey J. Salzgeber SA. The pyrethroids in general use are not considered teratogenic or to have significant reproductive toxicity (ATSDR. IARC considers deltamethrin and permethrin as not classifiable as to their human carcinogenicity.211(3):188-197.205(6):459-472. Transient dermal paresthesias have been reported among pesticide applicators after direct contact with certain types of pyrethroid pesticides. bioallethrin and deltamethrin.gov/toxprofiles/ tp155. Additional information about pesticides is available from U.35(2 Pt 1):227-237. Caudle WM. Varoli FM. 2005). Kang IH. Fourth National Report on Human Exposure to Environmental Chemicals 157 . fenvalerate.

1992–2001. Environmental Protection Agency (U. Marsh JR. Pesticides in the Nation’s Streams and Ground Water. Available at URL: http://www.S. Environ Health Perspect 2005. Reregistration Eligibility Decision for Cypermethrin.htm. 5/26/09 U. pdf. et al. resmethrin. Mechanisms of pyrethroid neurotoxicity: implications for cumulative risk assessment. Shafer TJ. 19962002. 5/26/09 U. Meyer DA.epa.htm. O’Malley M.gov/oppsrrd1/REDs/cypermethrin_red. Spencer J. Available at URL: http://pubs.S. 5/26/09 U. Rev Environ Contam Toxicol 2006.pdf. Available at URL: http://www. J Toxicol Clin Toxicol 2000. World Health Organization (WHO). and therapy.usgs.Pyrethroid Pesticides Ray DE. Geological Survey (USGS).gov/ circ/2005/1291/. Pyrethroid illnesses in California.S.186:57-72.epa. Permethrin. Toxicology 2002. EPA).S.gov/oppsrrd1/REDs/ factsheets/permethrin_fs. Permethrin Facts (Reregistration Eligibility Decision Fact Sheet). Developmental neurotoxicity of pyrethroid insecticides: critical review and future research needs. Soderlund DM. synergies. Pyrethroid insecticides: poisoning syndromes. Revised February 25. Environmental Protection Agency (U. Mullin LS.S. Clark JM. sumithrin synthetic pyrethroids for mosquito control. Available at URL: http://www. Crofton KM. Sargent D.22(8):983-991.S. June 2006b.gov/pesticides/ health/mosquitoes/pyrethroids4mosquitoes.171:3-59. EPA). March 2006. Lesser JE. Safety of pyrethroids for public health use. 5/26/09 158 Fourth National Report on Human Exposure to Environmental Chemicals .int/hq/2005/WHO_ CDS_WHOPES_GCDPP_2005.who.S. EPA). Forshaw PJ. Xenobiotica 1992. June 2006a.epa.10. 2005. 5/26/09 Woollen BH. 2007. Piccirillo VJ. U. Laird WJ. Available at URL: http://whqlibdoc.38:95-101. April 2002. Pesticide and Evaluation Scheme.113(2):123-136. Sheets LP. Environmental Protection Agency (U. The metabolism of cypermethrin in man: differences in urinary metabolite profiles following oral and dermal administration.

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

Survey Geometric mean (95% conf. which may vary for some chemicals by year and by individual sample.2. 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. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. population from the National Health and Nutrition Examination Survey. 160 Fourth National Report on Human Exposure to Environmental Chemicals .2 and 0.S.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. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. < LOD means less than the limit of detection.

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. population from the National Health and Nutrition Examination Survey. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.S. Fourth National Report on Human Exposure to Environmental Chemicals 161 . Survey Geometric mean (95% conf.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.

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

140 (<LOD-.630 (.52645-53-1 General Information Several pyrethroid pesticides are formulated as a mixture of cis.580-1.08) 947 1193 1004 1346 99-00 01-02 99-00 01-02 99-00 01-02 * * . cis-permethrin.790) .490-1.13 (.270-.600-1.262) * * * < LOD < LOD .570-.250-.580) 1.670-1.200) < LOD < LOD < LOD .210-.200) .630) .350) .380 (.680 (.910-5.330 (.740) 1.710) .790-1.07 (.2dichlorovinyl)-2. Similarly.2-Dichlorovinyl)-2. The cis-isomer of permethrin has more potent insecticidal activity than transpermethrin. In the body.2-dichlorovinyl)-2.490-.155-.600 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. The chemical trans-3(2.410) . 52315-07-8 CAS No..510 (.200 (.202 (. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.110-.530 (.890 (.340) .200) .630-.510 (.32) .210) .370-.21) . cis-3-(2. and ciscyfluthrin.250 (.740-1.730 (.260 (.380) .270 (.210) 90th . trans-permethrin.1 and 0.120-.80) .2-dimethylcyclopropane carboxylic acid Metabolite of cis-Permethrin.11) .850 (.610) .640 (.370 (.300-.240) .730 (. and cis-Cypermethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.300 (.180 (.410) .120-. Fourth National Report on Human Exposure to Environmental Chemicals 163 .330) .740 (. ciscypermethrin and cis-cyfluthrin.2-dimethylcyclopropane carboxylic acid that is formed in the environment from the degradation of these pesticides (George.110-.690) .270 (.380-.240) .43) .77 (.520) . 1985.380-.490-.570 (.670-2.2-dimethylcyclopropane carboxylic acid is a metabolite formed from trans-permethrin.500 (.or trans-3-(2.140 (.1. more of the trans-metabolite than Urinary cis-3-(2.15) . interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.460-1.960 (.610) .220-.400-.47 (.200-.870) 1. Cyfluthrin. but it can also reflect exposure to cis-3-(2.220-.Pyrethroid Pesticides Cyfluthrin the cis-metabolite is found in the urine.770-1.2dimethylcyclopropane carboxylic acid in urine not only reflects the metabolic transformation of any of the three pesticides.950-2. the presence of trans-3-(2.110 (<LOD-. Generally.890 (.780) .68 (.160 (. The presence of cis-3-(2.740-2.160 (<LOD-.280 (. 1999).380-.2-dichlorovinyl)-2.2-dimethylcyclopropane carboxylic acid in urine not only reflects the metabolic transformation of any of the three pesticides.650-1. Biomonitoring Information Urinary levels of cis. but can also reflect exposure to trans-3(2.180) .220) .490-1.220-.12 (.340) . Kuhn et al.2-dimethylcyclopropane carboxylic acid is a metabolite formed from cis-permethrin.430-.and trans-isomers.300 (. Kuhn et al.28) 468 580 667 831 816 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD . 1999).68) .790-1.730 (.28) 671 680 518 701 591 957 Limit of detection (LOD.440 (.10) size 1951 2539 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD 75th . trans-cypermethrin.35) 1.460 (.2dichlorovinyl)-2.630) .510 (.460-.35) . < LOD means less than the limit of detection.340-. population from the National Health and Nutrition Examination Survey.120-.470-1. 1985.2-dichlorovinyl)2.2-dichlorovinyl)- CAS No.300-.170 (.670-1.920) 1.120-. cis-cypermethrin.600) .270 (.680) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .54) .2-dimethylcyclopropane carboxylic acid formed in the environment from the degradation of these pesticides (George.550) .670 (.200-. which may vary for some chemicals by year and by individual sample.900 (.220-.2-dichlorovinyl)-2.S.110-.50) .44 (.68) ..820 (. transcypermethrin and trans-cyfluthrin.280-.770) .68359-37-5 Cypermethrin Permethrin CAS No.680-3.470 (.310) .880 (.700) .53) .420-.230) .150 (.790 (.160 (. and trans-cyfluthrin.08) .710-1. Survey Geometric mean (95% conf.500 (.24) 1.200-.

240 (<LOD-.220 (.440 (. 164 Fourth National Report on Human Exposure to Environmental Chemicals .230-.230-.340) ..440 (.200-.31) . the levels at 24-72 hours were slightly less than the 95th percentile in the NHANES 2001-2002 subsample (CDC.560) 1.680 (.500 (..390-..260) .190 (.170 (.67) . Urinary levels of the two chemicals in adults were similar to those in children in these studies (Heudorf et al.11 (.390 (.450 (.640-. representative NHANES 2001-2002 subsample (CDC.2-dichlorovinyl)-2.290) .900 (.S.03) size 1951 2538 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD 75th .190) .640-1.120 (.170 (.11) 947 1193 1004 1345 99-00 01-02 99-00 01-02 99-00 01-02 * * .and trans-3(2..570) . Schettgen et al.250-.08) 468 580 667 830 816 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD . 2006) and 1177 urban adults and children (Heudorf et al. 2006).700) .280-.260 (. Estimated daily pyrethroid intakes based on urinary levels in the German children were below the acceptable daily tolerances (Heudorf et al.2-dichlorovinyl)-2.580-1..220 (.560) .250) .33) .840 (.840 (.550) .11) .170) < LOD < LOD < LOD .210-.and trans-3-(2.21) .580) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.400 (.890 (. urinary levels of cis-3-(2.14) 671 680 518 700 591 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.S. 2004.530 (. In a study of volunteers.350) .2-Dichlorovinyl)-2.260 (.12-2.550) .59) .200-.380) .270 (.890) . 2006.700) .250-.300-. though the 95th percentile levels increased several fold after exposure to nearby pest control operations (Leng et al.440-.590) .420 (.710-3.750-1.59 (1.700-2.220) . Survey Geometric mean (95% conf.200 (.380-.810 (.300 (. 2004).710 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.11) .640) 1.190) .138 (.540 (. Other studies have provided evidence that urinary levels of cis.300) .180 (.680-1..430 (. In a study of urban residents in Germany (Berger-Preiss et al.450-1. 2001.640 (.150-.260-..37) .260 (.230-.. 2002).540) .370-.600 (.430-.540 (.180-.150-. median urinary levels of trans-3-(2.200) . 2005).2-dichlorovinyl)-2.410) .320-.550-1.59) .300) .690-1.390-. 2005).104-.290-.800 (.130-.400-1.250) 90th .230 (.Pyrethroid Pesticides 2.300 (.250) . These studies indicated that intake is mainly from the diet and that dermal absorption contributes little to intake (Heudorf et al.2dichlorovinyl)-2.640-1.2-dimethylcyclopropane carboxylic acid did not increase at 24-72 hours after exposure to nearby pest control operations (Leng et al.470-1.290 (.49) .12 (.33 (. 2005) In a small group of indoor pest-control operators.370-. 2006.340) .750 (. 2003).250-.182) * * * < LOD < LOD .2-dimethylcyclopropane carboxylic acid levels at the 95th percentile were about one-third of the 95th percentile in the NHANES 20012002 subsample (CDC. and cis-Cypermethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. 2005).440-.340-.550-1.2-dichlorovinyl)-2. In the same residents.250 (<LOD-.11) 1.2dimethylcyclopropane carboxylic acids at the 95th percentile that were similar or slightly less than the 95th percentiles in the U.2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of cis-Permethrin.270-.550 (.80) .680-1.780) 1.290) .370-.29 (. urinary trans-3-(2.270) .920 (.67 (.590 (.270) .2-dimethylcyclopropane carboxylic acids in children were related to residential pesticide use and house dust levels (Becker et al.2-dimethylcyclopropane carboxylic acid did not increase. Lu et al.520) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD . 2001) showed urinary levels of cis. the levels at 24-72 hours were slightly less than the 95th percentile in the NHANES 2001-2002 subsample (CDC.350 (.2dimethylcyclopropane carboxylic acid at the 95th percentile were about half the 95th percentile in the NHANES 20012002 subsample (CDC.24) ..320) .430-1.150-. 2002). post- Urinary cis-3-(2. 2003). the median and 95th percentile of urinary levels of cis-3-(2.160 (<LOD-.380 (.2dichlorovinyl)-2.830) .450-.510-1. Studies in Germany of 396 children and adolescents (Becker et al..280 (. 2005).03) 1.. Cyfluthrin. 2006).780 (. In these volunteers.140-.360-1.2-dimethylcyclopropane carboxylic acid reflect recent exposure to either their parent pyrethroid pesticides or their environmental degradates.080-.530 (.880) . population from the National Health and Nutrition Examination Survey.

5) 2.56) 2.550 (. Biomonitoring studies on urinary levels of cisor trans-3-(2.580 (.68-2.87 (1.89 (2.2-dichlorovinyl)-2.19 (3. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. interval) Selected percentiles ( 95% confidence interval) Sample 95th 3.17 (. Fourth National Report on Human Exposure to Environmental Chemicals 165 .810-1.77) 1.41-14.54 (1.01) 4.63) 1.12-6.37 (1.11-1.60) .28 (2.800-1.81) 2.940 (.25-3.77) 2.830-1.700) .2dichlorovinyl)-2.470 (.920-1.850-1.94 (1.760) .84 (1.610) 1. Finding a measurable amount of cis.520-.520) .60-4. The maximum post-application urinary levels.26 (.42) 1.490-1.22 (1.460-.20 (.560 (.08-6.68-3.560 (.410-.49-3.410-.400 (<LOD-.42 (2.500) .66) 691 680 518 690 595 954 Limit of detection (LOD.4 and 0.39 (1.460-.400-. population from the National Health and Nutrition Examination Survey.17 (.840-1.08-4.or trans-3-(2.440 (<LOD-.970 (.20 (.85) 4.77 (1.670) .410 (<LOD-.49-5.S. and trans-Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.58) 961 1184 1015 1341 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .66) 478 576 675 826 823 1123 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .710 (. Urinary trans-3-(2.39-5.780 (.68) 1. 2005).17-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. which may vary for some chemicals by year and by individual sample.55-4.95) 3.90) 1.76-4.09 (.25 (1.23) 2.62 (1.07 (1.69) 1.56 (1.63) 1. 2003) were similar to the 95th percentiles for adults in the NHANES 2001-2002 subsample (CDC.55-5.620) < LOD 2.660) 1.13) .55-3.530) .Pyrethroid Pesticides application median urinary levels of summed cis.420 (<LOD-.20 (.670) .2-Dichlorovinyl)-2.77) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD . were up to 27 times higher than the 95th percentile for adults in the NHANES 2001-2002 subsample (CDC.19 (2.910-1.68) 2.35) 1.56 (1.and trans-3-(2.820) .860) .76-3.16) 1.91 (1.50 (1.40 (1.7) 2.10) 2.11-2.48) 4.08) 1.70) size 1976 2525 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD 75th .500 (.01 (1.2-dimethylcyclopropane carboxylic acid (Hardt and Angerer.43) 2.68) 1. trans-Cypermethrin. however.14-2.500-.680-1.97-11.28 (1.490 (<LOD-.14-6.95) 2.64-4.570) 90th 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.59 (1. Survey Geometric mean (95% conf.69 (1.03-1.41 (1.56) 2.49-3.730) .2-dimethylcyclopropane carboxylic acid in urine does not mean that the level causes an adverse health effect.14) 1.07-3.470 (<LOD-.2-dichlorovinyl)-2.4. < LOD means less than the limit of detection.60) 1.23 (.910-1.2-dimethylcyclopropane carboxylic acid Metabolite of Cyfluthrin.66) .700-1.480-.19) 1.03-1.750) .27 (1.54) 4. 2005).560 (.410 (<LOD-.

34-3.770) < LOD 2.15-3.11) 691 680 518 689 595 954 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.12-1.15 (1.720 (<LOD-.720-1.15) 3.36) 2.86 (2.91 (1. and trans-Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.07-2.11) .22-2.00-5.47-2.07) 2.410-.700-.33-2.3) 2.540) .26 (1.44) 2.800-1.730) . 166 Fourth National Report on Human Exposure to Environmental Chemicals .820-2.33 (1.48-2.880 (<LOD-1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.470 (.60 (1.520 (<LOD-.80) 1.800-1.15-3.850-3.19) 961 1184 1015 1340 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .580 (.670) .760 (.530 (.880 (.39) 1.660) .91-11.60) 2.87) 1.35) 1.65 (2.55 (2.98 (1.480-.57) 3.87 (1.33-1.87-3.87-8.00) 1.2-Dichlorovinyl)-2.570-.40-2. Survey Geometric mean (95% conf.88) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 1.91) 1.07) 2.28) 2.45 (1.15-3.530 (<LOD-.31 (.00 (1.60) 2.900 (<LOD-1.19) .19 (1.470-.500-.87) 1.750) .81 (2.700 (.13) .64 (1.56-2.61) 1. population from the National Health and Nutrition Examination Survey.11) 478 576 675 825 823 1123 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .22-1.780) .41) 1.08 (.56-5.34-4.440-.07-1.08 (.29) 1.970 (.15) 2.31 (2.610-.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 .S.68) 3.31) 1.570 (.56 (1.850) .30-3.47-2.74) .42) 1.00) 1.89) 2.55 (2.22) 1.27-2.700 (.35 (1.74) 2.16 (1.65) 1.39 (1.560 (.850) 1.27-2.47 (1.30-6.57 (1.580) .36 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.55 (2.20-2. trans-Cypermethrin.42 (.67 (2.02-1.12 (.45-2.13) 1.640) .48 (1.Pyrethroid Pesticides Urinary trans-3-(2.07-3.780) 90th 1.930-1.740) .00) 5.780 (<LOD-.20 (1.37 (1.880-1.70 (.2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of Cyfluthrin.75 (1.720-1.570 (<LOD-.

Angerer J. J AOAC 1985. Idel H. Kolossa-Gehring M. Angerer J. Bravo R.206(2):85-92. Leng G. Hoppe HW. Leng G. Schulz C. Ranft U. George DA. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany.109(3):213-217. Pearson M. Drexler H. Berger-Preiss E. Sugiri D. Berger-Preiss E.Pyrethroid Pesticides References Becker K. Idel H. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. Bull Environ Contam Toxicol 1999. Seiwert M. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Environ Health Perspect 2001.134(1-3):141-145.77(1):67-72. Permethrin and its two metabolite residues in seven agricultural crops. Barr DB. Centers for Disease Control and Prevention (CDC). Heudorf U. Bartell S. Atlanta (GA). Butte W.209(3):293-299. Int Arch Occup Environ Health 2003.114(9):14191423. 2005. Angerer J. Ranft U. Int J Hyg Environ Health 2002. Fourth National Report on Human Exposure to Environmental Chemicals 167 . Idel H. Heudorf U. A longitudinal approach to assessing urban and suburban children’s exposure to pyrethroid pesticides. Int J Hyg Environ Health 2006. Angerer J. Pyrethroid exposure of the general population-is this due to diet? Toxicol Lett 2002. Levsen K. Third National Report on Human Exposure to Environmental Chemicals. Biological monitoring of workers after the application of insecticidal pyrethroids. Indoor pyrethroid exposure in homes with woollen textile floor coverings. et al. Int J Hyg Environ Health 2006. Angerer J. Drexler H.76(7):492-498. Environ Health Perspect 2006. Ball M. Angerer J. Int J Hyg Environ Health 2003. Heudorf U. Lu C. Hadnagy W. Wieseler B. Heudorf U. Sugiri D. Kuhn K. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides.68(6):1160-1163. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine.205(6):459-472.62:101-108. Int Arch Occup Environ Health 2004. Hardt J. Leng G.209(3):221-233. Schettgen T. Toxicokinetics of pyrethroids in humans: consequences for biological monitoring.

2-dimethylcyclopropane carboxylic acid is a metabolite of the pyrethroid insecticide deltamethrin. Baker et al. 2006) and estimated daily intakes based on urinary levels in children were considered to be below acceptable daily intakes (Heudorf et al. 2006) and 1177 urban adults and children (Heudorf et al.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. Thus.2-dibromovinyl)-2. 168 Fourth National Report on Human Exposure to Environmental Chemicals . in detection of cis-3-(2.2-dibromovinyl)-2. The peak mean levels in these children were more than 800-fold higher than the detection limit in the 2001-2002 NHANES subsample.2-dibromovinyl)-2.2-dimethylcyclopropane carboxylic acid at the 95th percentile ranged slightly higher (0. urinary levels of cis-3-(2. 52918-63-5 General Information Cis-3-(2.2dimethylcyclopropane carboxylic acid reflect recent exposure to deltamethrin or its environmental degradate.2-dimethylcyclopropane carboxylic acid of 0. Outside the U.2-dimethylcyclopropane carboxylic acid were below the limit of detection (CDC.2-dibromovinyl)-2.. Biomonitoring studies provide physicians and public health officials with reference values so that they can determine whether other people have been exposed to higher levels of deltamethrin than levels found in the general population.5 μg/L) than the detection limit (0..2-dimethylcyclopropane carboxylic acid in the environment (IPCS.. deltamethrin has been used against mosquitoes that carry malaria. in some situations replacing the use of DDT.S. Deltamethrin can degrade to cis-3(2.. 2004). 2005). 2001) showed that urinary levels of cis-3-(2.. Finding a measurable amount of cis-3-(2.39 µg/L.2-dibromovinyl)2. 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.2-dibromovinyl)-2.2dimethylcyclopropane carboxylic acid formed in the environment. mean peak urinary levels of cis-3-(2.Pyrethroid Pesticides Deltamethrin CAS No..2-dimethylcyclopropane carboxylic acid in urine does not mean that the level will result in an adverse health effect. (2004) reported a geometric mean concentration of cis-3(2. 1990). Biomonitoring Information Urinary levels of cis-3-(2.2-dibromovinyl)-2. In an analysis of 217 urine specimens from a nonrandom sample of United States residents. 2005).1 μg/L) for the NHANES 2001-2002 subsample (CDC.2-dibromovinyl)-2. In the NHANES 2001-2002 subsample. 2001. 2005).2-dibromovinyl)-2. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.2-dimethylcyclopropane carboxylic acid in the urine may reflect exposure to deltamethrin or to cis-3-(2. Following residential spraying with deltamethrin for malaria protection in Mexico.3-0.

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

S. 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. 170 Fourth National Report on Human Exposure to Environmental Chemicals .Pyrethroid Pesticides Urinary cis-3-(2. * 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.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.2-Dibromovinyl)-2.

[online] 1990. Environ Health Perspect 2005. Ball M. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides.209(3):293-299. 5/26/09 Ortiz-Perez MD. and genotoxicity in exposed children. et al. et al. Environmental Health Criteria 97. Heudorf U.209(3):221-233. Int J Hyg Environ Health 2006. Batres LE. Available at URL: http://www.org/documents/ehc/ehc/ ehc97. Environ Health Perspect 2001. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides. Int Arch Occup Environ Health 2004. Fourth National Report on Human Exposure to Environmental Chemicals 171 . Torres-Dosal A. Third National Report on Human Exposure to Environmental Chemicals. Grimaldo M. Butte W. Schulz C. Seiwert M. Angerer J. 2005. Kolossa-Gehring M. Int J Hyg Environ Health 2006. Drexler H.inchem. Atlanta (GA). Lopez-Guzman OD.77(1):67-72.109(3):213-217. Angerer J.113(6):782-786. Hoppe HW. Heudorf U. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. Carranza C. Heudorf U. International Programme On Chemical Safety (IPCS). Angerer J. Deltamethrin.htm. Centers for Disease Control and Prevention (CDC). toxicokinetics. Angerer J.Pyrethroid Pesticides References Becker K. Environmental health assessment of deltamethrin in a malarious area of Mexico: environmental persistence.

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

190-.340) .55 (1.560-.630) .18 (2.321 (.250-.44) 5.35) 1.64) 697 680 524 701 603 957 Limit of detection (LOD.355) .315 (.353 (.1) 3.238-.710 (.595) .90) 1.34) 8.62) 5.288-. Deltamethrin.320) .230 (.21 (2.510-.300 (.92-3.41-3.260 (.560-1.940) 1.230-.45 (2.250 (.35) 2.41) 3.780) 4.35 (1.25) size 1998 2539 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th .32-21.311 (.740 (.850) .850) .428-.62-6.83-11.320) .78) 6. interval) .454 (.288 (.26) 2.12) 4.54) 1.27-2.27-11.25-7.12 (.730 (.76 (1.490) .390) .271-.02-6.69) 3.870 (.226-.590-. Survey Geometric mean (95% conf.160-.590 (.227-.36) 1.1 and 0.960 (.28) 1.51-6.374) 99-00 01-02 99-00 01-02 99-00 01-02 .470-.336 (.52-4.1.41-2.38 (2. Fourth National Report on Human Exposure to Environmental Chemicals 173 .440) .75 (1.420) .65 (1.328 (.550-.30 (.298 (.32 (2.370) .276-.12) .49-2.560-.230-.230-.270 (.233-.387) .190-.35 (2.260 (.700 (.52-5.71 (1.820) .369) . population from the National Health and Nutrition Examination Survey.25-4.620-1.800 (.13 (.600 (.640 (.30) 3.340) 75th .49 (1.200-.530-.30 (1.295) .300 (.63 (3.14-6.25 (2.32 (1.270) .345) Selected percentiles ( 95% confidence interval) Sample 95th 4.79) 3.352-.277-.320 (.300 (.Pyrethroid Pesticides Urinary 3-Phenoxybenzoic acid Metabolite of Cypermethrin.38 (2.246-.43) 3.350-.273 (.434) .69 (1.430-.53) 1.27-2.990) .35) 2.490-.230 (.362) .650 (.60) .830-2.810) 1.260-.78) 1.04) .46) 2.34 (2.160-.700-1.253-.260 (.34-6.297 (.73) 1.04-5.200-.800) 1.601) .710 (.78 (1.56-5.S.680 (.427) .266-.330) .820) .180-.290 (.33) .18 (1.03 (3.65-2.300) .417 (.330) .16) 483 580 682 831 833 1128 99-00 01-02 99-00 01-02 .42-2.1) 3.320) .50 (2.16) 974 1193 1024 1346 99-00 01-02 99-00 01-02 99-00 01-02 .16-1.610) .265-.840-1.373) .29-1.750-1.280 (.267 (.62-8.586) .314 (.320) .292-.240 (.384) .250 (.16) 1.25 (2.507 (.325 (.93 (1.05) .78) 1.25-1.830) 90th 1.33 (1.240 (.210-.760 (.670 (.406) .8) 3.49-2.86 (1.81 (1.190-.63-3.23 (2.520 (.360) .48-2.13) .220-.570-1.210-.190-. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.510-.41 (1.51-3.750) .740 (.570-.26-2.430-.26) 2.364) .292 (.1) 3.750) .49 (1.45-5.05) 1. and Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.48-2.01 (1.450 (.39) 2.53-3.340) 1.530-.46) .33 (2.314) .200-.247-.89-71.250 (.72 (1.

246 (.Pyrethroid Pesticides Urinary 3-Phenoxybenzoic acid (creatinine corrected) Metabolite of Cypermethrin.362 (.700-1.95) 1.41-4.240-.03-1.264 (.423 (.490 (.27) 1.230-.290) .21-4.860 (.48 (1.48) 697 680 524 700 603 957 174 Fourth National Report on Human Exposure to Environmental Chemicals .91 (2.316 (.62) .330) 1.240-.190-.275 (.280 (.271-.299-.328) .200-.07) 2.320) .37) 1.36 (1.312 (.92) 483 580 682 830 833 1128 99-00 01-02 99-00 01-02 .55 (1.270 (.590) .05-3.02-1.730) .39) 1.670) .630) .860-1.44) 2.90) 3.210 (.860-1.234 (. Survey Geometric mean (95% conf.220 (.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 .19) 2.190 (.460-.00) 5.54 (1.400-.178-.365) 99-00 01-02 99-00 01-02 99-00 01-02 .730) .150-.67) 1.36-6. and Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.290) .202-.930) .350) .43-64.220-.410-.11 (.51-7.390-.160-.309 (.83) 1.17 (.400) .610 (.650) .35-3.17-1.210 (.274-.S.378 (.10 (2.53 (1.91) 9.510 (.41) 1.534) .304) Selected percentiles ( 95% confidence interval) Sample 95th 3.450 (.437) .540 (.274 (.300-.250) .07-5.61-2.52) 2.580 (.49-2.930) 1.0) 3.72 (1.550 (.272) .35) 1.311 (.280-.750-1.35) .37 (1.387) .357) .13 (.440-.490-.73) 1.677) .300-.309) .09) 3.80) 4.240 (.500) .09-2.370 (.81 (1.40 (1.22 (1.25-5.280) .335-.329) .173-.570) .13-1.278) .11 (.04 (.88-5.720) 90th 1.640 (.330) .280 (.52 (1.94 (1.740) . population from the National Health and Nutrition Examination Survey.16-4.253) .43 (2.270 (.270-.250 (.490 (.226-.261 (.530-.25) 2.240-.91-4.49) 3.55) 3.06-3.229-.216-.15-2.49) 1.67 (1.440-.580) .590) .19 (2.560 (.25-2.510 (.261-.290-.330) 75th .460-.550 (.280 (.840-1.480 (. Deltamethrin.63) 1.410) .49 (1.73-4.510 (.380 (.730-1.372) .19) 974 1193 1024 1345 99-00 01-02 99-00 01-02 99-00 01-02 .224-.60-4.380-.19-6.00) 1.530-.75-8.480-.240-.04 (3.350 (.200-.35 (1.190-.40) 2.640 (.67 (1.86 (1. interval) .230) .43) 1.225-.960-1.420-.43 (1.200-.310) .83 (1.446) .270) .550 (.590) .321-.230-.60) 1.590-1.09-2.91) .810) 1.240 (.74) 3.200-.401) .330 (.240 (.13-1.02 (2.240 (.400-.32 (2.270) .720 (.250 (.238-.64-5.670) 3.329) .63-3.280) .227 (.760) .370-.330) .09 (.44 (1.210-.84 (1.323 (.00) 1.03 (.96 (1.272 (.62) 1.21 (1.440-.

Ortiz-Perez MD. Carranza C. Int Arch Occup Environ Health 2003. Leng G. Sugiri D. Bravo R. Leng G. Hoppe HW. Idel H. Pearson M. Fourth National Report on Human Exposure to Environmental Chemicals 175 . Ranft U. Lopez-Guzman OD. 2005. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation.113(6):782-786. toxicokinetics. Bartell S. Torres-Dosal A. Int J Hyg Environ Health 2003. et al. Third National Report on Human Exposure to Environmental Chemicals. Kolossa-Gehring M. Deych E. Olsson AO. Hardt J.111(1):79-84. Levsen K. et al. Arch Environ Contam Toxicol 2004. Berger-Preiss E. Indoor pyrethroid exposure in homes with woollen textile floor coverings.206(2):85-92. Environmental health assessment of deltamethrin in a malarious area of Mexico: environmental persistence. Lapinski R.209(3):221-233.76(7):492-498.205(6):459-472. Angerer J. Environ Health Perspect 2006. et al. Barr DB. and genotoxicity in exposed children. Barr DB. Berger-Preiss E. Biological monitoring of workers after the application of insecticidal pyrethroids. Seiwert M. Centers for Disease Control and Prevention (CDC). Lu C. Int J Hyg Environ Health 2002. Hadnagy W. Int J Hyg Environ Health 2006. urban cohort. Liu Z. Idel H. Godbold J. Batres LE. Grimaldo M. Berkowitz GS. Obel J. Environ Health Perspect 2005. Atlanta (GA). GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Angerer J. Sugiri D.114(9):14191423. Environ Health Perspect 2003. Becker K.Pyrethroid Pesticides References Baker SE. Ball M.46(3):281-288. Ranft U. Isotope dilution highperformance liquid chromatography-tandem mass spectrometry method for quantifying urinary metabolites of synthetic pyrethroid insecticides. A longitudinal approach to assessing urban and suburban children’s exposure to pyrethroid pesticides. Exposure to indoor pesticides during pregnancy in a multiethnic.

250-.220-.130) < LOD .130 (.079-.430 (.310 (.140-.142) * Sample size 2276 2690 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .440 (.210 (.148-.100-.220) 95th .230 (.210) . 176 Fourth National Report on Human Exposure to Environmental Chemicals .420) .145 (. solder.114) .200 (.190-.140 (.260) .170-.140) .270-.260 (.150-.160) .280) .190 (. +3.320-.190 (. Two antimony compounds (sodium stibogluconate and antimony potassium tartrate) have been used as antiparasitic medications.130-.180-.440) .150) .120 (.140) .500) .340 (.150-.280-.110-.108-. distribution.120-. or other substances containing antimony is another means of exposure.190 (.250 (.100) .300-.154) .180) .210-. metal bearings.115-. and 03-04 are 0.190) .220-.207) .161) . Antimony enters the environment from natural sources and from its use in industry.180 (.180) .400) .080) .130-. respectively.140) .080 (<LOD-.110-.430 (.130 (.230 (.240 (.128 (.350) .190-.400 (.250-.04.220-.390) .080-. see Data Analysis section) for Survey years 99-00.120 (.100 (.300 (.07.200 (.154) .180 (.200-.330-.160 (.330 (.123 (.350) . Stibine is a metal hydride form of antimony used in the semiconductor industry.119) .270) .360-.410) .180 (.Metals Antimony CAS No.330 (.170-.220 (.115) .710) .430 (.143 (.190-.360 (.390) .093 (.120-.160-.230) .180-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.280 (.210) .160) .180-.210) .160 (.220) .400 (.350) .110 (.090-.090 (.200) .160) .230-.105 (.130) .240 (.220) .240) .530) .130-.137) .120-.180 (. Workplace exposures can occur at smelters.136-.280) .132 (.390-. and glass.120 (.340) . population from the National Health and Nutrition Examination Survey.350-.108 (.290 (.119-.178) .200 (. People are exposed to antimony primarily through food and.510) .132 (.190) . storage batteries.130 (.460 (.190-.560) .390 (.140) .350 (.137) .070 (<LOD-.230-.240 (.070-.390) .150-.117-.330) . fireworks.340 (.460 (. Dermal contact with soil.120 (. It is also used in paints. ceramics.320 (.128 (.200-.350 (.170-.169 (.290-.410) .250-.04.100 (. sheet and pipe metal.098-.140) .350) .150 (.270 (.410-.099 (. coal-fired plants.126-.310 (.210) .300-.220-.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 .350 (.154-.300) .070 (<LOD-.120-.197) .122 (.400 (.320-.095-.300 (.400) .145) Selected percentiles ( 95% confidence interval) 50th .250 (.175 (.156-.500) .230) .320) .103) .270 (.157) .250 (.600) .160-.320) 787 683 618 554 667 723 768 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. water.140 (.350 (. ammunition.126 (.090 (<LOD-.088-.130 (.150) 90th .260-.310-.350 (.440) . and refuse incinerators that process or release antimony.200) .160 (.150-.390-.260) .142 (.130-.400-.S.120) .270 (. Antimony can exist in one of four valences in its various chemical and physical forms: -3.260) .146 (.125 (.150) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.140 (.160-.290-.140 (.180 (.120-.280-.190 (.160) .210) .087-.141-.310) .134-.200-.190-.330 (.250) .300) .240 (.260 (.120-.300-.240-. and pewter.310 (.180 (.170 (.270) .110) .350-.176 (.120) . 7440-36-0 General Information Antimony is found in ores or other minerals. It is used in metal alloys.470) .120) .280-.310 (.200 (.320) 316 368 290 663 762 725 1297 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .080) .320-.230) . interval) . from air and drinking water.360 (.240 (.220-.158 (.117-.370-.160) .330) .190) .131-.130 (. 0.220) .200 (.160) .110-.470 (.320-.350-.130 (.280 (.230-. and excretion of antimony vary depending on its oxidation state.170) .280-.110-.490) .220-. The absorption.330) .135) * .230-.164-.130 (.460 (. < LOD means less than the limit of detection.170-. to a lesser extent.570) .310) .136) * .170 (.200) .270 (.120-.190) .470) .095 (.120-.230 (.370) .390-.320 (.180-.109-.144) . enamels.190 (.300) .130-.140) .320) Total .210-.210 (.400) .200-.170-.150-.130) .200) .230-.200 (.330-. castings.460) . Urinary excretion appears to be greater for pentavalent antimony Urinary Antimony Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.130) .120 (. 01-02.260 (. 0.130 (.390) .100-. often combined with oxygen to form antimony trioxide or with sulfur to form stibnite.134 (.250-.260-.310-.190) .120-.220 (.130-.490 (.330) .360) .133) * .112-.280-.150 (.090-.160-. and 0.120) . and +5.130-.280) .184) .090) 75th .180-.150) . which may vary for some chemicals by year and by individual sample.240-. and as a fire-retardant in textiles and plastics.150 (.280) .360) .

081 (<LOD-.125 (.444) .203) .104-.380 (.080 (.162-.114 (.321) .134) . Acute inhalation of antimony has been associated with irritation of the respiratory tract and impaired pulmonary function (Renes.125-.160 (.310) .129 (.086 (.188-.320) .300 (.228 (.107-.069-.429 (.148-.429) .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 .138 (.288 (.115) .076-.236 (.241-.333-.229-.267) .143 (.298 (.131-. interval) .320 (.121 (.188) .185 (.268) .253 (.121) . 1995).187) .132) .259 (.097-.357-.338 (. diarrhea.102-.092) .100 (.082 (<LOD-.471 (. and gastrointestinal symptoms such as vomiting. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.117-.200-.172-.727) . Human health effects from antimony at low environmental doses or at biomonitored levels from low environmental exposures are unknown.164 (.139 (.471) .130 (.278 (.226 (.209) .156 (.S.089) .209 (.115 (.179-. Pulmonary edema may occur in severe cases of inhalation exposure (Cordasco et al.087) .320-.308-.095-.137 (.333 (.278) .130) .192 (.139 (.164-.068-.126 (.385 (.153-.318-.333-1.107-. Dysrhythmias and T-wave changes on electrocardiogram have also been noted after both therapeutic (Berman.140) < LOD .133) .127) .235-. 1953).118 (.227-.109 (. 1954).430) .250-.173) .082) .352 (.163 (.272) . 1962). abdominal pain.313-.217 (.256 (.123) .143) 90th .061-.308) .741 (.241-.104-.263 (.343 (.238) .333 (. and ulcers (Werrin.300) .124-.173-.153 (.084) .192-.106-.741) .145) .112 (.255-.108-.400 (. 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.250-.146-.320 (. The toxicity of stibine after acute inhalational exposure is similar to that of arsine.163 (.112-.209) .205-.333) .075 (.239-.124-.200-.069-. Acute antimony poisoning may cause a metallic taste.214) ..149) .149-.295 (.175 (.146-.250) .152) .105-.131) .173 (.269 (.135) .300) .138-.250-. 1986).159-.146) .092-.444) .129 (.373) . and route of exposure (Elinder and Friberg.120 (.079 (<LOD-.266 (.222 (.117-.108 (.225 (.195-.204-.109 (.178-.417) .352) .122 (.130) .338 (.181) .135) .244-.114 (.095-.317) .225) .220) .193) .129) * . Inorganic antimony salts irritate the mucous membranes.178 (.136) .167 (.138) * .126) .161) .148) * .438) . species.250 (.151) .098) .196 (.500) .200-.144-.127) .128-.119-.156-.115 (.253-.102-..096-.315) .120 (.098-.271-.294) Total .130) .129) .181) .176 (.161) .233 (.075 (.238 (.Metals than for trivalent compounds (Elinder and Friberg.127) .480) .245) .208-.124) .131 (.108-.143) .120 (.364 (.074 (.261) .317) .122 (.247) .310 (.195-.117-.207) .257) .206-.194-. resulting in hemolysis with abdominal and back pain (Dernehl et al.213 (.414) .118 (.248) .116 (. 1988.159-.333-.081) .286 (.121 (.281-.127) .265-.150-.111 (.115-.167-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.171) .267-.167 (.276 (.182 (.126-.191 (.150-.250-.103-.255) . 1958) and occupational exposures (Briegner et al.195 (. 1973).143) .127 (.267 (.103-. An elimination half-life of approximately 95 hours has been estimated after occupational exposures (Kentner et al.109-. Fourth National Report on Human Exposure to Environmental Chemicals 177 .164) .185 (..248-.181) .152) .108-.115-.183) .242-.120 (.159-.208 (.086) 75th .277 (.189 (.082) .148-.199-.333 (.173 (.113) . myocardium.071-.317) .265 (. 1944).080 (<LOD-.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 . and eyes. and kidney have been demonstrated in high dose animal studies depending on the dose.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 .280 (. population from the National Health and Nutrition Examination Survey.185-.233) .228-.119 (.425) .085) .113-.068 (.107-.263-.417) .124 (.176 (.106-.209-.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..333-.167 (.224 (.280-.143) Selected percentiles ( 95% confidence interval) 50th .421) .147) .192) .391) . 1986).198) .138-.203) .076-.135) .310) . skin. Histopathologic inflammatory and degenerative changes in the lung.211) .371 (.238) . liver.170 (.098-.116-.391) .147-.140) .135 (.176-.154-.230) 95th .135 (.228 (.200) ..250 (.132 (.447 (.233-.357) .485) .111-.123 (.364 (.230-.077) .318-.099-.119-.320-.112 (.113-.193 (.115 (.099-.146-.078 (.30) .114 (.405) .186) . Ming-Hsin et al.338) .

arsenic. 1998. Finding a measurable amount of antimony in urine does not mean that the level of antimony causes an adverse health effect.Metals to antimony have been established by OSHA and ACGIH. Atlanta (GA). Wu M-T. Biomonitoring of a worker population exposed to low antimony trioxide levels. 1986.atsdr.158:165-190. Stocks J. Cullen A. and a drinking water standard has been established by the U. Nordberg GF. Information about external exposure (i.59:469-474. Mayne P. environmental levels) and health effects is available from ATSDR at: http://www. Leinemann M. Van der Venne MT. Antimony trioxide is rated by IARC as a possible human carcinogen. Ludersdorf et al. In: Friberg L. Industrial antimony poisoning. 1995. 1998). Third National Report on Human Exposure to Environmental Chemicals. Kuo-Juie Y. 2nd ed. and future strategies. Environ Health Perspect 1998.521-523. Mahieu P. Alimonti A. Chest 1973.. Pietra R. Handbook on the toxicology of metals. Yang C-Y. Hamilton EI. Rev Infect Dis 1988.48:93-97. Chia-Yu H. Sci Total Environ 1994. Nau CA. Sabbioni E. Friberg L.. eds. Liao Y-H et al. Int Arch Occup Environ Health 1995. 20012002. Pilgrim L. et al. pp. gov/toxpro2. O’Regan M. Pulmonary edema of environmental origin. plasma and urine and a critical evaluation of reference values for the United Kingdom population. Konings J.. 1997). Antimony. Dezateux et al. Industrial Medicine 1944.. 1990. 1998) or compiled reference ranges (Hamilton et al. Briegner H. Trace element reference values in tissues from inhabitants of the European community I. Element reference values in tissues from inhabitants of the European community. Semisch CW. Luedersdorf R.. Apostoli P.16: 33-39. Chemotherapy for leishmaniasis: Biochemical mechanisms. Pozzoli L. 26-42. Antimony in blood and urine of infants. Minoia C. Schaller KH.e. Chen J-R. Stead FM. Matthews T. and 2003-2004. Costeloe K.10(3):560-586. et al. Kentner M. VI. Gallorini M. Gebel TW. which may be due to methodologic. Bailly R.. and hydrogen sulfide. Lenert G. gallium. Dezateux C. Dunkelberg. Ho C-K. Centers for Disease Control and Prevention (CDC). stibine. EPA. Biological assessment of exposure to antimony and lead in the glass-producing industry. 1987).. Ming-Hsin H. HH. Mayer P.)1954. Review of elements in blood. Buchet JP. Carelli G. A study of 46 elements 178 Fourth National Report on Human Exposure to Environmental Chemicals . or exposure differences. 2002. Piatnek DA. Lauwerys R. Iavicoli et al. Stone FD. respectively. Kiberd B. et al. Kentner et al. 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.. Suchenwirth R. Levels of urinary antimony in infants appeared to be similar to those reported by CDC (2005) for young children (Cullen et al. 2004. Earlier measurements in general populations (Minoia et al.46:931-936.64(2):182-185. Wade A.S. Roland H. Arch Dis Child 1997. Chin Med J 1958.. Urinary antimony was not associated with locally elevated soil levels in a study of more than 200 German residents (Gebel et al. Weltle D. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. even when exposure levels were below workplace air standards (Bailly et al. Vouk VB. New York: Elsevier. Delves HT. Elinder CG. Cordasco EM. Fuchs A. Bolten C. Biomonitoring Information Levels of urinary antimony reflect recent exposure. Paschal et al. Skulsukai G. Sabbioni E. Br J Ind Med 1991. 1994) have reported values slightly higher than those in this Report. Caroli S.. Int Arch Occup Environ Health 1987..76(2):103-115.106:33-39. Mechanism and treatment of cardiac arrhythmias in tartar emetic intoxication. Schacke G. Stasney J. and antimony in optoelectronic industry workers. clinical efficacy.cdc.51:238-240. Arsine. External and internal antimony exposure in starter battery production..html. 1991. References Berman JD. J Clin Pathol 1998. Urinary antimony in infancy. Experimental and human studies on antimony metabolism: their relevance for the biological monitoring of workers exposed to inorganic antimony. Cheng-Wei L. Ju-Sun P. Iavicoli I. J Trace Elem Med Biol 2002.13:361-362. 2005. indium. J Occup Environ Med 2004. Dernehl CU. Liao Y-H. Human biomonitoring of arsenic and antimony in case of an elevated geogenic exposure. Yu H-S.76:432436. population. Delves HT.67:119-123. Shao-Chi C. Petrucci F. Biological monitoring of exposures to aluminum. Industrial Medicine and Surgery (Dec. Several investigations of airborne antimony exposures in workers have found urinary levels that are many times higher than those seen in NHANES 1999-2000.

95:89-105.99-108. Renes LE. 27:38-45.76(1):53-59. Antimony poisoning in industry. Chemical food poisoning. Quarterly Bulletin of the Association of Food and Drug Officials 1962. Industrial Hygiene and Occupational Medicine 1953. Pirkle JL. blood. Morrow JC. Paschal DC. Werrin M. and serum of Italian subjects. Ting BG. Fourth National Report on Human Exposure to Environmental Chemicals 179 . Sampson EJ. Environ Res 1998. et al. Trace metals in urine of United States residents: reference range concentrations. Sci Total Environ 1990. Jackson RJ.Metals in urine.

5 (40. and arsenates (oxidation states of -3.6) 618 722 1074 Limit of detection (LOD. a trivalent compound known as white arsenic) is a common natural and commercial form that can be released into the air during volcanic action.5) 95th 65.34-9.9) 21. lead.00-9.0 (15.13-8.1) 7. grain.8) 7.90) 75th 16.8 (48.8) 17.0 (43. and arsenosugars. The United States no longer produces arsenic from mining but imports about 22.90-8.29 (8. and as a cosmetic to lighten complexion.97) 8. aluminum.8) 7. Groundwater Urinary Total Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. psoriasis.7) 65.4) 60. 2001). Arsenic trioxide is approved to treat acute promyelocytic leukemia. it is found in over 200 crystalline or mineral forms. to a lesser extent. sodium arsenite. and foods.2-20.74.5 (36. lead hydrogen arsenate.000 metric tons annually.4-65.2-93. 2005). Survey years 03-04 Geometric mean (95% conf.70) 8.77) 6.6-141) 53.00 (6.90 (5. copper arsenates. arsenic compounds.Metals Arsenic CAS No.5-41. and monosodium methyl arsenate were used as pesticides but contemporary uses are restricted.9-62.08 (5.8) 34.1) 290 725 1542 03-04 03-04 9.9-46. cancers. from coal burning.80) 6. mental disorders.30 (6. and play sets.8) 30.30) 17. Since the 1940s.1) 1281 1276 03-04 03-04 03-04 9. alloys. meats. Arsenic is measurable in most soils.19-9.0 (14.8) 33.90 (7.8) 29.7) 90th 37.80 (5. Although it is still widely used in the United States.5 (23. 180 Fourth National Report on Human Exposure to Environmental Chemicals .9) 68. retaining walls. Arsine (AsH3) is a reactive.2) 46. the smelting of copper.2-17.4 (24.6 (32. cacodylic acid. though in some locations arsenite may be prevalent (WHO. Also.0-19. were used as treatments for syphilis.0 (11.6 (15.20 (8. Various forms of inorganic arsenic can occur in groundwater from natural sources or as a result of soil application or industrial waste. arsenites.5-19.90 (7. and indium arsenides are used in the semiconductor industry. arsenocholine.5-52.90-14.3-111) 78.34-10.90) 16. chromated copper arsenate (CCA) has been used to treat outdoor timbers and pressure-treated woods to prevent wood rot.6 (13. Roxarsone and other organic arsenicals are anticoccidial agents added to poultry feed.2 (12. Gallium.2 (51.6 (9.57) Selected percentiles ( 95% confidence interval) 50th 7.2-61. population from the National Health and Nutrition Examination Survey. pesticides. Arsenic trioxide (As2O3. In the last century.90-11. +3 and +5).9-34.10 (6. solders. and.5-178) 46. Arsenic can combine with such non-carbon chemicals as sulfur and oxygen to form arsenides.41 (7.8-77.55 (7.0 (22.5 (34.3-19. ocean and fresh waters.7-83. Before the 20th century.S.5) 41.2) 15.9 (8. see Data Analysis section) for Survey year 03-04 is 0. CCA-treated wood has been restricted since 2003 and no longer can be used in residential applications such as decks. and in lead-acid storage battery grids.6-43.66-8.7-95.9 (17.2 (13.3) 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 7.84) 8. and gray forms). and as homicidal poisons.90-8.5) 43.4 (48.10-7.1 (32.6-35.4) 13. particularly arsenic trioxide. or rarely as elemental metalloids (yellow. to a lesser extent.12-10. gaseous hydride manufactured in small quantities for use in the semiconductor industry. General population exposure to inorganic arsenic can occur through consumption of drinking water and.6) 11.70 (6. arsenic as elemental metalloids may be used in some ammunition.50 (8.3) 10. semiconductors.0-60.84) 8. and other metals.90-7.8-61.5) 66.4 (26.3-15. trimethylarsine oxide. as alloy in metal bearings.7) 24. Arsenic and its compounds have had many uses in the past and present as medicines.10-10.12 (6.27) 9. Water sources contain mostly inorganic arsenate. black. Arsenic can also combine with organic substances in nature to form such organic arsenic compounds as arsenobetaine. 7440-38-2 General Information Arsenic is an element that is widely distributed in the earth’s surface in small amounts.25-9.5 (14.80-9.7 (11.10) 10. Various arsenic compounds were used in paint pigments and for tanning animal hides.2 (41.50-14. interval) 8.4) 40.1) 15.1-18.1-40.02-8.70-9.4 (31. In nature. and produce. referred to as inorganic arsenic compounds.30 (7.4 (7.1 (38. mostly for use in wood preservation (ATSDR.40) 7. such as arsenopyrite (FeAsS) and realgar (As4S4).

and folate status (Chen et al.5) 290 725 1542 03-04 03-04 8.35) 7.7 (9. and contact with CCA-preserved wood structures.8 (27.1 (11.9) 618 722 1074 Fourth National Report on Human Exposure to Environmental Chemicals 181 . arsenocholine.0) 1281 1276 03-04 03-04 03-04 8.4 (40.1) 8.7-18.25 (6.1) 58. Direct exposure to DMA and MMA may result from use of the two pesticides.40) 8. arsenocholine is converted to arsenobetaine and also to small amounts of TMAO (Christakopoulos et al. NRC.0-26. U.30-9.8 (12. Though modest bioconcentration occurs in some aquatic life. Steinmaus et al. Inorganic forms of arsenic demonstrate high acute toxicity. arsenic does not show biomagnification in the food chain (WHO.12-10.9) 53. 2001).. Inorganic arsenic and its metabolites have elimination half-lives of approximately 2–4 days (Lauwerys and Hoet. 2001).1) 7.07-9.20-9. Fish.S.2) 40.1 (14.5 (9.64 (7.2 (12.81-9.7-17. Tseng.25-9. 2001).9 (45.9-56..11 (5. Survey years 03-04 Geometric mean (95% conf.01) 11.3 (24.6) 45.8) 22.32 (5.7-188) 27.5) 17.5) 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 8.75) 13.45) 5. 2006. TMAO is also formed in the environment from microbiological action and is a metabolite of arsenic in certain mammals. Gamble et al. These organic forms of arsenic from seafood are absorbed and quickly excreted in the urine (WHO. kelp.7-34. though some reduction may occur in the gut prior to absorption. WHO.6-17.2-15.7) 28. Inorganic arsenic is well absorbed from the gastrointestinal tract and absorbed to a lesser degree through inhalation.4 (12. 2001. 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. Ingestion of arsenosugars in kelp and algae can also lead to the excretion of DMA.88 (5. After absorption.7-35.0) 12. with trivalent inorganic arsenic (arsenite) being more toxic than pentavalent inorganic arsenic (arsenate) (NRC. have caused clinical arsenic poisoning.. 2006. dust.4) 32.10-8.0 (31. interval) 8.23-7.2) 90th 30.8 (21.4) 54.4-64.0-38. EPA.24 (7.06 (4.3-41. 1988).8 (20.86-17.0) 42.3-53.04 (5. organic arsenic can be converted back to methylated and inorganic arsenic. inorganic arsenic is widely distributed within the body.0-18. so exposure to the general population is extremely limited. are used in enclosed ultraclean operations within the semiconductor industry.1) 24.0 (17. and some other seafood can contain organic forms of arsenic including arsenobetaine.g.3-62.18 (5. gallium arsenide and indium arsenide.0) 14.1-36. 2001). Arsenate is reduced in the body to arsenite (oxidation state +3).. as observed in Bangladesh where millions of people have been exposed. 2001).6 (17.13) 8. 2007. mine tailings).2-46. Smoking tobacco is also a source of inorganic arsenic.04) 7.41) 6. Children may have additional exposures from ingestion of contaminated soils (e. In aquatic organisms. cacodylic acid and monosodium methyl arsenate. age.76 (6.75 (5.9) 13.5-17..3) 6.0-69. The semiconductor dopants. 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.7 (25.93-8.8-75. shellfish. 2007. 2001).66-8.01) 7.3) 9. population from the National Health and Nutrition Examination Survey.99-9. dose level.2) 15.6 (35.3 (27.47 (7. 2003. 2001).66 (7.33 (6. Chowdhury et al.51) 75th 14. Extremely high groundwater arsenic levels. 2001).8) 27.44-11. In aquatic sediments.93-9. but is poorly absorbed dermally (WHO.59) Selected percentiles ( 95% confidence interval) 50th 7.10-16.0) 33. EPA’s maximum contaminant level (Hughes. WHO.47 (6.6 (10.8-32.50 (6.44) 6.58-10. Arsenite is then oxidatively methylated to the monomethylarsonic acid (MMA) and dimethylarsinic acid (DMA) with subsequent excretion primarily in the urine (NRC. trimethylarsine oxide (TMAO).4 (42. 2007.28-7.S.1) 6.8-62.61 (7. 2001.Metals sources of drinking water often have measurable arsenic and several regions of the United States have naturally higher arsenic levels than the U.00 (6.47-6.38-10. selenium.88) 7.4 (11.31 (6.0) 26.33-10.S.66-8.5-120) 40.7 (11.7) 95th 50.3-64.96) 12. and arsenosugars..4 (24.8 (11.4 (26. Smelter workers can have significant inhalational exposures to airborne arsenic trioxide for which air standards have been established.

. it may have its own separate toxic action by substituting for phosphate in glycolysis and other pathways.50) 1. hypertension. 182 Fourth National Report on Human Exposure to Environmental Chemicals . and production of glutathione may be affected as well. OSHA and ACGIH have established workplace standards and guidelines for arsenic exposure and monitoring. The U. WHO. 2006. 2001). and by uncoupling oxidative phosphorylation (NRC. population from the National Health and Nutrition Examination Survey. peripheral vascular disease. cell transformations. WHO. Chronic elevated arsenic intakes have been associated with diabetes.10 (<LOD-1.. which may vary for some chemicals by year and by individual sample.. interference in signal transduction pathways. < LOD means less than the limit of detection. 2007. Cellular glucose uptake. see Data Analysis section) for Survey year 03-04 is 1.. hematocytopenias.. With chronic exposure. but additional or confirmatory research is needed (Kapaj et al.30) 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1. Acutely.30) 1. 2001). cytotoxicity. NRC.S. which can lead to dehydration and shock. including inhibition of numerous enzymes.10 (<LOD-1. and childhood neurodevelopmental effects in observational human studies. some of these effects may take years to develop. NRC.20 (<LOD-1. renal failure. 2001). noncirrhotic portal hypertension. arsenic trioxide) includes hemorrhagic gastritis with nausea. Chronic human intake of arsenic at less than acutely toxic doses.. 2007). 2001). Although arsenate is reduced in the body to arsenite. 2001. 2001. leading to a decrease in adenosine triphosphate energy production. drinking water have not been associated with increased cancer rates (Schoen et al.EPA.80) 1. and bladder cancer (IARC. and endothelial injury (Kumagai and Sumi. hepatotoxicity. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. and it also will inhibit succinate dehydrogenase.60) 1. apoptosis. fatty acid oxidation. Such actions may lead to decreased energy production. 2004.50) 621 725 1078 Limit of detection (LOD. can cause peripheral sensorimotor neuropathies..10 (<LOD-1. respectively. and peripheral neuropathy may also occur with large doses or after surviving an acute overdose.20 (<LOD-1. 2006) or when exposure occurs in smokers (Chen et al.. Laboratory studies using inorganic arsenic have shown chromosomal aberrations. Acute toxicity resulting from the ingestion of large amounts of trivalent arsenic (e. 1998. Survey years 03-04 Geometric mean (95% conf.S. food residue.0. Cohen et al. and hyperpigmentation of the skin (NRC. and diarrhea.10 (<LOD-1. including drinking water sources with elevated arsenic levels (e. WHO. gluconeogenesis.S. U.Metals +3) shows greater toxicity than arsenite itself (Aposhian et al.60) 1. 2006) and newly discovered thioarsenic metabolites may also be as toxic (Naranmandura et al. The organic forms of arsenic occurring in seafood have little known toxicity. 2006. vomiting. 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. Chile). arsenite will inhibit cellular pyruvate dehydrogenase by binding to the sulfhydryl groups of dihydrolipoamide.50) 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD 1. Arsenic has many actions demonstrated in cellular studies. and altered gene expression.. and DNA repair inhibition (Cohen et al..20 (<LOD-1. increased oxidative stress.20 (<LOD-1. Chronic arsenic exposure in humans is considered to be a cause of skin. Cardiac arrhythmias.g. WHO. Bredfeldt et al. 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. 2006.50) 2568 95th 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1.10 (<LOD-1.S. 2000. 2001). hyperkeratosis. Taiwan.. Bangladesh. The risk of lung cancer appears more pronounced when large environmental exposures start in childhood (Smith et al. 2001).EPA has established drinking water. substitution in phosphate metabolism. lung.. Raml et al.g. 2004). 2004). 2007. Studies of arsenic at levels typical of U. Acute unintentional inhalation of arsine gas can produce hemolysis of red blood cells.

. 2001).. WHO. In the German Environmental Survey III of 1998. 1986). 2006. Fourth National Report on Human Exposure to Environmental Chemicals 183 .. urinary arsenic levels have been accepted as a good biomarker of dose (WHO. 2000..atsdr.75 (<LOD-2. Consequently. though air levels of arsenic fume and dust are correlated with urinary arsenic levels at higher occupational inhalational exposures (Jakubowski et al..S. population in NHANES 2003–2004 (Schulz et al. and the FDA has established a bottled drinking water standard.. 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.. Offergelt et al.69 (<LOD-3. the median total urinary arsenic in about 200 people was approximately four times higher than that of the U. although urinary arsenic levels were not associated with CCA contact (Shalat et al.61 (<LOD-3.. 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... Caldwell et al. 2004. 2005) and Urinary Arsenic (V) Acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.. higher mean or median total urinary arsenic levels have been reported among people living in specific western areas of North America (Calderon et al. 2000).18 (<LOD-3. 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.. 1999.95) 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. 2004. 2008)..50) 1.00) 1. Pellizzari and Clayton 2006). 2003. Shalat 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. 1999. Josyula et al.S.04 (<LOD-3. Additional information about external exposure (i. Pellizzari and Clayton..80 (<LOD-4. Daily variation in creatinine-corrected urinary arsenic is relatively small when intake is constant (Calderon et al. 2006. Shalat et al. 2006).19) 3.. In animal studies.50) 2568 95th 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. Meza et al. 2006. 1998.33 (<LOD-3..html. Pellizzari and Clayton. DMA produced bladder cancer in some chronic rat studies (Cohen et al. arsenic has been fetotoxic and teratogenic..Metals compounds.. 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.70) 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD 2. 2008).41) 3.S.e. In a Nevada town where groundwater levels were naturally elevated. 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... 1992. Calderon et al. Vahter et al.cdc. median urinary total arsenic levels in 4052 adults varied with seafood intake. but generally only at maternally toxic doses (WHO. Compared with this Report.. Valenzuela et al..S.33 (<LOD-3.18) 3. 1999). Survey years 03-04 Geometric mean (95% conf. 2007. 2001). 2007. 2001). population (Rubin et al. and were about two-fold lower than those for the U.. Caldwell et al. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Though CCA-treated wood contains several thousand times more arsenic than untreated wood. IARC and NTP recognize inorganic arsenic and arsenic compounds as human carcinogens. 2006). had decreased since the prior 1990– 1992 survey. Levels of total urinary arsenic in the U. 2006).75 (<LOD-2. 2006).89) 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2. 2008. environmental levels) and health effects is available from ATSDR at: http://www. gov/toxpro2.

2 (6.10 (4.10) 8. as evidenced by trace or nondetectable levels of arsenobetaine and arsenocholine in the urine.30 (1. and urinary DMA represented about 67% of the total urinary arsenic (Hopenhayn-Rich et al. Total arsenic measured in the urine includes all species of inorganic and organic arsenic.70 (5. and TMAO were detected in only 7.20) 7. Caldwell et al.6 (13.7) 13.3 (9.05) < LOD . geometric mean levels were about 70-fold higher than for the U.6.0-23. 2008. see Data Analysis section) for Survey year 03-04 is 0. 2001.43-1. WHO.8-50. methylation capacity.28) 1.20) 3. 2008).0 (27.00-12. arsenite.40) 5..9) 13.6 (11. 184 Fourth National Report on Human Exposure to Environmental Chemicals .29 (1..20 (4.8) 35. 2000. Aposhian et al.74 (1. DMA has been the predominant metabolite composing the majority of measurable inorganic-related arsenic in the urine (i.00-6. 1.70 (3. and two methylated metabolic products.40-7.800 (.0 (26.900 (. Survey years 03-04 Geometric mean (95% conf.7) 15.9-23.9 (6.19 (.50-6.30) 10.1-51... 1996.. arsenocholine.5) 32.5 (26. Valenzuela et al.60-3. 2000.800 (.800) 1. Tseng et al.00-1.4. These associations are stronger at higher urinary levels. 2000.8 (17.4) 31. and other factors such as nutrition..Metals other areas of the world (Ahsan et al. 4.50) . arsenocholine.3 (21.400-.S.5) 621 725 1078 Limit of detection (LOD. 2008). * Not calculated: proportion of results below limit of detection was too high to provide a valid result. and peripheral neuropathy) have been associated with urinary levels as low as 50–100 μg/L in chronically exposed populations (ACGIH. 2005. with DMA.20 (2. vasospasm.66 (1. Caceres et al. After recent seafood ingestion.80 (4.8-40. 2003). median levels of urinary DMA were about 40-fold higher than the adult median reported in NHANES 2003– 2004.55 (1. Measurable organic arsenic species in this Report are three biologically generated environmental forms.1) 45.17-1.. interval) 1.2-38.93) 1.00) 3. 1990.70-21. population (Ahsan et al. population in the NHANES 2003–2004 subsample.S.5) 29.80 (. In the late 1980s.31-1. 2008).7-22. 2005.900-1.20-3.8. MMA. The higher percentiles of total urinary arsenic levels in the U.871-1.S.70-21.800-4.70) 6.3) 95th 35.700-1..g.500-1. Caldwell et al. Also. 2006). Median and mean total urinary arsenic levels for residents in some districts in Bangladesh were reported to be about 50-fold higher than respective levels in the U.6. < LOD means less than the limit of detection. Individually measurable species resulting from inorganic arsenic exposure are arsenate.80) 1.80 (3.9 (7.00 (.7 (13.800-1. in NHEXAS 1995–1996.1-25. 1985.50) .1-94. 2008. and TMAO.8 (12.3% of a representative sample of the U.700-1.30) 2.68) . Sun et al..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 * * 1.20 (..20-190) 31. Caldwell et al.00-4. arsenite.3) 1284 1284 03-04 03-04 03-04 1. Pellizzari and Clayton.40) 75th 5.62) 2. population (Sun et al.. a control population of 696 Tacoma residents had median urinary DMA levels similar to those for NHANES 2003–2004 (Kalman et al.. which may vary for some chemicals by year and by individual sample. respectively...20 (1. arsenobetaine. Blom et al.. Chowdhury et al.10) 4.2-35.45 (1.7 (21. 2007) with higher levels of arsenic in the drinking water.1) 18.4 (16. Urinary Arsenobetaine Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.6 (25..3-39. 2007). arsenobetaine and arsenocholine will greatly increase the level of total urinary arsenic and comprise the highest percentage of the total urinary arsenic level. China. dermal keratosis.6-44.50) 90th 16.. Arsenate. For residents of Inner Mongolia. In the residents of a Chilean town who consumed water with high levels of arsenic.48-2.90-7.. population showed a higher contribution of arsenobetaine (Caldwell et al.0) 4. Some noncancer effects of arsenic (e.30 (2. 2005.S. Levels of DMA and MMA increase in approximate proportion to the intake of inorganic arsenic.e. population from the National Health and Nutrition Examination Survey.90-29. when seafood organic arsenic is subtracted).83) Selected percentiles ( 95% confidence interval) 50th 1. Detectable levels of MMA reported in NHANES 2003–2004 were found only at the upper percentiles and. and 0.40-6.37 (1. 2008). DMA and MMA compose most (about 75%) of the total arsenic species measured in urine.5) 292 728 1548 03-04 03-04 1. When seafood intake is avoided.80-5.00 (1.600 (..0) 29.5 (14.3) 35. and arsenobetaine being the main contributors to the total urinary arsenic levels (Caldwell et al.S. 2001).4-35. In most human studies. and duration of exposure are also considered important.. DMA and MMA.4) 23.20) 18.60) 1.20-25. Great Lakes region residents had median urinary DMA levels that were slightly less than median levels in NHANES 2003-2004 (Caldwell et al.11-1.

5) 17.39-3.4 (11.5 (18.80-153) 17.12) < LOD ..76-27.Metals as with DMA..25 (..00 (3.4) 13. 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.45) 1. The 95th percentile of the U. 2003.6) 19.531 (. Survey years 03-04 Geometric mean (95% conf.7) 9.S..4-28. Information about the biological exposure indices is provided here for comparison.612-1. WHO. The American Conference of Governmental Industrial Hygienists (ACGIH) provides an occupational biologic effect index (BEI) for urinary inorganic arsenic plus metabolites equal to 35 μg/L (ACGIH.00 (1.67) 4.7) 17.15-1.30-1.40 (1.400-.1-36.6-46. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.88 (5.72) 12.909-1.29 (4.16 (.2 (4.68 (1. 1998. interval) 1.65 (1.9 μg/L.5) 26.9 (13.29-14.14 (1.3 (10.47 (2.28) 1.82) Selected percentiles ( 95% confidence interval) 50th 1. 2001).S.83) 8. 2008).61-6.877 (. Fourth National Report on Human Exposure to Environmental Chemicals 185 . Sun et al. 2001).37-2.18-1.10 (.4-21. these levels were much lower than those found in other studies where environmental exposures were highly elevated (Chowdhury et al.4-82.51-2.88) 2.73-6.786-1...3 (10.9 (25.50-15.44 (1. In recent years.9) 14.0) 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.8) 29.4) 292 728 1548 03-04 03-04 1.51) 5.32-7. Finding a measurable amount of arsenic in urine does not mean that the level of arsenic causes an adverse health effect.67) 1.91) 90th 16.1 (26.54 (1. 2006.1-18. population for the sum of inorganic related species was 18.11 (.91 (4.47 (1.15-1.5-20.638) 1.4) 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 * * 1.43) 75th 5.78-5.81 (4.0 (9.2 (12.53 (.83) 2.938-1. 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.959-1.6 (9.21) 5.9-18.15-4. Vahter et al.05) 1.50-7. 2007). not to imply a safety level for general population exposure.0-36.40) 1. 1986.43) 14.05 (.2 (12.55) 1.6-32.833-1.3-24.19-2.25-7.1) 26. 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.62-6.70) 5. Caldwell et al. 2008).2 (13.78 (3. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.9) 32.93 (1.4 (24.901-2.. population from the National Health and Nutrition Examination Survey. Offergelt et al. Biomonitoring studies of urinary arsenic can provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of arsenic than are found in the general population.4) 32.3) 95th 29.6 (6.13-39.82) 4.5 (18.64-29. which is below the ACGIH BEI (Caldwell et al.3) 1284 1284 03-04 03-04 03-04 1.30) 1.58 (3.. 1992. Urinary Arsenobetaine (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.36) 2.79 (1.6-29.7) 30.80) .

which may vary for some chemicals by year and by individual sample.6.Metals Urinary Arsenocholine Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.S. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th < LOD 90th < LOD 95th < LOD Sample size 2568 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. Urinary Arsenocholine (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.S. 186 Fourth National Report on Human Exposure to Environmental Chemicals . population from the National Health and Nutrition Examination Survey. see Data Analysis section) for Survey year 03-04 is 0. Survey years 03-04 Geometric mean (95% conf. < LOD means less than the limit of detection. Survey years 03-04 Geometric mean (95% conf. population from the National Health and Nutrition Examination Survey. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. interval) Selected percentiles ( 95% confidence interval) 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. population from the National Health and Nutrition Examination Survey.44) 2.00 (<LOD-2.Metals Urinary Arsenous (III) Acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. Survey years 03-04 Geometric mean (95% conf.80) < LOD 621 725 1078 Limit of detection (LOD. Survey years 03-04 Geometric mean (95% conf. which may vary for some chemicals by year and by individual sample.2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.08 (<LOD-4. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th < LOD 90th < LOD 95th < LOD Sample size 2568 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1.95 (<LOD-2.S.00) 1. population from the National Health and Nutrition Examination Survey. Fourth National Report on Human Exposure to Environmental Chemicals 187 .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. < LOD means less than the limit of detection.29) < LOD 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. 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 1.40 (<LOD-1. Urinary Arsenous (III) Acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.00 (<LOD-3.20 (<LOD-1.70) < LOD 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2.S. see Data Analysis section) for Survey year 03-04 is 1.

05) 5.00 (6.4 (7.00) 3.1-15.16-11.9 (11.84-8.00) 4.11 (3.03-6.00 (3.00-4.0) 14.0 (13.00-4.08 (2.49) 10.0) 292 728 1548 03-04 03-04 4.0 (12.89 (3.70) 5.00-4.09 (7.46 (4. population from the National Health and Nutrition Examination Survey.32-10.50-15.06) 5.57-5.80-3.60-7.69 (3.94) 3.00) 6.12-4.80-6. Urinary Dimethylarsinic Acid (creatinine corrected) Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.0 (10.70-4.98) 4.65-8.84-18.00) 6.0) 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 4.30 (7.7) 12.17 (2. Survey years 03-04 Geometric mean (95% conf.7) 1284 1284 03-04 03-04 03-04 4.17-6.05) 10.00-3.9) 12.34-4.00-7.10) 3.69-6.5) 95th 13.44 (2.0) 11.62) 4.00-15.59 (6.29-4.44) 5.4) 621 725 1078 188 Fourth National Report on Human Exposure to Environmental Chemicals .48 (2.0) 13.80 (4.20-12.7.9) 13.34-4.45) 3.65-6.7-16.00 (3.80-5.90) 5.0) 16.61-11.22) 4.79 (3.0-12.88 (4.69 (3.13-4.00 (4.05) 3.5) 12.70-3.45) 8.6 (9.67) 9.00 (3.78) 4.00-4.24) 3.3 (8.0) 12. interval) 3.69-3.80) 2.00) 5.0) 95th 16.0-17.11) 4.0-19.39-3.0) 16.38 (3.0) 13.00 (5.00-4.00-11.97-3.00-9.16 (2.00 (6.17-4.00-13.7 (10.60-6.0 (12.00) 3.20) 11.S.31-4.00-3.00-15.00-12.57 (3.5 (11.61-16.19) Selected percentiles ( 95% confidence interval) 50th 3.80) 7.0) 17.0 (8.95 (4.45 (8.8) 7.60-3.8) 7.6-18.00) 75th 6.6) 292 728 1548 03-04 03-04 3.0) 10.0 (9.0-17.32 (8.71) 3.82) 3.03 (3.0 (10.30) 3.12 (3.37 (2.0 (10.0 (11.0-16.00) 90th 11.20-4.34 (3.25 (4.00-8.82-9.24-4.S.0) 11.0 (14. interval) 3.0 (9.33-4.1-18.10) 6.0 (10.95-4.91) 75th 5.74) 90th 9.0) 9.00-15.95-3.00 (5.00 (6.72 (4.00 (3.77 (3.33) 3.0) 17.55 (2.9) 11.67) 8.9) 5.00 (7.27 (3.00 (7.14) Selected percentiles ( 95% confidence interval) 50th 3.00-22.Metals Urinary Dimethylarsinic Acid Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.00-11.27-5.90) 2.00-7.0-16.52) 3.0 (8. see Data Analysis section) for Survey year 03-04 is 1.9 (7.0 (13.85 (3.00) 12.3 (8.27-2.0) 621 725 1078 Limit of detection (LOD.0-25.50 (4.70 (3.31) 4. population from the National Health and Nutrition Examination Survey.00-7.1-22.7) 13.49-4.86-21.32 (4.0) 9.94-3.82-5.00) 7.8) 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 3.73 (3.18 (6.34 (3.73) 6.16 (4.86 (2.70-12.92) 3.81 (5.71 (4.3 (7.00-10.00-11.00) 6.00 (5.00) 9.0) 9.00 (5.48 (3.90 (3.0 (9.71-4. Survey years 03-04 Geometric mean (95% conf.00-5.28) 2.95-6.00) 6.14) 3.74 (2.00-12.0-18.00 (3.00-4.1 (8.15) 4.27 (2.50-5.6) 1284 1284 03-04 03-04 03-04 4.78 (4.92-12.34) 3.42) 3.00) 4.37 (3.86-7.00-7.60-4.71 (3.00 (5.2) 10.00 (3.

63 (<LOD-1. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th 1.14-1.70-2.45) 3.10-3.31-3.07-3.93) .37 (1.77) 1.00 (2.80) 1.60) 1. which may vary for some chemicals by year and by individual sample.62) 2.46 (1.30-2.20 (1.00-1.30) 1.28 (1.46-2.86 (2.00) 1.00) 2.40-2.79) 2.70-2.50) 1.11-1.70-2.90) 1.10 (1.00 (<LOD-1.50) 621 725 1077 Limit of detection (LOD.10) 2.10 (.00 (2.00 (1.88-2.80 (1.10 (1.20-1.73-2.16 (2.53) Sample size 2567 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.40) 1.07 (1.84-3.10-1.00) 2.35-3.00-4.40 (1.85) 2.80 (1.80-2.53 (1.80 (2.80) Sample size 2567 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.85) 1.60) 2.00) 1. population from the National Health and Nutrition Examination Survey.70-2.53-2.90) 2.07) 2.53) 1283 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.54) 90th 2.18-1.50 (1.80 (1.S.10) 95th 2.30 (1.40) 1.33 (1.20 (1.50 (<LOD-1.86) 3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.15-1.88 (1.60 (2.57) 95th 2.40-2.90 (2.10 (<LOD-1.60) 2.50 (2.58) 2.20 (1.53) 292 728 1547 03-04 03-04 * * < LOD < LOD 1.30 (1.90 (1.30-1.40-3.82-2.60) 292 728 1547 03-04 03-04 * * < LOD < LOD 1. Survey years 03-04 Geometric mean (95% conf.80 (1. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th 1.22 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.900-1.S.50-2. population from the National Health and Nutrition Examination Survey.96-2.60-2.23) 1.17) 2.80-2.20) 2.985) 1.40 (2.88 (1.10-1.70) 2.40-3.18-1.52 (2.30 (1.30) 2.816 (<LOD-.00-2.60) 1283 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.00 (<LOD-1.86) 2.20 (1.31 (1.70-3.86 (2. Fourth National Report on Human Exposure to Environmental Chemicals 189 .00-1.20 (1.80) 1.10 (.40) 2.Metals Urinary Monomethylarsonic Acid Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.30) 1.33 (1.36) 1.05-1.00) 1.61-3.9.853-1.60 (1.61) 2.71-2.30) 90th 1. < LOD means less than the limit of detection.82-2.36 (1.22) 3.75) 621 725 1077 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.43-3. Urinary Monomethylarsonic Acid (creatinine corrected) Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.81) 1.34) 2.50 (1.28 (1.20-3.00-2.90) 2. Survey years 03-04 Geometric mean (95% conf.30-1. see Data Analysis section) for Survey year 03-04 is 0.30 (2.20 (1.

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

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70) 1. Urinary Barium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.90) 1.86) 6. fireworks.30) 3.40 (5.65) 1.38 (1.00 (2.49-1.77 (3. such as brazil nuts.30) 2.90) 2.63 (2.76-2.95-6.60) 1.73) 1.34 (1.30-1.65-1.60-2.18 (6.85) 1.12.20 (3.70-5.20 (1.35 (3.11 (2.30) 8.14 (6. The general population can be exposed to low amounts of barium in air.77-3.21 (1.49) 8.27 (1.8 (6.44-2.86-4.60 (1.44 (1.12 (2.20-1.65-5.63) 1.40 (5.08-8. interval) 1.14-6.56) 4.30) 5.50-1.80 (2.42 (1.53) 2.30) 5.72) 75th 3.10 (2.8) 5.99 (4.43) 2.51) 2.65 (5.85) 1.63) Total 1.54) 1.02 (7.00) 4.30-2.62 (1.10 (4.48 (6.15-11.04-2. respectively.24-1.30) 5.40) 7.64 (1. Barium compounds are used by the oil and gas industries to make drilling muds.16 (1.10) 1083 1335 1281 1097 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.87-3.52 (4. were relatively well absorbed following inhalation (60-80% of a dose) or ingestion (11-32 % of a dose).90) 4.32) 8.40 (1.94-6.00) 6.16) 5.27) 2.28-1.50 (1.21 (1.45) 7. In single dose animal studies.38 (1.30 (1. bricks.39 (1.40) 3.55-3.54-1.90-2.15 (2.60-6.39) 4.82) 1.50 (4.80 (1.03 (1.67) 6.51 (1.71) 2.80) 7.26) 5.59-11.50 (2. 0.50 (4.17-1.60-3.37) 5. Ingested soluble barium General Information Elemental barium is a silver-white metal which comprises approximately 0.05% of the earth’s crust.70 (5.86-5.50-6. see Data Analysis section) for Survey years 99-00.01-7.80-7.27 (1.43) 297 368 290 621 762 725 1262 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 1.01 (4.34) 2.00 (1.60-6.70 (1.54 (6.50) 2.52 (1.70-8.80 (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 2.78) 1.53-5.60) 4.53) 1.80-2.31 (2.54) 2.80-3.15) 5.80 (2.30-5.30 (5.60) 3.80 (1.51) 1.00-76.38) 8.71-9.63 (1.76 (3.82-6.30 (3.40) 7.00) 1.86 (4.65-8.46) 1.54-8.36-1.62) 1.30 (5.56 (6.57) 3.40 (1.20-1.20-1.81-2.Metals Barium CAS No.12 (2.07 (2. barium sulfate is used as a contrast medium for taking radiographs of the gastrointestinal tract.4) 9.34 (1.33 (1.04-6.61 (2.73) 3.56 (1.84) 5.22) 6.91) 2.10) 3.90 (4.60 (2.09 (1.66 (4.54 (2.48-4.49-9.46) 1.62 (1.91 (2.50) 4.73 (5.11-1.57 (5.61-8.12) 6.26-7.87 (6.75) 2.49) 2. population from the National Health and Nutrition Examination Survey.25-1.91) 6.40 (4.74-2.65) 1.00) 1. water.29-5.77) 1. glass.95 (4.45 (1. Workers employed by industries that make or use barium compounds can be exposed to barium dust.49) 4.10-5.36 (1.78) 1.75-3.1) 9.11 (3..87-14.87-7.20) 2. Certain foods.51) 7.43 (1.50-6.09 (2.76) 1.49 (1.19-1.24-1.32-1.87 (5.40 (1.30-2.68 (1.72) 1.93 (4.50 (1.22-1.41-1.86 (4.88 (5.61 (1.59) 3. Barium salts have also been available as rodenticides.35) 5.50 (1.78-3.78-2.87) 7.54-1. it combines with other chemicals such as sulfur or carbon and oxygen.8) 9. whereas others are practically insoluble (e.70-6.69 (1.32-7.70-2.20-8.S.90 (6.70) 7.70) 5.06-2.15 (1.47) 4. and 0.70) 1. are high in barium (Genter.2) 6.48) 1.37) 1.50) 1.21-8.90 (1.88) 4.35 (2.15 (6.36 (4.15-1.31. depilatories.74) 3.36-1. Small amounts of barium can be released into the air during mining and other industrial processes.54) 1.41-3.70-3.80) 6.36) 5.10) 5. In nature.63 (8.56 (2.55-7.12. Fourth National Report on Human Exposure to Environmental Chemicals 193 .10 (3.60) 1.46-1.35-1.61 (3.08 (6. and 03-04 are 0.40-13.72) 4.63) 1.50 (3.70) 3.90-9.20-5.56) 1.60-10.93-2.35 (1.30 (2.80) 1.40 (5.50 (6.88) 7.65) 3.20 (4. 2001).44-5.06-1.34 (2. rubber.9) 5.96-2.00-3.61 (5.43) 6.73-5.25 (1.62) 1.20-1.48-4.21-2.92) 2.70) 4.18-1.73 (6.26-1.39) 1.49) 11.10-4. tiles.20-8.43 (5. such as barium chloride.37-8.61 (1.64-3.31-2.20-6.41) 1.4) 6.88) 1. soluble forms of barium.48) 1. and ceramics.80-5.66) Selected percentiles ( 95% confidence interval) 50th 1.99-5.80 (5.50 (1.30-3.90) 2.50 (5.12) 7.50 (4.29-1. 7440-39-3 Medically.15-1.g.22-1.85 (2.74-3.29) 5.24 (4.56 (1.18) 3.28) 90th 5. barium sulfate and barium carbonate).63 (5.05-2.76-3.71 (2.81-3.11 (3.53) 692 683 618 540 667 723 765 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.50-1.98) 1.71) 95th 6.47-1. Some barium salts are freely soluble in water.50 (1.50) 2.37-1.47-1.90-13.97 (1. and food.87-9.4) 7.76-7.30) 4.26) 2.00-8.57-7.70-2.39-1. 01-02.30-1.35-4.93-8.43 (1.82) 2.19) 2.71) 1.25-11.38) 2.37 (4.12-1. Barium compounds are also used commercially in paint.20-8.81-2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.14-1.39 (1.35-1.

39 (2.20-8.02 (3. water solubility.72 (2.67-6.38) 4. are not absorbed when administered.29-4.62 (2.22-4.25 (1.10) 6.62) 2.39-10.74) 1.70) 10.28-11.777-1.71 (5.50 (4.59) 1.68) 1.68 (2.96) 4. weakness.88 (2.00-7.26) 4.28) 5.04 (2. Chronic exposures to natural low levels of barium in drinking water have not produced general health effects or evidence of cardiovascular risk (Brenniman and Levy.61 (4.50) 2.80) 4.75) 1.75-22.97 (4.29-4.80) 3.54 (1.45-8.06) .00 (3.24-1.43-6.70) 1.915 (.86-7.880-1.41 (1.00) 1.51) 4.29 (1.2) 5.58 (2.87) 1.50) 1.19-1.35-1.65 (2. such as those used in medical radiographic procedures.79-5.20 (1.13-3.03-1.39 (2.55-5.44-2.50) 1.37-2.20) 4.57-5.57-10.51 (3.68 (3.3 (6.46 (2.90-2.66 (1.24-3.77) 5.21 (1.91) 2.34 (1.57) 2.58-6.68 (3.51) 6.35-3.59) 2.36-1.54) 2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.76) 1.82) 1.61) 2.60 (5.56) Selected percentiles ( 95% confidence interval) 50th 1.0) 5.8) 4.24-11. Insoluble barium salts.75) 1.56-3.22-1.45) 1.26-4.45) 95th 6.91-2.24-6.28 (1.881 (.55 (1.76-3.49-1. and route of exposure.39-5.703-1.81-6.26-1.60 (2.16-1.31-1. chemical form. interval) 1.Metals was eliminated primarily in feces and to a lesser extent.36 (1.97) 1.47) 10.77) 1.86 (2.39-1.11) .31 (1.83) 3.45 (3.20-1.34-3.45-6.47 (2.84-2.25) 4.48-5.60 (2.44-2.24-6.42) 1.40-1.36 (5.91 (3.96) 7.47-8. Following intravenous injection in animals.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. 1986).38 (4.03) 3.0) 7.51-3.76 (4.41) 4.19-1.710-1.30) 2.57-7.S.51 (1.73-4.04) 5.24 (3.32) 2.55 (5.33-4. NTP. about 75 % of a dose of soluble barium was eliminated within 3 days (Reeves.43) 1.2 (3.62 (1.69 (5.00 (5.963 (.3) 6.4) 5.62 (4. 1985. 2001).29-7.76 (2.74) 1.64) 7.64 (1.08-1.49-1.84 (3.00-1.31 (4.68-3.23-2.68-3. Urinary Barium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.25-11.18 (1.36-1. 1984.34-5. Perry et al.13-2.52-10.97-4.33 (1.73-2.19-2.51) 4.55 (1.84-5.37 (1.86) 5.01 (4.28-6.03) 2.76) 2.75) 2.38-5.24) 3.72) 4.00) 6.22-1.0) 6.12) 2.58) 1.41 (2.89) 90th 4.27) 7.91 (3.76 (3.28-1.23-1.31) 5.32) 2.49 (1.24 (5.11-2.905 (.56) 4.32 (1. diarrhea. Symptoms following acute high dose include perioral paresthesias.59 (1.48) 2.58) 75th 2.03-1.88 (6.64 (1.44 (1.33 (5. 1994.10-1.31-1.16) 11.81-7.33 (1.29) 1.32 (1.33) 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 2.38) 1. Toxicity from soluble barium salts is rare.65 (5.04) 1.15-4.39) 4.832-1.55-6.56 (1.02-5. The health effects of exposure to barium compounds depend on the dose.64 (1.891 (.59-7.49-1.60 (1.26-1.30 (1.10-2.81-6.96 (4.00 (2.00 (3.49 (1.79) 1.41) 5.92 (4.89 (2.72) 6.68) 3.36 (3. Human health effects from barium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.69-9.41 (1.63-4.39 (2.78 (2.48-1.52 (3.53) .00) 4.45 (1. 1990).52-4.09) 6.27) 692 682 618 540 667 723 765 1132 1074 Non-Hispanic blacks Non-Hispanic whites 194 Fourth National Report on Human Exposure to Environmental Chemicals .29 (3.42 (4.31-1.2) 6.96) 4. Barium blocks cellular efflux of potassium resulting in profound hypokalemia.05-1. hypertension.48-3.36 (3.70) 4.73) 2.56 (1. a benign condition that may occur among barite ore miners.20-2.38 (1.47 (5.54) 1.51 (1.06) 2.34-1.59 (1.10 (6. paralysis.84) 2.02) .36 (1.00) 4.39 (3.52) 7.54 (2.23-5..24-1.99) 1.38 (4. Chronic high doses in animals resulted in kidney damage (McCauley et al.45-1.75-3.48 (1.11) .83) 2.47) 1.46-22.77) 1.80-6.26-1.. Barium is not rated for human carcinogenicity.52) 1.38-1.96-6. vomiting.754-1. Chronic accumulation of inhaled barium dust in the lung tissue may cause baritosis.48 (1.921 (.99 (2.64 (1.58 (4.64) 7.52) 2.33) 6.38-7.42) 1.38) 1.47) 1..28-7.26-1. but can occur after intentional or accidental ingestion of barium carbonate in rodenticides (Genter.40 (1.40 (1.46) 3.19-1.96 (4.02) 4.37) 2. population from the National Health and Nutrition Examination Survey.40 (1.37 (1.74 (5.47) 4.97 (5.92) 2.50) 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 1.33-1.48 (1.4 (5.29-3. in urine.46) 2.36-2.57 (6.55) .03) 1.53 (2.53-21.27-1.01 (5.99 (4.34) 1.77) Total 1.60 (1.45-1. 1989).46) 1.35-1.08-2.55 (4.77) 1.32 (2.30 (1.39-1.18 (1.77-5.16 (1.14-2.76) 2.27 (2.37-1.22-2.85-5.58) 4.38 (1.82) 1.29-1.01) 1.10) 3.97-3.27-3. Wones et al.59) 1.75) 2.96) 4. and cardiac dysrhythmias.63) 1.98 (2.

Vouk VB. Princeton (NJ): Princeton Scientific Publications. p. 1986. ed. and 2003-2004 (CDC. Information about external exposure (i. patient population and literature reference intervals for urinary trace elements. Pirkle JL. Comparison of representative ranges based on U. 2000) to levels in NHANES 1999-2000 and 2001-2002. Magnesium. 231-249. Powell C.nih. Handbook on the Toxicology of Metals..296(1-2):71-90. Stadler BL. Barium. 1992).. Laurie RD. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Wones RG. Kopp SJ. 4/8/09 Paschal DC. In: Calabrese EJ. 5th ed.. Jr. 2nd Ed. 1998).gov/toxpro2. Centers for Disease Control and Prevention (CDC). Schaller KH.76(1):53-59. Douglas BH.gov:8080/cs. Ash KO. Weltle D. the welders had no obvious adverse clinical effects (Zschiesche et al. Reeves AL. 221-252 Komaromy-Hiller G. New York: Elsevier. [online]. Vol 2: Specific Metals. Pietra R. Fourth National Report on Human Exposure to Environmental Chemicals 195 . 2005. Levy. New York: John Wiley & Sons. environmental levels) and health effects is available from ATSDR at: http://www.gov/ntp/htdocs/LT_rpts/tr432. barium. 10326-27-9) in F344/N rats and B6C3F1 mice (drinking water studies). 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. et al. Epidemiological study of barium in Illinois drinking water supplies. References Brenniman GR. Biomonitoring Information Levels of urinary barium reflect recent exposure. 2005.64(1):13-23. Int Arch Occup Environ Health 1992. Jackson RJ.85:355-359.niehs. Clin Chim Acta 2000.. Cohressen B. ed. eds. Costa R. 1990.. and serum of Italian subjects. Barium levels determined in clinically submitted specimens were broadly comparable (Komaromy-Hiller et al. p. Princeton NJ: Princeton Scientific Publications. Urinary concentrations in acute poisonings are often hundreds to thousands of times higher than in this Report. Perry HM.95:89-105. EPA.nih. Trace element reference values in tissues from inhabitants of the European community I. Investigations into the effect of drinking water barium on rats. Howerton K. p. Welders of barium-containing electrodes had median urinary levels of barium that were 60 times higher than the median levels in this Report. Third National Report on Human Exposure to Environmental Chemicals. Patty’s toxicology. 2001.S.S. Sci Total Environ 1990. Atlanta (GA). Apostoli P. Finding a measurable amount of barium in urine does not mean that the level of barium causes an adverse health effect. McCauley PT. pp. Exposure to soluble barium compounds: an interventional study in arc welders. NTP. Pozzoli L. 2001-2002.28(3):373-388. 1989. Minoia et al.pd f&qt=barium+chloride+dehydrate+1994&col=020rpt&n=3&la= en.. Gallorini M. Paschal et al. Morrow JC. 1984. Frohman. Available at URL: http://ntp. Trace metals in urine of United States residents: reference range concentrations. Sampson EJ.. et al. 1985. Nordberg GF.atsdr. In Friberg L..e. PS. National Toxicology Program (NTP). et al. and radium In: Bingham A. Sabbioni E. Environ Res 1998. eds. LA. 84-94. A study of 46 elements in urine. strontium. Lack of effect of drinking water barium on cardiovascular risk factor. and a drinking water standard has been established by U. Ting BG. Zschiesche W. Hypertension and associated cardiovascular abnormalities induced by chronic barium feeding.html. 1994. technical report on the toxicology and carcinogenesis studies of barium chloride dehydrate (CAS no. Environ Health Perspect 1990. J Toxicol Environ Health.cdc.Metals Workplace standards for external air exposure to various barium salts have been established by OSHA. Inc.html?charset=iso-88591&url=http%3A//ntp. Genter MB. blood.niehs.. In: Inorganics in drinking water and cardiovascular disease. et al.197210. Perry EF. Advances in modern toxicology. Calabrese EJ. Studies reporting urinary levels of barium in general populations have found values generally similar to those reported in NHANES 1999-2000. calcium. Minoia C.

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 . coal.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. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. Low-level beryllium exposure in the general population can occur through breathing air. x-ray machines. In studies of laboratory animals. and machine-parts industries. Two types of minerals. soil. In medicine. bertrandite and beryl.13. are mined for commercial recovery of beryllium. Burning coal and oil can produce small amounts of beryllium dust that can be released into the air. inhaled insoluble beryllium sulfate was retained in the lungs and nearby lymph nodes. and refined beryllium is used in mirrors and special metal alloys for the automobile.170) < LOD < LOD < LOD < LOD 340 368 290 719 762 725 1406 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . and can be found in mineral rocks.S. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.13. and 03-04 are 0. 7440-41-7 General Information Pure beryllium is a hard gray metal. and volcanic dust. Beryllium compounds are commercially mined. aircraft. < LOD means less than the limit of detection. computer. 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 .130 (<LOD-. respectively. see Data Analysis section) for Survey years 99-00. population from the National Health and Nutrition Examination Survey. the lightest of all metals. 196 Fourth National Report on Human Exposure to Environmental Chemicals . less than one percent of the inhaled dose was slowly absorbed into the blood and eventually incorporated into the skeleton.130 (<LOD-. and 0. A half-life of 450 Urinary Beryllium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. or drinking water containing the metal. which may vary for some chemicals by year and by individual sample.13. 0. Beryllium is also used in the production of sports equipment such as golf clubs and bike frames. nuclear. and dental bridges. beryllium is used in instruments. near some hazardous waste sites. Exposure to beryllium occurs mostly in the workplace.Metals Beryllium CAS No.140 (<LOD-. electrical. eating food. 01-02. and from breathing tobacco smoke.

is a granulomatous interstitial lung disease that is caused by chronic beryllium inhalation and the resultant immunologic response. Air levels greater than 100 µg/m3 can result in erythema and edema of the lung mucosa. Skin exposure can result in delayed hypersensitivity reactions. More information about external exposure Urinary Beryllium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. which produces pneumonitis. 2003.346 (<LOD-. Fourth National Report on Human Exposure to Environmental Chemicals 197 . and drinking water and environmental standards have been established by U.. Chronic beryllium disease.281 (<LOD-. population from the National Health and Nutrition Examination Survey. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.Metals days has been calculated for beryllium elimination from the human skeleton (IPCS.S. Human health effects from beryllium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.333) < LOD < LOD < LOD < LOD 1227 1334 1281 1238 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . EPA. Genetic factors modify individual sensitivity to beryllium and susceptibility to developing chronic beryllium disease (McCanlies et al. The effects of occupational exposure to beryllium depend on the concentration of beryllium in the inhaled air and the duration of air exposure. S.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. 1990). or berylliosis. 2002). Workplace air standards and guidelines for external exposure have been established by OSHA and ACGIH. IARC has classified beryllium as a human carcinogen. NTP considers beryllium to be a known human carcinogen. including contact dermatitis and subcutaneous nodules. 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 . based upon excess lung and central nervous system cancers in studies of workers.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 . Maier.231 (<LOD-. respectively. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.

Biomonitoring Information Urinary beryllium levels represent recent and accumulated exposure. In other studies. McCanlies EC. 198 Fourth National Report on Human Exposure to Environmental Chemicals . Minoia et al. and the fact that most NHANES participant levels were undetectable.htm. which approximate this Report’s limit of detection.. Weston A. (1994) noted that analytical methods used in several general population studies appeared to have limits of detection that were insufficiently low (i. Paschal et al. Pirkle JL. Clin Chest Med 2002.gov/toxpro2. Third National Report on Human Exposure to Environmental Chemicals. 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. Given these results. 1990. References Apostoli P. blood. 1998). Howerton K.1 μg/L). less than 0. Atlanta (GA) 2005.15 μg/L in workers exposed at the recommended threshold limit value (Apostoli and Schaller. Ash KO. Costa R.Metals (i. Sabbioni E. 20012002.76(1):53-59. Apostoli P. Environ Res 1998.html. environmental levels) and health effects is available from ATSDR at: http://www. Maier L. Schaller KH.74:162-166. 2000.S. Ting BG. plasma and urine and a critical evaluation of reference values for the United Kingdom population.12 to 0.. Paschal DC.157:388-398. Genetic and exposure risks for chronic beryllium disease. Sampson EJ.296(1-2):71-90. 1990. Clin Chim Acta 2000. it is likely that urinary beryllium levels in the U.cdc. 2001).S. 3/27/08 Komaromy-Hiller G. and 2003-2004. Gallorini M. et al. Kriess K. Pietra R. VI.158:165-190. Trace metals in urine of United States residents: reference range concentrations. Pozzoli L. Morrow JC. HLA-DPB1 and chronic beryllium disease: a HuGE review. et al. Element reference values in tissues from inhabitants of the European community. 0. Van der Venne MT. urinary levels for general populations have been either undetectable or had different detection limits than in this Report (KomaromyHiller et al. Apostoli and Schaller (2001) stated that detection limits in earlier studies were inadequate to estimate nonoccupational exposures. Available at URL: http://www. population were generally undetectable in NHANES 1999-2000. Sci Total Environ 1990. Jackson RJ. population are lower than levels in workers. patient population and literature reference intervals for urinary trace elements. Centers for Disease Control and Prevention (CDC). Minoia C. Sci Total Environ 1994. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.23:827-839. Andrew M.. Urinary beryllium--a suitable tool for assessing occupational and environmental beryllium exposure. Beryllium [online]. They reported urinary beryllium levels ranging from 0. Sabbioni E..95:89-105.13 μg/L.e.e. Int Arch Occup Environ Health 2001.atsdr.S.org/documents/ehc/ehc/ ehc106. and the 95th percentile for males in NHANES 2001-2002. Trace element reference values in tissues from inhabitants of the European community I. Review of elements in blood. Levels of beryllium in urine for the U. Hamilton et al. 106. International Programme on Chemical Safety (IPCS).inchem. Hamilton EI. Environmental Health Criteria. A study of 46 elements in urine. Comparison of representative ranges based on U. Am J Epidemiol 2003. and serum of Italian subjects. Finding a measurable amount of beryllium in urine does not mean that the level of beryllium causes an adverse health effect..

400 (.900-1.usgs.300-.3.40-1.60 (1.367-.289-.20) 1.50) 1.900-1. Important sources of airborne cadmium in the environment are burning fossil fuels such as coal or oil.60 (1.60) 1.60 (1.40 (1.20-1.900 (.50-1.468 (.398) < LOD < LOD < LOD < LOD < LOD < LOD .400) .400-.200-. and 03-04 are 0.80 (1.800) 1.300-.200 (<LOD-.200 (<LOD-.40) 1.600) .900-1.700) 1.20) .400-.393 (.378 (.300-. EPA.600 (. malleable.00) .344) .600 (.00 (1.500-.700 (.200-.700) . The predominant commercial use of cadmium is in battery manufacturing.30) .900-1. during refining of lead and copper from sulfide ore.500 (.00 (.20-1.600) .300 (.441) * .424) * .20) 1.300-.400 (.10) 1.10) 1.400 (. 0.70) 2742 2268 2085 1842 2219 2292 2716 3806 3478 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.600 (.20) 1.313 (.400) .14.600-.900-1.300) .50 (1.366) * * .00 (.00-1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.420 (.300-.300-.600) 1.30) 1.300-.70) 1.500) .300 (.300 (<LOD-.10) 1.10 (1.500-.400) < LOD < LOD < LOD .300-.20) 1.400 (.400) . or copper smelters (U.400 (.460) .10 (.30-1.900-1.00-1.60 (1.200) .900-1.400) . which may vary for some chemicals by year and by individual sample.50 (1.20-1. lead.300) .30-1.400 (.30) 1.500-.600-1.500 (.700-1.600 (.600) .400 (.400) .513) . Blood Cadmium Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U.300 (.376-.300) .70) 1.449) Selected percentiles ( 95% confidence interval) 50th .400) .00 (.00 (.700) .368-.500-.300) .300 (.800) .296-. population from the National Health and Nutrition Examination Survey.400) .300) .600) .60) 1.600 (.10) 1.600 (. cadmium use has declined in response to environmental concerns (http:// minerals.700) .200 (.00-1.400) .300-.300-.900 (.700) .300-.400 (.300 (<LOD-.200-.500 (.10) 1.00-1. respectively.10 (1.283 (.500-.S. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.20-1.Metals Cadmium CAS No.600 (.700) .60 (1. see Data Analysis section) for Survey years 99-00.500-.500) .600 (. Fourth National Report on Human Exposure to Environmental Chemicals 199 .403 (.50 (1.304 (.S.400-.10) 1.700) .700-1.600 (.700) .900-1.500) .20 (.400) .300-. and 0.20) 95th 1.500-.320) Sample size 7970 8945 8372 Age group 1-5 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * .30 (1.400) .361-.200) .700-1.600 (.00 (.359-.500-. Cadmium also may be emitted into the air from zinc.500-.500 (.300-.300) .304-.500) .400 (.400 (.300 (<LOD-.600 (.400-.900-1. 01-02.500-.400) < LOD . Since 2001.362-. bluish-white metal that is obtained chiefly as a by-product of processing zinccontaining ores (principally sphalerite.400 (.300-.50 (1.255) .300) .300) .400) .20) .700) .300) .500-.382 (.40 (1.80) 1.333 (.300-.300 (.20 (1.50-1.40 (1.10) 1. Other uses include pigment production. interval) .40-1.10 (1.70) 1.00) .600 (.452) .500 (.425 (.500-.400 (.30) 1.20-1.300) 1.326 (.500) .400 (.500-.421 (.00-1.600) .10 (1.00 (1. coatings and plating.200-.300-.400-.216-.300) .800) .70) 1.800-1.400-.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 . plastic stabilizers.235 (.00 (.300 (.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 .10 (1.300-.30-1.20-1.00 (.40 (1.50-1.400-.400-. U.00-1.500 (.500-.gov/minerals/pubs/commodity/cadmium).426-.400 (.427) * .60-1.20) 1.800 (. 7440-43-9 General Information Cadmium is a soft.400-.20) 1.331) .300) .395 (.600) .400) .300) .300 (<LOD-.30-1.600 (.500) .300-.600 (.60) 1.800-1.00 (.300 (.20) 1.500 (.300 (.S.60) Total * .30-1.200-.400) < LOD .400 (.403) .400) < LOD .300) .400 (.200 (.500-.20-1.300 (.400-. and nonferrous alloys.300 (.20) 1.400 (.50) 1.40) 1.500 (.300 (.275-.00 (.50-1.400) .600) .600) .10) 1.40 (1.300) 75th .309-.3.500 (.600) 90th 1.00-1.300 (.386-.470) * . and incineration of municipal waste materials.304 (.500-.600-.900-1.400-.300-.500-.300-.00-1.337) .50) 1.80) 1.500) . < LOD means less than the limit of detection.300 (.600) .300-.40 (1.266-.300 (.800 (.90) 1.40 (1.500-.378-.400) .200 (.10 (1.300-. as zinc sulfide) and to a lesser extent.412 (.00 (.600-.00-1.

37) 1121 1335 1277 1136 1355 1266 Females 99-00 01-02 03-04 Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 .210 (..233) . The kidney is a critical target and shows the earliest sign of cadmium toxicity.545 (.203) .061 (<LOD-.38) .148) .433-.087-.381-.25 (1.350 (.763-. About one-third to one half of the total body burden accumulates in the kidney tissues (Nordberg and Nordberg. a factor that may contribute to the higher absorption of cadmium by women (Diamond et al.447 (.01) .310) .680 (.336) .211-.151-.17 (.080 (.210 (.262) .189-.135 (.235) .980) .12-1.128 (.153-. To a lesser extent. potatoes.539) . and 03-04 are 0.230) 75th . Diamond et al.766 (. 1994).306 (..430-.249-.170-.440-.07-1.260-.38) 1.121 (.255) .748-1.366-.211 (.83) 1.15) 1.257-.279 (.196-.855-1.810-1.194-.960) 1.10 (1.253-.313) .450 (.519) .455 (.580) .394-.858 (. including many food crops such as cereal grains.109-.320) .17) .510-.48 (1.686-.19) 1.277 (.476-. population from the National Health and Nutrition Examination Survey.169-.790 (.101) .175 (.135-.257) . however.01 (.20) 1.061-.202 (.229) .092 (.177-. interval) .82) 1. 2004a.109 (. Renal tubular and glomerular damage.282 (.090) .329 (.09-1.01-1.470-.330-.157-.189) .229-.263) .191-.233) .260 (. For nonsmokers who are not exposed to cadmium in the workplace.226) Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 * . calcium.200-.270 (.249) .202-. 200 Fourth National Report on Human Exposure to Environmental Chemicals .47) 1. Horiguchi et al.067-.15 (..610) .20 (1.753-.239 (.192-.210 (.234 (.790 (.** Survey Geometric mean (95% conf.150-.339) .700-.167-.366-.222) .110-.445 (.160-.918-1.221) .17 (. whose body burdens of cadmium can be approximately twice that of nonsmokers.20-1.220-.243-.261-.836-1.498-.480) .13) .43) 1.806) .507) .251) .170 (.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 . drinking water is a source for cadmium intake.227 (.199 (. Urinary Cadmium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.289-.214-.216 (.283 (.203 (.220) .38) 1.717-.114-.210 (.741-1.02-1.207-.818 (.607) .260-.892 (. 2003).820 (. Cadmium in soil is absorbed by plants.713) .193 (.25) 1.886) .839 (.372) .126) .20 (1.820) 1.285-.550 (.479) . and various seeds.490) 1.26) size 2257 2690 2543 Total years 99-00 01-02 03-04 50th .112-.192-.310 (.430) .03) .284) .115-. individual values vary and are affected by factors such as dietary intake of essential nutrients (iron. wheat.316 (.400-.173) .. 2001).57) 1. ingestion through food is the largest source of exposure.238) .28) 1.067-.390 (.190-.26) 780 683 614 546 667 717 760 1132 1070 Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 03-04 Limit of detection (LOD.06-1.200-.201 (.270 (.06-1.302 (.220-.265) .466 (.20 (1.530 (.210) .219 (. The gastrointestinal absorption of dietary cadmium is about 5% in adult men and 10% or higher in women (Diamond et al.30-1.366) .436-.187 (.700-.200 (.06.875 (.165-.462 (.960 (.210) .22 (.272-.890 (..060-.730-.238-. rice.74) 1.596) . 2003).295) .Metals 2000).210 (.452 (.198) .890-1.230) .393-.482) .300) . 01-02. Cadmium absorption may be increased with iron deficiency (Berglund et al.700-.28 (1.623) .445 (.229) .181 (.458 (.191-.195-.972 (.540) .13-1.875) .226) .892-1.240-.500) .28-1.500) 90th .171-.450 (.184-.440 (.327 (.04 (.175 (.362) .589 (.219 (.860) 1. With chronic exposure. The estimated half-life of cadmium in the kidney is from one to four decades (ATSDR.183-. 0.322 (.160) .351-.733) .308) .980-1.221 (.231) .06.800-.817 (.220 (.280 (.100-.290-. cadmium accumulates in the liver and kidneys where it is bound to metallothionein.510) .160) .354) .246) .400-.140 (.530) .081) .136) .977) .230 (.193-.813 (.963-1.800 (.148-.640) . 1999.191 (. zinc.980 (.078 (.273 (.490) .090) .255) . see Data Analysis section) for Survey years 99-00.390-. **All results are corrected for molybdenum oxide interference in the ICP-MS method.281 (.237-.475 (.72) 1.190-.15) .219 (. an inducible metal binding protein..209 (.232 (.220) Selected percentiles ( 95% confidence interval) Sample 95th 1. respectively.733-.06) .157) .41 (.520-. 2003.52 (1.423-.519) .32 (1.190-.107-. and 0. Kikuchi et al.170-.440 (.247) .360) .559 (.232) .240) .990) .817 (.134) .065-.51 (1.24) 1.820-1.493-.980) .06.130 (.206 (.13 (.551) .22 (1.077 (. Cadmium is absorbed via inhalation and ingestion.092) .299) .919) .120 (.989-1.200 (.412) .705-.633 (.714-1.077 (.843-1.551 (.326) .880) .141 (.178-. Inhalation of cigarette smoke is a predominant source of exposure in smokers.150) .300 (.633-1.179-.261-.265 (.180 (.S.426 (.848 (.390-.36) 1.17 (.208-.206) .387) .189-.940-1.481) . 2003).12 (.492 (.456-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.04 (.388-. copper) and protein.870) .980-1.223 (.241) .255) .204 (.38) .160 (.34) 1.886-1.

090 (.162 (.191) .873 (.192) .189-.261) . 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.215 (.** Survey Geometric mean (95% conf.238) .13) .091 (.607) . 2002.716) .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.168 (.487 (.183) .826-1.667) .267 (.221-.223) .985 (.418) .876-1.404) .111-.668-.253 (.382-.500-.206-.263-.491-.209) .077-.143-.071 (.415) .827) .325 (.716-.181) .481 (.551) .289) .051-.094) .159 (.143-.. 1999).316 (.210 (.097) . During the 1950’s and 1960’s.278) .431) .207) .826-1.282 (.261-.208-.767 (.220 (.802 (.666-.950) .686 (.440) ..631) .533) .091) .274) 1.136-.256-.240) .147 (.247-.931 (.687-.174-.470) .078 (.38) .874-1.297) .470) .112) . 1996.250) .350) .067-.906) .909-1.919 (.157-.123-.137 (.. 1999). Horiguchi et al.238-.173 (.828) .769 (.288) .144-.690 (.02 (.538) .182) .156-.479 (.377-.712 (. Staessen et al.267 (.170 (.779 (.316) .221 (.693 (.940-1.331 (.518) .940 (.438-. 2004). Fourth National Report on Human Exposure to Environmental Chemicals 201 .281) .472) .283 (.098) .101) .113-.168-.700 (.856 (.146-.789 (.00 (.754) ..818) .185) .083-.719 (.767) .183 (.135) . 2000.929) .783) .501 (.645-.678 (.247-.296 (.917 (.181 (.391-.962) .941 (.182) .239-.150-.440) .387-.209) Selected percentiles ( 95% confidence interval) Sample 95th .170-.096) .226) 75th .830) .423 (.184) . However.303) . most often a result of occupational exposure (Roels et al.16) 1.199-.536 (. Noonan et al.161-.107) .205 (.085-.074-.865 (..225) .075 (<LOD-.187-.329 (.093 (.147-.085 (. 2002.727-.218) .850) .289) .234) . Olsson et al.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 .078-.148 (.219 (.182) . Jarup et al..234-.212 (.441-.856) .175-.199 (.270 (.07 (.614) . 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.261 (.178-.156) .156 (.191 (.00 (.541) .191-.09 (.158-.318 (.387 (.175 (..200 (.426-.321) .293-.201-.484 (.247-.617 (.137-.184-.228-.757) .131-.288-.084-.130-.266) . two studies in Japan did not find an association between cadmium in urine and renal biomarkers (Ezaki et al.433-.136-.16) . a condition known as “itaiitai” (“ouch-ouch”) affected postmenopausal women living in a cadmium-polluted region of Japan.207-.106) .850) .700) .273 (.304-.381-.388-.336-.198) .718 (.194-.233 (.663 (.423-.674-1.449) .591 (.05) 1.792 (.300-.190 (.311) .075-.173-.229) . 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.678-.806-1.729 (.688-.063-..740 (.263 (.998) .653) .100 (.227-.104) .222-.185 (.545) .04) size 2257 2689 2543 Total years 99-00 01-02 03-04 50th .304) . 2003.338 (.235) .154 (.414 (.210 (.308 (.795) 1.163) .507-.12) 1.240) .208 (.473 (.140-.06 (.211 (.181-.166 (.224 (. interval) . **All results are corrected for molybdenum oxide interference in the ICP-MS method.434 (.839) .196 (.438) 90th .414-.691-.412 (.340) .757 (.159 (.622 (.184-.884) .163 (.696-.202 (.335 (.281) .178) .255-. At lower environmental exposures.234 (. 1999).490 (.253) .171-.308) .157-..086 (.288 (. 2002.210) .190 (.091 (.446) .818) .176 (.813-.236-.216-.559-.08) .421 (.219 (.17) .245 (.123-.140-.197-.531 (.084 (.126 (.722-.175 (. 2004b).650-.232) .266-.382) .418-.917) .177) .187) .398-.352) .252 (.537-.476) .154-.725-1.147-.813-1.927-1. population from the National Health and Nutrition Examination Survey.232) .364) .242) .444-.219) Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 * .343-. can result from high dose chronic exposure.168-.562-.Metals manifested by irreversible proteinuria and progressive reduction in glomerular filtration rate.690-. 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.292) .268 (.647-.830-1.560-.10) 1.14) 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 .104) .708-1.122 (.687 (.630-.07) .979 (. 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.784) .783 (.833-1.225) .432 (.404 (.176 (.280 (.690-.516-.S..181 (.241) .204-.143) .

Olsson et al.. Horiguchi et al. Moriguchi et al.1 mg/L (Alfven et al. Occupational standards are provided here for comparison only.... as may occur from welding cadmium-alloyed metals.. EPA. 2004.html. potentially fatal pneumonitis (Fernandez et al.. decreased bone density was correlated with mean urinary cadmium levels of approximately 1 mg/gram of creatinine (Staessen et al. Becker et al. pituitary gland and kidney tumors in animals and has been associated with lung cancer in humans in occupational epidemiologic studies... 2003). 2002. 2004). 2006). Information about external exposure (i. 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. 2005. 2000. 2004b)..26 and 3. In postmenopausal women.. 2004. Biomonitoring studies on levels of cadmium provide physicians and public health officials Fourth National Report on Human Exposure to Environmental Chemicals ... 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). and drinking water and environmental standards have been established by U.. Jin et al.... 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.. Olsson et al. 2004. Women had higher blood and urine cadmium levels compared to men of similar ages.. 1999. 2000. 2006. Staessen et al. Olsson et al...46 mg/gram of creatinine) (Ezaki et al.. 2003. Cadmium can produce lung.. Zhang et al. 1996. 2002. intermediate in former smokers and lower in never-smokers (Becker et al. Both IARC and NTP consider cadmium a human carcinogen. Wilhelm et al. 2000).. Jarup et al.. Surveys of populations not known to have increased cadmium exposure have reported similar urine and blood levels (Becker et al.atsdr. Animal studies have demonstrated reproductive and teratogenic effects. blood cadmium was also slightly higher in Mexican Americans and participants 20 years and older (CDC.gov/ toxpro2. Ezaki et al.e. Friedman et al. approached these values associated with subclinical changes in renal function and bone mineral density. has resulted in severe. 2002). Becker et al. 2003.S. Noonan et al. maternal blood or maternal urine and birth weight (Nishijo et al. Ezaki et al. 2002. 2005. environmental levels) and health effects is available from ATSDR at: http://www. Workplace exposure to airborne cadmium particulates was associated with decreases in olfactory function (Mascagni et al. 2002) and length at birth (Nishijo et al. respectively. Salpietro et al.S.. data (CDC. Waalkes (2003) provides an overview and summarizes potential mechanisms for carcinogenicity. Wennberg et al. Biomonitoring Information Blood cadmium reflects both recent and cumulative exposures.. with peak values observed in the fifth to sixth decades (CDC. 2003. Small epidemiologic studies have noted an inverse relationship between cadmium in cord blood. For NHANES 19992000. In adults aged 60 years and older. 2002. 2002). 2003. In the typical environmental exposure. People who are occupationally exposed may have blood and urine cadmium levels that are higher than those of the general population. Wennberg et al. 2002). 1996). Further research is needed to address the public health consequences of such exposure in the United States... urinary cadmium reflects both cumulative exposure and the concentration of cadmium in the kidney... Horiguchi et al. 2002). Blood cadmium levels are about twice as high in smokers compared to nonsmokers (Becker et al.cdc. the risk of low bone mineral density increased by nearly three-fold when the blood cadmium exceeded 1. Suwazono et al. Staessen et al. CDC. 2000. 2006).. Finding a measurable amount of cadmium in blood or urine does not mean that the levels of cadmium cause an adverse health effect. 2003. Workplace standards and guidelines for air exposure to cadmium have been established by OSHA and ACGIH. 1999).Metals greater urine cadmium levels may have an increased risk for bone fracture and diminished bone mineral density (Alfven et al. Creatinine-corrected urine cadmium values in U. Jarup et al...S. 2005. 2002. Chronic inhalation exposure to cadmium particulates was associated with changes in pulmonary function and chest radiographs that were consistent with emphysema (Davidson et al. In this Report the urinary and blood cadmium levels at the 95th and 90th percentiles. 2006. 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). 2005). 1999).. Becker et al. 1988).. 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. Acute and heavy exposure to airborne dusts and fumes. Mannino et al. 2004b. 2004. 2005.. Komaromy-Hiller et al.. Blood and urine cadmium levels are typically higher 202 in cigarette smokers... respectively. Staessen et al.. However. 2003.. 2002. not to imply a safety level for general population exposure.

J Occup Health 2003. No clear-cut evidence for cadmium-induced renal tubular dysfunction among over 10. Jin T. Uemura T. Sanz P.000 women in the Japanese general population: a nationwide large-scale survey. Cadmium and lead in blood in relation to low bone mineral density and tubular proteinuria. Int J Hyg Environ Health 2003.html. Machida M. Urinary cadmium levels predict lower lung function in current and former smokers: data from the Third National Health and Nutrition Examination Survey. diabetes mellitus. Pharmacokinetic/ pharmacodynamics (PK/PD) modeling of risks of kidney toxicity from exposure to cadmium: estimates of dietary risks in the U. Jones RL. Stock AL. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Occup Environ Med 2000. Clin Chim Acta 2000. Neurotoxicology 2003. Lundh T. Machida M. Becker K. Kikuchi Y. and cadmium burden on dietary cadmium absorption in cadmium-exposed female Japanese farmers. Miyamoto K. Howerton K. 2005.110:699-702. Tsukahara T. Grubb A. Agency for Toxic Substances and Disease Registry (ATSDR). Thorax 2004. Lison D. Lukyanova EM.296(1-2):71-90. Anthropometric. Wang H. et al. Elinder CG. Diamond GL. Lancet 1999. et al. Ikeda Y. Holguin F. Oguma E.1(8587):663-667. Available at URL: http://www. Jarup L. Alfven T. Chiappino G. et al. Ukai H. Fayers PM. Bellerup P.atsdr.45:43-52.gov/toxprofiles/tp5. Low level exposure to cadmium and early kidney damage: the OSCAR study [published erratum appears in Occup Environ Med 2002. Choudhury H. Serra J. Hotz P. Tsukahara T. Occup Med 1996. 196:114-123. Fourth National Report on Human Exposure to Environmental Chemicals 203 . Moriguchi J. J Toxicol Environ Health 2003.13(11):1627-1631. Lauwerys R. Taylor AJ.S. Vahter M. Bernard A.46:372-374. Nordberg G. Berglund M. Gadea E. Becker K. Renal effects of low-level environmental cadmium exposure: 5-year follow-up of a subcohort from the Cadmibel study. Olfactory function in workers exposed to moderate airborne cadmium levels.354:1508– 1513. Environ Res 2004b.59:194-8. Sasaki S. Fatal chemical pneumonitis due to cadmium fumes. environmental. et al. Greves HM. Friedman LS. Sasaki S. 206:15-24. Mannino DM. Horiguchi H. Nomiyama T. Carlsson MD. Schulz C. Environ Health Perspect 1994. Seiwert M. iron deficiency. Thayer WC. et al. Venables KM. Dietary exposure to cadmium at close to the current provisional tolerable weekly intake does not affect renal function among female Japanese farmers. Intestinal absorption of dietary cadmium in women depends on body iron stores and fiber intake. 4/8/09 Alfven T. Toxicol Lett 2004. a1-Microglobulin as a promising marker of cadmium-induced tubular dysfunction. Kaus S. Environ Res 2006. Savage-Brown A. Toffoletto F. Comparison of representative ranges based on U. Fukui Y. et al. et al. Seiwert M. Int Arch Occup Environ Health 2003. et al. Miyamoto K.24:717-724.59:497]. Atlanta (GA).57:668-672. Akesson A. Ezaki T. Bo M.96:353-359. Furuki K. Davison AG. Mascagni P.66(Pt A):2141-2164. Tubular and glomerular kidney effects in Swedish women with low environmental cadmium exposure. Osteoporosis and renal dysfunction in a general population exposed to cadmium in China. Consonni D.S.102:83-89. Oguma E. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Furuki K. Krause C. Ye T. Kumagai N. Nermell B. patient population and literature reference intervals for urinary trace elements. Lidfeldt J. Toxicol Appl Pharmacol 2004a. Palomar M. Hellstrom L. Environ Health Perspect 2005.148(1-2):11-20.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. Ash KO.95:20–31. Mucha A. Environ Health Perspect 2002. Seifert B. Dekio F. Ezaki T. Takebayashi T. Moriguchi J. Schulz C. Comprehensive study of the effects of age. Centers for Disease Control and Prevention (CDC). et al. Uptake of cadmium in meals from the digestive tract of young non-smoking Japanese female volunteers. et al. Horiguchi H. ShkiryakNizhnyk AZ. Toxicological profile for cadmium update. Chislovska NV. Costa R. Int J Hyg Environ Health 2002. Darbyshire J. Kundiev YT. Lepom P.205:297-308.76:186-196. Kaus S. Okamoto S. Zhu G. et al. Komaromy-Hiller G. Vahter M. Cadmium fume inhalation and emphysema. Fukui Y. 102:10581066. and dietary predictors of elevated blood cadmium levels in Ukranian children: Ukraine ELSPAC group. Bregante G. Lancet 1988. Third National Report on Human Exposure to Environmental Chemicals. References Akesson A.cdc. 1999 [online]. population. possibly better than b2microglobulin. Jarup L. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Fernandez MA. Nerbrand C. Buchet JP. Pickering CA. Persson B. Environ Res 2004. Ikeda Y.

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98 (7.90-10.S.27) 4.70-5.3) 10.5 (10.5) 10.6) 10.98 (7.1 (11. and high-power gas-ion devices.62) 4.81 (4.13 (7.30) 5.14.60) 7.07-11.7) 10.73-11. population from the National Health and Nutrition Examination Survey.32-5.60) 7.00) 6.26 (3.4) 12.40) 5.10 (8.56-11.74 (4.97) 4.6) 1226 1335 1281 1238 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 4.63 (4.81) 9.3) 9.77-8.45-8.99-6.2-12.86-12.22 (4.29 (4.00-4.64 (4. 2004).9) Total 4.90-10.99-11. and 03-04 are 0.2-13.8-13.7) 884 683 618 568 667 723 821 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.94 (4.70 (6.3) 10.12) 5.9 (11.2-14.81) 4.52-9. although cesium was generally of low toxicity when given to animals.6) 11.14 (4.2-13. Little is known about the health effects of this metal.0-15.30-5.40) 5.8) 11.25) 4.42-7.71 (8.40 (4.35 (4.95-4.1) 11.17 (6.1) 9.4 (10.7 (11.63) 6.55-11.89) 5.40) 7.71) 4.54-11.20-7.3) 10.59) 7.80-11.59-5.90) 7.20) 5.7 (10. respectively.70) 5.42) 7.10 (8.57-5.44 (8.26) 4. scintillation counters. nausea.60-6.70 (4.71-8.20-5.2-13. cesium hydroxide is corrosive and irritating at high concentrations.96 (6.60-6.0) 10.35-5.71-9.36 (6.95 (3.13 (5.08 (6.25-5.95) 5.72-7.61) 7.70) 5.94-4.10-9.5-14.08) 7.39) 7.7 (9.6 (11.05) 5. 7440-46-2 General Information Cesium is a silver-white metal that is found naturally in rock.70 (8.50) 5.89-5.04 (4.0 (9.43 (5. semiconductors. 0.32) 4.59-5.9 (10.90 (6.97 (7.80 (4.05-5.90) 9.40-5.80 (8.17-6.7-14. infrared lamps.26-11.05) 5.77 (4.56 (4.13-8.54) 4.1-12.79 (4.5) 12.33 (6.20 (6.4) 10.84-9.3) 10.80-6.05-5.7) 11.1 (10.60-7.27-5.4 (9.00) 4.29) 4.36) 3.84-5.12-11.64-10.84) 8.34) 9.33 (5.3-15.92-13.40-5. and cardiac arrhythmia (ATSDR.6 (9.64) 5.4) 10.70 (6.60 (7.49) 4.8) 12.4) 9.8) 12.20) 7.90-10.31-8.90-12.20-4. For absorbed cesium salts. Radioactive 137Cs has been used medically to treat cancer.77 (9.33-5.2.90) 5.74-5.08 (7.37) 7. Case investigations of ingestions of large doses of cesium chloride have reported decreased appetite.04) 7.87 (4.0 (10.0-13.7 (9.60 (8.5-16. and 0. and clay.03 (4.8) 12.87 (4.45-5.60-7.90) 4.90 (4.01-6.5) 9.70-8. and as polymerization catalysts.87-7.93 (4.00-8.09) 5.61-6.87) 5.12 (4.8 (10.27 (7.10-5. Urinary Cesium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. Fourth National Report on Human Exposure to Environmental Chemicals 205 . Whether cesium compounds are carcinogenic is unknown. see Data Analysis section) for Survey years 99-00.40-5.55 (4.80 (4.4 (9.68 (7.0) 9.64) 5.50 (4.07) 4.94) 4.7 (8.30 (6.16-6.50 (4. Inorganic cesium compounds are used in photomultiplier and vacuum tubes.60) 5.17) 4.80 (8.02 (4.73-5.9 (11.38) 5.2 (9.25 (3.20) 8.03 (4. soil.10-7.71 (4.81-14.23-4.Metals Cesium CAS No.59 (5.66 (7.08-5.09-5.00-10.70 (9.01) 7. However.35 (4.5-13.50 (4.1) 10.56 (4.6 (9.47-4.52) 7.83-4.7 (9.24) 4.26) 7.34 (4.2) 12.10 (6.20-8.55 (7.3 (8.9 (10.7 (10.4-13.1) 11.01-8.0) 11.50 (7. interval) 4.00-8.99-11.00 (7.16-6.03-4.42) 6.60-12.8) 11.0) 12.62 (5.99) 9.80 (4. Workplace guidelines for cesium hydroxide are available from ACGIH and NIOSH.37) 5.90-12.62 (5.74) Selected percentiles ( 95% confidence interval) 50th 4. the body half-life is estimated to be 70-109 days based on 137Cs exposures.68) 9.97) 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 4.90-8.84 (4.9 (11.30 (6.20 (4.8) 9.81) 4.53-11.7) 10.4) 12.21) 90th 9.50 (6.9) 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 4.2) 11.3 (8.21 (4. 01-02.20) 4.49 (5.10-8.8) 9.94 (4.63-4.60-5.77 (9.00) 7.32 (3.90) 5.47-8.6 (11.70 (5.9 (11.2 (9.64) 4.4) 11.97-7.49) 75th 7.49 (4.70 (8.1-12.80-10.89) 4.10 (6.59-5.13 (8.7) 11.1) 9.23) 9.3-13.72) 4.1-13.40-7.82-4.6 (9.30-10.30) 7.67 (4.64-5.53 (6.88 (8.50) 9.8 (11.0) 11.36 (3.83) 6.80-10.80 (8.91 (7.8 (10.40-11.82) 5.14.86 (7.80-10.00-9.08-5.70) 7.46) 7.3-13. diarrhea.5 (8.7 (10.91-8.40-5.12-5.50-7.76-6.84) 5.4) 95th 11.22-4.1 (9. photographic emulsions.71-5.15-8.43-8.6 (9.69-6. Most human exposure to cesium occurs through the diet.39-4. Human health effects from cesium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.3) 12.80-13.40-11.86-11.99) 7.9) 11. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.0) 12.9) 8.56) 5.5-14.9) 12.87 (4.80) 7.0) 12.

47 (7.56) 4. 1990).64) 5.S.47) 4.3-15.64-6.53 (6.16) 5.54 (5.00-4.49) 3.67 (5.95) 8.33-3.98) 5.29) 5.08-7.19-3.13-9.43 (4.18 (7.55-5.61-3.5) 7.17) 9.44 (4.50) 4.77) 4.27-6.63 (7.10 (3.25) 4.22 (3.02-4.0) 7.10) 7.60 (5.28 (5.12-6.47) 7.11 (5. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.46-4.91-9.10-4.00-5.29) 4.04-5. population.68) 6.3 (9.83-7.95-6.84-7. Two small studies of European populations reported urinary cesium levels similar to U.Metals Biomonitoring Information Urinary cesium levels reflect recent exposure.8) 6.29-3.08 (5.78 (3.96) 4.66 (5.6) 6.88-4.79) 9..12) 3..90-8.99 (3.33 (5.74) 3.3) 9.87-4.59-8.96) 4.04) 5.82) 7.30 (3.56) 3.77 (7. Using clinically submitted specimens.42-4.81 (4.38 (3.31-6.58) 3.76-6.44) 3.18) 8.10 (3.37-3.27 (8.09 (4.53 (4.54 (4.45 (4.08) 3.91-7.42 (4.77-5.07) 8.43 (4.29) 4.93-7.64 (4.74 (5. population from the National Health and Nutrition Examination Survey.99-4.08) 4.20-4.68) 4.35 (4.51 (3.28) 7.39) 5.73-4.22) 6.46 (8.58 (6.64) 9.68 (4.37) 4. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.94 (5.68) 3.50 (7.24 (3.84-9.43 (3.05-4.05-3.99-9.60-10.5) 9.36-3.74-11.96-4.7) 10.S.21-4.03) 5.16-5.04) 6.98 (7.79-5.15) 95th 8.74 (4.30-4.73 (3.72-5.70) 6.90-8.91) 5.66 (6.89-4. 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.41 (4.3) 11.7-12.30) 10.90 (7.47 (4.70) 7.05-3.87) 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 5.34 (5. 2005.65 (6.2) 11.24-4.07-4.53) 6. 2004).41) 9.88-10.16-8.64) 4.63 (6.33 (5.27) 4.81 (4. (2000) found urinary cesium levels that were slightly lower than those reported for the U.85-4.82-4.71) 6.14) 4.63 (4.97) 8.91-6.13-9.2 (8.09) 8.30 (7.08 (3.42-4. interval) 4.78) 4.50 (5.0 (7.57) 3.31 (4.62-8.18-6.86 (4.41-4.18-7.65-3.14-4.9) 10.50) 4.15 (7.84-7.75 (7.78 (3.56 (4.04-11.08) 4.6 (9.36-6.54 (4.2 (8.06 (3.00-9.16-8.20) 5.98 (6.99) 4.35-7.91 (5.21-3.83-6.70 (7.43) 8.95 (5.87 (5.50-5.77 (4.03-5.58 (4.84-9.59) 4.26 (3.0) 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 .46-8. population results shown in this Report (Alimonti et al.91) 4.23 (7.08 (6.95) 4.95 (3.00-10.39 (5.41-7.3) 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 3.20-4.46 (7.22-11.44 (8.12 (3.9 (9.11 (5.8) 10.41 (5.56-10..60) 3.79 (5.79) 4.42 (5.66-6.28 (4.51 (4.31-4.72) 4.80) 6.40) 7.44-9.99-9.65-4.91 (5. and were also roughly similar to those in this Report.06) 4.94) 7.93-9.24-10.02 (5.06 (5.28) 8.15-11.79) 6.27 (6.13) 7.38-7.95-12.48) 7.48) 90th 7.76-9.51 (7.1) 11.92) 3.2) 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 3.20-8.51) 4.87) 5.6 (9.25) Selected percentiles ( 95% confidence interval) 50th 4.56) 4.50 (6.40-5.54 (3.97-4.13 (3.58) 8.29-3.63) 6.05 (4.63-6.71 (7.03) 6. Komaromy-Hiller et al.97-5.48-6.17 (6.30-4.27-4.51 (3.0) Total 4.45-6.26-6. Finding a measurable amount of cesium in the urine does not mean that the levels of cesium cause an adverse health effect.55 (3.3 (8.17) 4.50) 4.74) 75th 5.S.07) 8.38) 10.38 (3.47) 6.31 (4.75-11.06) 5.35 (3.91) 5.35) 3.05) 6.8 (9.00) 6.85) 4.7) 10.4) 10.05) 3.42-6.41) 4.03-6.96-4.83) 8.52-5.50) 8.5) 9.00-8.09) 4.67) 5.60-20.41 (8.44-5.85) 5.63-6.43-11.61 (7.19-6.47) 6.58-5.10 (5.98) 5.38-12.95) 10.64 (8.43-6.46) 6.15-4.72 (4.39) 8.14) 4.14 (6.08-3.51 (4.9 (10.75 (6.21-5.55) 4. Minoia et al.40) 6.92 (5.21 (2.5 (9.68-11.62) 5.66 (5.01-8.14-7.78) 4.20-4.35-11.3 (10.26 (4.96 (4.43 (8. Urinary Cesium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.00 (8.90-3.84-11.17-4.00-5.77 (6.30) 10. Urinary cesium levels were similar in a group of forest fire fighters and residents living near the fire area (Wolfe et al.33-8.8) 5.07 (5.53) 3.36-10.67 (6.14-6.30 (4.27 (6.60 (3.

95:89-105. Komaromy-Hiller G.296(1-2):71-90. Toxicological profile for cesium. Gatti A.Metals References Agency for Toxic Substances and Disease Registry (ATSDR).S. Mincione G. Forte G. Uncertainty of inductively coupled plasma mass spectrometry based measurements: An application to the analysis of urinary barium. Trace element reference values in tissues from inhabitants of the European community I.cdc. Rapid Commun Mass Spectrom 2005. patient population and literature reference intervals for urinary trace elements. cesium. Ronchi P. et al. Voorhees RE. Wood CM. Sci Total Environ 1990. New Mexico. Spezia S. Pietra R. Costa R.atsdr. Paschal D. Mott JA. Apostoli P. Available at URL: http://www. Sabbioni E. 2000. Comparison of representative ranges based on U. Gallorini M. Assessment of urinary metals following exposure to a large vegetative fire. et al. Minoia C. Pozzoli L.html. Ash KO. antimony and tungsten. Atlanta (GA) 2005. Wolfe MI. and serum of Italian subjects.2004 [online]. Third National Report on Human Exposure to Environmental Chemicals. 4/8/09 Alimonti A. Fourth National Report on Human Exposure to Environmental Chemicals 207 . Sewell CM. et al. Howerton K. J Expo Anal Environ Epidemiol 2004. blood.14:120-128.19:3131-3138. Clin Chim Acta 2000. A study of 46 elements in urine.gov/toxprofiles/tp157. Centers for Disease Control and Prevention (CDC).

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 .331-.465) .680 (.750 (.460) .13) 1.25-1.04-1.22 (1.530) .430 (.37-1.690 (.490-. Medical uses include joint and dental prostheses and radioactive cobalt in cancer chemotherapy.03 (.870 (.850) 1.910-1.42) 1.81) 1.470) .430 (. Cobalt is used as a drying agent in paints.519 (.430) .515 (.435 (.750 (.830-1.370-.620-.15 (1.Metals Cobalt CAS No.386) .67) 1.26-2.590-.03) 1.540-.259-.340-.430-. hard metal (alloys of cobalt and tungsten carbide).590 (.900-1.570) .416) . large appliances.460) .290-.410 (.770) . respectively.540) 1.08-1.400-.16 (1.371 (.350-.790-.450-.68 (1.373-.16-1.581) .450) .01-2.12) 1.29 (1.700) .410 (.410-.580 (.373) .564) .417) . interval) .24 (.630-.379 (. 01-02.375 (.414) .950 (.640) .810) .450) .270-.890-1.800) .380-.359 (.600) .460 (.348-.660-.348-.930) .419) Selected percentiles ( 95% confidence interval) 50th .434 (.340 (.900) .07.21) 1.440-.45 (1.427-.46 (1.420) .50) 1.420) .09 (.16-1.630 (.570-.316-.334) .690-.270-.640) .26) Total .940 (. population from the National Health and Nutrition Examination Survey.690-.379 (.960-1.380 (.790) .550 (.394) .06 (.610) .540-.680) .48) 1.410 (.388-.550-.840) .490-. 7440-48-4 General Information Cobalt is a magnetic element that occurs in nature either as a steel-gray.32 (1.270-.670-.03) 1.496) .420 (.370) .372) .610) .523) .338-.07.367 (.48) 1.17 (1.16) 1.02-1.352 (.340) .760 (.17 (1.08) .340) .410) .00) .370-.580 (.327-.03) . and inks.59 (1.650-.99) 1.20 (1.47 (1. blue-colored pigments.364-.398) .410) .680 (.47 (1.319) .04 (.03 (.370 (.03-1.393-.520-.310-.461 (.28-2.53) 1.313) . 0.600 (.900) .339 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.700) .22) 1.04) 1.380 (.710 (.355-.350-.07-1.56) 1.300 (.33-1.510) 1.294 (.940-1.350-.36) 1.630 (. Cobalt compounds are used as catalysts in producing oil and gas.520) .424) .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 .410-.320 (.23) .390 (.28 (1.374 (.50 (1.418 (.540-.890-1.380-. seawater.310 (. steel-belted radial tires.64) 1.487) .530 (.16) 1.01 (.790 (.350) 75th .580 (.316 (. 208 Fourth National Report on Human Exposure to Environmental Chemicals .520 (.431) .800-.760) .17 (.16 (1.460) .S.950-1.520 (.350 (.430) .308-.14-1.740-.860 (. varnishes.520) .543) . and in synthesizing polyester and other materials.01 (.620) .920-1.800-.590) .650 (.660) .32 (1.26-1.333-.450) .08.740-.520-.399) .370-. Cobalt compounds are also used in manufacturing battery electrodes.09) .05) 1.520 (.65) 1.280-.460-.850-1.336-.17-1.530-.01-1.890) .60 (1. It is emitted into the environment from burning coal and oil and car and truck exhaust.450) .285 (.620-.19) .480 (.670 (.28 (1.398 (.28 (1. shiny.369 (.291-. and soil.452 (. and 0.520 (.390 (.75 (1.570-.92) 1.23-2.810) .26) 1.330) .570) .880-1.499 (. and fertilizers.340-.16 (.06-1. It is also a component of porcelain enamel applied to steel bathroom fixtures.410-.09 (.950-1.52 (1.880 (.360-.680) . and 03-04 are 0. industry is imported or obtained by recycling scrap metal that contains cobalt.12) 1.301 (.610 (.05 (.560 (. automobile airbags.33 (1.620-.450-.410 (. and kitchenware.520-.810-.410 (.710) .540-.380 (.930 (.07 (.950) .820 (.81) 1.920) 1.570 (. see Data Analysis section) for Survey years 99-00.06 (.980) .390-.32) 1.300-.390 (.940-1.39) 1.32) 1.14) .404) .470 (. hard metal or in combination with other elements.980-1.73) 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 .73) 1.22-1. Usual human exposure is from food sources. and magnetic recording media.710) 1.330-.47) 1.850) .05 (.870-1.670 (.305-.740 (.469-.460 (.670 (.890-1.430 (.820 (.750 (.660) . Among its many uses are manufacturing superalloys used in gas turbines in aircraft engines.463-.670-.04-1. diamond-polishing wheels.32-2.590-.04-1.26) 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.454 (.343 (.730) 1.360-.44) 1.480-.610-.405-.583) .750-.640) . The cobalt used in U.500 (.502) .330 (.950 (.428-.24 (1.390) . 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.650 (.500) .480 (.870 (.360-.820 (.520-.890) 95th 1.07-1.550) 90th . Cobalt occurs naturally in airborne dust.900) .333-.930-1.377-.600-.431) .S.47) 1.850-1.900-1.15-1.

848 (.50) 1.323) .599) .50) 1.905) .444 (.606 (.963-1.777-.400 (.756 (.488) .313 (.33) 1.03 (.513) .960 (. A nutritional requirement for cobalt other than that contained within dietary cobalamin has not been established.417 (. or using diamond-polishing wheels that contain cobalt metal.487-.215-.593) . 1994.616-.337) .298 (.534-.640) .990) .829-1.29 (1.917) .457 (.738 (.611) .00 (.44 (.594) .634-.00 (.895-1.23 (1.361 (.736-.844 (.547 (.259) .515 (.361 (. 1994).529 (.00 (. an essential human nutrient.550-.274-.365) .723 (.435 (.522) .294-.362-. Cobalt is absorbed by oral and pulmonary routes.275-.449) .73) 1. A portion of cobalt retained for long periods is concentrated in the liver.630-. Once absorbed and distributed in the body.363) .282 (.00 (.407 (.378-.534 (.326-.786-.12-1.842) .290 (.388 (.16 (.932-1.281) .737 (. Cobalt constitutes 4% by weight of vitamin B-12 (cobalamin).296-.343-.479-.781-1.271 (.543) . Lung retention of relatively insoluble cobalt compounds such as cobalt oxide may be prolonged.609) .542 (.425) .574-.314 (.361-.14 (.683-.355) .938) .563-. Smith et al.25 (.439) .929) .29 (1.369 (.500-.19) .689 (.392 (.955) .630-.760-1.304) .04 (.476-.471-.328 (.352) .306) 75th .247 (.829) .279) .248-.792 (.560-.523 (.237-.378-.286) .16 (.495 (.387) .851 (.591 (.327-.481) 90th .313-.983-1.976 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.850-1.508-.704-.00) .673-.352 (.513 (.303-.781) 95th 1.433) .327 (.317 (.313-.626-. population from the National Health and Nutrition Examination Survey.833-1.503-.11-1.635 (.895-1.419) .384) .35) 1.257-. Workplace standards and guidelines for external air exposure to cobalt and several of its compounds have been established by OSHA and ACGIH.393 (.243-.372) .425-. Urinary Cobalt (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.282-.333-.362) .963-1.272-.33) .60) 1.279 (.703-.615) . but with a minor fraction (10-15 %) exhibiting a half-life of several years (Mosconi et al.847) . cobalt is excreted predominantly in the urine.694) .333 (.324-.02 (.28) 1.707) . and to a lesser extent.824 (.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 . Elimination reflects a multi-compartmental model dominated by compartments with half-lives on the order of several hours to a week.306 (.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 .316 (.27) 1.358 (.455 (.660-.523 (.471-.360) .10 (.349) .429) 1.728 (.391) Selected percentiles ( 95% confidence interval) 50th .435-.581) .331-.248-.679-.850 (.964 (.15 (.259 (.600-.691 (.785) .309) .16 (1.983) .388 (.36) 1.821 (.457) .15) 1. 2003).329 (. 1972).324) . refining or processing alloys..750-.500-.391 (. interval) .396) .461) .595) .938-1.408 (.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 .300) .348) .10) . Exposure in the workplace may come from electroplating.733-1.428-.471 (.00) .16) .857-1.09) 1.442-..407) .280-..60) 1.35) .469-.10) Total .452-.949) .378-.582-.662) .396) .291 (.49) 1.821-3.402 (.268 (.585) .334) .11-1. 1972).339-. in the feces.313-.353-.898 (.290 (.700 (.838 (.365-.475 (.667-1.319-.963) .990-1.343 (.302-.278 (.404-.744) 1.250) .426 (.537 (.479) .861 (.872 (.Metals fabricated from cobalt alloys (Lhotka et al.738 (.740-1.30 (1.911-1.830 (.975 (.753-.368) .251-.393-..500 (.487-.337 (.552 (.278-.27) 1.963) .750) .598 (. respectively.259-.24) .17) .277-.04-1. Recent inhalation exposure to soluble cobalt compounds can be monitored by measuring cobalt in urine or blood (Lison et al.290 (.468) .289) .449-. Human studies with 60Co administered as soluble cobalt chloride have reported oral absorption ranging from approximately 1 to 25 % (Smith et al.513-.313-.376 (.29) .632-.54) 1.33) 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 .257 (.329-.342-.29 (1.394) .275-.368) .861-1.310) .467-.647) .368 (.256-.611) .346 (.561) .826-1.900-1.727 (.328) .533 (.937 (.297) .554 (.608 (.386 (.382-.55) .239-.335 (.296) .728) .25 (.667-1.462) .548 (.304-..03-1.774 (.381) .273 (.352 (.12 (.644 (.353 (.700 (.457-.879-1.S.313-.333-.463-.361-.297-.421) .562) .438) .83) 1.753) 1.50 (1. with pulmonary clearance half-lives of from one to two years (Hedge et al.409) .554 (.333-.00-1.792-1.06 (.328 (.417) .708) .562) .955) .301) .57) 1.378 (. 1979).434-.757-1.293 (. using hard metal cutting tools.301-.638-1.669) .952 (..380-.29) 1.804) 1.344-.10-1.505) .362 (.36) 1.234 (.

Lisi. 1985. Cobalt compounds elicited numerous genotoxic effects in both in vitro and in vivo assays (De Boeck et al. For workers exposed to cobalt in the air.. Occupational exposure to cobaltcontaining dusts has caused occupational asthma (Pisati and Zedda.. et al. not to imply that the BEI is a safe level for general population exposure. Toxicol Sci 1999. A clinical and pathological study of twenty-eight cases. Centers for Disease Control and Prevention (CDC).. 1994). 1998).. Atlanta (GA).. Linnainmaa and Kiilunen. 2006. 2001. Sills RC.S. 1988). The ACGIH biological exposure index (BEI) for inorganic forms of cobalt (except insoluble cobalt oxides) is 15 mg/L. White and Sabbioni.S. Blood and urinary concentrations as estimators of cobalt exposure. 1992). has been associated with exposure to dusts that contain cobalt. 1994.. Morgan WKC.53:395417. 210 2006. with mean levels that were about 15-20 times higher than in the general U.. Case reports have also suggested a link between occupational cobalt exposure and cardiomyopathy (Jarvis et al. An industry-wide study of hard metal workers in France observed an increased mortality from lung cancer (Moulin et al. 4/3/08 Christensen JM. Smaller population surveys of European adults reported urinary cobalt levels that were roughly similar U. Information about the BEI is provided here for comparison. 2003) and produced lung cancer in rats and mice after chronic inhalation (Bucher et al..atsdr. 2005 [online].50(13):95-104. Lauwerys and Hoet. 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. Am J Med 1972.. 1993).html. Grumbein SL. 1999). environmental levels) and health effects is available from ATSDR at: http://www. 1990). an interstitial lung disorder with findings that range from alveolitis to pulmonary fibrosis... 1994. Cobalt was once added as a foaming agent to beer. Sci Total Environ 1994..gov/toxpro2. Cobalt compounds appear to stimulate erythropoietin production and were formerly used in the treatment of anemia (Goldberg et al. “Hard metal” disease. 2003. usually in combination with tungsten carbide (Cugell et al. Information about external exposure (i. population results in this Report (Kristiansen et al. Urinary measurements mainly reflect recent exposure. Cobalt-beer cardiomyopathy. population (CDC.cdc. Iavicoli et al. Cobalt compounds are a recognized cause of allergic contact dermatitis (Dickel et al. Finding a measurable amount of cobalt in the urine does not mean that the levels of cobalt cause an adverse health effect. Haseman JK. The respiratory Fourth National Report on Human Exposure to Environmental Chemicals . Thomassen et al. Correlations between air exposure levels and urinary cobalt levels in hard metal fabricators are well documented (Ichikawa et al. biological levels and health effects following exposure to soluble or insoluble cobalt compounds in cobalt blue dyes.e. Small studies of patients with hip replacements using metal alloy prostheses reported increased urinary cobalt concentrations. Bucher JR... Cugell DW. 1972).. A 1982-1992 surveillance programme on Danish pottery painters. MacDonald et al. Dunstan et al. 1989). Available at URL: http://www... 2005.cdc. 1997. 2003). Alexandersson R. Biomonitoring Information Urinary levels of cobalt decline rapidly within 24 hours after exposure ceases (Alexandersson et al. The extent to which cobalt exposure alone causes interstitial lung disease is unknown (Linna et al. 2001. References Alexander CS. IARC has classified cobalt metal with tungsten carbide and other soluble cobalt salts as possibly carcinogenic to humans.. Daniel et al. 2005..gov/ exposurereport/. 1988).49:56-67. Krause et al. 1993). Shirakawa et al. Lison et al. Exposure to soluble cobalt salts will produce proportionately higher urinary levels because they are absorbed better.. 1997). Swennen et al.. Arch Environ Health 1988. a distinction is made between soluble and insoluble (oxides and metallic) cobalt (Christensen and Poulsen. Third National Report on Human Exposure to Environmental Chemicals. Inhalation toxicity and carcinogenicity studies of cobalt sulfate. Roycroft JR. Pharmaceutical preparations of cobalt used in the past as hematinics were associated with the development of overt hypothyroidism (Kriss et al. 2001)... Poulsen OM. Hailey JR. 1998).Metals Toxic effects of cobalt have been encountered in workplace settings. 2003.43(4):299-303. 2001. 1955).. although substantial occupational exposures have produced elevated urinary levels for many weeks. A subclinical decrease in thyroid production was observed in a study of cobalt production workers (Swennen et al. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.. Rubin A. and this caused outbreaks of cardiomyopathy among heavy drinkers in the mid-1960’s (Alexander et al. Persons with occupational exposure to cobalt often have urinary cobalt levels that are many times higher than those of the general population. Perkins DG.

Bozec C. Bourne RB. a study of 13 elements in blood and urine of a United Kingdom population. Sabbioni E. Leghissa P. Hammon E. Chess DG. Metal ion levels after metal-on-metal proximal femoral replacements: a 30-year follow-up. Ghat IS. Cleland D. Toxic trace element reference levels in blood and urine: influence of gender and lifestyle factors. Pradhan C.45:246-247. Laippala P. Barnaby CF.150. Palmroos P. Sci Total Environ 1997. and cobalt metals. Weber A. Kusaka Y. Shirakawa T.20(1):25-31. J Orthop Res 2003. Epidemiological survey of workers exposed to cobalt oxides. Unwin P. Cobalt cardiomyopathy. Ziaee H. Uitti J. Edmonds CJ. Lauwerys R. Kirsch-Volders M. Kiilunen M. Wild P. Blunn G. Cobalt-specific T lymphocytes in synovial tissue after an allergic reaction to cobalt alloy joint prosthesis. Clin Orthop Relat Res 2003. Lung cancer risk in hard-metal workers. Kuska Y. Boca Raton (FL): Lewis Publishers. Health Phys 1972. et al.150(1-3):167-171. Sabbioni E. Stanescu D. Respiratory health of cobalt production workers. Swennen B. Swennen B. Fujimura N. Meyer zum Buschenfelde K-H. X. Lhotka C. Cobalt and antimony: genotoxicity and carcinogenicity. Hoet P. 1985. Goto S.150:177-183.69(3):193-200.55(4):269-276. A report of two cases from mineral assay laboratories and a review of the literature. 3rd ed. Schramel P.36:732-734. Schank M. Buchet JP. Robinson C. Hoher T. Moulin JJ. Thabe H.58(10):631-634. Kriss JP. Dunning SP. Long-term clearance of inhaled 60Co. J Bone Joint Surg Br 2006. Gross RT. Kraus T. Four-year study of cobalt and chromium blood levels in patients managed with two different metal-on-metal total hip replacements. Heki S. Vitali MT. Fourth National Report on Human Exposure to Environmental Chemicals 211 . Occupationallyinduced “isolated cobalt sensitization. Outcome of occupational asthma due to cobalt hypersensitivity. Linnainmaa M. Arch Intern Med 1990. Sanghrajka AP. Goto S. Lasfargues G. Schaller KH. Metal-on-metal versus polyethylene in hip arthroplasty: a randomized clinical trial. Daniel J. Linna A. White MA. et al. oxides. Science 1988. Cannon SR. Biological monitoring of cobalt exposure based on cobalt concentrations in blood and urine.204:147-160. Lison D. Radulescu M. cobalt salts. Peltier A. HoffmannB.Metals effects of cobalt. Bacis M. Thakker DM.88(4):443448. Trace element reference values in tissues from inhabitants of the European Union. Occupational asthma from cobalt sensitivity in workers exposed to hard metal dust. Jarvis JQ. Carnes WH. MacDonald SJ. Sci Total Environ 1994. Meier R. Bunn HF.87(5):628-631. Buchet JP. Urinary cobalt as a measure of exposure in the wet sharpening of hard metal and satellite blades. Dickel H. Dunstan E. Lison D.(1-3):133-139. et al. Sci Total Environ 1994. Biological monitoring of workers exposed to cobalt metal. Co-sensitivity between cobalt and other transition metals. The release of metals from metal-onmetal surface arthroplasty of the hip.51(7):447450. Regulation of the erythropoietin gene: evidence that the oxygen sensor is a heme protein. Iversen BS. J Rheumatol 2001. Sci Total Environ 1998.148:241-248. Cresti R. Diepgen TL. J Trace Elem Med Biol 2006. Contact Dermatitis 2003. et al. Exposure assessment in the hard metal manufacturing industry with special regard to tungsten and its compounds. Salvatori S.95:29-37. Industrial Chemical Exposure: Guidelines for Biological Monitoring. The effect of the diameter of metal-on-metal bearings on systemic exposure to cobalt and chromium. Br J Ind Med 1993. Absorption and retention of cobalt in man by whole-body counting. Mosconi G. Iavicoli I. Weyher I. Cobalt excretion in urine: results of a study on workers producing diamond grinding tools and on a control group. and hard metal dust. Int Arch Occup Environ Health 1997. Tilley S. Am J Epidemiol 1998.216:253-270. Zweymuller K. Christensen JM.34:620-626. DeSantis V. Hedge AG.406:282-296. Am J Ind Med 2003. Lison D. Molders J. Ichikawa Y. Occup Environ Med 1994. salt. Zhuber K. Salama A. Romazini S. Health Phys 1979. Lauwerys R. Smith T.28(5):1121-1128. Zobelein P. Rorabeck CH. Mutat Res 2003. Sabbioni E.242:1412-1415.48:172-173. et al. Lisi P.22:359367. De Boeck M. Goldberg MA. Roto P. Kristiansen J. J Bone Joint Surg Br 2005.44:124-132. Steffan I. Pisati G. McCalden RW. Int Arch Occup Environ Health.50(9):835-842. Chest 1989. Lauwerys RB. Oksa P. 2001. Alessandrelli M. Szekeres T. Thomassen H. Hypothyroidism and thyroid hyperplasia in patients treated with cobalt JAMA 1955.157:117121.533:135-152.” Contact Dermatitis 2001. Zedda S. Kato M. Angerer J.21(2):189-195. Falcone G. Occup Environ Med 2001. McMinn DJ. et al. J Occup Med 1992.

00) 3.50-1.60-4.55-1.96-2.30 (4.51 (1.10) 3.40-6.90 (3.52-1.60-1.30) 2742 2268 2085 1842 2219 2293 2716 3806 3478 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. brass.60-1.20 (2.60) 2.50-2.80-3.30 (2.00) 1.40-2.25) 1.80 (1.80) 1.02) 1.50 (1.75-2.00) 1.70) 4.30-1.80 (5.65 (1.30-1.40 (2.30 (1.20 (3.40) 2.87) 1.70 (1.20) 3.20) 1.60-4.43 (1.10 (2.66) 1.80-2.60) 2.62) 1.80) 1. 0.09) 1.10-3.80) 2.30) 1.36-1.70-1.75) 1.39) 1.80 (1.40) 5.60 (1.14-1.80) 1.20 (1.30-1.60 (2.10) 1.01 (1.60 (4. Aerosolized lead is either inhaled or ingested after it is deposited on surfaces and food crops.50) 5.68-1.00) 2.60) 1.50) 4.60 (1.50 (4.20-1.50 (2.30 (4.50-1.81) 1.90) 1.49-1. 01-02.80) 1.10) 2.50 (3.62 (1.40-6. the main source of lead exposure for the general U.69 (1.10) 1.70) 1.80 (2.00) 3.20-4. and 03-04 are 0.00-1.75-1.60-6.60) 723 898 911 905 1044 856 2135 2231 2081 4207 4772 4525 6-11 years 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 2.37-1. 7439-92-1 General Information Elemental lead is a soft.20 (2.20-1.50 (3. interval) 1.70 (1.70) 2.10-2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.30 (1.69) 1.20 (3.90) 2.20 (3.70) 4.60-1.50) 3.00 (2.00-4.40) 2.90) 3.20) 4.60) 4. 212 Fourth National Report on Human Exposure to Environmental Chemicals .90 (4.30-4.00-5. and for radiation shielding.00-2.70) 1.50-1.900-1.50) 1.900 (.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. malleable. Lead has a variety of uses in manufacturing: storage batteries.50-6.40-5.50 (1.10) 3.48) 1.50-2.70) 1.00) 4.60) 4.50) 1.60) 2.80-4.90-4.60 (2.70-5.70-1. plastics.60) 2.23 (1.90 (1.40) Total 1.30 (1.10-4.10-1.39-1.30 (2.60 (2.20-3.40) 1. Lead was used in plumbing for centuries and may still be present.70 (2.43-1.70) 1.60 (3.10 (1.50 (1.00 (3.70 (2.30-1.10-4.10-6.31) 1.10 (3. antique-molded or cast ornaments.50-4.70) 4.00) 1.70) 3.50-2.40-1.69 (1.80 (1.20 (4.30-5.60) 3. metal alloys (e.20-3. ammunition.45-1.60) 2.40-1.00-4.70 (3.50-5.20) 90th 3.80 (4.19 (1.30 (2.20) 2.10 (2.90-2. see Data Analysis section) for Survey years 99-00.40) 1.80-4.10-3.90) 2.80) 3.10) 1.40) 2.95) 1.20) 4.60) 1.20) 5.40) 3.90-4.70) 1.20 (1.53) 1.50 (2.87 (1.50-1. leaded glass.10-6.10-2.90) 3.80 (1.30 (2.70 (1.00 (4.20-2.00 (6. In the past.90) 1.50) 7.60 (1.80-4.40-3.50-2.80 (1.14-1. bronze).3.70-3.20 (1.37 (1.90-2.70) 3.50) 5.32-1.90 (3.S.50 (2.30-2. such as lead phosphate and tetraethyl lead.40 (1.899-. blue-gray metal that occurs naturally in soils and rocks.40-1.72) Selected percentiles ( 95% confidence interval) 50th 1.60 (1.10-2.10-2.20 (3.91) 1.66 (1.80 (4.52-1.89) 1.10-1.70-4.20-6.93-2.00-1.40-4.70) 3.40 (5.20 (1.22 (1.20 (1.50) 1.36-1.70-2.37 (1.60 (1.90-4.90 (2.70-6.30 (3.00) 1.10 (1.56 (1.50) 2.800-1.00 (1.60 (1.17) .00-4.50 (2.60) 5.14-1. population from the National Health and Nutrition Examination Survey.60) 4.00) 2.70 (2.30-6.36) 1. Since lead has been eliminated from gasoline.30 (2.80) 2. dense.34-1.00) 5.60 (2.40 (2.40-3.50-3. and 0.80) 2.60-2.90) 2.32-1. solders.30) 5.986) .52 (1.50 (1.30-2.80) 3913 4339 4132 4057 4606 4241 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.60) 3.40-2.86) 1.90-4. Lead is most often mined from ores or recycled from scrap metal or batteries.80) 2.60) 5.30) 2.Metals Lead CAS No.70-2.50) 1.20 (3.43 (1.04-1.30-2.60 (2.60) 1.40-3.80 (5.60-1.30) 2.77 (1.90-2.40-1.30 (1.90 (3.60) 4.10) 2.70-2.43) 1.30-2.20 (3.00) 1.25 (1.30-1. Elemental lead can be combined with other elements to form inorganic and organic compounds.40-1.60) 3. lead was added to gasoline and residential paints and used in soldering the seams of food cans.60) 1.00) 2.28.20) 3.50) 4.69) 1. Before the 1980’s.00 (5.80 (3.80 (2.878-1.90 (2.30) 95th 5. respectively.10-8.70 (3.40 (4.20-2.40-1.10-2.90 (1.00 (4.S.00) .46 (1.62-1.75 (1.80-3.10-3.50-4.90) 2.60) 3.70) 4.30 (2.90) 5.900 (.40 (1.20) 3.10 (4.80 (2.90-2.80-3.60) 1.g.90-6.00 (1.10-1.10 (1.90) 2.40) 2.60 (2.40 (1.90) 1.10) 4.90 (3.30-1.50-3.51) 1.60 (3.83 (1.90-3.10-2.70 (1.20-3.40) 4.20 (3.50) 75th 2.80 (1.00) 6.10) 3.25 (1.55 (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.80) 1.30) 2.50-1.90 (3. ceramic glazes.70 (5.60 (1.10-3.55-1.30 (4.50 (2.30 (2.50-5.40 (3.20-3.40 (1.12-1.78 (1.50) 2.40) 1.20) 3.20) .80-5.60 (3.00) 2.10) 5.80-3.71-1.45 (1.10 (2.40-2.43) 1. population was aerosolized lead emitted from combustion engines that used leaded gasoline.3.50 (4.60 (3.00-6.946 (.942 (.70-1.60-2.00) 4.60-3.

50) 2.785) .20 (1. Less common sources of incidental or unique lead exposure are numerous: lead-glazed ceramic pottery.02) 1.10-1.90 (2.808 (.00) .00 (1.51) 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.00 (2.660) .600) .800) .00-2.800-1.40) 3.52-1. 01-02.30) .82 (2.20) .757-.90-3.31 (1.04 (.60 (1.40 (1.50-1. or water contaminated by mining or smelting operations.30) 2.900-1.14 (1.10 (.960-1.04-2.820-1.10) .80) 2.558 (.695 (.07 (.573 (.800) .710-.20 (2.690) 75th 1. lead-based painted surfaces undergoing renovation or demolition.700-.700) .500-.10-1.78-2.10 (1. dust.940 (.70-2.700 (.749) .20 (3. see Data Analysis section) for Survey years 99-00.800 (.753 (.40 (2.10) 2.637-.50) 2.800 (. stained glass framing.540 (.790 (.40) 1.20-1.40) 1.23) .90) 2.800 (.80-3.700-..738) .50 (2.20-1.29 (2.18-1.700) 1. interval) .60 (1.90-2.35 (.50 (2.49 (1.11) 2. However.700-.40) 1.75) 3.833-1.955-1.78-2.Metals occupational (e.80 (1.60-3.700 (.604 (.640-.10 (.935) 1.50-2.730 (.14-1.579-. respectively.1.659 (.30-1.10 (1.40 (2.708-.60 (2.591 (.600-.931) .960 (.564 (.800-.19 (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 1.20 (1. Lead is absorbed into the body after fine lead particulates or fumes are inhaled.70 (2.910-. and contact with soil.75) 4.70 (2.41) 2.815 (.80) 3. Approximately half of the absorbed lead may be incorporated into bone.89) 2.50 (1.80-2.40) 2.90-2. imported children’s trinkets and toys.20 (1.50 (2.990) 2..70) 1.800) .60) 2.66 (2.00-1.10-3.30-1.91) 2.00-2.20) .651) .70) 1.526-. Fourth National Report on Human Exposure to Environmental Chemicals 213 .44-2.30 (2.00) 2.73 (1. In the blood.86) 95th 2.52 (1.90 (1.1.30 (3.60 (1.24-1.480-.10-3.80-2.30) 1.80) 2.30-3. which is the site of approximately Urinary Lead Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.900) .30 (1. pewter utensils and drinking vessels.90-4.752 (.80) 1.20) .00-1. 1991).800) .642 (.20-1.40) 2.560-.00 (1.59-2.848 (.990) 1.90 (2.50-2.10-3.00) 2.06) .72) 1.13) .900 (.30) 1.650) 1.80) 2.40-1.900) .30) 1.636 (.00 (1.10) 1.828) Selected percentiles ( 95% confidence interval) 50th .900 (.10-5.40 (1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.857) .572-.589-.20 (1.33 (2.40 (1.78-2.710-1.70) 2.70-3.40 (1.40-2. absorbed lead is bound to erythrocytes and then is distributed initially to multiple soft tissues and eventually into bone.33-2.795 (.20-2.680) .11 (1. Small amounts of environmental lead also may result from burning fossil fuels (ATSDR.09) 1.30) 1.00) .90-3.80) 1.60-3.14 (1.90) 2. 0.52-1.20) 1.20 (1.700-1.620) 1.40 (2.745-.30-1.595-.677 (.90 (2.600-. lead-contaminated dust in indoor firing ranges.600-.40) 1.680-.600 (.70 (2.64) 2.00 (.900) .30) 2.13-3.900) .30-2.90 (1.07-1.700 (.50) 3.30-1.40 (2.613) .32 (1.718) .915-1.862) .50 (1.900 (.553-.40) 1.31-3. 2000).840 (.50) 1.800-.27 (1.731 (.920 (.620 (.90-2.986) .86 (1.800 (.30) 1. older plumbing systems with leaded pipes or lead soldered connections.628) 1.800-1.59) 1.80 (1.04) 2.10-1.80) 2.00) .20) .590 (.70 (1.80) 3. population from the National Health and Nutrition Examination Survey.20 (1.03-2.900) .680-.900) .20 (2.40) 2.10 (1.86-2.570-.80) 2.920 (. CDC.27) 1.49) 340 368 290 719 762 725 1406 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .40 (1.625-.20 (2.20) 1.70) 3.60-2.600) .40-5.50) 1.641-.90 (1.20-2.90-2.850 (.900-1.50-3.70) 1.661-.40-1. the primary source of exposure in children is from deteriorated lead-based paint and the resulting dust and soil contamination (Manton et al.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. and 03-04 are 0.00) 1.579-.90) 2.600-.30) 2.506-.29) 2.700 (.610 (.40) 2.04) .S. battery and radiator manufacturing) and recreational sources.700-.691-. lead-containing folk remedies and cosmetics.86) 1.616) .33.90) 1.60-1.700 (.822-1. 2007.82 (1.535-.540-.g.10 (1.70) 3.40-1.630 (.23-4.810-1.605) .40-1.923 (.50-2.04 (.10-1.818) .700 (.80) 1.960-1.40-3.600-.00-2.970-1.66 (2.10) 2.21 (2.688 (.640 (.02 (.900-1.20) 1.700-. 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.773) .50) 1.10) .12) 90th 2. Children may also be exposed to lead brought into the home on the work clothes of adults whose work involves lead.00-1.729-.600 (.556-.900-1.22) 1.00) .10 (.625 (.17 (1.60 (1.671-.701) . or after soluble lead compounds are ingested.30-5.80 (2.674) 1.03 (1.62) Total .00 (1.941) . bullet fragments retained in human tissue.70 (2.62-4.97) 4.833 (.10-1.60-2.580-.766 (.800) . and 0.

05 (. 1991.82) 1.731-.31 (1.83 (2.44) 1. 1995.608 (.725) .02) 1.04) 2.07-1.659-. hair.981-1. and iron.708 (.65 (1.696 (.63) 1.43) 2.375 (.404-.77) 2.28) 2.22) 1.41) .571-.50-2.34-1.26) 2.70 (1.918 (.87) 1.03) 1.07 (.24 (1.469 (. with lesser amounts eliminated via the feces.688) .535) .62-2.606-.62-1.988 (.78-4.975-1.638 (.632 (.66 (1.98) 2.380-.01 (.617-.52) 1.603-.15-2.655) 75th 1.26) Total .55 (1.61) 1. and through binding to ion channels and regulatory proteins.645-.38 (2.61) 3.59-3. In 1991.914 (.592-.400) .75-2.882-1.876-1.408-.43 (2.03) 2.06) 1.828-1.709 (.793-1.841-1.00 (.746) . BLLs and associated toxic effects differ in children and adults.10 (1.36-2.92) 2.342-.85) 1.41-1.594-.38 (2. population from the National Health and Nutrition Examination Survey.893) .43) 1.639) .53-1.639 (.625 (. and approximately 40 to 70% of lead in blood comes from the skeleton in environmentally exposed adults (Smith et al.11 (1.79 (1. with a half-life of years to decades. interval) .608-.07) .03 (.67-4.971 (. kidney injury.561-.681-.97) 1.774 (.492-.607-.990 (. BLLs near 10 µg/dL can affect blood pressure in adults and neurodevelopment in children (Bellinger.03) .28-1..644) .85 (1.957-1. 1993.66 (1.703) .37-1.579-.50-2.79) 1.11 (1.38 (2.20) 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 .648 (.918-1.790) .20-3.39-1.09-1.946-1.838) .05-1.86 (1.88) 1.31) 1.781-1.594-.609 (.03-2.46 (2.45 (1.677) .62-3.44 (1.615 (.06) .588-.645-.977) 1.56 (1.828) .68 (1. Schwartz.00 (1.667-. 1995).06 (.47 (2.657) 1.618 (.88-2.508) .670) 1.588-.702-.700-.09-1.61) 1.649 (.569 (.03) 90th 1.621 (.22-2. abdominal pain.19) 1.03) 1.03 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. Lead is cleared from the blood and soft tissues with a half-life of 1 to 2 months and more slowly from the skeleton. based on prospective population studies.20) .718) .914-1.404 (. Approximately 70% of lead excretion occurs via the urine.25-1.56) 3.644 (.436) .11) 1.64-2.71 (1.914 (.02-1.676) .50 (1.96 (1.862-.722 (.988-1.917-1.920-1.05 (1.730) 1.383-.27 (1.702) .739) .870 (.679-.43-1. The toxic effects of lead result from its interference with the physiologic actions of calcium.667-.671 (.22) .601-.47 (1.992-1.83) 1.94 (1.755 (.603-.50-1.763) .992-1.11) .74 (1.08) .18) .72) .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. the Centers for Disease Control and Prevention (CDC) established a BLL of 10 Urinary Lead (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.09) 1.73-2.98 (1.673) .56-3.683-.89-2.09-1.69 (1.639 (.49 (1.88 (1. CDC.79) 2.734) . Lead can cross the placenta and enter the developing fetal brain. 1996).00 (1.667) .655-.702) .56-2.529-.938-1.979 (.64) 2.926 (.03) 2.681-.11 (. Nash et al.633 (.00) .652 (.15-3.62) 2.622 (.698) .898) .587-.933) .963-1.541-.796-1.586-. and nails (Leggett.677 (.88) 2.61) 1.Metals 90% of the body lead burden in most adults.701 (.35) 2.812-1.25-1.765) .571-.938 (.851) .933-1.720 (. Staessen et al. Equilibrated blood lead levels (BLLs) after chronic intake are associated with certain toxic effects.15) 1.64) 95th 2. seizures.559-.48 (1.496 (. 2007).61) 1.94-2.51) 1.78 (2.06 (1.623 (.18) 2.460-.0) 3.88) 2.52 (1.593 (.654) . 2004.89-5.40-1.47) 1.31 (1.97 (1.10) 1.43 (1.641 (. and paralysis.461) .712 (.66) 2.693 (. 1993).55 (1.722 (.758) .04-3.686) .97) 1.962 (.615 (.28) .98-2.583-.15-2.718) 1.64 (1.635 (.01) . encephalopathy.15) 1. 2003.03 (. zinc. Large amounts of lead in the body can cause anemia.17-1. For instance.11-1.682) .58) 1. The skeleton acts as a storage depot.710) .11 (.742) Selected percentiles ( 95% confidence interval) 50th .97-18.10 (.900 (.72-2.605-.551-.S.46 (1.940 (.721 (.510-. through the inhibition of certain enzymes.655) ..37-1.800-.997-1.63) 4. O’Flaherty.18 (1.432 (.853-1.604-.73) 2.50-2.33-1.51 (1.810 (.41 (1.08-2. Additional mechanisms include generating reactive oxygen species and altering gene expression (ATSDR.44 (1.85-2.22-1.753) .14) 1.18) 1.404 (.677-..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 .603 (.612-.65-2.33 (1.698) .887 (.679) 1.33) 2.53) 1.75 (2.31) 1.72-2.29 (1.05-1.428) .623 (.18) 1.00 (1.17 (.658 (.08) .03 (1.720 (.03) .71-2.701) .50) 1.33) 1.31 (2.20) .742) .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 . scant amounts are lost through sweat.725) .85-2.12-1.14 (1.668-.707 (.23 (1.19-5.639 (.22) 1.

Schwartz et al. Pirkle et al. Workplace standards and guidelines for lead exposure and monitoring have been established by OSHA and ACGIH. and low family income (CDC... Schwartz. Fourth National Report on Human Exposure to Environmental Chemicals 215 . subtle or nonspecific neurocognitive effects have been reported at BLLs as low as 20-30 µg/dL (Mantere et al. Telisman et al. and organic lead compounds not classifiable with respect to human carcinogenicity..cdc. reduce sperm count. CDC. 2003. More recently. Biomonitoring Information Blood lead measurement is the preferred method of evaluating lead exposure and its human health effects..000 adults. when the geometric mean BLL was 2. environmental levels) and health effects is available from ATSDR at: http://www. Jones et al.g.. 2000).9 µg/dL) and percentage of children with BLLs greater than 10 µg/dL (1. Temporal declines in children’s BLLs have been found in other developed countries (Wilhelm et al. 1996. Information about external exposure (i. Muntner et al. with overt encephalopathy.. 2005b. 1998).....xls). including minority race or ethnicity. Overall.3 million children tested had BLLs of 10 mg/dL or higher (http://www.atsdr. The U..Metals µg/dL or higher as the level of concern in children. 1995. High dose occupational lead exposure. Korrick et al. 2006). 1999). 2002.. Both drinking water and ambient air standards for lead have been established by the U. premature delivery.S. 1996. Data submitted through state public health programs from 2006 showed that 1. 2007). 1995) and associations between increased bone lead concentrations and blood pressure (Hu et al. the prevalence rate has declined annually since 1994 (CDC.6%) were lower than those from NHANES 1991-1994. adults in the 1999-2000 NHANES sample. Staessen et al. Jones et al (2009) showed that the prevalence of BLLs of 10 µg/dL or greater decreased from 8. respectively. 2001). 2005a).e. adult population has similar or slightly lower BLLs than adults in other developed nations (CDC. 2000). Results of studies of adults with either occupational or environmental lead exposure have shown consistent associations between increased BLLs and increased blood pressure (Nash et al. In occupationally exposed adults. BLLs greater than 10 µg/dL continue to be more prevalent among children with known risk factors. which is an 84% decline. 2002). both the geometric mean (1..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. 2005b). approximately 11.cdc... 2009). EPA.. 1987. though there is greater individual variation in urine lead than in blood and greater potential for contamination. urban residence. residing in housing built before the 1950’s.html. A decrease in BLLs is evident also in adult NHANES results reported over past decades (CDC. Borja-Aburto et al.5 per 100. 1984. 2002a).7 µg/dL and 4. 2003.6% in NHANES 1988-1991 to 1. 1994).S. IARC considers inorganic lead compounds probable human carcinogens. 2006). seizures.. However. the national prevalence rate for adults with BLLs 25 mg/dL or higher was 7.S.4% in NHANES 1999-2004. NTP considers lead and its compounds reasonably anticipated to be human carcinogens. and decrease fertility (Alexander et al.gov/nceh/lead/surv/database/State_ Confirmed_byYear_1997_to_2006. 1991. Urine levels may reflect recently absorbed lead. A general population survey of adults in Italy tested in 2000 found BLLs slightly more than double those reported for U. A general population survey of adults Germany in 1998 reported a geometric mean blood lead concentration of 3.gov/toxpro2. 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.S. Recent studies have suggested that neurodevelopmental effects may occur at BLLs lower than 10 µg/dL (Canfield et al.07 µg/dL (Becker et al. At low environmental exposures. Bellinger 2005. Surveillance data reported by U. higher than 100-200 µg/dL). Low level environmental lead exposure may be associated with small decrements in renal function (Kim et al. 1999). usually with BLLs greater than 40 mg/dL. almost double the geometric mean of 1.S. the geometric mean BLL was 3.S. 2003. Lanphear et al. adult residents. lead in women may be associated with hypertension during pregnancy. and peripheral neuropathy generally occurring at much higher levels (e. and spontaneous abortion (Baghurst et al... BLLs higher than 40 mg/dL can result in proximal tubular dysfunction and decreased glomerular filtration rate leading to interstitial and peritubular fibrosis when high body burdens persist.. Payton et al. 2003). Many animal studies have established the multiple neurotoxic effects of lead (ATSDR. For example. 1996. 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. BLLs reflect both recent intake and equilibration with stored lead in other tissues.. adults in the 19992000 NHANES sample (Apostoli et al. In NHANES 1999-2002 in children 1-5 years old.0 µg/dL in females (Soldin et al.75 µg/dL in U.21% of approximately 3...4% of children had BLLs of 10µg/dL or higher (CDC. particularly in the skeleton. may alter sperm morphology.2 µg/dL in males and 3.

Jones RL. Wager C.8(3):395-401. Angle CR. IARC Monogr Eval Carcinog Risks Hum 2006. 2003-2004. et al. Meyer PA. A longitudinal study of low-level lead exposure and impairment of renal function: the Normative Aging Study. Cognitive deficits with blood lead concentrations < 10 µg/dL in US children and adolescents. 4/14/09 Centers for Disease Control and Prevention (CDC). Kim R. JAMA 1996.1542/peds:2007-3608. Speizer FE. Toxicological profile for lead. Occup Environ Med 1996. Jusko TA. Pediatrics 2009. Jacobson JL.htm. Trends in blood lead levels and blood lead testing among US children aged 1 to 5 yeas. Environ Health Perspect 1993. Lead.atsdr. Environ Res 2000. Leggett RW. Recommendations from the Advisory Committee on Childhood Lead Poisoning Prevention. Borja-Aburto VH.150(6):590-597.87:1-471.123:e376-e385. Korrick S.htm. et al. Semen quality of men employed at a lead smelter. et al. Lanphear BP. Rotnitzky A. Kaus S.115:521-529. Birth Defects Research (Part A). Available at URL: http://www. Atlanta (GA). Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Roberts RR. Neri A.275:1177-1181. Kaufman JD. Cox C. Lead and hypertension in a sample of middle-aged women. Atlanta (GA). Hertz-Picciotto I. Blood lead and chronic kidney disease in the general United States population: 216 Fourth National Report on Human Exposure to Environmental Chemicals . Muller CH. Baj A. Batuman V. Am J Epidemiol 1999. Vimpani FB. Cox C. 2005b. Adult blood lead epidemiology and surveillance—United States.gov/nceh/lead/publications/ books/plpyc/contents. Blood lead reference values: the results of an Italian polycentric study. Weiss ST.10:43-50. Muntner P. 1988-2004. Weiss ST. MMWR Morb Mortal Wkly Rep 2006.cdc. Public Health Rep 2000. Reese YR. Ganzi A. van Netten C. 2002 [online]. Auinger P. Hänninen H. Available at URL: http://www. Inorganic and Organic Lead Compounds. 4/14/09 Centers for Disease Control and Prevention (CDC). Aug 2007 [online]. Lanphear BP. Bavazzano P. Bellinger D. Farias P. Blood lead levels—United States. 4/14/09 Centers for Disease Control and Prevention (CDC). Blanco J. Neurotoxicol 1987. doi:10. Ga.htm. Wigg NR. gov/mmwr/preview/mmwrhtml/mm5420a5. References Agency for Toxic Substances and Disease Registry (ATSDR). Rotnitzky A. Chiodo LM. Becker K. Checkoway H. Pirkle JL.89:330-335.26:359-371. Intellectual impairment in children with blood lead concentrations below 10 µg/dL. Schulz C. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Aro A. Third National Report on Human Exposure to Environmental Chemicals. Int J Hyg Environ Health 2002. Robertson EF. JAMA 1996.cdc.275(15):1171-1176. Hu H.348:15171526. N Engl J Med 2003. CDC. Rios C. Seiwert M. Available at URL: http://www. Kuehnemann TJ. The relationship of bone and blood lead to hypertension.gov/mmwr/preview/mmwrhtml/ mm5532a2. Atlanta. et al. MMWR Morb Mortal Wkly Rep 2005a. Korrick SA. Scand J Work Environ Health 1984. 4/14/09 Alexander BH. Jacobson SW. Apostoli P.cdc. Bellinger D. Hunter DJ. Rojas LM. Lepom P. Hu H. Mantere P.53:411-416. Krause C. Managing Elevated Blood Lead Levels Among Young Children.htm.73:409-420. Ronchi L. Centers for Disease Control and Prevention (CDC).287:1-11.cdc. Acquisition and retention of lead by young children. Homa DM.html. Pediatrics 2004. 4/14/09 Centers for Disease Control and Prevention (CDC). Sparrow D.205:297-308. Preventing Lead Poisoning in Young Children.gov/nceh/lead/ CaseManagement/caseManage_main. Age-specific kinetic model of lead metal in humans. Coresh J. Sci Total Environ 2002.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. Canfield RL. Caldwell KL. Henderson CR. Dietrich K. Baghurst PA. Hu H. Ewers TG. Am J Public Health 1999.101(7):598-616. Payton M.gov/toxprofiles/tp13. 1991 [online]. Available from URL: http://www. McMichael AJ.54(20):513-516. Vupputyuri S.113(4):1016-1022. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. The Port Pirie cohort study: lead effects on pregnancy outcome and early childhood development.55(32):876-879. Cory-Slechta DA.cdc. Luukkonen R. Available at URL: http://www. Manton WI. Teratogen update: lead and pregnancy. Hernberg S. 1999-2002. Brody DJ. Neurodevelopmental effects of postnatal lead exposure at very low levels. Stanek KL. Sparrow D. et al.82:60-80. A prospective follow-up study on psychological effects in workers exposed to low levels of lead. 2005. Neurotoxicol Teratol 2004. Blood lead levels measured prospectively and risk of spontaneous abortion.

Soldin OP. Weiss ST.327:109-113. J Hum Hypertens 1995.209:301305. Use of endogenous. Kaufmann R. Semen quality and reproductive endocrine function in relation to biomarkers of lead. and mercury in blood or urine of children: basis for validation of human biomonitoring data in environmental medicine.Metals results from NHANES III. Paschal DC. Jurasovic J. Flegal AR. Low-level lead exposure and renal function in the Normative Aging Study. Rubin R.S. et al. Rocic B. Environ Health Perspect 1998. Kinetics of lead disposition in humans. Revised and new reference values for arsenic. Nash D. Brody DJ. Cvitkovic P. Blood lead. Lauwerys RR. Schulz D. Gunter EW.289(12):1523-1531. and tibia lead with neurobehavioral test scores in South Korean lead workers. lead. Soldin SJ. JAMA 2003. Environ Health Perspect 1996. Telisman S.140:821-829. Gavella M. Am J Epidemiol 2001. Amery A. Lead. Exposure of the U. Payton M. Hwang KY. IV.106:745-750.118:16-29. Kidney Int 2003. Physiologically based models for bone-seeking elements. Low-level lead exposure and blood pressure. Hickman T. zinc. Sparrow D. dimercaptosuccinic acidchelatable lead. Toxicol Appl Pharmacol 1993. Int J Hyg Environ Health 2006. Stewar WF. Sherwin R. population to lead: 1991-1994. cadmium. Blood lead concentrations in children: new ranges. Lee BK. O’Flaherty EJ.63:1044-1050. Schwartz J. and hypertension in perimenopausal and postmenopausal women.153(5):453464. Lustberg M. Wilhelm M. Kaufmann RB. stable lead isotopes to determine release of lead from the skeleton. Lee GS. and copper in men. blood pressure.9:303-327. Osterloh JD. Roels H. Clin Chim Acta 2003. Schwartz BS. et al. Arch Environ Health 1995. Staessen JA.104(1):60-66.108(1):45-53. 50:31-37. Lee SS. Hu H. Environ Health Perspect 2000. Fourth National Report on Human Exposure to Environmental Chemicals 217 . Am J Epidemiol 1994. Smith DR. Schwenk M. Magder L. cadmium. Hanak B. blood pressure and cardiovascular disease in men. Pizent A. Pirkle JL. Association of blood lead.

inorganic.500) . and organic forms.574) .900) 1.927) .60) 1.00 (.g.300 (.672) . thermometers..363-.300) .800-1.753-1.20-4.776 (.00 (. 218 Fourth National Report on Human Exposure to Environmental Chemicals . see Data Analysis section) for Survey year 03-04 is 0. Atmospheric elemental mercury can be deposited on land and water.500 (.00 (2.30) 4132 4241 03-04 03-04 03-04 .400-.903) Selected percentiles ( 95% confidence interval) 50th .50-3. 1994.40 (3.60-5.00) 1. Woods et al. elemental mercury is absorbed mainly by inhaling volatilized vapor. 7439-97-6 General Information Mercury is a naturally occurring metal that has elemental (metallic). synthetic organomercury compounds were once used in pharmaceutical applications.80) 1. with the highest concentrations occurring in the kidneys (Barregard et al..326 (.g.10-3.800-1.60-6. and mining and smelting.30) 3.800-1.70) 911 856 2081 4525 03-04 03-04 .700) .00 (1. Inorganic mercury exists in two oxidative states (mercurous and mercuric) that combine with other elements.714-.80 (3. 1980. Metabolism of mercury by microorganisms in aquatic sediments creates methyl mercury.90) 90th 3.40 (3.80 (1.90) 3. thermostats and switches).40 (4. constitutes the main source of dietary mercury exposure in the general population.90) 95th 4.40-1. sulfur. solid-waste incineration.800-1.80 (1.900) 1.00) 4.20-4.10) .563 (. Elemental mercury is released into the air from the combustion of fossil fuels (primarily coal).860-1. water can be contaminated by the direct release of elemental and inorganic mercury from industrial discharges.50) 4.800 (.700-.20) 2.400-.S.655-.50) 5. Also. merbromin). IARC. which create an episodic potential for volatization and inhalation of mercury vapor.484) .700-.500-. Hursh et al.40) 1. electrical lamps.S.781 (.60-2.60 (1. such as chlorine (e.50) 2..50-2.30) 1. population from the National Health and Nutrition Examination Survey.80) 3.80 (1..419 (.30-4. Elemental mercury is a shiny.490 (.30) 3. 2007). Imported folk and alternative medicines occasionally are contaminated with inorganic mercury. Other major uses include electrical equipment (e. Inhalation of elemental mercury volatilized from dental amalgam is a major source of mercury exposure in the general population (Halbach.40-1..418-.00 (. phenylmercuric acetate) or topical antiseptics (e. 1993).60-6.877 (.40-2. or oxygen.50) 1.979 (. 1999 .400 (.00) .60) 2085 2293 3478 Limit of detection (LOD.800 (.372) .700-.00) 3.500 (. Inorganic mercury compounds such as mercuric oxide are used in producing batteries and pigments and in synthesizing many organic chemicals.500-. an organic form of mercury. which can bioaccumulate in aquatic and terrestrial food chains. it is oxidized in Total Blood Mercury—2003-2004 Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U. 1998. The kinetics of the different forms of mercury vary considerably.00 (2.00 (2. Elemental mercury is used to produce chlorine gas and caustic soda for industrial applications.2.90-3..60 (1.50-1.. interval) .70 (1.70 (1. Accidental spills of elemental mercury. and mercury compounds are still used as preservatives (e.Metals Mercury CAS No.703-. After elemental mercury is absorbed.40 (4.797 (.900) .814 (. predominantly from fish and other seafood..30) 1.60) 1.919) .90 (1. elemental mercury is used in rituals practiced in some Latin American and Caribbean communities. mercuric chloride).800-1.30-2. have often required public health intervention (Zeitz et al. silver-white liquid (quicksilver) obtained predominantly from the refining of mercuric sulfide in cinnabar ore.12) .30 (2. Survey years 03-04 Geometric mean (95% conf.00-5.g.40) 3.70 (3.02) . thimerosal.70 (4.900) 75th 1. and is distributed to most tissues. Kingman et al.700-. The ingestion of methyl mercury.00-1.90 (4. Poorly absorbed from the gastrointestinal tract.300-.80) 4.600 (.886) .20 (2.700) . and dental amalgam.800 (.60 (2.g.70-2.60-3.90 (1..30 (1.700-. Apart from methyl mercury.285-.40-3.800 (. to form inorganic mercury compounds or salts. may contain inorganic mercury.30-5. sphygmomanometers and barometers. 2002).40-2.00 (.700 (.900) 1. Some cosmetic skin creams from countries other than the U.600) 1. In addition.900 (.689-.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 .30-6.30) 5.472-.20-3.00) 1.

1993)..00 (2. with most elimination occurring through in the feces (Sherlock et al.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 .30-6.90) 90th 1. 1996.900 (.664-1.70) 4.30 (.30) 3. 1973).06-1. 1992.23) . 1993).700 (. for both acute and chronic exposures.256-. 1995.3) 4.. and a useful marker of exposure in epidemiologic studies (Grandjean et al.500-.Metals the tissues to mercurous and mercuric inorganic forms.919) .10) 1.50) 2.700) 2. 1992 and 1999.300) .800 (. 1971).300 (.265-.40) 2.369) 1.40-1. Methyl mercury is incorporated into growing hair.343 (.400-.90 (1. 1991.407) .80 (1.60) 1.600) . 1992)..02 (.10) .200-.825-1..90 (4.70-5..20 (.00-2.700 (. 1969. Geometric mean Survey years (95% conf.800 (.726-1.20-2.80 (3.10 (.820 (.20-3.60 (1..374) . 1994).940) Race/ethnicity (females. interval) Selected percentiles (95% confidence interval) 50th .90) 5. Less than 15% of inorganic mercury is absorbed from the human gastrointestinal tract (Rahola et al.300) .80-3.00) 1.200-.27) .00) 2.30-4.824) 1.70) 1... 2004.70-3.30) 1.800) 1.40 (1. Smith et al.10 (1. 1975..10 (1.70 (1.10 (.00) 4.30 (1.500 (.475) . 1996).329 (.30) 1..00-1.800 (.00 (1.90) 2.317 (. Sandborgh-Englund et al.200-.20-3.70-5.00) . Mercury levels in the cord blood are higher than in the mother’s blood (Stern and Smith.500-.00-2.60) 3.20) .50) 1. thereafter.700-.. 1999-2002.00-6. Human pharmacokinetic studies indicate that methyl mercury declines in blood and the whole body with a half-life of approximately 50 days. 1990).500-1.800-1.800-1.0) 4.20) 1.30-6.50) 1.70 (1.50-12. Smith and Farris.7) 4..300) ...700 (.500-.377) . 2003).20 (2.20) .307 (. population.900 (.200-.541-.667 (.833 (.14 and 0.60 (3.700-.70-6.80) 579 527 370 436 588 806 Limit of detection (LOD. Fourth National Report on Human Exposure to Environmental Chemicals 219 . The slow-phase half-life may be several weeks longer in persons with chronic occupational exposure (Sallsten et al.30-11.300 (..70-3.395) .50) 95th 2.30 (1.50 (2.200 (.60) 1.10) .73) 1.90 (1. Vimy et al.600) .30-2.. Excretion occurs by renal and fecal routes.697-.900-1.60 (2.30 (1. After exposure to elemental mercury.00-2.70) 4.00 (3.500 (. 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. 1998). 16-49 years) Mexican Americans Non-hispanic blacks Non-hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .297-. 2003).299-.871-1.00-3.00 (2.800) .300 (. Myers et al..60 (3.50) 3.10-1.40) 5. and peak urine levels can lag behind peak blood levels by days to a few weeks (Barregard et al. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.01) .40) 1. and the newborn’s levels decline gradually over several weeks (Bjornberg et al.50-2.10 (5.00) 1.50-3.10-3.900 (. a measure of accumulated dose (Cernichiari et al. Vahter et al. excretion of mercury occurs predominantly through the kidney (Sandborgh-Englund et al.60) 2.06 (..14.600 (.20-11. 1998).80) 1.800) . McDowell et al.90) 2.10 (1.90 (4..500-.200-. 1999).70 (1.30-3. 1994.90) 3.300) .00) 6.268-.30-6.40-2.944 (.300) . 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.700-1.738-.900-1. The fraction of methyl mercury absorbed from the gastrointestinal tract is about 95% (Aberg et al.377 (.29) .300) .60 (1.200 (. Transplacental transport of methyl mercury and elemental mercury has been demonstrated in animals (Kajiwara et al.30-5.500-.35 (1.318 (.40-2.00 (2.300 (.00) 7. National Health and Nutrition Examination Survey. Jonsson et al.800) 75th . The half-life of inorganic mercury in blood is similar to the slow-phase half-life of mercury after inhalation of elemental mercury. 2005).S. Methyl mercury enters the brain and other tissues (Vahter et al. urinary mercury levels decline with a half-life of approximately 1-3 months (Roels et al.200-. Suzuki et al.700-1. Lesser penetration of inorganic mercury occurs through the bloodbrain barrier than occurs with either elemental or methyl mercury (Hattula and Rahola..50 (1.. Inorganic mercury and methyl mercury are distributed into human breast milk in relatively low concentrations.60 (1..800-1.269-.700 (.30-4. 1984. Miettinen et al.90 (3.800) 1.10 (3.40 (1. 1994) and then undergoes slow dealkylation to inorganic mercury.20-3.

220 Fourth National Report on Human Exposure to Environmental Chemicals . hypertension. 1987).700-.700-. interval) Selected percentiles ( 95% confidence interval) Sample 95th . and a drinking water Inorganic Blood Mercury Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U. Sakamoto et al. gingivitis. Survey Geometric mean (95% conf.700 (. Rissanen et al. 2006. Oskarsson et al.700-.Metals may be more efficient for inorganic mercury (Grandjean et al. 2004.600 (.600-.500-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Mercury levels in breast milk also decline in the weeks after birth (Bjornberg et al. 2004). 1983).600 (. DeRouen et al.800) . typically after a latent period of weeks to months. Overt poisoning from methyl mercury primarily affects the central nervous system.800) . and progressive constriction of the visual fields.700) 2007 2240 3406 Limit of detection (LOD.500-. Occupational exposure to elemental mercury vapor has been associated with subclinical effects on biomarkers of renal dysfunction (Cardenas et al.600-.500-. which may vary for some chemicals by year and by individual sample.500 (.. maculopapular rash. 1996). dysarthria.500 (. Stern 2005. Although recent investigations have suggested a possible link between chronic ingestion of methyl mercury and an increased risk for cardiovascular disease. Once absorbed.500 (<LOD-. sensory impairments. and pinkish discoloration of the hands and feet (Tunnessen et al. 1995. Acrodynia is a sporadic and predominantly pediatric syndrome historically associated with calomel (mercuric oxide) in teething powders and occasionally other inorganic forms of mercury. Salonen et al. Vupputuri et al. and neurocognitive and behavioral disturbances.500-. fatigue.600) .600) . Bellinger et al... At levels below those that cause acute lung injury. high-dose exposure to elemental mercury vapor may cause severe pneumonitis. depression. 2002.800) 792 842 2060 4453 03-04 03-04 * * < LOD < LOD < LOD < LOD . limb deformities..700) . Low-level exposure from dental amalgams has not been associated with neurologic effects in children or adults (Bates et al.500) . 2005). < LOD means less than the limit of detection. 2003).. Smith et al.800) 4015 4132 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD . the existence of a causal relation is unresolved (Chan and Egeland.. 1963).42.600-.. causing parasthesias. 1993). hearing impairment.600) . 2000.600-.500-..600) * 03-04 03-04 03-04 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .600) . Rice.700 (.. 2005.600) .500-.600) . insomnia..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 . dysarthria. irritability. cerebellar ataxia.500 (<LOD-. 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.700 (..500-.600 (. 2006. Sakamoto et al. overt signs and symptoms of chronic inhalation may include tremor. 2004. 2004).700 (. 1998.600 (. and sleep disturbance (Bidstrup et al. 1995. Inorganic mercury exposure usually occurs by ingestion. Large amounts may cause irritant or corrosive effects on the gastrointestinal tract (Sanchez-Sicilia et al.. The constellation of findings may include anorexia.600) . 2000. Acute. 1951. short-term memory loss. the most prominent effect is on the kidneys where mercury accumulates and may lead to renal tubular necrosis. particularly irritability. Smith et al... In recent epidemiologic studies.. Factor-Litvak et al. 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. High-level prenatal exposure may result in a constellation of developmental deficits that includes mental retardation.600 (. anorexia.600 (..600) . altered physical growth. 2000). population from the National Health and Nutrition Examination Survey. Drexler and Schaller.700 (. 1970.. ataxia. and cerebral palsy (NRC.600) .500-. pain in the extremities..700 (. see Data Analysis section) for Survey year 03-04 is 0. Workplace standards for inorganic mercury exposure have been established by OSHA and ACGIH.600 (.S.600 (.500-.

88 (1..19 (2.330-. A cohort of 1127 U.23) .46) 3.00) 1.76-4.405-. 2006).700 (.66) 3. IARC considers methylmercury to be a possible human carcinogen and elemental and inorganic mercury to be unclassifiable with regard to human carcinogenicity. Sanzo et al. see Data Analysis section) for Survey year 03-04 is 0.442-.520) .440 (. 2003).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 .840) 1. Benes et al.396-.530) . 1995.930-1..60) 619 713 1066 Limit of detection (LOD. Survey years 03-04 Geometric mean (95% conf.S.29) 1. Total blood mercury levels increase with greater fish consumption (Dewailly et al.S.250) .570) .441 (..30) 3. 1998).430 (..430 (.13-2.840-1.S.42) 95th 3. 2009). 2001. population from the National Health and Nutrition Examination Survey.413-. although non-Hispanic black females had higher levels than non-Hispanic white or Mexican American females.05) 3.610-1.495 (.534) .gov/mercury and from ATSDR at: http:// www. Information about external exposure (i.Metals standard for inorganic mercury has been established by U.26 (1..408) . who participated in a 1998 representative population survey (Becker et al. Grandjean et al.00 (.19 (1. 1998).24 (2. Schober et al.cdc.99-6. These men had no occupational exposure to mercury but previously had received dental amalgams at military facilities (Kingman et al.530) . Mahaffey et al.89) 3.88) 287 722 1529 03-04 03-04 .58 µg/L for 4645 adults. 2001.96 (1.46 µg/L for children.55 µg/L.34-3.67-2. 1997. total blood mercury geometric mean levels in females aged 16-49 years did not change. 758 children. Urinary Mercury—2003-2004 Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. range 40 years to 78 years) had an average total blood mercury concentration of 2.08 (1.960 (.33 (2.14.67-3.890 (.90) 2.03-4.atsdr.16 (.430) . Among the three racial/ethnic groups.420 (.93 (1. Kingman et al.509) .08 (1.420 (..480) 75th 1..370) . total blood mercury levels declined slightly in non-Hispanic black and Mexican American children.07 (.24) 1.. Urinary mercury consists mostly of inorganic mercury (Cianciola et al. et al.463) .09 (2. These distinctions can help interpret mercury blood levels in people. slightly higher total blood mercury levels were found in U. average age 33 years.77-2.330-.60 (1. Over the NHANES 1999-2006 survey periods.509) .460 (.530-.14-2.05) 1. the developing fetus may be the most susceptible to the effects of ongoing methyl mercury exposure (NRC. Biomonitoring Information In the general population. the median concentration of blood mercury was 0.840-1.97) 2.16 (1.476 (. However.96 (1. EPA.770-1..350-.31) 2. Urine mercury levels increase as more occlusal surfaces of teeth are filled with mercury-containing amalgams (Becker et al.20 (1.76-3. Clinically observable signs of ataxia and paresthesias may occur when blood mercury levels increase to approximately 100 µg/L after methyl mercury poisoning.28) 1.870-1.39-3. average age 9. environmental levels) and health effects is available from the U.580) . 2003).S..360 (.65) 1. interval) .68 (2.360-. particularly methyl mercury.358 (.447 (. From 1996 through 1998. adult women in several ethnic subgroups (Hightower et al. In Germany the geometric mean for blood mercury was 0..290-.61) 1.340-. 2004. During the same survey periods..78 µg/L for adults and 0.330 (.700-1.12 (.870-1.382-.555) .88-3.e.480 (.gov/toxprofiles.9 years).78-2..304) .433 (.200 (.254 (.160-. and the age-related changes differed across the groups (Caldwell et al.213-.54 (2.416 (. military veterans (mean age 52.460) .280-. In NHANES 19992002.63-2.76-3.313-.epa.60-2.. Fourth National Report on Human Exposure to Environmental Chemicals 221 .360-.14) 90th 2. aged 18 to 69 years.410-.31) 1266 1272 03-04 03-04 03-04 . (2000) studied 1216 blood donors in the Czech Republic (896 men and 320 women.23) 2. and increased slightly in non-Hispanic white children (Caldwell. 2000).8 years. the total blood mercury concentration is due mostly to the dietary intake of organic forms. EPA at: http://www.330-.18) 2. A cord blood mercury level of 85 µg/L (lower 95% confidence bound = 58 µg/L) is associated with a 5% increase in the prevalence of an abnormal Boston Naming Test (NRC.85-2.52) 2.406-.492) Selected percentiles ( 95% confidence interval) 50th .940 (.549) . 2009).01 (.S.400 (. 2002). total blood mercury increased with age.

392-.64-2.358) . 2003).447 (. Finding a measurable amount of mercury in blood or urine does not mean that the level of mercury causes an adverse health effect. ACGIH recommends that the blood levels due to inorganic mercury exposure in workers not exceed 15 µg/L.67 (1.545 (.391) . a biomarker of perturbation in renal tubular function.276 (.90) 618 713 1066 222 Fourth National Report on Human Exposure to Environmental Chemicals .00) 286 722 1529 03-04 03-04 .04-3.Metals 2000). 2006.00) 90th 1.587 (.56) 1266 1271 03-04 03-04 03-04 .463 (.306 (.455-.16) 1.09) 1.400-.30) 1.28 (. among workers with urinary mercury concentrations of 25-35 µg/L or greater (Barregard et al. reversible increase in urinary N-acetyl-glucosaminidase.51-2.196-.343 (.301-.S.476 (.964-1.85) 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 .54 (2.508 (.30) 2.63) 1.86) 95th 2.40 (1.76 (1.376-. Information about the biological exposure indices is provided here for comparison.280-.208-. 2002). DeRouen et al..225-..78-4. 1988..1 µg/L. et al.480) .46-2.12-3. Langworth et al.365 (.599) . and Italian (Apostoli et al.800-1.25 (.417) .217 (.455) .535) 1.522-.65 (1.06 (.07) 1.44) 1.40-1.385-. military veterans with dental amalgams. 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.368) .77 (2.443 (. An expert-panel report recently prepared for the U.S. Urinary mercury levels in recent German (Becker et al. 2002) adult population surveys were similar to those in a U. and on average.62 (1.275) .970 (.S.532 (.79) 1.400) . Czech (Benes et al. Levels in U. Blood mercury levels of women and children in NHANES 19992006 were also below levels established as occupational exposure guidelines (Caldwell.333-.21) 1.455-.785-1. Survey years 03-04 Geometric mean (95% conf. Department of Health and Human Services noted that several studies have observed a modest.307-.32-2.404-.11) 1.88-2. 1992).687) .347) .784) 1.486) Selected percentiles ( 95% confidence interval) 50th .714-1.619-.79 (1.06 (.31 (1.13 (1. representative sample of women aged 1649 years reported in NHANES 1999-2006 (Caldwell.265-.620-. 2009).00 (.667-1..13-2.297 (.566) .969-1.909 (..255 (.525 (.88 (1. Biomonitoring studies provide physicians and public health officials with reference ranges so that they can determine whether people have been exposed to higher levels of mercury than are found in the general population.362 (.18-1.35 (1.11-2.246-. In the study of U.. et al. Biomonitoring data will also help scientists plan and conduct research on exposure and health effects.537) .365 (. Urine mercury and the number of dental amalgams were correlated.01) 2..652) .447-..498) 75th .23-2. The ACGIH (2007) currently recommends that urinary inorganic mercury in workers not exceed 35 µg/g of creatinine. 1998).384 (. population from the National Health and Nutrition Examination Survey.616) .990) .588) .39) 1.. women of childbearing age have generally been much lower than these levels (CDC.32 (1.88-2. Urinary Mercury (creatinine corrected)—2003-2004 Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. 2009).1 µg/L for each surface with a dental amalgam (Kingman et al. the urine mercury increased by approximately 0.03) 2.87) 2.41-2.11) 2.768 (..485 (. interval) . 2005).67 (1.875-1.391-.630) .S.61) 1.696 (.464 (.S. not to imply a safety level for general population exposure.309-.289) .87 (1.472-. mean urinary mercury was 3. 2006).

00 (3.42) 90th 2.23-1.966) .S.832-1.56 (1.420-.22-3.84 (2. 16-49 years) 99-00 01-02 .76) 2.686) .98 (5.45) 2.37) 1.806) .30 (1.650 (.87-4.15-1.54) 595 531 381 442 594 826 Limit of detection (LOD.45 (1.21 (2.658 (.76-5.13 (2.615 (.68-3.27-1.46) 3.709) . 1999-2002.41 (2.09-1.07-2.569-.605-. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.520-.94) 1.30-2.699) 1.508-.32 (1.426-.721 (.774) .41-6.657 (.772 (.99) 1.68) 3.870) .14-2.00 (2.46-4. Geometric mean Survey years (95% conf.846) .639 (.69 (1.05 (2.45-3.410-. Urinary Mercury (creatinine corrected)−Females Aged 16-49 Years Old.63) Sample size 1748 1960 Age group (females) 16-49 years Race/ethnicity (females.Metals Urinary Mercury−Females Aged 16-49 Years Old.522 (.579-.03-2.65) 1.18) 3.47) 1.70 (2.664) Mexican Americans Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .59-5.05 (3.10-2.540-.664) .52) 3.97) 2.77) 2.42-3.99 (2.685 (.39-3.53) 595 531 381 442 594 826 Fourth National Report on Human Exposure to Environmental Chemicals 223 .44) 3.670) 75th 1.92) 3.09-1. 16-49 years) 99-00 01-02 .84 (2.909-1.850-1.526-.35 (1.32) 2.16-5.56) 4.62 (1.580-.55-3.46 (1.61) 1.502-.57-4.892) .520-.56) 3.18 (3.724 (.92) 4.24) 6.97) 2.14 and 0.97) 2.69-3.77) 1.38) 4.582-.81-6.95 (2.06 (.665) Mexican Americans Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .13-4.81 (3. 1999-2002.50 (2.596 (.07) 1.79) 1.691) .03 (.710) 1.99 (3.790) . 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.578-.28 (1.557-.910) .500-.744) 1.32-3.68 (3.650) 1.61-6.31-1.21-3.41 (1.14-1.97 (1.62 (4.665) .565 (.83-3.48 (2.553-.72) 1.99-2.45) 95th 3.930) .00) 2.600 (.04-1.14) 3.719 (.831) .616-.624-.27 (2.30 (2.91-7.30 (2.S.622-.91 (2.824) .650 (.450-.592 (.37 (1.45-2.55) 90th 3.79) 3.04-10.25) 2.22 (.475-.76 (1.620 (.710 (.07-5.723 (. population.655 (.636-.03 (.831) .43-1.560 (.85) 4.631-.53-3.709) 75th 1.62 (3.706 (.31 (1.3) 5.632 (.833) .50-4.51) .45) 2.14. interval) Selected percentiles (95% confidence interval) Survey years 50th .580 (.21 (1.387-.47) 1.51 (3.89 (2.540 (.50 (1.92) 2.16) 5.740 (.41 (1.65-4.799) .742-1.10-4. Geometric mean (95% conf.760 (.501-.39) Sample size 1748 1960 Age group (females) 16-49 years Race/ethnicity (females.27 (1. 1999-2002 Geometric mean and selected percentiles of urine concentrations (in µg/L) for females aged 16 to 49 years in the U.15 (2. population.23-1.42) 2.560-.85-3.656-. National Health and Nutrition Examination Survey.710 (.637) .24-1.810) .35) . interval) Selected percentiles (95% confidence interval) 50th .606 (.17) 95th 5.610-.809) .516 (.03) 1. National Health and Nutrition Examination Survey.

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Toxicol Appl Pharmacol 1996. et al. et al. Leroux BG. Leitao JG.289(13):1667-1674. Mooney TF. 1993-1998. Turner MD. Hislop D. Stern AH. Aguinagalde FX.31:687-700. Farris FF. Smith JC. Methyl mercury pharmacokinetics in man: a reevaluation. Osterloh J. Arch Environ Health 1993. Baser M. An assessment of the cord blood: maternal blood methyl mercury ratio: implications for risk assessment. Environ Res 2005.Metals Sanzo JM. Takahashi Y. Dorronsoro M. Pediatrics 1987. DeRouen TA. Lind B. Sinks TH. Acrodynia: exposure to mercury from fluorescent light bulbs. Smith AE. Amurrio A. Speciation of mercury in the primate blood and brain following long-term exposure to methyl mercury. Maternal-fetal distribution of mercury (203Hg) released from dental amalgam fillings. Smith PJ. Sandler DP.40:413-419. Guo S. Hall LL. Azpiri MA. Lorscheider FL. Kaye WE. Effects of exposure to mercury in the manufacture of chlorine. Imai H. McMahon KJ. Nakazawa M. Longnecker MP. Allen PV.258(4 Pt 2):R939-945. Environ Health Perspect 2002.4(5):981-988. The contribution of dental amalgam to urinary mercury excretion in children. JAMA 2003. Toxicol Appl Pharmacol 1994. Matsuo N.2:117-131. Br J Ind Med 1983. Public Health Nutr 2001. Estimation and validation of mercury intake associated with fish consumption in an EPIC cohort of Spain. Suzuki T. Hum Toxicol 1984.128(2):25125-25126.48(4):221229. Smith JC. 1999-2000. Environ Res 2005. Am J Physiol 1990. Public health consequences of mercury spills: hazardous substances emergency events surveillance system. Toxicol Appl Pharmacol 1994. Hongo T.79:786789. Tunnessen WW.115(10):1527-1531. 226 Fourth National Report on Human Exposure to Environmental Chemicals . Goldberg J. Fisher HL. Environ Health Perspect 2007. et al. Topping G. Bolger PM. Amiano P. Friberg L. Am Ind Hyg Assoc J 1970.97(2):195-200. Burbacher T. Woods JS. Environ Health Perspect 2003. The kinetics of intravenously administered methyl mercury in man. Daniels JL. Yoshinaga J. McDowell M. Mottet NK. Most B. Blood mercury levels in US children and women of childbearing age. Bernardo MF. A review of the studies of the cardiovascular health effects of methylmercury with consideration of their suitability for risk assessment. Vimy MJ. Vahter M. Schober SE.98(1):133-142. Martin MD. Stern AH. The hair-organ relationship in mercury concentration in contemporary Japanese. Patil LS. Newton G.110:129-132. Blood mercury level and blood pressure among US women: results from the National Health and Nutrition Examination Survey 1999-2000.111(12):1465-1470. Orr MF. Vupputuri S. Zeitz P. Whittle K. Vorwald AJ. Effects of occupational exposure to elemental mercury on short term memory. Shen DD.37:245-252.124:221-229. Smith RG. Langolf GD. Sherlock J. Jones RL. Elevation of mercury in human blood from controlled ingestion of methyl mercury in fish.

0 (41.6 (43.2-91.4-61. 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.0) 54.3 (53.9) 62.3 (46.4) 45.1-88.7 (37.4) 76.0) 97.3-91.2 (69.7 (73. 2001).0-110) 90.7 (44. The recommended dietary allowance for adult men and women is 45 µg/day (IOM.7) 86.5-52. respectively.6 (73. 01-02.2) 48. chemical reagents in hospital laboratories.7-47.2 (49. semiconductor and battery industries have begun to use molybdenum.6) Selected percentiles ( 95% confidence interval) 50th 50.8 (67.2) 37.0 (81. Fourth National Report on Human Exposure to Environmental Chemicals 227 .6 (55. 0. Gastrointestinal absorption of molybdenum averages 8893% for dietary intakes of 22-1490 µg/day.2 (63.1-52.6-55.1) 82.6-111) 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 52.9 (40.1-52.5 (74.5) 80. Molybdenum is a nutritionally essential trace element that enters the body primarily from dietary sources.2-59.1-55.9 (73.7) 45. lubricants.5) 60. and 1.5-41. aldehyde dehydrogenase. and xanthine oxidase (Kisker et al.7 (58. At a daily oral molybdenum dose of 24 µg.3 (84.7) 77.8-106) 88. and 03-04 are 0.9 (78.2 (49.7-41.0-56.1 (34.1) 59.7) 78.8 (42.1 (38.4 (34.7 (71.4) 41.6) 121 (103-139) 133 (113-155) 121 (106-143) 153 (126-188) 132 (121-147) 117 (109-129) 135 (119-154) 117 (108-129) 107 (99.6 (40.3) 41.8-90.6-58.0-85.8.8.4-52. hard metal widely used to add strength and hardness and retard corrosion in metal alloys.2 (40.6) 53.5) 85.6) 71.5-52.3-108) 215 (161-278) 169 (145-194) 148 (136-163) 154 (132-180) 158 (130-177) 127 (114-139) 1121 1335 1281 1136 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 47.7-60. 7439-98-7 General Information Elemental molybdenum is a silver-white.3-75.3 (79.7 (36.7-39.0-65. Compounds of molybdenum are also used as corrosion inhibitors.9-83.4 (79.0-53.9 (44.2 (38.9-56.9 (32.5 (49.7-84.2) 150 (128-187) 130 (120-141) 119 (112-130) 119 (105-138) 115 (104-128) 101 (97.7-92.6) 51.0-100) 63.7-122) 93.6-96.7) 51.0) 55.6-46.3 (64.2) 41.7) 46.8) 48.1) 126 (106-147) 109 (94.3) 54.0-77.0 (76.5 (43.2 (55.3-44.2) 40.0 (46.2-59.7-50.2) 52.2-53.0 (43.0-38.7 (50.4) 52.7) 78.6) 71.5-66.7 (45.8) 75.8-108) 87.6 (40.3) 37.2-70. WHO.2 (83.7-68.4-82.5-68.6-82.9-82.3 (47.8-49. 2001. urinary excretion over six days CAS No.0) 62.7-51.2-37.7) Sample size 2257 2690 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 78.1-59. see Data Analysis section) for survey years 99-00.9 (34.3-47. hydrogenation catalysts.8) 46.0-101) 82.4 (80.5 (37.5-124) 108 (92.0 (42.3 (55.3 (71.4) 49.6 (52.1-63. population from the National Health and Nutrition Examination survey. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.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 (98.3) 90th 135 (125-146) 124 (117-130) 111 (105-118) 95th 180 (154-216) 165 (145-176) 138 (133-146) Total 45.9 (33.9 (52. 1997).1) 46.3 (73.3) 65.5.7-73.3-115) 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) 79.9) 67.3) 83.3) 85.2-42.0-62.7 (51.9 (37.5-46.7) 57.9-109) 97.Metals Molybdenum or ore deposits.S.9) 34.8-46.0-71.1-48.0 (48.8) 39.1) 60. which exert homeostatic regulation over molybdenum balance.8-94.9-55.3) 47.2 (61.1-44.4 (48.2) 53.9-55.2-79.5 (48.6 (55.8 (82.6-72.1) 57. Excretion occurs predominantly via the kidneys.5 (41.4 (48.0 (42.4-75.3 (38. inks.9-85.0) 60.5) 47. and in pigments for ceramics.8 (85.1) 35..4 (72.5 (41.4) 56.5) 80.2 (56.1 (91.8) 44.3 (37.8) 40. In humans.6) 93.1-51.0) 39. interval) 45.7-91.1 (71. and paints.5) 44. molybdenum is a cofactor for three enzyme classes— sulfite oxidase.5-91.7-96.5-65.6-62.4) 42.0) 84.5 (67.6-42.5 (81.7) 75th 84. 1996). and the average dietary daily intake of molybdenum is approximately 100 µg/day (IOM.7-105) 69.3 (55.0) 45. More recently.

6 (36.6-61.9-96.6-78.4) 61.4-106) 85.9-45.1 (42. of the ingested dose (Turnlund et al.8-46. 2001).6-61.5-92.6-63.9) 44.5 (50.2-40.8) 61.1) 37.2 (33.3) 61.3) 57.9 (64.5) 73.7 (77.9-87.3-115) 98.1 (49.3 (71.9-71.2-47.S.1-45.6) Selected percentiles ( 95% confidence interval) 50th 41.9 (49.4-185) 106 (94.2 (40.4 (67.5-45.5) 63.9) 92.0-56.3 (55.9) 79.8) 71. 1997).0) 95th 144 (125-171) 130 (120-149) 120 (107-135) Total 42. and urinary levels reflect intake from all sources.0) 44.0 (74.7) 115 (93.5 (40.8 (37.9-118) 91.4) 40.2) 42.3) 56.0) 72.9-40.1-41.2-46.5 (39.8-42.4) 89.8-67.8) 39.6-41.3 (37.3-52.4-41.5 (78.8-47.9 (40.9 (35.5-70.1) 56.4-118) 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 . A long term inhalation bioassay of molybdenum trioxide in mice yielded “some evidence” of carcinogenicity (NTP.4 (78.1-81.4 (40.2 (52.5 (41.5) 71.7) 41.9 mg/kg/day and established a tolerable upper intake level of 0.0-46.6-63.3 (58.5-50. U.5 (83.6 (42.9 (73.0-103) 103 (90.2) 39.1) 101 (83.1-109) 89.5 (40.5-97.6 (36.7-40.0 (58.2-103) 131 (112-179) 123 (107-155) 118 (100-139) 152 (122-181) 136 (117-169) 122 (115-142) 1121 1334 1281 1136 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 42.1) 43.1 (30.0-133) 119 (88.2) 37.1-43.0) 39.2) 37.3) 44.0 (35.2-96.4) 116 (101-126) 104 (88.7-43.2) 55.3-102) 122 (116-147) 123 (109-139) 118 (101-134) 310 368 290 648 762 725 1299 1559 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 40.4) 77.2-41.2 (50.3-59.0) 36.5 (35.1) 65.2 (37.8) 38.9 (64.6 (57. 1999).1 (39.5 (36.9 (36.1 (82.8 (75.7-62.5-99. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.8-47.0-46.7) 45.2-80. at daily oral doses of 95 µg and 428 µg.4-66.2 (69.6-45.3 (51.2) 43.1 (38.6) 43.6) 36.3-44.0) 38.1-34.3 (71.5 (59.4) 47.7) 75th 63.6) 39. Based on studies finding adverse reproductive effects in rats and mice.5) 214 (154-1040) 185 (165-219) 160 (129-257) 112 (78.2 (73. urinary excretion over six days rose to 50% and 67%.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. the Panel on Micronutrients of the Institute of Medicine identified a no observed adverse effect level (NOAEL) of 0.4 (55. In industry.1 (38.1-112) 78.2-65.2) 42.4 (53.1-100) 86.2 (40. Levels of molybdenum Urinary Molybdenum (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.5 (80. and clinical or epidemiologic evidence of adverse effects is limited.4) 60.5-60.7-137) 129 (109-155) 112 (97. interval) 43.6 (71. Molybdenum is generally considered to be of low human toxicity.4) 48.1 (44.7 (66.7) 57.0-120) 85.3) 37.5) 72.8-66.6 (59.5 (65.4 (59.5 (54.1 (37.7-120) 87.0 (80.1-127) 90.5-35.0) 33.5 (34.1 (33.8 (36.5-48.5 (38.1-38.2 (40.9 (39.9) 31. dust and other fine particles produced during refining or shaping of molybdenum or molybdenumcontaining alloys are inhalational pathways of exposure. Chronic exposure to very high levels may result in higher serum uric acid levels and a gout-like illness (Koval’skiy et al.4) 122 (107-133) 109 (99.3) 64. One case-control study suggested a possible link between occupational exposure to molybdenum and lung cancer (Droste et al. EPA.3 (37.0-38.6 (38.7) 62.8) 62.5-69.7-93.3 (36.3 (53.7-38.2-96. but available epidemiologic data are scant.9) 41.1 (54.5-62.7-52.4-76.1-43.3 (83.5 (79.4-42.1) 40.2 (57.. population from the National Health and Nutrition Examination survey.3) 40.4-107) 85.9 (79.2) 38.8-52.2 (36.6-76.9-45.5 (39.9-117) 57.9-42.Metals was 18% of the ingested dose.6-88.7) 42.4) 44.0) 88.3) 41.0-41.4-39.7) 53.4 (37.6) 48.0) 53.1-39.4) 58.3-43.9-61.2-49.9) 173 (130-243) 159 (129-170) 132 (107-158) 85.4 (56.8) 38.2-121) 107 (92.5-119) 90.8 (90..5) 90th 108 (97.3) 43.8-118) 81. respectively.3-46.7 (75.5 (37. Human health effects from molybdenum at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 1993).5 (35.8-84.5 (37.1-79.8) 37.5) 60.03 mg/kg/day in humans (IOM.8) 45.8 (56.S.9) 40.8) 79.7) 112 (95. Biomonitoring Information Molybdenum is an essential element for health.9-68.0) 39.7-100) 77.1-67.9-41.1-40.3-68.3-56.1-39.4 (44.8 (57. 1995).2) 58.3-141) 109 (81.2) 39.5 (65.0) 62.1) 37.5-46.6) 39.5-44. 1961..7 (30.4-120) 101 (84.9 (39.1 (40.7-44.3-45.5 (41.2 (43. and molybdenum has not been systematically evaluated for carcinogenicity by IARC.8-65.3 (36.

S.S. Inductively coupled plasma mass spectrometric determination of molybdenum in urine. Available at URL: http://www. Inductively coupled plasma mass spectrometric determination of molybdenum in urine from a Danish population. Kristiansen J. Kisker C. Sci Total Environ 1998. Turci R. Atlanta (GA). nickel. Food and Nutrition Board. et al. molybdenum. Turnlund JR. Occup Environ Med 1999.. cfm?objectid=070A72C6-E9C1-AE67-4BFAB97AD0F427E8. 2001. vitamin K. Geneva: WHO. these levels were comparable to those reported for adults in smaller European population surveys (Iversen et al. EPA). Yarovaya GA.S. 1313-27-5) in F344 Rats and B6C3F1 Mice (inhalation studies) 1997 [online]. Occupational risk factors of lung cancer: a hospital based case-control study. Aprea C. Minoia et al. Am J Clin Nutr 1995. Sabbioni E. Schleyerbach U. Analyst 1998. 4/14/09 White MA.htm.nap. and retention studied with stable isotopes in young men at five intakes of dietary molybdenum. 2005). manganese. References Centers for Disease Control and Prevention (CDC). boron..123(1):81-85. Molybdenum 1993 [online]. Molybdenum-cofactorcontaining enzymes: structure and mechanism. Sciarra G. 1996. Vermeire PA. TR-462. 144-154. Keyes WR. van Sprundel MP. Zhurnal Obshchey Biologii 1961. iron.php?record_id=10026&page=420. 4/14/09 Iversen BS.. (DC): National Academy Press.66:233-267. Available at URL: http://ntp. 2001). Molybdenum absorption. 4/14/09 Sievers E. 2005. pp. 420-441. Fourth National Report on Human Exposure to Environmental Chemicals 229 . Menne C.216:253-270. Shmavonyan DM. Rees DC. Sabbioni E. White MA. excretion. Trace element reference values in tissues from inhabitants of the European Union. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Rapid Comm Mass Spectrom 2002. Finding a measurable amount of molybdenum in the urine does not mean that the level of molybdenum causes an adverse health effect. Peiffer GL.Metals in urine for the U. edu/openbook. pp. 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. Molybdenum. Available at URL: http://books.epa. U. 1998). In: Trace elements in human nutrition and health. Ann Rev Biochem 1997.gov/index. A study of 13 elements in blood and urine of a United Kingdom population. Standing Committee on the Scientific Evaluation of Dietary Reference Intakes.gov/iris/ subst/0425. Schaub J.22(3):179-191. X. National Toxicology Program (NTP).niehs. Minoia C. Ronchi A. arsenic. Environmental Protection Agency (U. Toxicology and carcinogenesis studies of molybdenum trioxide (CAS No. Koval’skiy GA. White and Sabbioni. Third National Report on Human Exposure to Environmental Chemicals. Changes of purine metabolism in man and animals under conditions of molybdenum biogeochemical provinces. chromium. vanadium. 56:322-327. Gatti A. population were well characterized in NHANES 1999-2000 and 2001-2002 (CDC. Weyler JJ.62(4):790-796. Molybdenum in infancy: methodical investigation of urinary excretion. Van Meerbeeck JP. J Trace Elem Med Biol 2001. 16:1313-1319. 1998.15(2-3):149-154. iodine. copper.nih. silicon. Institute of Medicine (IOM). Washington. Urinary molybdenum concentrations in infants may be slightly lower than those in other age groups (Sievers et al. Schindelin H. Christensen JM. Droste JHJ. and zinc: a report of the Panel on Micronutrients. 2002. World Health Organization (WHO). Dietary reference intakes for vitamin A.

Survey years 99-00 01-02 03-04 Geometric mean (95% conf. 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. as oxidation catalysts in chemical manufacturing. 1998). 230 Fourth National Report on Human Exposure to Environmental Chemicals . see Data Analysis section) for Survey years 99-00. thick-film circuits printed on ceramic substrates.07. carboplatin) in the treatment of cancer. < LOD means less than the limit of detection.04.Metals Platinum CAS No. cisplatin.g. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th < LOD < LOD < LOD 90th < LOD < LOD < LOD 95th < LOD < LOD < LOD Sample size 2465 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.S. copper. Human health effects from platinum at low environmental Urinary Platinum Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. 01-02. Platinum-rhodium and platinumpalladium crystals are used as catalysts in petroleum refining and in vehicular catalytic converters to control exhaust emissions. which may vary for some chemicals by year and by individual sample.. and high catalytic activity. Platinum compounds are used in electrodes. Platinum-rhodium compounds are also used in glass and glass-fiber manufacture and in hightemperature thermocouples. Higher environmental soil concentrations of platinum from vehicular emissions have been found near roadways (Farago et al. and iron. dental alloys. respectively. 7440-06-4 General Information Platinum is a silver-gray.04. lustrous metal found naturally in extremely low amounts in the earth’s crust and is typically associated with sulfide-ore bodies of nickel.. however. 0. population from the National Health and Nutrition Examination Survey. and 03-04 are 0. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. strength at high temperatures. jewelry. Important properties of platinum are resistance to corrosion. and as drugs (e. and 0.

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

9:152-158. Schulz C. Schierl R. Platinum-industry and precious-metal workers had urinary concentrations about one-thousand times higher than general populations (Schierl et al. ruthenium. Blanks R. 1997. Pethran A. New York: John Wiley & Sons.. Levels of platinum in urine for the U.10:63-71. Gromiec JP.. and platinum. Environ Res 1975a. Stara J: Preliminary studies on the toxicity and metabolism of palladium and platinum. Saindelle A. Influences on human internal exposure to environmental platinum. Raab W. Part 1: monitoring of urinary concentrations. Biomonitoring Information Urinary platinum levels reflect recent exposure. International Journal of Hygiene and Environmental Health 2003. Environmental Health Criteria 125. Urinary platinum levels associated with dental gold alloys. Stara J: Biological fate of a single administration of 191Pt in rats following different routes of exposure.19:685-691. 2003. Hauff K.. 1991 [online]. Jankofsky M. et al.htm. 1999. eds. 232 Fourth National Report on Human Exposure to Environmental Chemicals . Wilhelm M. Fries HG.org/documents/ehc/ehc/ehc125. et al. Stilianakis NI. Schierl R. 289-380. Arch Environ Health:1969.13(1):24-30. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.. Several studies have shown that background concentrations in general populations were usually less than 0. which elevate urinary platinum by five to twelve-fold (Begerow et al. Hebert R. J Expo Anal Environ Epidemiol 2003. Ruff F: Histamine release by sodium cholorplatinate. Kulka U. van de Weyer C. and gold excretion of patients after insertion of noble-metal dental alloys. Schierl R. Occup Environ Med 2004. Czerczak S. Herr et al.. 1998). In: Bingham E. Schierl et al... Powell CH.. rhodium. 2003. 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. Finding a measurable amount of platinum in the urine does not mean that the level of platinum causes an adverse health effect. Revised and new reference values for some trace elements in blood and urine for human biomonitoring in environmental medicine. 2001).Metals the International Programme on Chemical Safety at http:// www. Petrucci F. Kuster W. Platinum. Gieler U.61(7):636-9. Ruff F: Platinum and platinosis. palladium. Cohrssen B. Seiwert M. Campbell K. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. International Programme on Chemical Safety (IPCS).inchem. Iavicoli I. 206:15-24. Allergy and histamine release due to some platinum salts. Biomarkers 1999. Br J Pharmacol 1969. Senofonte O. Carelli G.76(1):5-10. 3/31/08 Moore W Jr.htm. Schierl. Pethran A. Farago ME. Wilhelm et al. Grimm CH. Platinum concentrations in urban road dust and soil. One study found that traffic-control officers had no greater urinary platinum concentrations than office-based control subjects (Iavicoli et al. population were below the limit of detection (0. Nowak D. Parrot JL. Turfeld M. 2003. 2000.123(3):451-454. 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. Begerow J. Ensslin AS. 2004).04 µg/L) in this Report. Fruhmann G. Ewers U.4(1):27-36. Pethran et al.70(3):205-208. 5th ed. Gold-platinum dental restorations were correlated with increased urinary platinum concentrations. Patty’s Toxicology. Int Arch Occup Environ Health 2003. Occup Environ Med 1998. Kelly J. Rommelt H. 2004. Kaus S. et al.. Neuendorf J. Kazantzis G. Hall L. Schierl R. Angerer J. pp. Hysell D.S. osmium.. Schulz C. Bocca B. Int J Hyg Environ Health 2004. Arch Environ Health 2001. Biomonitoring of traffic police officers exposed to airborne platinum. References Becker K. Kavanagh P.005 µg/L (Iavicoli et al. and in blood and urine in the United Kingdom. Moore W Jr. Nickel. Crocker W. Boos KS. Biological monitoring of hospital pharmacy personnel occupationally exposed to cytostatic drugs: urinary excretion and cytogenetic studies.35:313-321. Saindelle A. 1998).org/documents/ehc/ehc/ ehc125. Analyst 1998. Int Arch Occup Environ Health 1997. Alimonti A. Urinary excretion of platinum from platinum-industry workers. et al. Thornton I.207(1):69-73.. Herr CE. Duneman L:Long-term urinary platinum. Uptake of antineoplastic agents in pharmacy and hospital personnel. 2003).inchem. Available at URL: http://www. Environ Health Perspect 1975b. Hysell D.01 µg/L (Becker et al. Seifert B.55(2):138-140. palladium. Huber R. Herr et al.56(3):283-286. 2004) or less than 0.

140-.390-.390) .240-.160-.280) .280 (.160 (.440) . Elimination from the body tissues occurs slowly through urine and feces (Blanchardon et al.360-. Thallium exposure occurs primarily from industrial processes such as coal-burning and smelting.280-.360 (.S.200) .230) .290 (.560) . see Data Analysis section) for Survey years 99-00.150-. the latter being the current major industrial consumer of thallium in this country.134-.350) .280 (.202 (.159 (.190 (.180 (.170-.160 (.400 (.330-.176 (.260 (.190 (.380 (.154-.290) .243) .340-.250-.450 (.430) .197 (.360) .170 (.410-..450 (.185 (.400) .197-.520) .170 (.190 (.181-.220) .330-.470) .270-.172) . 7440-28-0 General Information Elemental thallium is a blue-white metal found in small amounts in soil and in sulfide-based minerals.400-.400 (.270-.400-.190-.167 (.640) .172 (.145-.500) .230) .470) .350 (.370 (.410 (.02.280) .430) .450 (.290-.460) .460) 861 675 618 561 657 723 801 1114 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.340-.210-. Fourth National Report on Human Exposure to Environmental Chemicals 233 .270) .220-.410-.470 (.220) .450) .175) .330-.160-.340-.202 (.350) .240) .350-.430-.390-.218) .260-.280) .290) 90th .179-.163) . thallium was obtained as a by-product of smelting other metals.187-.270) .370-.410-.173) .360-.350-.250 (.250-.300) .200-.210 (.171 (.390) .200 (. 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.510 (.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 .137-.360 (.200) .410-.410 (.217 (.180-.420-. In the past.215) .690) .450 (.177) .170) .320) .420) . Human health effects from thallium at low environmental CAS No. From these and other sources.330-.300-. respectively.230-.420) .200-.490) Total .420) .145-.200-.260) .220 (.170-.225) .430 (.300) .183) .290-.200) .180 (.170-.320-.380-.170-.420) .173) .200 (.145 (.157-.330-.340 (.170-.330) .370) .156-. and 03-04 are 0.240) .500) .146 (.310) .270-.420-.220 (.167-. representing distribution into other tissues.240-.149 (.160-.300 (.Metals Thallium depilatory cosmetics.183) .420-.150-.190 (.156) .300 (.330) .360-.270 (.430 (.147-.270 (.440) .290 (.170) .200) .440 (.260-.400) .230-.430 (.188) .350-.330-.250-.190 (.320) .180-.192) Selected percentiles ( 95% confidence interval) 50th .210 (. It is still used in relatively small amounts in pharmaceutical and electronics manufacturing.220 (.191 (.220 (.160-.440 (.250-. thallium readily crosses the placenta and also distributes into breast milk.410 (.173-.370 (. interval) .390) .185-.230-.200-.250-.590) .470 (.150-.410 (.460-. 2005).400) 95th .196) .155 (.158) .520) .490) .370-.170) .490 (. however.156) .380 (.320) .420-.350-.180 (.220) .400) .630) . 01-02.430-.220) .135-.196) .400) .250) .200 (.310 (.160 (.206) .280-.147-.340) .500) .520) .470) .133-.420) .160-. In addition.370) .400 (.270 (.260 (.200 (.280 (.370 (.162-.360 (.144 (.370 (.230) .239) .184 (.200 (. 0.147-.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 .190 (.160 (.550 (.02.240) .250-.390) .350 (.390-.150-.330-.170 (.210) .290) .410 (.350-.201 (. Thallium disappears from the blood with a half-life of several days.330) .370-.310-.218) .300) .410-.410 (.220) .370 (.420 (.460 (.390-. In the United States.260-.290 (.480) .520 (.390 (.250-.490) .440 (.182-.400-.480) .510) .165) Sample size 2413 2653 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .400 (.360-.320 (.300) .350-.300 (. thallium is produced in a fine particulate form that can be absorbed through inhalation or ingestion.200) .217) .450 (.400 (.148-.159 (.450 (.02.170-.200) .420) .370-.165 (.260 (.180-.380) .220) .490) .480) .360-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.310 (.270 (.160 (.250 (.250-.410) .202) .230 (.430-.390 (.420) .440-.260-.180) 75th .153-.480) .290 (.170-.159 (.430 (.201 (.480) .167-.590) .440 (.260-.370 (.450 (.380-.172 (.450 (.410-.230) .290) .440) . it has not been specifically mined or refined in the United States since 1984.330) .310 (.178) .240-.180-.360 (. and 0.290) .180) .400-.290 (.450 (.150-.340) . population from the National Health and Nutrition Examination Survey.200 (.500 (.400-.220 (.270 (.290 (.340-.370 (.150-.

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

Available at URL: http://www.47(3):223-231. Investigations of thallium-exposed workers in cement factories. Finding a measurable amount of thallium in urine does not mean that the level of thallium causes an adverse health effect. These urine levels are generally comparable to levels observed in earlier studies of general populations (Brockhaus et al. Toxicological profile for thallium.95:89-105. et al.265 people living near a thallium-emitting cement plant in Germany. Minoia et al. Int Arch Occup Environ Health 1981.216:253-270. Long term retention and excretion of 201Tl in a patient after myocardial perfusion imaging. Investigation of a working population exposed to thallium. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.S. Schaller KH. Soddemann H.35(1):4-9. 7/15/09 Blanchardon E..atsdr. 2005. Minoia C. Jackson RJ. Centers for Disease Control and Prevention. 1985). Sabbioni E. 1990. Challeton-de Vathaire C. References Agency for Toxic Substances and Disease Registry (ATSDR). Schmidt M. with concentrations ranging up to 76. Gallorini M. 1992 [online]. 2005.gov/toxprofiles/tp54. population) are thought to correspond to workplace exposures at the threshold limit value of 0..76(1):53-59. Paschal et al. Paschal DC. Schaller et al. Seventy-eight percent of the urine specimens in that study contained greater than 1 μg/L. Pozzoli L. Pietra R. Raithel HJ.Metals (CDC. Morrow JC. Wiegand H. blood.html. Sci Total Environ 1998. Valentin H. Fourth National Report on Human Exposure to Environmental Chemicals 235 . Int Arch Occup Environ Health 1980. Manke G. Intake and health effects of thallium among a population living in the vicinity of a cement plant emitting thallium-containing dust.113(1):47-53. Environ Res 1998. A study of 46 elements in urine. Trace metals in urine of United States residents: reference range concentrations. J Soc Occup Med 1985. Apostoli P. 2005) and are shown with results from NHANES 2003-2004 in this Report. Martin J-C. Cassot G. White MA. Brockhaus A. White and Sabbioni.cdc. and serum of Italian subjects. (1981) studied 1. Urinary concentrations of 100 μg/L in asymptomatic workers (500 times higher than median levels in the U.. et al. Dolger R. Buhlmeyer G.48(4):375-389. Nearby residents were exposed by eating garden plants that had been contaminated by the thallium. 1998).5 μg/L. Sampson EJ. 1980. et al. Trace element reference values in tissues from inhabitants of the European Union. Trace element reference values in tissues from inhabitants of the European community I. 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. Marcus RL.1 mg/m3 (Marcus. Brockhaus et al. Sci Total Environ 1990.. 1981. X. 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. Kramer U. Boisson P. Celier D. Pirkle JL. A study of 13 elements in blood and urine of a United Kingdom population. Radiat Prot Dosim. 1998. Ting BG. Sabbioni E. Ewers U. Third National Report on Human Exposure to Environmental Chemicals. Atlanta (GA).

340) .570 (. respectively.060-.100 (.073 (.300) .140 (.380 (.204) .270-.350 (.210 (.090-.290-.056-. 236 Fourth National Report on Human Exposure to Environmental Chemicals . 0.113 (.082 (.490 (.460) .080) .050-.092 (.180-.250) .410-.200-.250) .180 (.060 (.130) .04.620) .130-.113 (.090 (.070-.00) .230) .280-.410 (.220) .260 (.120-. which is used in the steel industry.260-.470) .270-.101-.088 (.076 (.340-.260-.068) .180-.110-.060 (.210-.270 (.088) .080-.060-.200 (.210 (.062 (.070) .310 (.107 (.070-.080) .110 (.071 (.120) .065 (. 7440-33-7 General Information Tungsten is a steel-gray to tin-white metal that occurs naturally in the earth’s crust.105 (.310-.210 (. Urinary Tungsten Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.460 (. their illness may stem from exposure to cobalt mixed with tungsten carbide rather than to tungsten alone.340-.250) .340-.120) .320 (.116) .190-.470 (.420-.120-.133) .050-.070-.170-.190 (.330-.132) .110) . 01-02.100) .310-.810) .190-.360 (.160 (.330) .230 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.110 (.250-.370-.280 (.120-.310-.084) .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 .160) .520) .400 (. Most background environmental exposures to tungsten are from the soluble forms such as tungstate salts that may occur in drinking water.100) .090-.060-.078) Sample size 2338 2652 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .260) .04.230-.190 (.160-.150 (.690) .650) .350-1.104) .056-.410) 790 680 618 562 649 723 802 1117 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.270 (.050-.100-.100-.350) .087) .560) .095-.320) .140 (. Evidence is lacking for the carcinogenicity of tungsten.590) .090 (.180) . Although workers occupationally exposed to tungsten carbide may develop serious lung disease (“hard metal disease”).062 (.097-.430 (.081 (.100) .350) .53) .111-.220-.190) .430 (.120) .250) .310-.570 (.250-.620 (.050-.300 (. interval) .370 (.064-.069-.180-.080 (.220) .300-.160-.130 (.560) .126) .640 (.090-.550) .093 (.230) .210 (.500 (.310-.250) .060 (.110-.180) .060-.520) .070 (.090 (.076 (.170) . and for producing ferrotungsten.093) .480) Total .130) .270-. and as catalysts in the petroleum industry.110 (.070) .250) .560) .380-.160-.093-.110 (.270 (. Tungsten compounds are used as lubricating agents.670) .550) .140-.090) .140 (.230-.130) .078-.470-.120 (.330 (.084 (.400 (.800) .130) .360-.330-.500) .430-.130-.290-.160) .380-.082-.220) .470 (.160 (.122) .560) .130 (. Little information is available on the toxicity of tungsten.090-.630) . Tungsten is used mainly for producing hard metals.830) .280 (. mainly as scheelite (CaWO4).123-.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 .077-.510 (.370 (.400) .100 (.080 (.530 (. Human health effects from tungsten at low environmental doses or at biomonitored levels from low environmental exposures are unknown.170) .100) .370) .240-.420-.120-.110 (.220 (. and 0.130-.360 (. Occupational exposure is from dusts released during grinding or drilling of hard metals.160 (.440) .430-.090-.080) 75th .210) .470) .Metals Tungsten CAS No.113 (.080 (. bronzes in pigments.084-.230-.190-.800) .380-.070 (.082 (.105) .113 (.290) . see Data Analysis section) for Survey years 99-00.360-.500 (.490) .160 (.090-. which are used in rock drills and metal-cutting tools.082) .120) .290-.095-.04.290) .074-.390) .550 (.160 (.060 (.110) .065-.071-.160-.151) .400-.070 (.100 (.080-.320-.310) .170) .360 (.150) .130) .530 (.100) Selected percentiles ( 95% confidence interval) 50th .092) .560 (.370-.137 (.260-.101 (.120-.180 (.096 (.080) .120-.080-.620) .450-.430 (.080 (.091) .320-.550) .110-.300 (.510-1.070-.170 (.520) .090-.450 (.130-.058-.260 (.070-.086 (.140) 90th .158 (.200) .390 (.092 (.090) .460 (.100) .460 (.580) .770 (.270-.170) .069) .150-.210 (.073-.380-. population from the National Health and Nutrition Examination Survey.073) .400 (.060-. filaments for incandescent lamps.150 (.330) .300) 95th .510-.090-.320 (.080 (.180) .S.135) .060-.100 (.380 (.140-.120) .109) .230-.360) .180) .070) .096-.150 (.790) .070) . and 03-04 are 0.170 (.090) .240 (.530 (.370 (.073-.400 (. and it has not been classified with respect to its carcinogenicity by either IARC or NTP.380) .180-.290 (.190-.460) .090) .140 (.087-.300 (.066-.060 (.350) .950) .430) .120) .100-.

465) .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 .217-.436-1.085-.063-.085) .080-.250-.091 (.081 (.067 (.245-.285) .880) .169 (.279 (.089) .131-.154) .308) .180-.053-.144 (.103-.079) . similar to those in this Report (Schramel et al.209-.Metals Workplace air standards for external exposure have been established by ACGIH and recommended by NIOSH.158) .216 (.823) .055-.431) .170-.167) .155-.057-.066 (.255 (.116 (.214) .176-. population from the National Health and Nutrition Examination Survey.078 (.354) .302-. or exposure that a control group of non-metal workers had mean levels differences.462) .258-.197-.634 (. 1997).060-.086-.233-.090-.253-.075-.500) .061-.099-.739) .064-.078) .077-.605) .146) .200-.130 (.190) .088) .075 (.317 (. Using neutron activation analysis to 2000.283) .145 (.098-.278-.152-.231 (.201) .169) .146 (. 2005).216 (.054-.293 (.064-.174) .497 (.333-.090-.058-.108) .179-.439) Total .075) .067 (.436) .054-.360 (. population in the NHANES 1999-2000 slightly higher values than those found in NHANES 1999.070 (.359 (.28) .301) .074 (.068 (.158) .072 (.081-.151 (.122 (.096) .214-.138 (.333 (.326) .333 (.086) .061-.237) .216-..168 (.538) .121-.098-.071) .727) .107-.240-.073 (.554) .331-.059 (.275 (.. Biomonitoring Information median urinary levels were as much as 15-fold higher than median levels in the U.555 (.133) .353 (.199 (.136-.062 (.167-.200-.339 (.093-.077) .375) .086) .069 (.074) 75th .294 (.065 (.082) .347 (. interval) .167-.255 (.197 (.153-. 2003.203-.124 (.329-.138) .077) .383 (.079) .098-.148) .100) .066 (.215) .150 (.329 (. A study of 14 unexposed adults yielded values that were similar to the 95th percentiles in this Report.081) .143-.136 (.079) .136-.056-.237) .222-.059-.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 .060 (.186 (.126-.094-.358) .080 (.122-.255-.339 (.098 (. (1987) found possibly due to methodologic.136-.124-.120) .063 (.167) .143 (.125) . 2001).198-.084 (.057-.439 (.340 (.072-.139-.075-. 1998).(Kraus et al.065-.063 (.073 (.250 (.426) .091) .059-.133) .431) .459) .071 (.157) .084 (.S.078) .116-.049-.130-.138 (.258 (.308) .299 (.300-.287) .176-.216-.059-.085 (.279 (.069 (.069-.125 (.284) .300-.091) . 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. Workers involved in grinding operations that released tungsten metal into the air had elevated urinary levels that Levels of urinary tungsten reflect recent exposure.071 (.091 (.261-.105 (.111 (. A were more than 900 times higher than the overall geometric nonrandom subsample from NHANES III demonstrated mean of the U.088) .379 (.063-.197) .158 (. Nicolaou et al.158) .104-.083-.217-.091) .452-. population (CDC.224) .084) .139 (.165) .100 (.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 . population.216-.087 (.179-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.286-.301) .231-.333 (.344-.222) .079 (.S.065-.093) .300) .078-.083 (. and 2003-2004 (Paschal et al.797) .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 .136-.667 (.184 (.150-.150-.071 (.083) .106 (.465) .333) .267-.270 (.414) .174 (.094) .070 (.164 (.086) .253 (.077-.392) .265 (.198) .079 (.333 (.122-.187) .341 (..359 (.074) .199 (.120) .065-. measure urinary tungsten.081 (.154) .105 (.385 (.117) .148 (.087) .201 (.267) .095-.364 (.206-.109 (.109-.410-.063-.082) .117 (.056-.121 (.061-.144-.208-.215 (.075 (.079) .094) .060-.188-.453) .426) .301) .078 (.484) .091) .119 (.582) .279 (.072-.119-.139) .484 (.412 (.080-.116) .667) .068-.300 (.161) .133) 90th .205-.237-.181 (.218 (.146 (.197) .211 (.071) .386) .071) .074-.092) .084) .272-.108-.354-.083) . Patients with medically-inserted tungsten found at increased levels in drinking water.073 (.089 (.333) .S.353 (.100) . 2001-2002.063-.095) Selected percentiles ( 95% confidence interval) 50th .083 (.065 (.333-.071-. In whereas the tungsten-worker group had mean urine levels a Nevada community where tungsten was measured and 35 times higher.098) .250 (.431) .306) .073 (.153) .317-.082 (.302-.080 (.315-.439 (.075) .381) .482 (.253) 95th .065) .074-.317) .067-.

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

020) . the primary exposure sources for nonoccupationally exposed persons are dietary (especially root vegetables) and drinking water.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 .005-.016) .007-.053) .009) . or processing.038) .009-.026 (.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 .005-. 0.034-.006-.008) .017-.046 (.041 (.022-.067) .008 (.006-.028 (.043) .006-.023 (.054) .030 (.013 (.010) .017) .015 (.036) .009) .060 (.008-. Natural uranium is a mixture of three isotopes: 238 U (greater than 99%).007-.026) .021 (.007) .016) .031-.008 (.011) .010) .006-.019 (.044 (.009) .040 (.055 (.028-.027 (.008 (.009-.038 (.035) .007-. 235U (about 0.007 (.010 (.018) .022-.008-.006-.031 (.009) * .009-.009 (.036 (. Fourth National Report on Human Exposure to Environmental Chemicals 239 . Since the 1990’s.018 (.036) 883 683 618 568 667 722 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.009-.027 (.062) .011-.012-.027-. and 0.016-. In workplaces that involve uranium mining.006-.033 (.017) .051) .018) .033) .009) .069) .039) .023 (.009) .017) .010-.008 (.026-.020 (.008 (.047 (.158) .008) .008 (.010) * .010) .021) .009) .011 (.006-.016) .007 (.013 (.022 (.007-.007) .009 (. 7440-61-1 General Information Uranium is a silver-white metal that is extremely dense and weakly radioactive. 01-02.064 (.045) .009 (.007-.020-.006-.008 (.017) .020-.037) Total .016 (.035) .040) . Variable concentrations of uranium occur naturally in drinking water sources.027-.017-.019-.007-.026 (.024-.Metals Uranium CAS No.010) .008 (.006 (.026) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.008 (.007 (.012 (.026-.011-.009 (.027) .009) . Thus.050) .041 (. and 234U. including nuclear weapons. see Data Analysis section) for Survey years 99-00.011 (.008 (. and 03-04 are 0.009) .029-.006-.022) .040-.008-.015 (.S.016) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.040 (.019-.009-.010-.037) .037-.088) .006 (.010-.065) .028 (.030-.072) .031 (.018) .056) .010) .025-.018) .017 (. 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.006 (.042 (.036-.007 (.114 (.046 (.016) .005-.036 (.014 (.018 (.007-.008-.007-.012 (.021 (.020-.046 (.015 (.010) .008 (.012-.018-.009 (.013) 90th .005-.007 (.011-.027) .013 (.036-.012) .056) .023) .009 (.010 (.013-.008 (.023-. It usually occurs as an oxide and is extracted from ores containing less than 1% natural uranium.012) .008 (.72%).027 (.014 (.008) .007-.009-.021-.005-.054) .021 (.008-.010-.005.021) .009-.012-.009-.024-.019-.049) .022-.023) .009-.031 (.028 (.011) .013-.034-.010) .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 .011) .011-.007) 75th .007 (.023) .008-.279) .017-.010 (.015 (.007-.028-.037) .007 (.010) * .008-. in some ceramics.007-.006 (. respectively.046 (. Exposure to DU may occur in military personnel from retention internal shrapnel that contains DU or exposure to dust generated from ammunition Urinary Uranium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.021) .031 (.007) .007-.019-.009) Selected percentiles ( 95% confidence interval) 50th .067) .023 (.040-.021-.030 (.013 (.073) .017-.026) 95th .008 (.007 (.012) .006-.006-.065) .045) .009) .034) .027-.052 (.024-.007) .014 (.033 (. DU has been used by the military in armor-piercing ammunition and as a component of protective armor for tanks.027) .007-.036) .014 (. nuclear fuel.029 (.042) .009) .007-.016-.017 (.035-.009) .039) .127) .037) .040) .011) .027 (.017-.048 (.029-.009 (.015-.009 (.015) .031 (.020) .011-.011-. and as an aid in electron microscopy and photography.010 (.012-.009 (.014 (.014 (.027) .054-.046) .009) .053 (.024 (.049) .066) .011) .030 (.030) .012-.004.048) .007-.007-.008) .016-.007-.017-.004.020-.033-.046-.012-.020-.043 (.010 (.007 (.011-.007 (.008 (.026 (. interval) . population from the National Health and Nutrition Examination Survey.010-.006-.013) .013 (. Uranium has many commercial uses.013 (. human exposure occurs primarily by inhaling dust and other small particles.006-.015) .008) .008 (.007-. milling.012 (.039-.010-.012) .013-.037 (.012 (.009-.023-.007 (.009) .023-.016) .009 (.012 (.050) .032 (.011) .011) .023-.063) .010) .012 (.013 (.007) .017) .008 (.

006) .007-.014) .017-.027) .039) .007 (.006-.012-.022-.016-.008 (.008-.005 (.008) .080) .027 (. Health effects from uranium exposure result from chemical toxicity to the kidney. 1992).013 (.013 (.015 (. 240 Fourth National Report on Human Exposure to Environmental Chemicals .012) .008-.007 (.018-.028) .008) .146) . Soluble forms of uranium salts are poorly absorbed in the gastrointestinal tract.054) .024 (.027-.008) .005 (.008-.006) .023-.029) .010-. After long term or repeated exposure.009) .006-.012 (.005-.059 (. Radiation risks from exposure to natural uranium are very low.007 (.027 (.011 (.008 (.009) .008) .056) .008 (.028-.024 (.005-.012-.011-.006) .024-.037 (.100 (.015-.012 (.009) .020 (..011) .007 (.024) .010) .031-.012 (.021 (.010) .014 (.042-.007 (.006-.006-.017-.013 (.040 (.007 (.018-.018-. where limited absorption occurs (less than 5%).006-.024) .010-.017 (.007) . interval) .012) .024) .017-.011 (.011-.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 .007 (.006-.008) .015-.008) .027) .030-.009 (.009-.032) .016-.018) .008) .024-..013 (.022-.051) .016) .007 (.022 (.019-.008 (.009 (.043 (.005-.009) Selected percentiles ( 95% confidence interval) 50th .009-.007-.024) .029) .1%-6% of an ingested dose may be absorbed. kidneys.028) .039) . about 50% of the absorbed dose is eliminated in the urine within the first 24 hours.009-.017) .030 (.019) . After inhalation.061) .007 (.010-.016 (. population from the National Health and Nutrition Examination Survey.005 (.024-.025-.020-.007-.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 . Human health effects from uranium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.035 (.010-.022-.006) .006 (.007 (. 2003).007 (. which represents distribution and excretion.047) .006-.019-.006-.008-.015-.009 (.020-.008) 75th .053) .015-.017 (.025-.016) .007 (.042) .009) .008 (.006-.013 (.006-.026 (.050 (.008) .009) .013 (.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.012 (.007 (.025 (.032) .013) . 0.034 (.016) .006-.009) .008-.006 (.020-.006-.058) .014 (.033) .021 (.010-. Uranium is eliminated in feces and urine.010-.007-. the shrapnel acts as a source of chronic.010-.008 (.010-.008 (.009) .010-.029 (.074) .019) .033 (.015-.008) . liver.045 (.011) * .034 (.026 (.009) .019-.021 (.014) .016-.034-.030 (.016-.024 (.011-.015) .051) .016) .009) .006-.034) .022 (.012 (.028) .006-.019 (.034-.020 (. the initial half-life of uranium is about 15 days (Bhattacharyya et al.017) .009-.020 (.051 (.007-.005-.028 (.013-. Depending upon the specific compound and solubility.010) .009 (.005 (.020) .007 (.006-.009) .008) . low level exposure.007 (.007-.007 (.021) .006-.058) .013) .014) .006-.034 (.014-.006-.033 (.026) .050) .012 (.007-.014-.010 (.008 (.030 (.025) 95th .009) . 2005).009-.027-.044) .025-.012 (.015 (.024) .017) .016) .013 (.015) .025-.007 (.008-. and bones can accumulate uranium with the largest amounts being stored in bones (Li et al.028 (.026 (.006-.020-.004-.006 (.006-.010 (.010) .053) .015 (.006-.008 (.. After exposure to soluble uranium salts.011-.007 (. Studies of persons with chronic exposure to soluble uranium salts in drinking water have not shown kidney Urinary Uranium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.042) .028) .009) * .026-.007 (.005-.021-.010-.048) .011-.007 (.013 (.014-.009-.011) .010) .007-.039) Total .051) .004-.016) .015) .010) .270) .016) .010 (. Inhaled uranium-containing particles are retained in the lungs. In cases of retained DU shrapnel.029 (.034 (.063) .019-.008) .015 (.006 (.019 (.006-.010 (.014) 90th .030) .041) .007-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.005-.029) .018 (.007) .015) .010 (.018-.011) .011-.007 (.016) .011-. with much slower elimination from bone.Metals impact.018-.010) * .013 (.006 (.035 (.005-.050) . the half-life of insoluble uranium in the lungs is several years (Durakovic et al.033 (.027 (.021 (.012) . which can occur occasionally from high occupational exposure.029) .029 (.039) .006) .011-.011-.013) .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 .007) .006 (.019-.027-.S.006-.067) .031 (.077) .025 (.013 (.027-.017-.033 (.022 (.007-.022) .006-.034 (.010-.048) .008 (.030) .030-.019 (.009 (.

cdc. Six workers in a depleted uranium program showed concentrations of 0. 2006). 2002). soldiers evaluated before. 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.110 to 45 μg/L (Ejnik et al. 2004). Vol. Drinking water and other environmental standards have been established by U.e. Older studies have demonstrated urinary uranium concentrations that are consistent with levels in the U. Fourth National Report on Human Exposure to Environmental Chemicals 241 . Finding a measurable amount of uranium in urine does not mean that the level of uranium causes an adverse health effect.S. In a study of 105 persons exposed to natural uranium in well water. Durakovic A. Carmichael AJ. respectively. Uranium content of blood. the median urinary uranium concentration was 2. 2006). Hamilton et al. during. soldiers who had been injured and had embedded DU shrapnel for as long as eight years. Biomonitoring Information Levels of urinary uranium reflect recent and accumulated exposure. Health Phys 2000. A previous nonrandom subsample from NHANES III (n = 499) (Ting et al.atsdr. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 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..61 μg/g creatinine.S.62:562-566. 2006). but in whom no shrapnel was embedded. Guidebook for the treatment of accidental internal radionuclide contamination of workers. Workplace air standards and guidelines for external exposure to soluble and insoluble uranium compounds have been established by OSHA and ACGIH. Karpas et al. Horan P. 28 soldiers who may have been exposed to DU by inhalation.011 μg/L (McDiarmid et al. and no consistent effects on multiple endpoints of kidney function were found.. 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. NRC.55 μg/L (median 0. Health Phys 1992. 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. Volf V. Mil Med 2003. Tolmachev et al. Benedik L. McDiarmid M.S. environmental levels) and health effects is available from ATSDR at: http://www. 2006. although slightly increased during and after deployment.. Dietz LA. References Bhattacharyya MH. Sci Total Environ 1991. Stradling GN. Urinary uranium measurements in 103 Canadian military personnel showed mean urinary levels slightly less than geometric mean in this Report (Ough et al. the geometric mean urinary uranium concentration was 0.S. 2004).078 μg/L (ranging up to 5. 2000). 41 (1).107:143-157.78:143-146. Pullat VR.. Zimmerman I. Third National Report on Human Exposure to Environmental Chemicals. Thomas RG.066 μg/g creatinine (Gwiazda et al. 2006).. Determining the normal concentration of uranium in urine and application of the data to its biokinetics. Kent (England): Nuclear Technology Publishing.1996. Nuclear Regulatory Commission (NRC) has set an action level of 15 μg/L urinary uranium to protect people who are occupationally exposed (U. (May et al. The U. A cohort of 46 U.. Boyd P. 1994. Byrne AR. Recent studies of veterans have been conducted to examine concerns about DU exposure during military conflicts.S. McDiarmid et al.65 μg/L). Galletti... Metivier H. Information about external exposure (i. eds. 1978).Metals injury associated with elevated urinary uranium levels (Kurttio et al. Determination of the isotopic composition of uranium in urine by inductively coupled plasma mass spectrometry. et al. Breitenstein BD. Komaromy-Hiller et al. In the same study..168(8):600-605. In: Gerber GB. pp. 2002. Squibb K. Radiation protection dosimetry. EPA. 1-49. Atlanta (GA). Eighty-five percent of those levels were above the 95th percentile of the NHANES 1999-2000 population. IARC and NTP have no ratings for uranium human carcinogenicity. population. with emphasis on quality control.162 μg/L) (Orloff et al. 1991. the median urinary concentration was 0. 2000).... Centers for Disease Control and Prevention (CDC).. Ejnik JW. had a mean urinary uranium concentration of 0.. 2003. Pillai KC..1992.. 2004). 2001-2002. Muggenburg BA. Hamilton MM. In 17 U. Dang HS. In two studies of a Finnish population with high natural uranium concentrations in their drinking water. 2005.html. In a much larger study of 446 Gulf War veterans who were concerned about past exposure to DU. 1999) and other small populations have shown urinary concentrations that are similar to those in NHANES 1999-2000.. in that the levels were below their respective detection limits (Byrne et al. (Kurttio et al. 2004). urine and hair of exposed and non-exposed persons determined by radiochemical neutron activation analysis. and 2003-2004 (Dang et al. urinary levels of uranium were as high as 9. or wound contamination.. 1992. ingestion.gov/ toxpro2.

Marino R. Paschal DC. U. et al. Cordero S. Environ Health Perspect 2002. Human exposure to uranium in groundwater.S.94:319-326.81:45-51. J Toxicol Environ Health A 2004.47(6):972-982. VI.296(1-2):71-90. Van der Venne MT. Auvinen A. May LM. Clin Chim Acta 2000. and inexpensive method for determination of uranium in urine and fresh water: comparison with LIF. Uranium daily intake and urinary excretion: a preliminary study in Italy. plasma and urine and a critical evaluation of reference values for the United Kingdom population. Howerton K. Health Phys 2004. Kidney toxicity of ingested uranium from drinking water. Kane R. Pekkanen J. Engelhardt SM. Wahl W. Li WB. Lewis BM. Kuwabara J. Squibb K. McDiarmid M. Saha H. et al. Pinto V. Health Phys 2004. Inductively coupled plasma mass spectrometry as a simple. Uranium and thorium in urine of United States residents: reference range concentrations. Noguchi H. Health Phys 2002.110(4):337-342. Biokinetic modeling of uranium in man after injection and ingestion. Gucer P. Kurttio P. Gwiazda RH. Costa R. Scott K. Salonen L.44:29-40. Jarrett JM. Pirkle JL. concentration and daily excretion of uranium in urine of Japanese. July 1978. Shelly T. Ough EA. Squibb K. Roiz J. et al. Charp P. et al. Lorber A.22–Bioassay at uranium mills. Health Phys 2006. Radiat Environ Biophys 2005. Kurttio P. Hancock RG.Metals Galletti M. Bennett LG. Sci Total Environ 1994. McDiarmid MA. NRC). Am J Kidney Dis 2006. Hamilton EI. Roth P. Oliver M.67(8-10):697-714. Englehardt SA.87:51-56.S. Andrews WS. Ash KO. Biological monitoring and surveillance results of Gulf War I veterans exposed to depleted uranium. Detection of depleted uranium in urine of veterans from the 1991 Gulf War. Health Phys 1996. Kalinsky V. Halicz L. Katorza E. patient population and literature reference intervals for urinary trace elements. Health Phys 2003. Int Arch Occup Environ Health 2006. D’Annibale L. Hollriegl V. et al.85:228-235. Jackson RJ. Wilson PD. Paretzke HG. Element reference values in tissues from inhabitants of the European community. McDiarmid MA. Heller J. Cremisini C. Comparison of representative ranges based on U. Karpas Z. Makelainen I. Komulainen H. Environ Res 1999.79(1):11-21. Oberbroekling KJ. Renal effects of uranium in drinking water. rapid. 242 Fourth National Report on Human Exposure to Environmental Chemicals .86:12-18. Auvinen A. Sampson EJ. Smith D. Orloff KG. Sabbioni E. Mistry K. Nuclear Regulatory Commission (NRC) Guide 8.S. Review of elements in blood. Salonen L.71(6):879-85. Oeh U. Nuclear Regulatory Commission (U. Washington (DC): NRC. Karpas Z. Harmionen A. Komaromy-Hiller G. U. et al. Ting BG. An examination of uranium levels in Canadian forces personnel who served in the Gulf War and Kosovo.82(4): 527-532. Tolmachev S. Ejnik J. Military deployment human exposure assessment: urine total and isotopic uranium sampling results. Marko R.158:165-190. Environ Res 2004. Biologic monitoring for urinary uranium in Gulf War I veterans. Saha H.S. Metcalf S.91(2):144-153.

00) 3.70-12.50-3.05.90 (2.0) 13.0) 1335 1229 1485 1293 01-02 03-04 01-02 03-04 01-02 03-04 4.80 (3.30 (5.10-11.20 (8.70-3.40 (8.50 (8.0 (9. 2001-2002 performed on surplus samples (variable unavailable of NHANES website) Fourth National Report on Human Exposure to Environmental Chemicals 243 . fabric dyeing.40) 6.49-3.0 (12.40-6.50) 11.0) 9.40) 2.30) 6. laboratory analysis.70-11.0 (11.21 (2. Survey years 01-02 03-04 Geometric mean (95% conf.60 (4.00-5.02 (3.90) 5.0 (9. potassium.30) 6. In addition.81-16.0 (11.30-17.50) 5. The ammonium salt of the perchlorate ion has been manufactured in the military defense and aerospace industries primarily for use as an oxidizer in solid propellant systems for rockets and missiles.93-3.45-4.51 (3.87-3.01 (2.90 (4.0 (9.0) 9. certain catalytic metals.50-7.50) 6.60-7.0-17.0 (11.50) 3.80) 7.70) 3.80-4.40 (4.0-15.93-4.00) 7.81) Selected percentiles ( 95% confidence interval) 50th 3.40-4.0 (12.40-5.0-17.20 (2.90-11.51 (3.40-4.10-7.S.75 (3.90-12.50-4.0 (10.0) 19.22-5.10) 3.0 (8.38) 5.50 (5.0 (12.80) 75th 6.0 (9.40) 3. 2005).10 (6.0-17.30-6.96 (3.40 (4.0-15. Drinking water.60 (7. small amounts of perchlorate can form naturally in the atmosphere (Dasgupta et al.20) 4.0-17. It is normally found and produced as the anion of a sodium.10) 3. 2002).70 (3.50 (3.30-19.0) 13. but has strong oxidant properties in the presence of concentrated acids.62 (3.60 (4.20 (5.90 (3.30 (5.0-29. Animal and human studies have shown that perchlorate can inhibit thyroid hormone production (NAS.40) 90th 10.31) 2.40 (3.00) 5.0 (11.0) 15.0) 11.0-17..67-5.0) 14.80) 12.26 (2.00-6.46) 3.0 (9.80 (6.20 (4.0-18.0) 13.0-14.70 (3.20-12.70-6.40-13.0) 13.0) 10.0-23.10 (5.0-18.40 (5.0 (11.40 (5.18-3. leather tanning.80-8.60) 5.56) 3.66) 3. Perchlorate is excreted unchanged from the human body with an estimated elimination half-life of about 7.19 (3.0) 11.44-4.0-17.74-3. 2006) and accumulate in nitrate-rich mineral deposits mined for use in fertilizers Urinary Perchlorate Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.70-7.0 (8.55) Sample size 2820 2522 01-02 03-04 01-02 03-04 01-02 03-04 4.90-10.20) 7. 1998).50-4.0) 8. Other manufactured uses include fireworks. 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.11) 3.80-15.70-5.10-12. matches.20-4.30-7.S.54 (3.0 (9. and electroplating.0) 13.20-3.0 (8. Perchlorate has been characterized as a mobile and persistent ground and surface water contaminant. lettuce) can be the main sources of intake for humans (FDA. or ammonium salt.0) 14.80) 3.39-4.0) 10.0) 374 314 828 721 1618 1487 01-02 03-04 01-02 03-04 4.90-9.70-9.93 (4.80-4.07-4.0) 13.30 (2.05 and 0.50-11.11) 4.0) 14. and reducing agents.90-6.20-11.90 (5.0 (11.19-4.40-7. 2007).79 (2.10 (2.00) 4.03) 3.0) 9.0) 95th 14.0 (11.10-11.90 (5. Perchlorate is stable under most environmental and physiological conditions.80-12.00) 3.65) 3.90-3.20-4.0 (12.90 (5.10 (6.0) 12.12) 3.50) 5.80-6. 2005)..16) 3.05 (2.0 (11.10 (7.40) 3.g.47-4. Large doses of perchlorate have been used as a medicine to treat hyperthyroidism and to diagnose disorders related to thyroid or iodine metabolism. Perchlorate was added to the U.0 (9. population from the National Health and Nutrition Examination Survey.80 (7.20) 3.76) 4.0-19.0 (11.90-9.0) 8.60-6. milk.90-11. see Data Analysis section) for Survey years 01-02 and 03-04 are 0.0) 13.0) 10.00-6.0) 15.0 (8.09) 3.20 (4.89-3.5 hours and has a small estimated volume of distribution (Crump and Gibbs.0) 9.20 (7.40) 3.32 (3.0 (13.0) 9.10) 5.30-7.10) 5.0) 9. 7601-90-3 General Information Perchlorate is an inorganic chemical containing one chlorine and four oxygen atoms.0-18.0) 13.68) 4.0) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites 3.S.80 (3.90-3.10) 12.30 (2.88) 3.60) 8.75-3.0) 708 617 681 652 1228 1092 Limit of detection (LOD. interval) 3. and certain plants with high water content (e. and limited applications in pharmaceutics.29-3. EPA’s Contaminant Candidate List (CCL) for drinking water in 1998 following discoveries of its presence in drinking water supplies throughout the southwestern United States (U.Perchlorate Perchlorate (Urbansky.70 (3.0 (11.20 (2.40-11.40 (5.76 (3.0-20.0) 16.EPA.35 (3.0) 11.08-3.0 (8.60) 3.70-3.10-4.22 (2.40) 4.40 (3.90) 6.84) 14.20 (6.

20 (6.50) 9.10-7.0 (11.02-4.40) 3.0) 13.1-14.S.20-9. levels and sufficient in most participants (Tellez et al.00 (2.81-3.80-3. in a representative sample of U.51-4.50) 5.91) 4.35 (2.96) 2. menopausal status.95 (2.46-13.70-5.47) 2.1-16.0-14.4) 8.20 (7.3) 12.83 (5.50) 6.40) 5.25 (3.50) 95th 12.70 (2.50) 2.10-3.52 (8. population from the National Health and Nutrition Examination Survey.46 (3. However.08) 3. In these small short-term experimental studies on males and studies of male perchlorate workers with doses or estimated exposures thousands-fold higher than known environmental exposures. Survey years 01-02 03-04 Geometric mean (95% conf.64-3.60-11.50 (3.00 (4.24 (4.6) 12.61-10.74) 7.15-12.76 (3.35) 3.40 (3..30 (3. 2005).51 (3.4 (10.04-3. 2005.0) 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 .09) 3.20-3.98) 3.43) 6.Perchlorate inhibition (RUI).76-3.60-11.0-14. women with urinary levels of iodine less than 100 micrograms per day. Lamm and Doemland.02) 3.58) 2. Short term human studies of the effect of perchlorate on RUI have been used for risk estimation (Greer et al.60-5.0 (8.20 (4.10 (4.00-11. 2002).80 (4.EPA.20) 3.0 (8.03 (2.1 (8.5) 8.60 (3.18-3. levels.3 (10.99 (5..70) 2.7 (11. chronicity of exposure.54 (2.10 (2.32) 5.90-11.60-15.0-44.0-19.90 (4.87-3.60-8..6) 20.35 (4.3-14.30-10. gender.89-3.56 (3.90-20. Greer et al.25) 5.0) 10.39-4.00) 4.60) 10.0-17.87) 2.50) 2.08 (3.60-3.30) 3.S.24-2.1-22.39 (3.04-3.0) 12.S.80 (7.2) 8.59) 3.40 (7. 2003.S..0) 6.77 (3.22 (2.45-2. During gestation and infancy. NAS.37 (4.S. perchlorate is negative in most genotoxic assays (U.0) 9.60-8.20) 8.39) 2.50-5.33 (7.72 (3.37-13. dietary iodine intake.22-4. 2005).30-5.89 (2..8 (11.93-5.66) 3.3) 8. Li et al.90-15. 2005). Lawrence et al. suggesting its tumorgenic effect is a result of a chronic increase in thyroid stimulating hormone indirectly resulting from iodine uptake inhibition. 2002. it is known that maternal and congenital hypothyroidism adversely effects neurological development and decreases learning capability.90-2.30-5.46-4.4 (11. Though it produces follicular cell thyroid tumors in animal studies at goitrogenic doses.0) 7.3) 11.60-6.44) 3.60) 3. and the presence of other substances known to affect thyroid function (e.90 (2.33-6.42 (3.33-12.40-10. urinary perchlorate at environmental exposure levels were inversely associated with thyroxine levels and positively associated with levels of thyroid stimulating hormone (Blount et al.0) 12. 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.5 (13.80 (7.20 (3.90 (2.93-7.93-8. 2006..0 (11.82 (5.0) 12.90) 5. congenital hypothyroidism is a condition for which nearly all newborn blood is screened. 2001.22-6. nitrate.61 (5.34-3.60-5.87 (7.26) 4.90-9.10 (4.30) 90th 9.10) 3.0 (9.2) 8.09 (7.00 (6.S.0) 11.12 (6.12-2. 1999. interval) 3.60) 8.1) 8.1 (11.64) 5. thiocyanate.0) 13.10) 13.53 (2.50 (6. Also.41-9.93-5.87) 7.EPA.75) 3.70-15.40) 17..g.97-5.87 (5. 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.26 (3.0 (9. 2005. medications).67) 5.90-3.40 (4.54 (3.4 (8.6-17.70-3.45) 3. 2007). up to 68% RUI has been demonstrated. age. Ecologic studies from screening programs with elevated perchlorate in the regional drinking water have indicated no increased prevalence of abnormal neonatal screening tests for this disorder in these regions (Kelsh et al.80-3. 2002.70 (2.21 (2.16-3.0) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites 3.22-4. although iodine intake was higher than U. U.40 (3.70-4.90 (7.56-3.80) Selected percentiles ( 95% confidence interval) 50th 3.20-10.25) 5. but without effects on serum levels of thyroid stimulating hormone or thyroxine (Braverman et al.00-2.41) Sample size 2818 2504 01-02 03-04 01-02 03-04 01-02 03-04 5.4 (11.4-16.05 (4.00) 9.20-3.70) 10.14 (2.30 (6.52-9.25) 5.29-6.0) 4.99-3.0 (9.0 (10..44-6. Many factors may be important in consideration of perchlorate action on the thyroid: dose. Steinmaus et al.19-6.10 (1.00-3.00) 3.61-5.0 (11.36 (8.0) 1335 1220 1483 1284 01-02 03-04 01-02 03-04 01-02 03-04 3.07 (2.0) 374 313 827 715 1617 1476 01-02 03-04 01-02 03-04 3.10 (6.1-13.29) 2.30) 5. In the U.0) 14.10) 6..50-9.19-10.86) 4.70 (4.20-4.0) 9.30) 75th 5.50-3.S.73) 3.20 (2.30 (5. 2000).84) 2..10) 4.71 (5.4) 13.0) 12.93) 3.

115(9):1333-1338. and nitrate on thyroid function in workers exposed to perchlorate long-term. Sesser DE. Tellez RT. Health Implications of Perchlorate Ingestion.gov/toxpro2. 2001-2002.S.46(5):509. Finding a measurable amount of perchlorate in urine does not mean that the level of perchlorate causes an adverse health effect.11(3):295.42(2):200-205.10(8):659-663. et al. Crump KS. CFSAN/Office of Plant & Dairy Foods. EPA reference dose (Blount et al.Perchlorate be unlikely to occur without overt perturbation of thyroid homeostasis.EPA at: http://www. He X. Erratum in: Environ Health Perspect 2005.html and from ATSDR at: http://www. 6/2/09 Greer MA. When these NHANES 2001-2002 urinary levels of perchlorate are used to calculate daily oral intakes for the U. May 2007. 2005). Kelsh MA.S. Li Z. Environ Health Perspect 2002. et al.113(8):10011008.. Cross M. Blount et al. Valentin-Blasini L.S. Gibbs JP.. Lamm S. National Research Council of the National Academies. Li FX. Miller MD. References Blount BC. Abarca CR. Rutherford GW. Urinary perchlorate and thyroid hormone levels in adolescent and adult men and women living in the United States. Richman K. et al. most of the population is considered to be below the U. 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. Food and Drug Administration (FDA). Long-term environmental exposure to perchlorate through drinking water and thyroid function during Fourth National Report on Human Exposure to Environmental Chemicals 245 . Greer SE. population. Environ Health Perspect 2006. The effect of short-term low-dose perchlorate on various aspects of thyroid function. Doemland M. Additional information about exposure and health effects is available from the U.114(12):1865-1871. Lamm SH. Crump KS. J Occup Environ Med 2000. Lamm SH. Valentin-Blasini L.atsdr. Byrd D. Lamm SH. Jackson WA. Blount BC. newborn thyroid function. Pino S. Pleus RC. Compared to a previous study of pregnant women in three Chilean communities with varying perchlorate levels in the drinking water. Analysis of relative source contributions to the food chain. 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. Has perchlorate in drinking water increased the rate of congenital hypothyroidism? J Occup Environ Med 1999. thiocyanate. Washington (DC): National Academy Press. J Occup Environ Med 2003. Thyroid 2000.cdc. Dyke JV. Steinmaus C.40(21):6608-6614. Pino S. Daaboul JJ. Buffler PA. 2007).45(10):1116-1127. Preliminary Estimation of Perchlorate Dietary Exposure Based on FDA 2004/2005 Exploratory Data. Lawrence J. Page Last Updated: 05/28/2009. Lawrence JE. 2005. Neonatal thyroxine level and perchlorate in drinking water. National Academy of Sciences (NAS). Perchlorate in the United States. Skeels MR. Braverman LE.gov/safewater/ccl/perchlorate/perchlorate.gov/Food/FoodSafety/ FoodContaminantsAdulteration/ChemicalContaminants/ Perchlorate/ucm077653. 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. Low dose perchlorate (3 mg daily) and thyroid function. Chacon PM. Howd R.110(9):927-937. Primary congenital hypothyroidism. Magnani B. epa. Osterloh JD. Landingham CB.htm. Braverman LE. Deyhle GM. Pirkle JL. and environmental perchlorate exposure among residents of a Southern California community. Environ Health Perspect 2007. J Clin Endocrinol Metab 2005. Thyroid 2001.html. Environ Sci Technol 2006. Available at URL: http://www. Goodman G. J Expo Sci Environ Epidemiol 2007.41(5):409-411. Blount BC. et al. 2005). Barnard JC. Mauldin JP.90(2):700-706. Perchlorate Exposure of the US Population. Benchmark calculations for perchlorate from three human cohorts.fda. Impact of smoking and thiocyanate on perchlorate and thyroid hormone associations in the 2001-2002 national health and nutrition examination survey. Environ Health Perspect 2005. Erratum in: J Occup Environ Med 2004. Also. Pirkle JL. Braverman LE. Lau EC. Caldwell KL. Kirk AB. Health effects assessment for environmental perchlorate contamination: the dose response for inhibition of thyroidal radioiodine uptake in humans. The levels seen in NHANES 20032004 show a similar pattern to NHANES 2001-2002. Biomonitoring Information Urinary perchlorate levels reflect recent exposure. Dasgupta PK.113(11):A732. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.. The effect of perchlorate.17(4):400-407. (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. Osterloh JD.

Environmental Protection Agency (U. Environ Sci Pollut Res Int 2002.15(9):963-975. Urbansky TF. Perchlorate as an environmental contaminant. Doc. Integrated Risk Information System (IRIS).S. EPA). Drinking Water Contaminant Candidate List. EPA/600/F-98/002 Washington (DC). Perchlorate. 246 Fourth National Report on Human Exposure to Environmental Chemicals . 1988.epa.S. No. EPA).S.9(3):187-192. Available from URL: http://cfpub. Thyroid 2005.gov/iris/quickview.Perchlorate pregnancy and the neonatal period.1/15/06 U. U. cfm?substance_nmbr=1007. Revised 2/11/05.S. Environmental Protection Agency (U.

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

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

. Two recent cross-sectional human studies observed a negative correlation of birth weight with serum levels of PFOA (Apelberg et al. 2007a.900 (. which may vary for some chemicals by year and by individual sample. Slightly higher levels of PFOS and PFOA in males than females have been noted in several other studies (Calafat et al. 1999.50) . 2004). 2004b). 2003a).800) 1.3. possibly related to lung immaturity (Lau et al. Olsen et al. 2007b.400-1. EPA. PFOS.. 2003). 2007. development in offspring was stunted and hypothyroxinemia was observed.400-1. 2007a. perfluorohexanesulfonate (PFHxS). Olsen et al.500) .80) 485 538 962 Limit of detection (LOD. see Data Analysis section) for Survey year 03-04 is 0.400) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.300 (<LOD-. elderly and children. and changes in thyroid hormone concentrations (Grasty et al. A study of workers chronically exposed to primarily PFOA showed no biochemical evidence of hepatotoxicity or hormonal changes (adrenal. 2003.400 (<LOD-. 2003a. Harada et al.Perfluorochemicals and testicular tumors in high dose animal testing (Biegel et al.500-1.20) ..300 (<LOD-.600 (.500) .S...S.400-. 2004.10) .500 (.600 (. Olsen et al.00 (. Cook et al.400-1. PFOA.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 . 2004a. and other PFCs have not been classified as to human carcinogenicity by IARC or NTP..700 (.400 (<LOD-.800 (. 2003). Fei et al. 2003). PFOA.500) ..S.500) . population from the National Health and Nutrition Examination Survey. Survey Geometric mean (95% conf. 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. Twelve different PFCs were measured in the sera of NHANES 2003-2004 participants.500-1.500-1. 2007)..400 (<LOD-. EPA.500-. population.500 (<LOD-1. and humans. 2003. and no substantial age trends were seen within adults ages 20-69 (Olsen et al. or increased cancer rates (Alexander et al.500-1.800 (..108 times higher than background serum levels in humans (Butenoff et al.10) * 03-04 03-04 * * < LOD < LOD < LOD .40) ..400-1. the median PFCs values tend to be roughly similar in these age categories (Olsen et al.S.. Biomonitoring Information Serum levels of PFCs (particularly PFOA and PFOS) tend to reflect cumulative exposure over several years. 2005). and there was no clear evidence of excess all-cause or diseasespecific mortality. 2003a. monkeys. 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. reproductive. At high but non-toxic maternal doses of PFOS. Effects on serum liver enzymes in limited observational studies of human occupational exposures are unclear.. 2003a. 2007b). At doses causing maternal toxicity..600 (.00) . animal and human serum PFOA levels have been compared: serum levels associated with toxic effects in animals are 66-11. 2005). 2003. Kennedy et al. thyroidal).00) . Serum Perfluorodecanoic acid (PFDeA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U. developmental and teratogenic effects were demonstrated in offspring.600-2.300 (<LOD-. However. Roughly similar levels of PFCs in serum have also been measured previously in other samples of the U. U. and perfluorononanoic acid (PFNA) are detectable in a high percentage of the participants and PFOS levels are generally 3-10 times higher than PFOA levels (Calafat et al. 2001. 2003a). U..400-.800) 1... 2004.00) . < LOD means less than the limit of detection.10) ..300-1.900 (.700) .. Due to marked intergender differences in the elimination of PFOA in rats and substantial differences in the half-life of PFOA in rats. In comparing three separate reports on adults. Thibodeaux et al.. interval) Selected percentiles ( 95% confidence interval) Sample 95th . Lau et al.500) 90th . the potential to estimate risks to humans from animal doses is uncertain. 1992. PFOS.500 (.80) 640 1454 03-04 03-04 * * < LOD < LOD ..800 (. Animal studies of PFOS have demonstrated weight loss.10 (.20) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD .500-3. 2004). Late gestational exposure to PFOS in animal studies has also demonstrated early neonatal lethality.800 (. hepatotoxicity.400-1. In such studies.900 (.. Fourth National Report on Human Exposure to Environmental Chemicals 249 .

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

which may vary for some chemicals by year and by individual sample.600) < LOD . Survey Geometric mean (95% conf.400) . see Data Analysis section) for Survey year 03-04 is 1. Survey Geometric mean (95% conf. Serum Perfluoroheptanoic acid (PFHpA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U. interval) Selected percentiles ( 95% confidence interval) Sample 95th .300-. see Data Analysis section) for Survey year 03-04 is 0.500-. < LOD means less than the limit of detection.3. population from the National Health and Nutrition Examination Survey.400 (<LOD-. population from the National Health and Nutrition Examination Survey.600 (. < LOD means less than the limit of detection. Fourth National Report on Human Exposure to Environmental Chemicals 251 .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 . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.900) < LOD 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD .300 (<LOD-.Perfluorochemicals Serum Perfluorododecanoic acid (PFDoA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.500 (<LOD-.600) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .S.300 (<LOD-.S.400 (<LOD-.0. which may vary for some chemicals by year and by individual sample.400 (. 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.500) 485 538 962 Limit of detection (LOD. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.900) < LOD .

80-4.17 (1.40 (1.30-9.90 (4.80-2.900-1.852 (.50 (2.05-2.60-2.00 (1.50 (1.30-6.30) 03-04 03-04 .Perfluorochemicals Serum Perfluorohexane sulfonic acid (PFHxS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.80-12. Survey Geometric mean (95% conf.16) .70-6.963 (.60-2.90 (1.10) 6.50-10.50) 6.00) 3.60) 1.70 (1.80-6.50-6.90 (2.80) 3.966 (.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) 1053 1041 03-04 03-04 03-04 .20) .80-3.20) 03-04 03-04 2.30) 3.40 (1.40-3.00-1.826-1.50 (1.80 (4.70) 13.10 (.90 (1.00 (1.900-1.20 (1.10-9.90-19. population from the National Health and Nutrition Examination Survey.09 (.50 (6.00-6.800 (.30) .S.00 (2.70) 2.20) 485 538 962 Limit of detection (LOD.1.62-2.44 (2.86 (1.900-1.70) 3.90 (4.90-2. Survey Geometric mean (95% conf.00-8.80) 5.93 (1.00) 1.60-3.900-1.900) 1.700-1. interval) .30 (2.90) 1.42 (1.834-1.50) 2.20-3.60-4.S.60-4.70-10.800-1.26) 2.70 (2. population from the National Health and Nutrition Examination Survey.10 (.10) 75th 3.50) 2.40-1.10-5.56-1.10 (4.10 (.80-8.80 (1.70) 1.70-2.60 (6.809) 1.14 (.70) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 1.40) .70-5.90) 90th 5.50-3.586-.30 (1.700 (.87-2.20) 1.80) 4.70) 2.30 (6.816-1.60 (1.900-1.90 (1.73-2.80) 1.80) 90th 2.80-3.17-1.03) 1.20 (6. see Data Analysis section) for Survey year 03-04 is 0.72 (1.01 (1.90) 3.10) 1.10) 1.10) 5.900 (.10) 8.20-2.54) .90) 8.60) 3.0) 1053 1041 03-04 03-04 03-04 1.10) 4.20) 2.90) 1.1) 485 538 962 Limit of detection (LOD.50-6.16) Selected percentiles ( 95% confidence interval) Sample 95th 8.912-1.30 (1.00 (1.04) .600-.50 (1.80-7.51) 1.689 (.60-7.20) 1.60-2.00 (.12) .10) 4.30 (1.40) 1. 252 Fourth National Report on Human Exposure to Environmental Chemicals .40) 1.90) 1.10) 6.900 (.10 (1.80 (1.72) 1.30) 3.14) Selected percentiles ( 95% confidence interval) Sample 95th 3.60 (1.80-4.50 (4.60) 2.80-7.67-2.40 (1. interval) 1.697-1.27) 1.721-1.30-12.20-1.30 (7.00 (5.861 (.30 (3.40) 2.30-2.40) 640 1454 03-04 03-04 1.10-9.40-1.60 (1.80-8.5) 5.70) 1.00-1.20 (1.40 (1.60-8.20 (6.3 (9.984 (.00 (.30 (2.900-1.50 (4.91) 2.20 (1.00-7.20-1.60) 9.10 (4.90-10.00) 1.0) 8.20-1.20-1.77-2.70-2.10) 75th 1.30 (1.70-7.6) 7.20 (1.835-1.08) 2.5) 8.40) 4.40 (2.00 (1.80-4.50 (6.40) 640 1454 03-04 03-04 2. Serum Perfluorononanoic acid (PFNA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.60-3.00) 2.30) 3. see Data Analysis section) for Survey year 03-04 is 0.50 (1.90 (1.3.92 (1.

8-22.37 (2.9-38.65-4.3) 42.9) 9.20) 5.35) 3.6) 35.60 (7.4 (19.67-4.6) 21.6-45.00 (5.0) 21.20) 5.1) 15.0 (27.90 (7.6 (42.4-42.9) 27.3) 485 538 962 Limit of detection (LOD.95 (3.40 (6.40 (4.6) 42.S.6-24.90 (7.8 (45.6 (35.30-11. population from the National Health and Nutrition Examination Survey.60 (6.8-30.84-3.8-22.1-52.60 (4.1-24.80-4. interval) 3.6) 18.70-9.5-21.90-12.3) 41.60-13.3-61.2) 640 1454 03-04 03-04 4.30 (3.90-4.0-16.4) 75th 30.80 (7.7 (43.10-3.20) 4.20) 7.30-5.8 (34.6) 7.50-6.5) 7.8-78.30) 7.1-36.0-66.30) 6.40-6.1.3 (17.2-22.30-3.1) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 4.9) 22.30 (3.21-3.30-6.0) 23.1 (24.0) 90th 41.7 (35.20 (4.5) 57.80-9.9-23.53) 3.96 (3.7-53.20-4. Fourth National Report on Human Exposure to Environmental Chemicals 253 .6-50.2 (28.85-4.1-33. Survey Geometric mean (95% conf.S.4 (23.7 (35.20 (4.50-13.40) 3.2-57.99-3.1 (19.70-7. population from the National Health and Nutrition Examination Survey.40) 5.2 (16.90) 6.40-6.3) 28.70 (3.1-25.90 (7.7 (7.10 (3. Survey Geometric mean (95% conf.1) 57.50) 4.7-69.2 (19.47 (4.2 (21.5) 18.7 (13.8 (37.27) 4. see Data Analysis section) for Survey year 03-04 is 0.4) 20.9 (17. Serum Perfluorooctane sulfonic acid (PFOS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.2 (27.2) 30.50 (3.70 (5.5) 8.4) 56.5) 1053 1041 03-04 03-04 03-04 14.6 (44.40) 90th 7.8-81.7) 39.70) 6.50-4.60 (6.4 (28.30-8.89 (3.70-5.70-7.5) 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 21.5-62.7 (43.4) 21.7-33.7-49.10 (3.9 (19.3 (44.0) 03-04 03-04 19.60-14.Perfluorochemicals Serum Perfluorooctanoic acid (PFOA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.0) 21.2) 45.7 (19.47-4.70-10.00 (3.5 (28.0 (20.10) 5.40) 75th 5.60-9.82) 4.3) Selected percentiles ( 95% confidence interval) Sample 95th 54.00 (5.60) 03-04 03-04 3.9 (22.20) 10.80-12.8) 46.9) 22.60 (3.0) 36.70 (5.11 (2.8) 27.90 (5.8) 32.3 (35.20-5.60 (5.79) 4.4.0) 485 538 962 Limit of detection (LOD.2 (18.90-4.6) 9.5-23.3 (28.1-35.18 (3.50 (4.2) 30.6) 62.20-9.80 (5.4 (19.07-4.4 (17.8-35.6 (19.40-10.40-17.27) Selected percentiles ( 95% confidence interval) Sample 95th 9.0-70.0) 43.30 (5.5) 19.80 (6.5 (28.9 (13. see Data Analysis section) for Survey year 03-04 is 0.5-33.10 (6.20) 7.4) 640 1454 03-04 03-04 23.8-22.1 (23.91) 3.70) 4.80) 8.5) 32.60-6.5) 9.70) 3.50) 7.60) 8.80 (6.9-19.6) 1053 1041 03-04 03-04 03-04 3.3-22. interval) 20.40-14.4-17.0-20.00) 3.3 (35.4-25.7-23.7-30.

population from the National Health and Nutrition Examination Survey.300) .300 (.300 (.300-.200-. < LOD means less than the limit of detection.200-.200-. interval) Selected percentiles ( 95% confidence interval) Sample 95th . < LOD means less than the limit of detection. which may vary for some chemicals by year and by individual sample. Survey Geometric mean (95% conf.500) .4.200-. 254 Fourth National Report on Human Exposure to Environmental Chemicals .300) .200-.300 (.300) . which may vary for some chemicals by year and by individual sample.500) < LOD 485 538 962 Limit of detection (LOD.300 (.300 (.S.400) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th 90th . see Data Analysis section) for Survey year 03-04 is 0.300-.200-.400 (<LOD-.400) 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD .200-.300 (.300) .300) .200 (<LOD-.500) . Survey Geometric mean (95% conf. see Data Analysis section) for Survey year 03-04 is 0.200-.300 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.300 (.500) .300 (.300 (.300) . population from the National Health and Nutrition Examination Survey.Perfluorochemicals Serum Perfluorooctane sulfonamide (PFOSA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.300-.300 (.300-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.500) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .S.300 (.300 (.500) 485 538 962 Limit of detection (LOD.300 (.200-.300) * 03-04 03-04 * * < LOD < LOD < LOD < 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 .2.300) . Serum 2-(N-Ethyl-perfluorooctane sulfonamido) acetic acid (Et-PFOSA-AcOH) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.200-.

see Data Analysis section) for Survey year 03-04 is 0.50 (1.20) 1.900-1.40) 1.900-1.20 (1. Survey Geometric mean (95% conf.30) 1.10) .300 (<LOD-.30) .80) 1.900-1.20-1.10-1.900-1.700) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .00 (.900-1. population from the National Health and Nutrition Examination Survey.10 (.800) .00 (.30) 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.900-1.10) . Fourth National Report on Human Exposure to Environmental Chemicals 255 .700 (<LOD-.900) 485 538 962 Limit of detection (LOD.300 (<LOD-1.600) .30) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th < LOD 90th * 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD .30 (1. population from the National Health and Nutrition Examination Survey.10) * 03-04 03-04 * * < LOD < LOD .700 (<LOD-.70) 1.500 (<LOD-.30 (1.80) 1.10 (1.50) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD 75th .700 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Survey Geometric mean (95% conf.800 (<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.40) < LOD < LOD .10 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th .S.6. which may vary for some chemicals by year and by individual sample.700) 1.900-1.30 (1.700 (<LOD-.700) 90th 1. Serum Perfluoroundecanoic acid (PFUA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.800) . < LOD means less than the limit of detection.600 (<LOD-1.700) . which may vary for some chemicals by year and by individual sample. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.900) .900 (<LOD-1.700) 1.60) 640 1454 03-04 03-04 * * < LOD < LOD .00 (.10-1.10-1.40) 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD .10-1.80) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD .900) 1.900 (.600 (<LOD-. see Data Analysis section) for Survey year 03-04 is 0.700 (<LOD-.300-2.00) < LOD .60) 485 538 962 Limit of detection (LOD.600 (<LOD-1.400 (<LOD-.400 (<LOD-1.90) .700 (<LOD-.600 (<LOD-1.50 (1.00-1.10 (.10) 1.00 (. < LOD means less than the limit of detection.700 (<LOD-2.3.S.10) 1.10-1.

7(4):371-377.34(4):351-384.134(1):18-25. Kuklenyik Z. Yun SH. Tully JS. Kamiyama S. Hurtt ME. Mandel JH. Olsen GW. McLaughlin JK. Saito N.179:99-121. Calafat AM. Environ Res 2005. Yoshinaga T. Hurtt ME. Mohotti KM. Biegel LB.38(10):2857-2864. Kuklenyik Z. Mandel JH. Perfluorinated chemicals and fetal growth: A study within the Danish National Birth cohort. Needham LL. Taniyasu S. Toxicol Sci 2001. Grey BE. Jarnberg U. Holmstrom KE. Calafat AM. Reidy JA. Chlorinated. Bookstaff RC. and perfluorinated contaminants in livers of polar bears from Alaska.Koizumi A.41:2237-2242. Reidy JA. Laane RW. Moore JA. in vivo. Harada K. sex and geographic factors on levels of perfluorooctanesulfonate and perfluorooctanoate in human serum over the last 25 years. Environmental and toxicity effects of perfluoroalkylated substances. Olsen GW.104(2):322-333. Kudo N. Seneviratne HR.68(6):465-471. Perfluorinated compounds in the plasma of loggerhead and Kemp’s ridley sea turtles from the southeastern coast of the United States. Falandysz J. Toxicol Appl Pharmacol 1995. J Occup Health 2004.99(2):253-261. Characterization of risk for general population exposure to perfluorooctanoate.and perfluorinated acids. Bandai N. Fillmann G. Yamashita N. Taniyasu S. and ex vivo studies. Cord serum concentrations of perfluorooctane sulfonate and perfluorooctanoate in relation to weight and size at birth. Hurtt ME.60(1):44-55. Environ Health Perspect. Chemosphere 2006b. Mechanisms of extrahepatic tumor induction by peroxisome proliferators in male CD rats. Keller JM. et al. Witter FR. Day RD. Chem Biol Interact 2000. Kennedy GL Jr.38(17):4489-4495. Reidy JA.60(10):722729.40:21282134. population: Data from the National Health and Nutrition Examination Survey (NHANES) 1999–2000. Androgenic deficiency in male rats treated with perfluorodecanoic acid. Birth Defects Res B Dev Reprod Toxicol 2003. population: data from the National Health and Nutrition Examination Survey (NHANES) 2003-2004 and comparisons with NHANES 1999-2000.S. Environ Sci Technol 2006a. O’Connor JC. et al. Biegel LB. Lau CS.39(23):9101-9108. Perfluorinated organic compounds in human blood serum and seminal plasma: a study of urban and rural tea worker populations in Sri Lanka. Caudill SP. 256 Fourth National Report on Human Exposure to Environmental Chemicals . brominated. Hekster FM. Effects of ammonium perfluorooctanoate on Leydig cell function: in vitro. Rodricks J. Toxicol Appl Pharmacol 1990. Crit Rev Toxicol 2004. Herbstman JB. Burris JM.39(1):80-84. Cook JC. Evans TJ. Sasaki S. Frame SR. Environ Health Perspect 2007. Cook JC. Ingall GB. Perkins RG. Fei C. de Voogt P. Yamashita N. Temporal trends of PFOS and PFOA in guillemot eggs from the Baltic Sea. Corsolini S. Regul Toxicol Pharmacol 2004. Environ Sci Technol 2004. Olsen GW. Environ Sci Technol 2005. Needham LL. The toxicology of perfluorooctanoate. Perfluorooctanesulfonate and related fluorochemicals in human blood from several countries. et al. Environ Health Perspect 2007. Murray SM. Rogers JM. Fluorotelomer alcohol biodegradation yields poly. Loganathan BG. Katakura M. Halden RU. Kannan K.46(2):141-147.39(23):9057-9063. et al. Mandel JS. Toxicol Appl Pharmacol 1992. Rev Environ Contam Toxicol 2003. Wong LY.S. Wijeratna S.115(11):1670-1676. Environ Sci Technol 2005. Bignert A.1968--2003. Caudill SP. Edwards EA. Moore RW. Mabury SA.124(2):119-132. O’Connor JC. Environ Sci Technol 2004. Occup Environ Med 2003. Morikawa A. Yoshinaga T. Kannan K. Tully JS. Liu RC. The influence of time. Induction by perfluorinated fatty acids with different carbon chain length of peroxisomal beta-oxidation in the liver of rats. Cook JC. Calafat AM. Perfluorinated chemicals in selected residents of the American continent. Calafat AM. Kuklenyik Z. Butenhoff JL. Kawashima Y. Needham LL. Mortality of employees of a perfluorooctanesulphonyl fluoride manufacturing facility. Butenhoff JL.115(11):1596-1602. Inoue K. Koizumi A. Induction of Leydig cell adenomas by ammonium perfluorooctanoate: a possible endocrine-related mechanism. Needham LL. Renal clearance of perfluorooctane sulfonate and perfluorooctanoate in humans and their species-specific excretion. Apelberg BJ. et al. Suzuki E.63:490496.113(2):209-217. 2007b. Guruge KS. Peterson RE. Harada K. Environ Sci Technol 2007a. Kannan K. Serum concentrations of 11 polyfluoroalkyl compounds in the U. Frame SR. Kumar KS. et al. Olsen J.Perfluorochemicals References Alexander BH. Prenatal window of susceptibility to perfluorooctane sulfonate-induced neonatal mortality in the Sprague-Dawley rat. Calafat AM. Seacat AM. et al. Ye Y. Perfluorochemicals in pooled serum samples from United States residents in 2001 and 2002. Dinglasan MJ. Grasty RC. Environ Sci Technol 2005. Tarone RE. Inoue K. Gaylor DW. Saito N. J Environ Monit 2005.39(3):363-380. Polyfluoroalkyl chemicals in the U. Reidy JA. Arendt MD. Aguilar-Villalobos M. Kuklenyik Z.115(11):1677-1682. Watanabe T.

Chemosphere 2007b. U. fast foods. Rogers JM. Case MT. Pepper K. J Occup Environ Med 2003b. et al. Mandel JH. Perfluorooctanesulfonate and other fluorochemicals in the serum of American Red Cross adult blood donors. Burris JM. birds. Peterson RE.54(11):1599-1611. Stanton ME. Toxicol Appl Pharmacol 2004. J Occup Environ Med 1999. Coordinate induction of acyl-CoA binding protein. Seacat AM. fate and transport of perfluorocarboxylates. Toxicol Sci 2002. Horii Y. A global survey of perfluorinated acids in oceans. II: postnatal evaluation. Chemosphere 2004a. J Children’s Health 2004b. perfluorooctanoate andother fluorochemicals in human blood. Burris JM. Available from URL: http://www. Mandel JH. Cousins IT. Kannan K.111(16):1900) Olsen GW. Environ Sci Technol 2003. Mandel JH. fish. Church TR. Preliminary evidence of a decline in perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) concentrations in American Red Cross blood donors. EPA). Hansen KJ.55:3203-3210.Perfluorochemicals Kudo N. Hansen KJ. Olsen GW. Hansen KJ.74(2):382-392.1177(2):183-190. Kannan K. Historical comparison of perfluorooctanesulfonate. Cao XL et al.82(1):359. Helzlsouer KJ.perfluorohexanesulfonate. Hanson RG. Butenhoff JL.S. Prevedouros K. Gamo T. fatty acid binding protein and peroxisomal beta-oxidation by peroxisome proliferators. Hanari N. (Erratum in: Toxicol Sci 2004.37(12):2634-2639. htm.198(2):231-241. 2003a. I: maternal and prenatal evaluations. Fourth National Report on Human Exposure to Environmental Chemicals 257 . Hanson RG. Seacat AM. Environ Sci Technol 2006. Petrick G. Olsen GW. Froehlich JW. Sterchele PF.26(1):47-51. Barbee BD. Olsen GW. Half-life of serum elimination of perfluoroo ctanesulfonate. Yamashita N. J Ag Food Chem 2007. Ellefson ME. fish. Grey BE. Environ Health Perspect 2003a.111(16):1892-1901. Burris JM. Olsen GW. Toxicol Sci 2003. Biol Pharm Bull 2003. and perfluorooctanoate in retired fluorochemical production workers. Butenhoff JL. Burris JM. Buck RC. et al. Dietary exposure of Canadians to perfluorinated carboxylates and perfluorooctane sulfonate via consumption of meat. Bronson R. Exposure to perfluorooctane sulfonate during pregnancy in rat and mouse. Zobel LR. Sources. Huang HY. et al. Horii Y.2(1):53-76. Hansen KJ.68(1):249-264. Moisey J. Miller JP. Church TR. Reagen WK. and humans from Japan. Thibodeaux JR. A survey of perfluorooctane sulfonate and related perfluorinated organic compounds in water.115(9):1298-1305. Thibodeaux JR.epa.68:105–111. Rogers JM. Lundberg JK. Nesbit DJ. Taniyasu S. Olsen GW. Butenhoff JL. 2007a.40(1):32-44.45(3):260-270. Quantitative evaluation of perfluorooctanesulfonate (PFOS) and other fluorochemicals in the serum of children. Epidemiologic assessment of worker serum perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) concentrations and medical surveillance examinations. Korzeniowski SH.S. (Erratum in: Environ Health Perspect. Olsen GW.74(2):369-381. et al. Butenhoff JL.51(8-12):658-668.gov/opptintr/pfoa/pfoara.113(5):539-545. Mar Pollut Bull 2005. Rogers JM. Serum perfluorooctane sulfonate and hepatic and lipid clinical chemistry tests in fluorochemical production employees. Butenhoff JL. Exposure to perfluorooctane sulfonate during pregnancy in rat and mouse. Burris JM. et al. Environmental Protection Agency (U. Hansen KJ. Richards JH. Lau C. Grey BE. Biochim Biophys Acta 1993.. Subchronic toxicity studies on perfluorooctanesulfonate potassium salt in cynomolgus monkeys. The developmental toxicity of perfluoroalkyl acids and their derivatives. Toxicol Sci 2003. Kawashima Y. Burlew MM. Washington. Mandel JH. et al. Ehresman DJ. Church TR. Yamashita N. Lau C. Seymour C. Butenhoff JL.) Tittlemier SA. Mair DC. van Belle G. Thomford PJ. Taniyasu S. Preliminary Risk Assessment of the Developmental Toxicity Associated with Exposure to Perfluorooctanoic Acid and its Salts. Ehresman DJ. 2003. Olsen GW. 1/15/06 Vanden Heuvel JP. Environ Health Perspect. Olsen GW. Serum concentrations of perfluorooctanesulfonate and other fluorochemicals in an elderly population from Seattle. Induction of triglyceride accumulation in the liver of rats by perfluorinated fatty acids with different carbon chain lengths: comparison with induction of peroxisomal betaoxidation. Larson EB.41(9):799-806. and food items prepared in their packaging. Lundberg JK. Environ Health Perspect 2005.

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

Dirven HA. The Handbook of Environmental Chemistry. Information about external exposure (i. at very high levels. High doses of di2-ethylhexyl phthalate (DEHP).niehs. 2002). but similar findings were not present in young Swedish men with comparable or higher median levels of urinary metabolites (Jonsson et al. A biomarker approach to measuring human dietary exposure to certain phthalate diesters.cdc. Environ Health Perspect 1982. van der Broek PH.. 2000b. 2001.New York.. Assessment of critical exposure pathways. Phthalate urinary metabolite levels in men evaluated at an infertility clinic were associated with several measures of sperm function and morphology (Duty et al. 2001). reducing estrogen production. dibutyl phthalate (DBP). Needham LL. at higher doses. Herbert AR. Kessler et al.html. 1986). Castle L. phthalates produced anti-androgenic effects by reducing testosterone production and. However.cdc. Peck and Albro. and benzylbutyl phthalate (BzBP) during the fetal period produced lowered testosterone levels. Also. 2001.. The National Toxicology Program’s Center for the Evaluation of Risks to Human Reproduction (NTPCERHR) has reviewed the developmental and reproductive effects of specific phthalates (http://cerhr. 2004. J Chromatogr B 2004. In Staples CA (ed). Slakman AR. In animals. Hoppin et al. Hauser et al. Calafat AM.. Massey RC. Matthews HB. The proportions of each metabolite for a given phthalate may vary by differing routes of exposure (Liss et al.cdc. Sauer MJ. Biomonitoring Information Urinary levels of phthalate metabolites reflect recent exposure to the parent phthalate diester. 2005. Available at URL: http://www. Cousins IT. Albro PW and Lavenhar SR. Vol. atsdr. interactions with macromolecules and species differences in metabolism of DEHP. Environ Health Perspect 1997. Jongeneelen FJ. Hauser et al. 227-262. Drug Metab Rev 1989.. Silva MJ.gov/ reports/index.21:13-34. testicular atrophy.nih. 2006). Toxicological profile for di(2-ethylhexyl)phthalate update [online].gov/toxprofiles/ tp135. peroxisomal proliferation may not be a relevant pathway in humans (Rusyn et al. 1982. which may be a pathway to the development of liver toxicity and cancers in these animals.. 2003. 4/20/09 Albro PW. Automated solid phase extraction and quantitative analysis of human milk for 13 phthalate metabolites. 2007.html. 2000c. 2004). 2000a.. variation also occurs in the same person during repetitive monitoring (Fromme et al. 2004. Mackay D. 2004. Springall C. Clark K. McDonnell DP. 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.. 2006). environmental levels) and health effects is also available for some phthalates from ATSDR at: http://www. 2002). pp. Part Q: Phthalate Esters.atsdr. Determination of four metabolites of the plasticizer di (2-ethylhexyl) phthalate Fourth National Report on Human Exposure to Environmental Chemicals 259 . Scotter MJ. Silvapathasundaram S. McKee et al. 4/20/09 Agency for Toxic Substances and Disease Registry (ATSDR). gender... Anderson WA. Connor C. Corbett JT. The monoester metabolites are thought to mediate toxic effects for some of the phthalates. Lovekamp-Swan and Davis.3.45:19-25. Dave M.. Rhodes et al. Toxicological profile for di-n-butyl phthalate update [online]. efficiency of intestinal absorption.. Pharmacokinetics. Food Addit Contam 2001.18(12):10681074.. Available at URL: http://www.. 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.atsdr.gov/ toxprofiles/tp9. Coldham NG. 2004. and race/ethnicity (Silva et al. Population estimates of concentrations of specific phthalate metabolites may differ by age. 2003. and extent of metabolite conjugation to glucuronide (Albro et al.Phthalates and metabolites have been tested. 1985.html.. ovarian abnormalities in the female animals (Jarfelt et al. Springer. Schroeder JL.e.805:49-56. Evaluation of a recombinant yeast cell estrogen screening assay.gov/toxpro2. effects that may be mediated by inhibiting testicular and ovarian steroidogenesis. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Metabolism of di(2-ethylhexyl) phthalate. Variation occurs from person to person in the proportions or amounts of a metabolite excreted after similar doses (Anderson et al. 105:734-742. phthalates have been shown to induce peroxisomal proliferation in rodents. but there are known species-related differences in the hydrolysis of diester phthalates. and Sertoli cell abnormalities in the male animals and. 2005).. 2007). Jordan S. NTP-CERHR. These differences may contribute to species-specific differences in toxicity (ATSDR. 2002. 1982). References Agency for Toxic Substances and Disease Registry (ATSDR).html).

Environ Health Perspect 1997. Hagmar L. Meeker JD. Silva MJ. Yoshimura M. Decreased serum free testosterone in workers exposed to high levels of di-n-butyl phthalate (DBP) and di-2-ethylhexyl 260 Fourth National Report on Human Exposure to Environmental Chemicals . Leffers H. Environ Health Perspect 1995. Chahoud I. Duty SM. Am Ind Hyg Assoc J 1985. Antiandrogenic effects in male rats perinatally exposed to a mixture of di(2-ethylhexyl) phthalate and di(2-ethylhexyl) adipate.19(4):505-515.niehs. Csanády G. Mortensen GK. Hoppin JA.html. Draft Update Monograph on the Potential Human Reproductive and Developmental Effects of Di(2-ethylhexyl) Phthalate (DEHP). The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. Mechanisms of phthalate ester toxicity in the female reproductive system. A variety of environmentally persistent chemicals including some phthalate plasticizers are weakly estrogenic. and infant formula by tandem mass spectrometry (LC-MS-MS). Hass U.112(17):1734-1740. 6/2/09 Okubo T. Reprod Toxicol 2004. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Calafat AM.46(11):643-647. Boehmer S. Hauser R. Urinary phthalate metabolites and biomarkers of reproductive function in young men. Albro PW. Rylander L. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. NTP-CERHR. Kano I.64(8):555-560. Henttu P. Yokoyama Y. Int Arch Occup Environ Health 1993. Hanaoka T. Environ Health Perspect 2002. McKee RH. Reprod Toxicol 2005. Reproducibility of urinary phthalate metabolites in first morning urine samples.niehs. Stringer WT. Zhang S. et al. Jonsson BAG. Duty S. Nielsen J. Ladefoged O. Research Triangle Park (NC). Milligan SR. Ryan L. 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Malek NA. Reidy JA.58:339349. Orton TC. Parks LG. Silva MJ. Crit Rev Toxicol 2006. Urinary levels of seven phthalate metabolites in the U. Peck CC. et al. Bratt H. Toxicol Sci 2000. Klinefelter GR. Ostby JS. Pratt IA. Toxicol Sci 1998.112(3):331-338. Zacharewski TR. 112(5):A270].Phthalates phthalate (DEHP): a cross-sectional study in China. Comparative pharmacokinetics and subacute toxicity of di(2-ethylhexyl)phthalate (DEHP) in rats and marmosets: Extrapolation of effects in rodents to man. Modes of action and species-specific effects of di-(2-ethylhexyl)phthalate in the liver. Jackson SJ.65:299-308.45:11-17. Cunningham ML. Peters JM. Toxic potential of the plasticizer di (2-ethylhexyl) phthalate in the context of its disposition and metabolism in primates and man. et al. Barlow NJ. Examination of the in vitro and in vivo estrogenic activities of eight commercial phthalate esters.114(11):1643-1648. Abbott BD. Fielden MR. Batten PL.36:459-479. Environ Health Perspect 1986. Wu ZF. Barr DB. Environ Health Perspect 2004. Environ Health Perspect 2006. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Hodge CC. Clemons JH. Fourth National Report on Human Exposure to Environmental Chemicals 261 . Albro PW.S. et al. Environ Health Perspect 1982. Rhodes C.46:282-293. Lambright CR. Caudill SP. The plasticizer diethylhexyl phthalate induces malformations by decreasing fetal testosterone synthesis during sexual differentiation in the male rat. Meek MD. Rusyn I. Matthews JB.

8 (21.5) 65.4) 35.4 (32.Phthalates Benzylbutyl Phthalate CAS No. residents (Blount et al.1-16.7-13. and diet is the major source for general population exposure.5 (76.9 (28.2) 15.3) 94.3-161) 99.2 (14.1 (19.8 (80.8-18. particularly male animals (McKee et al. 2001-2002.5-36.4-16.5 (57.6 (21.1) Selected percentiles ( 95% confidence interval) 50th 17.9-28.7-15.5 (13.5) 16.2-115) 113 (91.7 (82.3) 15.2) 66.7-119) 99.1-120) 52.7 (53. and 0.8) 28.8 (71.2) 78. 01-02.8-133) 89.5 (61.3-88.9) 49.0) 20.0 (14.4) 49.8 (38.7) 38.4 (48. including MBzP.3-130) 122 (88. sealants.1-15.3 (13.6-150) 94.6) 25. People exposed to BzBP will excrete mono-benzyl phthalate (MBzP) and small amounts of mono-n-butyl phthalate in their urine.1-116) 122 (93.1) 13.6-72.5 (47. 2004.5-33.3-122) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.8) 328 393 342 752 742 729 1461 1647 1534 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 16.2) 33.8 (28.9-14.5-94.5 (67.7-17.9 (12. some personal care products.8-17.0-106) 58.0 (34.6-92.5) 27.4-92.2) 13.3) 54.8 (50.9-16.1) 68.6) 35.9 (13.2) 22. and 03-04 are 0.3) 63.8 (10.2) 32. Food crops take up BzBP.8) 63.1 (55.3-74.4-120) 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 13.5) 82. 0.8 (86.7-172) 103 (74.8 (30.6-92.4) 12.7-35.1.2) 14.5) 214 (108-399) 235 (183-330) 255 (146-365) 125 (93.2-33.2-183) 101 (78.1-35.3-34.1-214) 166 (116-191) 145 (110-213) 88. High dose BzBP and its monoester metabolites.1) 67.1) 29.6-38.7 (80.7) 23.0) 34.2) 69.7-170) 169 (134-198) 152 (99.9) 14.9) 12.5-84.1 (14. it can be released into the ambient air during use or disposal of the products.8-13.3-18.9) 15.4) 75th 35.1) 12.1 (32.9) 18.6) 14.S.7 (13.1-61.2-16.4-62.6 (12.7-82.6) 35.0 (11.3 (12.6-116) 122 (102-142) 101 (85.5-14. interval) 15.9 (11.0 (55.2-16.4-25.7) 40.8-41.6-132) 103 (84. 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.4 (10.9-190) 86.3-27.3 (54.2 (10.3 (30.2) 12. 2000). 2000).1 (14.2-38.4 (29.1 (13.3) 37.4-127) 80.6) 37.1-18.8-16.8) 24.6 (32.8-14.5 (66.5) 15.8 (14.7 (51.1-39. respectively.1) 14.6) 13.9) 13.3-82.7 (15. can produce developmental and reproductive toxicity in rodents.4) 51.4 (13.8 (53.5-97.8-98. car care products.5) 30.4) 35.2-155) 91. BzBP can be released into the environment during its production and.6) 29.0 (33.9-27.3 (29.8-48.5-36.5 (26.6-17.4-24.4 (63.7 (12.7-16.7 (70.6-29.4) 98.3-125) Total 15.3-43. vinyl tile. Biomonitoring Information The median levels of MBzP in NHANES subsamples from 1999-2000.6-39.6) 13.4) 80.0 (20.3) 23.4 (59.5-41.6) 16.4) 33.0) 23.1 (13.8) 33.8-76.0) 16.5-40.8-16.4 (32.0-85.9) 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 39.0 (43.8.5-62.2 (19.4) 65. see Data Analysis section) for Survey years 99-00.4) 129 (98.0-130) 101 (86.6-79.1-90.1 (58.0) 32.4) 108 (96.6) 67.6) 14. and 2003-2004 were generally similar those reported in U.3 (29.6) 50.2 (19.5-25.2 (43.4) 38.1) 76.6-43.9) 11.6-18.3 (44.7-16.6 (53.0 (15. because it is not bound to products in which it is incorporated. population from the National Health and Nutrition Examination Survey.2-19.5-18.9) 43.8) 14.7-16.3-21.3-12.2) 14.0) 90th 67.9-87.0) 33.9-47.2 (11.6) 24.1-38.2-31.0) 70.4 (27.6) 63.4) 14.6 (13..5) 23.8-121) 79.2-39.6) 15. 262 Fourth National Report on Human Exposure to Environmental Chemicals .5 (55.2-116) 122 (102-143) 101 (84.0 (15.1 (10.4-15.0-26.6 (41.9 (70.0 (12.1-16.9-30.4) 71.3.1) 32.9 (12.0 (26.9 (39. IARC considers BzBP not classifiable with respect to human carcinogenicity.3-75.7 (11.8 (12.7-25.7-14.4 (53.8-64.9 (22.8-14.0-55.3) 13.3 (33.0 (30.9) 14.5-35.S.6 (66.0 (30.0) 24.3-18.4 (68.8-17.6 (13.2-40.1-15.1 (20.3-91.6 (13.2-17.1) 31.5 (27.8 (71.5) 55.3 (12.5-145) 138 (106-241) 143 (127-179) 120 (99.5) 15.8-72.2 (47.3) 13.2-20.9-62.0 (23. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. 85-68-7 General Information Benzylbutyl phthalate (BzBP) is a solvent and additive used in products such as adhesives.4) 81.9 (16.8-35.4 (53.6 (13.4 (10. NTPCERHR.3 (12.2) 17.7-58.1-43.4 (31. and to a lesser extent.2 (25.0 (27.3 (22.9 (21..6) 95th 103 (94.9-49.

8 (50.0) 24.2) 11.1) 142 (99.1-58.7) 11.7 (11.. adolescents compared with adults. 2004).8 (69.4-42.8) 71.6-81. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.1 (25.5-26.8 (10.9) 11.8) 26.5-16.4) 12.3) 89.9-13.6 (11.9-69.8-69.1-79.8) 68.3) 12.6) 38.5 (12.0-27.95-14.1 (9.5) 46.0) 15.4) 104 (89.1 (18.8) 108 (75.7 (13.7 (54.0) 49.7 (38.5-29. 2002.1-14. 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.2-15.0) Selected percentiles ( 95% confidence interval) 50th 13.7-56.8 (30.5) 20.6) 25.8) 15.4) 50. 2003).5-57.4 (33.1-35.8-39. and in a small sample of German residents (Koch et al.7) 46.1 (23.S.7-15.4) 25.1 (21.5-58. interval) 14.6 (14.3 (60.6) 12.2) 15.4 (25.8) 56.9 (24.6-86.1) 24.4 (21.2) 11.0 (13.6) 53.5) 41. Weuve et al.1 (53.2 (69.4-14.0-53.8) 54.5-61. in men attending a Boston infertility clinic (Duty et al.9) 12.8 (49.5) 17.2-117) 95.5 (9.4 (60.2) 26.9 (51.5) 14.0) 24.3) 14.5 (35.9-13.7 (19.1) 80.0-26.9-23.4 (11.9 (9.4 (69. 2002).2-26.7-61.0-51.2-12.5-42. 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.3-16.9 (39.4 (12.1 (41.0 (38.9) 24.8) 24.7-15.8-60.9 (15.4 (26.2-13.0) 11. DC reported median urinary MBzP levels that were about twice the levels of adults and females reported in NHANES 1999-2002 (CDC.0 (49. 2003).7-31.3) 55..4 (11.1 (15.6) 73.8) 46.2) 11.9) Total 14.1-27.9) 12.9 (43.5 (10.8 (13.3 (23.6 (22.5) 16.0 (12.1 (21.9-16.Phthalates York City (Adibi et al.6) 75th 25.1) 24.4-99.1-12.3 (39.8 (46.9) 42.4-27.6-13.8-27.2 (40.0-109) 65.2 (41.2-15.9 (15.5) 95th 77.4-23.1 (21.6) 13.8-42.6-12.6 (19.4 (34.2-13.5 (11.7-90.4) 44.4-79.6-15.3 (13.0-15.1) 23.5-31.2-21. A small study of African-American women in Washington.6-20.0-90.3) 73.1 (13.1) 17.1-125) 86.4-116) 73.7-19.9 (55.4) 51.6 (11. 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.8-13.3) 18.8) 16.9 (54.3) 90.9) 52.3 (15.7) 25.4 (10.3 (38.4) 13.6-99.5-23.7-69.9 (22..7-29.3-11.3-73.9 (29.3) 67.1 (46.2) 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 12.1) 35.7-123) 77.6-40.3) 14. 2005).7-19. 2005.8-34.3) 36.0 (10.4) 17.0 (41.5-213) 49.6 (24.4-60.1 (13.7 (21.3-64.5-58.4) 14.4) 60.3 (35.8-15..9 (10.1 (14.4-19.8) 80.5 (42.9) 100 (80..5 (48. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.1-12. In an annual sample of German university students.1 (11.7 (23.6) 58.3-34.1 (19. and females compared to males (Silva et al.9) 11.9 (24.4) 15.1-120) 77.4-102) 70.3 (12.5 (49.9 (12.0-48.8) 13.9 (10.8 (11.5) 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 .1 (21.7 (11.6-26.0) 60. Hauser et al.8-13.4) 90th 50.7 (55.2) 32.8 (64.9-115) 57.7 (12.8-80.69-11.6 (15..6 (30.9-83.2) 12. the adjusted geometric mean levels of urinary MBzP were significantly higher in several subgroups: children compared to adolescents and adults.6 (51.0 (12.9-28.8-173) 195 (121-305) 229 (99.4) 13.5 (56.5-79.4-14.2-57.4 (46.1 (34.7 (14.8-13.8-16.73-12.8) 53.2-51.8) 11.3) 29.0 (41.0) 12.7-397) 70.7-14. 2004.2-78.9-104) 62.8-64. median urine levels of MBzP were about one-half the median levels in NHANES subsamples from 1999-2002 (Wittassek et al.5) 10.7-20.4-93.7) 38.6) 30.6 (30.6 (36.5-38.6-47..8-14.4) 28.5-26.1) 27. population from the National Health and Nutrition Examination Survey.1) 12.5) 13.3) 13.0) 13.6 (11.7 (11.3 (24.3) 37.4 (11.5-13.0 (62.7) 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 40.7 (18.2) 67.8) 33.3) 16.2-49.2-17.7 (13.8-48.2 (27.7-14.6) 12.5) 78.6 (34.4) 328 393 342 752 742 729 1461 1647 1534 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 12.3) 21. 2007). Hoppin et al.0 (67.7 (59. 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.9) 12.8-14.5-99.8 (12.6 (57.8-85. 2007).9-40. 2006).3) 13...3) 13.8) 34.4-142) 134 (116-176) 136 (85.4-15.1-29.7-20.4 (63. In NHANES 1999-2000. in young Swedish men (Jonsson et al.0 (33.2 (56.7-12.9-14.4 (74.1 (43.9) 64.4) 21.4 (13.7) 19.4-17.4-90.8-15.5) 23.3-38.1) 39..5-76.0 (11.9 (12.8) 53.8 (57.7) 56.6-116) 74.9-62.4-18.5 (10.8) 33.

NTP-CERHR. 264 Fourth National Report on Human Exposure to Environmental Chemicals . Blount BC. Hilborn ED. Silva MJ. Environ Health Perspect 2003. Int J Hyg Environ Health 2007. et al. Environ Health Perspect 2006. J Androl 2004.18(1):122. et al. Dobler L. Phthalate monoesters levels in the urine of young children. Koch HM.25(2):293-302. Environ Health Perspect 2004. Hoppin JA. Reproducibility of urinary phthalate metabolites in first morning urine samples. Caudill SP. Exposure to phthalates in neonatal intensive care unit infants: urinary concentrations of monoesters and oxidative metabolites. Richthoff J.16(4):487-493. Gans G. Levels of seven urinary phthalate metabolites in a human reference population. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. Bull Environ Contam Toxicol 2002. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters.210(3-4):319-333. Urinary levels of seven phthalate metabolites in the U. Environ Res 2003.68:309-314. Research Triangle Park (NC). Reidy JA. Needham LL. Available at URL: http://cerhr. Sanchez GN. Hauser R. Calafat AM. McKee RH. Reprod Toxicol 2004. Green RA. Drexler H. Hum Reprod 2007. Centers for Disease Control and Prevention (CDC). Wittassek M. Ryan L. Epidemiol 2005.Phthalates References Adibi JJ. Camann DE. David RM. 112(5):A270]. Jacek R. Davis BJ.niehs. Sampson EJ. Duty S. et al. Giwercman A. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites.nih.gov/ chemicals/phthalates/bb-phthalate/bbp-eval. Pirkle JL. et al. Butala JH. et al. Prenatal exposures to phthalates among women in New York City and Krakow. Weuve J. Silva MJ. 2005. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Jedrychowski W. 4/20/09 Silva MJ. Eckard R. Silva MJ. Caudill SP. Barr DB.108(10):979-982. Rylander L. Poland. Chen Z.html. et al. Hagmar L. Atlanta (GA). Third National Report on Human Exposure to Environmental Chemicals. Needham LL. Meeker JD. Silva MJ. Calafat AM. Wiesmuller GA. Schettler T. Hodge CC. Environ Health Perspect 2002. Brock JW.114(9):1424-1431. 2000 [online]. Duty SM.110(5):515-518. Caudill SP. Brock JW. Baird DD. et al. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Brock JW. Environ Health Perspect 2000. Monograph on the Potential Human Reproductive and Developmental Effects of Butyl Benzyl Phthalate (BBP).112(3):331-338. Singh NP.93:177-185. Internal phthalate exposure over the last two decades—a retrospective human biomonitoring study.S. Barr D.22(3):688-695. Jonsson BAG. Angerer J. Ryan L. Malek NA. Rossbach B. Perera FP. Urinary phthalate metabolites and biomarkers of reproductive function in young men. Hu H. Helm D. Koch HM.111(14):1719-1722.

OSHA has established a workplace air standard for external exposure to DBP.50) 7. People exposed to dibutyl phthalates will excrete mono-n-butyl phthalate (MnBP) and mono-isobutyl phthalate (MiBP) in their urine.6 (11.7-31.50 (6.7 (7.8 (9.20 (7.7-31.20-6.6) 17.3 (11.55) 2.10-2.9 (16. 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. Fourth National Report on Human Exposure to Environmental Chemicals 265 .59) 3.50) 18.20) 4.5-16..40) 5.2-22.00-9.19-3.6-34.17 (2.67 (5.3) 18..90) 12.3 (13.80) 75th 5.10 (4.30-13.90 (6. interval) 2. Small amounts of mono-3-carboxypropyl phthalate are also produced from di-n-butyl phthalate.0-25.1 (8.6) 16. 2005).6 (13. 2003).4-12.1-20.3-19.0) 24.5) 18.3-30.70-4. 2005)..17) 4.80 (2.3-20.56 (3.6-14.50 (3.5 (10.91) 4. Koch et al. pharmaceutical coatings. 2005.7 (9. 2004.30-7.11-3.37) 6.7 (18.3.6) 10.60-6.46 (3. When total DBP metabolites have been measured.7 (17.70 (2. DBP can produce reproductive toxicity in male rodents (McKee et al.40-5.40 (7.90-4.7) 7.70-4.50-2.10-9.63) 3.50-6.90 (4.1) 16.24-8.70 (5.8) 40.8) 677 652 703 699 1216 1088 Limit of detection (LOD.1 (13.56) 3.2) 5.5-24.20-9.8) 21.10 (3.40-4.30 (1.30) 10.96) 3.5) 18.30 (3.5-29.00) 6.. 2001-2002 and 2003-2004 subsamples were similar to MBP levels reported in U.22 (3.7) 15.2 (11.00 (5.80-5.20 (6.80 (2.5 (11.3 (16.00) 4.56-4.70) 5.6) 16.5) 25. 2007).02) 4. 2004.10) 8.60 (5.0-38.30-6.1) 22.6-26. Compared with the median for 6 to 11 year olds in NHANES 1999-2004 (CDC.40-17.7 (16.90-4.30-11.0) 1371 1250 1411 1355 01-02 03-04 01-02 03-04 01-02 03-04 3.9) 15. Neither IARC nor NTP has evaluated dibutyl phthalates with respect to human carcinogenicity.50) 2.50) 5.0 (13. and in a small sample of Japanese adults (Itoh et al. 2000.6 (9.40 (6.5-16. Hauser et al.73 (2.3-48.9 (16.44-2.26 (2.0 (11.00) 10.55 (3.60 (2.30 (4.40-4.0) 20. 2000).2-33.20-12.5 (27..1-17.94) Selected percentiles ( 95% confidence interval) Sample 95th 17.0) 12.50) 8.5 (20.7-20. Biomonitoring Information Median concentrations reported in the NHANES 19992000.0) 9.46-5.0) 393 342 742 729 1647 1534 01-02 03-04 01-02 03-04 2.84) 4.66) 2.30) 6.80-5.6 (13. population from the National Health and Nutrition Examination Survey.7 (17.56 (5.6 (29.90-2.50-4.40-9.00) 7. NIOSH and ACGIH have established guidelines for workplace air exposure to di-n-butyl phthalate.6 (14. about 65% to 80% of a dose is eliminated in urine within 24 hours.5) 19.60) 3.1-25.40-3.0 (13. Studies of children found age-related differences in urine MBP levels.6 (10.90 (3.6-20.3 (19.5) 22. in men attending a Boston infertility clinic (Duty et al.70-8.80 (3.0) 13. residents (Blount et al.85-6. 84-69-5 General Information Dibutyl phthalates (both di-n-butyl and di-isobutyl phthalates.6) 12. 2001). in a small sample of pregnant women in New York City (Adibi et al.S. and insecticides..40-3.9) 10.43) 6.50) 90th 12.4) 12.4) 22.3-24.4-27.40 (3.0-14.6 (10.40 (2.3-18.71 (2.10) 3.7) 18.10) 11.4) 5.90-7.6) 26.9-23.3 (16.46) 2.82-3. 84-74-2 Di-isobutyl Phthalate CAS No.97-7.5) 23.00-11.6) 17.07 (3.00-4.46 (2. Median MBP levels in two European studies were about two to six times higher than median levels in this Report (Jonsson et al.81 (3.2 (12. Survey Geometric mean (95% conf.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 2.33 (2.4 (20. mostly as MnBP (Anderson et al.50-10.40-12.. referred to as DBP) are industrial solvents or additives used in many personal care products such as nail polish and cosmetics.6-18.3) 3.80 (5.90 (4.20-2.72-3.97) 4.6 (14.68 (2.20) 7.97) 2.7) 4.5) 12.7-18. NTP-CERHR.20 (3.10) 2.25) 01-02 03-04 01-02 03-04 01-02 03-04 4. Following oral administration of DBP to humans.30-2.10 (4.1) 25..4 (14.28-5. 2005).5) 14.3 (13.7) 14. and also in some printing inks.2-14.10) 9. exposure to benzylbutyl phthalate (BzBP) will also result in small amounts of mono-n-butyl phthalate appearing in the urine.30) 5.0 and 0. CDC.30-3.22) 3.30) 2.3) 33.1-12.00) 4.. they have been referred to as monobutyl phthalate (MBP).20-12.49-2.0 (19.30) 10.40 (2.60 (8. see Data Analysis section) for Survey years 01-02 and 03-04 are 1.00 (7.60 (4.73-5.80 (5.48 (2.3 (18.2 (8.00-6.S. In addition.5 (17.Phthalates Di-n-butyl Phthalate CAS No.00-6. 2003).70) 3.0-18.30-6.9-14.3-43.10-9.

2) 8.39-3.20-2.56-15.7 (11.98 (2.75 (4.65-4.9-40.7) 1371 1250 1411 1355 01-02 03-04 01-02 03-04 01-02 03-04 3.53-5. up to four and 13 fold.72) 5.15) 3.43) 3.54 (2. respectively.36-2.0) 3.11-2.Phthalates for neonates was lower (by about half) and the median for toddlers was higher (by about sixfold) (Brock et al.7) 19.51) 2.6-19.2 (11.80) 7.10-5. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.31 (7..9) 12.6) 13.11) 5.18) 3. while MnBP declined (Wittassek et al.5) 13.68 (2.94-12.99) 7. the students’ median values for MiBP levels remained relatively unchanged..00-3. 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.00-7.84 (4.21) 10. 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..1-25.74-3.07-5.28 (4.2) 9.3) 13.1-24.8 (8. Differences in urinary MBP population estimates by gender have also been shown (Silva et al.93-6.81 (3.62 (6.38 (6.13 (2.62-12.0 (10.64-7.54 (4.25) 5. An analysis of NHANES 2001-2002 showed similar age.79 (4.11 (5. 2005).30 (6.1-12.17) 90th 8.7 (9.1) 4.1) 10.24) 3. 2006). samples from German university students had consistently higher median urine levels of MnBP and MiBP.31 (2.56-4.20-4.33) 3.1-15. 2007).04) 3.08) 75th 4.43) 3.6-19.4) 23.94) 6.26-2.4 (12.94 (5.39) 5.6 (9.04-5.4) 7.8-18.9-26.38-10.07 (2.46-11..14 (4.66 (8. 2007).1) 15.20-3.2-13. Survey Geometric mean (95% conf.31) 2.86) 6.00) 01-02 03-04 01-02 03-04 01-02 03-04 4.68) 5.3) 13.69) 6.3) 18.1) 11.68) 3.0) 15.33 (2.47 (3.89-5.55-6.0) 393 342 742 729 1647 1534 01-02 03-04 01-02 03-04 2.2 (10.6 (12.81 (6.7 (21.78) 9.91-6.26 (2.33-9.. to about two to fourfold higher (Fromme et al.7) 3.8-13.84 (8. ranging from more than one-tenth the NHANES median (Itoh et al.8 (10..66) 10.79-8.1) 677 652 703 699 1216 1088 266 Fourth National Report on Human Exposure to Environmental Chemicals .0-18.20 (7.8 (9.76-3. Studies measuring urinary MnBP have reported variable median values compared to the NHANES 2001-2002 and 2003-2004 subsamples.6 (8.6 (15.8-18.46 (2.22 (2.5 (9.9 (9.61-3.64-7.79-6.97-2.86-4.69-7.0) 7.05) 2.19 (2. population from the National Health and Nutrition Examination Survey..43) 3.65 (4.89 (3.46) 3.37) 3.21 (5.02 (7.20 (2.32) 7.69 (2. 2002.83 (2.and gender.18 (4.73) Selected percentiles ( 95% confidence interval) Sample 95th 12.3 (13.47-5.65-11.27-12.67-5.2) 24.41 (2.30) 2.75 (6.1 (10.18-4.74 (4.51) 5.6 (10.32 (3.7) 11.28-13.57 (3.18) 4.57 (3. 2005).9-16.4) 15.34 (3.52-20.7) 10.6) 11.47-12.56) 5.S.53-4.52) 3.82 (4.58-3.related differences in the adjusted geometric mean levels of urinary MiBP and MnBP (CDC. Over this time.99-4.6) 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 2.17-12.57-4.7-28.95) 10.31) 2.72-7.7 (13.03-7.85 (2.35) 3.80-3.5-19.95) 2. Between 1998 and 2003. than adults in NHANES subsamples during the same time period.1) 13.76 (3.3 (17.82) 4.3) 16. In an analysis of NHANES 1999-2000.2-15.89) 6.0 (8.56) 2.20 (2. 2004).00-3.09-2.08-2.45) 3.64-10.3) 28.78) 8. interval) 2.29-3.8-36.59 (4.32 (7.42) 2.95-3.0 (12.18 (1.00 (3.88 (2.54) 2.44 (3.01-2.73 (5.6 (8.80 (3.53-3.18-10.0) 11. Weuve et al.5 (11.13-6. 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.9 (11.17 (2.51) 15.66) 2.1) 7.58-4.33 (3.66) 4.52-3.76-3.4-16.96 (3.29-8.52 (2.76-15.36-7.04) 7. 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.69) 4.5) 15.9 (15.92 (7.15-4.1 (11. 2004).03-11.81) 4.8) 10.02-10.03 (5.81) 9.78-8.

1) 23.8) 75th 51.S.9 (17.6-36.1-75.2-32.9-42.1) 31.6-48.6-143) 127 (99.6 (26.6) 46.0) 21.9 (79.7) 74.3-60.2) 62.7 (51.7 (28.8-25.1 (17.7-53.0-24.2-87. referred to as monobutyl phthalate (MBP).0) 20.3-76.7 (33.6-49.6 (61.9 (79.7-42.3 (42.8) 23.7-34.3-85.2-93.8-165) 167 (143-197) 138 (110-184) 144 (115-168) 142 (111-161) 107 (89. 01-02.5) 65.1) 23.7-26.5) 36.1-80.1) 17.1.7-92.1-51.4 (35.7 (24.2-33.1 (36.0-19.9 (17.2) 38.9) 18. see Data Analysis section) for survey years 99-00.6-40.8 (19.4 (35.0-19.3) 23.3) 19.3) 18.0 (78.6 (65.3 (37.7 (38.1-20.7-127) 328 393 342 752 742 729 1461 1647 1534 12-19 years 20 years and older 99-00* 01-02 03-04 Gender Males 99-00* 01-02 03-04 99-00* 01-02 03-04 22.2 (18.7) 92.8-119) 90.3) 36.2-21.7) 52.0 (25.5) 95.2-63.7 (22.2-56.1 (21. concentrations of mono-isobutyl phthalate and mono-n-butyl phthalate were measured together and expressed as a combined value.0 (45.3 (60.0-26.9.5 (59.1 (19.0-51.2) 32.0 (23.4) 64.3 (30.1) 23.4 (25.7-20.5) 78.6-113) 108 (90.9-22.6) 35.4-44.4 (36.7 (64.6 (32.7-91.5) 40.4-25.4 (35.0-21.8) 48.0 (18.3 (17.6-29.2 (25.4-20.3) 40.7 (16.9) 36.1) 36.2) 42.0) 120 (98.9-101) 77.1 (26.6 (90.6-29.4 (19.7 (19.3-24.9-92.2 (78.7 (70.3 (36.8) 43.5) 31.2 (58.3-136) 137 (107-162) 119 (90.6 (16.4) 22.5) 85.1) 46.4) 52.2-23.5 (59.9) 29.2 (21.0-24.5) 37.7) 28.4-26.8-42.0 (17.3-96.5) 20.6) 80.4-18. population from the National Health and Nutrition Examination Survey.3-145) 85.6-44.0 (72.5-47.6-31.4 (21.2 (21.0) 84.3-21.3-79.4 (38.6) 71. respectively.2 (19.3) 24.8-123) 101 (90.0) 38.1 (62.2-114) 73. interval) 24.6) 21.1 (16.1 (58.3) 26.4-42.1-122) 122 (104-137) size 2541 2782 2605 Total years 99-00* 01-02 03-04 50th 26.9) 71.5-27.8-29.1) 25.0) 30.9-53.0-58.8-132) 95.1-92.8) 62.7-124) 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.1-27.6) 20.7-117) 118 (108-143) 93.1 (51.4 (71.7 (18.7-106) 69.3 (23.1-22.0) 31.7-111) 64.9) 21.8-111) 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 (41.5 (28.4 (72.9-87. and 0.5) 47.2 (75.7-24.6-33.6-24.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.0 (20.1 (19.9 (20.4 (23.6 (19.3-67.5-60.0) 117 (104-131) 112 (84.5) 26.6-69.5 (74.1) 20.4-31.8 (57.5-53.2) 20.5-42.7 (18.8) 58.0) 27.7-42.5-117) 95.7) 124 (98.5) 19.7) 42.1 (19.2) 68. 1.1 (54.5 (30.7-34. Fourth National Report on Human Exposure to Environmental Chemicals 267 .7-116) 95.0 (36.8-22.9) 26.4 (84.4-60.6) 39.0-73.9-79.6) 38.1-24.6) 17.4.3) 21.5-44.1) 19.2-22.2-159) 92.2 (59.2-24.1 (28.2) 90th 98.4) 20.9-114) 116 (97.9-28.1 (19.9) 75. Survey Geometric mean (95% conf.1-29.6-37.1) 47.7 (43.0 (31.3 (30.4 (35.4) 59.1 (34.1 (18.2) 26.6) 166 (127-279) 159 (110-290) 191 (150-243) 165 (121-227) 148 (106-185) 134 (110-158) 143 (117-161) 95.5-47.3 (23.4) Selected percentiles ( 95% confidence interval) Sample 95th 150 (121-169) 108 (94.5-43.2 (79.1) 30.2 (20.0 (15.9-33.5) 36.0-32.5) 24.3-40.4-159) 107 (84.6 (48.8) 19.5 (29.5) 17. and 03-04 are 0.5-121) 106 (94.3 (51.5) 21.6 (44.0 (30.2 (74.6 (22. *In the 1999-2000 survey period.9) 46.7-121) 97.1-82.3 (56.6 (55.5) Age group 6-11 years 99-00* 01-02 03-04 99-00* 01-02 03-04 41.2-49.2 (17.9-22.6-20.5) 34.1 (31.

6-92.6 (19.8 (50.4 (16.9 (35.7 (16.7-51.1 (56.9 (35.5) 90th 68.7 (28.8) 34.7-20.3) 33.6-22.0 (71.0) 70.6) 23.6-27.6) 83.2-22.7 (81.3) 35.9) 20.5 (64.6-50.3-32.1 (21.2 (38.3 (55.1) 53.9 (30.9 (16.6) 39.2 (19.5) 91.4 (23.0 (15.3 (19.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.5-142) 89.3 (17.8 (17.5) 60.4) 21.9-34.4) 51. concentrations of mono-isobutyl phthalate and mono-n-butyl phthalate were measured together and expressed as a combined value.5) 21.7-19.8) 20.5-76.9-68.5-30.0) 29.0-60.9-36.9-70.3) 33.6-19.4-76.0) 53.1 (32.1) 35.2-22.7 (60.0-92.5-37.9 (64.6-155) 91.2-18.8) 75th 38.6 (25.8-32.2) 59.0 (43.9) 30.0 (52.9-38.6-24.3) 18.0) 35. population from the National Health and Nutrition Examination Survey.0) 94.8) 28.4-103) 117 (83.5-142) 81.5) 17.1-62.8-24.6) 38.3-81.4 (18.6) 34.8) 63.9) 52.8) 35.0-113) 104 (83.8 (16.2 (16.7-39.5-22.2 (35.3 (17.4 (37.0 (70.3) 17.5 (14.0 (26.6 (27.4-72.9) 19.3-21.9 (30.6 (41.8) 17.4) 16.7) 19.1-99.6-28.3-38.5) 134 (93.5 (18.6-23.8 (25.4) 62.4 (17.0 (34.2) 159 (102-263) 147 (93.3-78.9-26.4 (53.4) 20.2) 16.6-23.6 (31.6) 24.4-61.8) 30.2-22.9-84.4 (20.6-43.4) 15.7 (54.5-64.9 (30.1-21.3-39.8) 40.3) 52.2) 21.8) 22.6-32.3) 67.5 (81.3 (16.2-106) 64.7-23.5 (15.7) 20.5 (18.7 (19.6 (61.3) 19.2-16.7 (60.4 (45.0-38.3 (52.0 (19.3 (24.0) 59.3 (71.9-68.S.7 (12.1 (61.9 (21.2-179) 84.0-19.5-41.4-65.6) 18.7 (20.0) 25.3) 20.6-128) 96.6) 25.5 (30.8-235) 137 (108-198) 88.4 (47.0) 108 (71.7 (27.9 (20.7-19.6 (25.5-70.9 (73.4 (56.9-100) 86.8) 17.2-21.8 (18.2-27.4 (31.4 (19.3) 19.9) 39.3-21.2-28.0 (16.8 (33.0) 81.4 (33.7-26.1-115) size 2541 2782 2605 Total years 99-00* 01-02 03-04 50th 21.2-61.0) 75.1) 37.3-26.6-42.6 (72.8-23.7 (43.2) Age group 6-11 years 99-00* 01-02 03-04 99-00* 01-02 03-04 41.3 (52.4) 19.8 (18.4 (13.4 (68.6 (57.9) 91.7-80.3-18.8 (13.4) 53.1) 21.1-128) 97.1-18.2-73.7 (14.5) 84.6) 24.5) 39.6) 37.6-26.8) 17.6-44.1) 61.6-24.4-164) 96.6-44.4 (17.0) 28.4) 15.2) 65.3-49.4 (50.6-119) 63.1) 44.0 (50.0-90.1 (34.7-37.1) 22.6) 65.6-16.1) 42.8) 19.2 (83.1-23.2 (19.1-99.3-114) 328 393 342 752 742 729 1461 1647 1534 12-19 years 20 years and older 99-00* 01-02 03-04 Gender Males 99-00* 01-02 03-04 99-00* 01-02 03-04 17.4-24.6-74.6 (29.0) 55.9 (39.2-48.8 (65.5-16.1-32.2) 74.0 (18.6-139) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00* 01-02 03-04 99-00* 01-02 03-04 21.3 (42.8) 34.8) 13.3-40.0 (69.1 (15.1-83.3 (28.6-53.3-106) 74.3 (76.4-135) 71.5-23.7 (57.5) 82.7) 36.9 (19.6) 64.3 (46.3) 59.3 (17.2-108) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites 99-00* 01-02 03-04 *In the 1999-2000 survey period.8) 20.4 (16.1) 17.4-34.4) Selected percentiles ( 95% confidence interval) Sample 95th 97. interval) 22.4 (31.4 (50.2) 31.8-24.7-21.0) 26. Survey Geometric mean (95% conf.9 (56.9-105) 85.7-78.3-23.0-17.9) 14.0 (18.9 (37.7) 42.5-18.9) 62.6 (17.9) 24.6 (74.7 (73.3 (21.3-17.1) 20. 268 Fourth National Report on Human Exposure to Environmental Chemicals .3 (48.0-47.9) 49.3-71.0 (20.7-28.9) 28.5-15.4-131) 81.7-42.6) 14.6) 31.3 (60.0 (61.8) 23.4-47.9-14.0-75.0) 41.4 (31.1) 50.8 (18.3 (69.1) 20.3) 21.1 (46.0-41.8 (22.9 (58.0 (27.2-86.5-21.9-49.9-56.2-85.8-43.0) 19.3-20.1 (29.

Levels of seven urinary phthalate metabolites in a human reference population. Pirkle JL. et al. Duty S. Anderson WA. et al. Environ Res 2003. David RM. Brock JW. Monograph on the Potential Human Reproductive and Developmental Effects of Di-n-Butyl Phthalate (DBP). Rossbach B.210:21-33. Koch HM. Silva MJ.111(14):1719-1722. Jedrychowski W. Caudill SP.208:237-245. 112(5):A270]. Food Addit Contam 2001. Urinary phthalate metabolites and biomarkers of reproductive function in young men.niehs. et al. Sanchez GN.html.108(10)979-982.S. Masunaga S. Silva MJ. Scotter MJ. NTP-CERHR. Butala JH. Springall C. Perera FP. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Yoshida K. Atlanta (GA). 2000 [online]. J Androl 2004. 2005. Hu H. Barr DB. Boehmer S. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Caudill SP. Angerer J. Hagmar L. Massey RC. Hauser R. Drexler H. Meeker JD.Phthalates References Adibi JJ. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. et al. Brock JW.22(3):688-695. Phthalate monoesters levels in the urine of young children. Calafat AM. Duty SM. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. Silva MJ. Hum Reprod 2007. Environ Health Perspect 2000. Reprod Toxicol 2004. Schettler T. Eckard R. Weuve J. Castle L. Chen Z. Environ Health Perspect 2003. Int J Hyg Environ Health 2007. Richthoff J.nih. Koch HM. Drexler H. Reidy JA. Angerer J. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Singh NP. Wiesmuller GA.18(1):122. Prenatal exposures to phthalates among women in New York City and Krakow. Jacek R. Int J Hyg Environ Health 2005. Needham LL. Evaluation of the effect ofa governmental control of human exposure to two phthalates in Japan using a urinary biomarker approach. Malek NA. Centers for Disease Control and Prevention (CDC). Third National Report on Human Exposure to Environmental Chemicals. Silva MJ. Blount BC. Jonsson BAG. McKee RH.112(3):331-338.18(12):10681074. Gans G. Exposure to phthalates in neonatal intensive care unit infants: urinary concentrations of monoesters and oxidative metabolites. Green RA. Ryan L. Epidemiol 2005.93:177-185. Hilborn ED. Bolte G.68:309-314. Dobler L. A biomarker approach to measuring human dietary exposure to certain phthalate diesters.114(9):1424-1431. Ryan L. Internal phthalate exposure over the last two decades—a retrospective human biomonitoring study. Needham LL. Bull Environ Contam Toxicol 2002. Helm D. Koch HM. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. Available at URL: http://cerhr. Barr D. Calafat AM. et al. 4/20/09 Silva MJ. et al. Environ Health Perspect 2004. Wittassek M. et al. Int J Hyg Environ Health 2007. Environ Health Perspect 2006. et al. Camann DE.gov/chemicals/ phthalates/dbp/dbp-eval.16(4):487-493. Research Triangle Park (NC). Fromme H. Sampson EJ. Rylander L. Urinary levels of seven phthalate metabolites in the U. Occurrence and daily variation of phthalate metabolites in the urine of an adult population. Giwercman A. Caudill SP.25(2):293-302. Itoh H. Hodge CC. Poland.210(3-4):319-33. Fourth National Report on Human Exposure to Environmental Chemicals 269 .

3.300-. People exposed to DCHP will excrete mono-cyclohexyl phthalate (MCHP) in their urine.10 (<LOD-2.70 (1.200-.00 (<LOD-1.600) < LOD .80) .300-.700) .200-.600) .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.500 (.2.9.600) . and 03-04 are 0.500) < LOD 1.400-.S.500-.300 (.400 (.500 (.300 (.400 (<LOD-.500 (.200-.400 (<LOD-.200-.500) .400) size 2541 2782 2605 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .300 (.400) < LOD < LOD .400) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.500) < LOD < LOD .400 (.300-.400 (. Survey Geometric mean (95% conf. only levels at or above the 90th percentile could be characterized. resins.10) . see Data Analysis section) for Survey years 99-00.400) < LOD 1.500) .50) .400 (<LOD-. 01-02.400) 1.400-.400) 1. 0. and 0.70) .500 (.300) 328 393 342 752 742 729 1461 1647 1534 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .400 (.20) . interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.400 (.300) < LOD .300-.300) < LOD .00 (<LOD-1.Phthalates Dicyclohexyl Phthalate CAS No.500) .600 (.600) . including nitrocellulose.500) < LOD < LOD . 270 Fourth National Report on Human Exposure to Environmental Chemicals . 84-61-7 General Information Dicyclohexyl phthalate (DCHP) is used to stabilize some rubbers.300-.700) .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. and polymers.500 (.600) .70 (1.10 (<LOD-1. In this Report.500) .00 (<LOD-1.500) 1.200-.300 (. < LOD means less than the limit of detection.500 (. which may vary for some chemicals by year and by individual sample. population from the National Health and Nutrition Examination Survey.700) .70) .50) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.300 (.300 (.500 (.10 (<LOD-1.300-.500) 1.300-.400-.400-.200-.10 (.00-3.200 (<LOD-.00) .300 (<LOD-.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 .500) 1.300-.500 (. respectively. and polyvinyl chloride.300-. Neither IARC nor NTP has evaluated DCHP with respect to human carcinogenicity. polyvinyl acetate.600) . 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.400-.400 (.400-. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.900-1.400 (<LOD-.300-. Biomonitoring studies on levels of urinary MCHP provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of DHCP than are found in the general population. Finding a measurable amount of MCHP in urine does not mean that the levels of MCHP or the parent compound cause an adverse health effect.300 (.500 (.00-2.90) .400 (.

530 (.17) .500) size 2541 2782 2605 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .310) < LOD .500 (.400-. Survey Geometric mean (95% conf.410 (.490) .420-.530) 1.360-.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) .690) < LOD < LOD .590 (.660) < LOD < LOD .620) < LOD .11) .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 .660) .54-6.590 (<LOD-.390 (.480 (.220 (<LOD-.370 (<LOD-.33 (<LOD-3.33) .630 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.690) < LOD 2.74) .54 (<LOD-2.400-.530-.790-1.910 (.00 (<LOD-3.500-.16) .450 (.34) .470) 3.10) .170-.00) .670 (<LOD-.16 (<LOD-3.510 (.500) 3.43 (1.310-.510-.270) < LOD .610 (.530-1.710) .690-1.44) .36-1.350-.05) .06) .420-.470 (.380 (.22 (<LOD-1.S.670-1.770-1.380-.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.830) 1.67 (1.240-.82 (1.560) 1.53) . interval) Selected percentiles ( 95% confidence interval) Sample 95th 3.910 (.54) .18) .880 (.910 (.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.800-1.770 (.14 (<LOD-3.940 (.53) .330 (. population from the National Health and Nutrition Examination Survey.910 (.250 (.12-1. Fourth National Report on Human Exposure to Environmental Chemicals 271 .770-1.420-.740) < LOD < LOD .770) < LOD 2.590) 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 .770-1.450 (.740) .330 (.630 (<LOD-.82) .260-.950 (.690 (.290-.

S. and 03-04 are 1.9 (61. population from the National Health and Nutrition Examination Survey. In contrast.3 (82.. 272 Fourth National Report on Human Exposure to Environmental Chemicals . shampoos.3-110) 211 (160-278) 197 (159-243) 225 (187-270) 190 (164-219) 191 (171-214) 205 (176-238) 75.3 (74. Workplace air guidelines for external exposure to DEP have been established by ACGIH and NIOSH. 2002). respectively.4 (62. soaps. particularly those containing fragrances. 01-02. colognes.8-111) 85. 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. 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. and also in men attending a Boston infertility clinic (Hauser et al.5) 81. 0. 2003) and African-American women in Washington.1 (71. deodorants. People exposed to DEP eliminate mono-ethyl phthalate (MEP) in their urine. 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.4.2. a sample of young Swedish males entering the military had median urinary MEP levels that were somewhat higher than males in the NHANES subsamples.7 (70. Biomonitoring Information MEP levels in the NHANES 1999-2000. and hand lotions.9-92.1-93..Phthalates Diethyl Phthalate CAS No. see Data Analysis section) for Survey years 99-00. Neither IARC nor NTP has evaluated DEP with respect to human carcinogenicity. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. Products that may contain DEP include perfumes. and 0. 2007). 2001-2002. 84-66-2 General Information Diethyl phthalate (DEP) is a solvent used in many consumer products.9.. DC (Hoppin et al.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.2-102) 95.7) 71.

6 (77.9 (82. In an analysis of NHANES 1999-2000.7-110) 81.. 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. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.. Other population estimates also differed by sex and race ethnicity (Silva et al.0 (66. This age-related trend is opposite the direction seen for other phthalates.5-113) 122 (93. 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..3-105) 87. 2004). Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 2003) were slightly lower than levels found in NHANES 2001-2002.0-156) 140 (111-180) 150 (123-184) 154 (136-177) 160 (146-182) 177 (147-202) 165 (127-208) 177 (135-224) 180 (145-203) 364 (275-495) 330 (249-409) 363 (292-485) 390 (336-452) 419 (363-486) 512 (423-632) 341 (219-554) 512 (290-802) 470 (310-596) 879 (676-1260) 808 (590-1100) 791 (589-1080) 1010 (803-1460) 1060 (884-1320) 1230 (989-1610) 625 (400-784) 843 (512-1320) 719 (470-1330) 1760 (1000-2000) 1330 (868-1840) 1470 (987-2220) 2170 (1790-3350) 2120 (1520-2790) 2290 (1770-3200) 328 393 342 752 742 729 1456 1647 1534 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 141 (124-159) 148 (130-168) 154 (139-171) 187 (165-211) 187 (166-210) 211 (180-248) 120 (107-134) 126 (110-147) 127 (108-150) 158 (142-179) 171 (148-188) 181 (148-217) 324 (249-415) 352 (282-425) 390 (341-465) 377 (307-495) 407 (355-473) 508 (379-634) 1000 (693-1480) 1100 (839-1480) 1070 (852-1360) 822 (697-1170) 860 (712-1100) 1120 (889-1400) 1950 (1460-2900) 2120 (1490-3030) 2000 (1610-2410) 1930 (1170-3410) 1430 (1190-2010) 2250 (1440-3330) 1214 1371 1250 1322 1411 1355 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 164 (142-190) 213 (182-249) 241 (213-271) 208 (183-236) 247 (226-271) 254 (225-287) 149 (135-165) 157 (142-173) 165 (144-189) 154 (136-174) 199 (164-242) 233 (202-270) 196 (166-228) 227 (185-270) 212 (188-246) 128 (111-142) 136 (124-150) 135 (120-158) 382 (314-472) 461 (396-572) 533 (417-665) 443 (390-505) 557 (478-618) 619 (476-791) 313 (239-387) 338 (288-402) 386 (338-485) 814 (673-974) 1080 (860-1650) 1230 (956-1610) 1030 (762-1700) 1240 (961-1480) 1530 (1200-1970) 856 (655-1390) 919 (712-1160) 989 (831-1330) 1330 (974-1920) 1940 (1410-2630) 2270 (1810-3140) 1920 (1230-2590) 2090 (1550-2800) 2590 (2160-3500) 1950 (1480-2740) 1590 (1320-2170) 1920 (1400-2780) 813 677 652 603 703 699 908 1216 1088 Non-Hispanic blacks Non-Hispanic whites Fourth National Report on Human Exposure to Environmental Chemicals 273 . with adjusted geometric mean levels of urinary MEP that increased with age (CDC.0-117) 142 (119-169) 152 (126-184) 168 (141-201) 179 (161-199) 181 (164-200) 197 (174-223) 79.2 (66. Urinary Mono-ethyl phthalate (MEP) (creatinine corrected) Metabolite of Diethyl phthalate (DEP) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.5-114) 101 (87. Analysis of NHANES 2001-2002 showed similar findings. 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. 2002). 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. 2005).9-110) 96. Median MEP levels found in a small sample of German residents (Koch et al. population from the National Health and Nutrition Examination Survey.6 (65.Phthalates 2002 (Brock et al.S.

Poland. Angerer J. Silva MJ. Koch HM. Ryan L. Reidy JA. Brock JW.110(5):515-518. Camann DE. Brock JW.22(3):688-695. Baird DD. Jedrychowski W. Singh NP. Environ Health Perspect 2003. 2005. Environ Health Perspect 2002. Perera FP. et al. et al. Barr D. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Prenatal exposures to phthalates among women in New York City and Krakow. Rossbach B. Silva MJ. Hilborn ED. Silva MJ. Phthalate monoesters levels in the urine of young children. et al. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Barr DB. 112(5):A270]. Duty S. Reproducibility of urinary phthalate metabolites in first morning urine samples.112(3):331-338.111(14):1719-1722. Meeker JD.Phthalates References Adibi JJ. Third National Report on Human Exposure to Environmental Chemicals. Jacek R. 274 Fourth National Report on Human Exposure to Environmental Chemicals . Centers for Disease Control and Prevention (CDC). Hum Reprod 2007. Davis BJ.68:309-314. Needham LL. Environ Res 2003.S. Environ Health Perspect 2004. Hoppin JA. Caudill SP. Atlanta (GA). Caudill SP. Hauser R. Urinary levels of seven phthalate metabolites in the U. Hodge CC. Drexler H.93:177-185. Malek NA. Bull Environ Contam Toxicol 2002.

.50-14.7) 18.60) 7.4) 23.0 (14.24-4.40-9. Four metabolites were measured in this Report: mono-(2-ethyl-5-hexyl) phthalate (MEHP).69) Selected percentiles ( 95% confidence interval) 50th 3.60) 9.8) 17.0-19.0) 328 393 342 752 742 729 1461 1647 1534 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 3.90-5.90) 3.5) 43.6) 15.61 (3.40 (4.50 (7.70) 2.80) 13.5 (18.70-3.90 (1.9-57.60) 4. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.80 (8. toys.50-5.8-36.60) 8.30-11.80-27.5 (30.98) 2.46) 3.1-27.4-20.94-3.57-7.0) 23.3 (24.77 (2.50-5.10 (6.40-9.50 (3.9 (17.10 (5.9-19.7-58.3 (19.80-3.5) 32.1982).20 (1.00) 5.5-28.70-2.9.40-11.50-2.10-2.90) 4.10-5.4) 22.4-27.26-2.5 (31.6) 14.4 (21.83) 2.2) 42.15 (1.42) 3.2-17.90-4.50-6.9) 27.20 (3.60 (6.9) 5.90-3.40-12.32 (3.89-3.5 (12.6) 14.50) 4.50-3.9 (15.40-8. which is used for many consumer products.42-5.10 (2.00-3.10) 3.60 (5.0) 31.9 (13.6-28.91-3.70-4.00) 2. see Data Analysis section) for Survey years 99-00.39) 3.4) 22.10 (3.31-4.3-64.30-6.63-4.20 (3.7) 27. mono-(2-ethyl5-hydroxyhexyl) phthalate (MEHHP) and mono-(2-ethyl5-carboxypentyl) phthalate (MECPP). packaging film.6-23.41) 3.60) 10.40 (4.2.1) 25.16 (2.79) 2.70 (3.60-7.0 (18.10) 2.4) 13.70 (2.12 (4.7-32.30-13.27) 2.0 (21.30 (7.60) 90th 14.70-5.40 (4.2-35.10) 3. DEHP present in medical devices and parenteral delivery systems results in the diester rather than the monoester form being directly introduced into the blood.0) 39.51) 4.92-5.40) 4.10) 3.50 (2.6-25.84 (2. DEHP is metabolized to more than 30 metabolites which are rapidly eliminated in urine.6 (41.5-36. and 03-04 are 1.9) 15.00 (7.1 (8.70 (1.86) 2.2 (31.9-49.0-18.00 (5.2) 6.37-4.5 (18.5-17. MEHP is primarily formed by the hydrolysis of DEHP in the gastrointestinal tract and then absorbed.1-29.6 (9.00) 9.8-47.41 (3.85) 4.5 (24.90-11.30 (4.00-4.9-29. and in humans.92) 4. 2002.23) 3.49 (3.00) 11.2 (7.0) Total 4.9 (29.3-25. and 0.0 (17.1) 19.68 (3.6 (20.9 (29.86) 2.40) 11.0 (13.8 (19.84-4.50-3.50-16.10 (4.85 (3.9 (26.40) 75th 7.0.90-8.96-5. Urinary Mono-2-ethylhexyl phthalate (MEHP) Metabolite of Di-2-ethylhexyl phthalate (DEHP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. and blood product storage and intravenous delivery systems.4) 5.10) 8.S.70 (8.1-17.30) 2.50-2.6) 95th 23.5) 40. DEHP has been removed from or replaced in most toys and food packaging in the United States