2009

Fourth National Report on Human Exposure to Environmental Chemicals

Fourth National Report on Human Exposure to Environmental Chemicals

2009

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

Contents

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

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

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

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

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

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

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

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Introduction

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

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

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2'.1-Dichloroethane 1.3-Dichlorobenzene (m-Dichlorobenzene) 1.4'.4.html.3.gov/exposurereport/chemical_selection.4.5.5'-Hexabromobiphenyl (BB 153) Volatile Organic Compounds (VOCs) Benzene Chlorobenzene (Monochlorobenzene) 1.1-Dichloroethene (Vinylidene chloride) cis-1. Table 1. The process for selection is described at http://www.5-Pentabromodiphenyl ether (BDE 99) 2.and p-Xylene o-Xylene 2 Fourth National Report on Human Exposure to Environmental Chemicals .3'.4.4'.2-Dichloroethane (Ethylene dichloride) 1.3.2'.4-Tribromodiphenyl ether (BDE 17) 2.5'-Hexabromodiphenyl ether (BDE 153) 2.5'. Paradichlorobenzene) 1.6.3-Tetramethylbutyl] phenol) Triclosan (2.2-Dichloroethene Dichloromethane (Methylene chloride) 1.4'.4.2'.6-Pentabromodiphenyl ether (BDE 100) 2.4'.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'-Tribromodiphenyl ether (BDE 28) 2.2-Dichlorobenzene (o-Dichlorobenzene) 1.6'-Hexabromodiphenyl ether (BDE 154) 2.1.4.2'.4.1-Trichloroethane (Methyl chloroform) 1.1.What’s New in this Report What’s New in this Report In this Fourth Report.4.4.2-Dichloropropane 2.2-Tetrachloroethane Tetrachloroethene Tetrachloromethane (Carbon tetrachloride) Toluene 1. Chemicals reported for the first time in the Fourth National Report on Human Exposure to Environmental Chemicals.4.4’.4’-Trichloro-2’-hydroxyphenyl ether) Non-dioxin-like Polychlorinated Biphenyls 2.5’.2'.2'4.5.3.3.5'-Tetrachlorobiphenyl (PCB 49) 2.1.2-Dichloroethene trans-1. 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 (2.6-Heptabromodiphenyl ether (BDE 183) 2.4.cdc.2'3.4'-Pentabromodiphenyl ether (BDE 85) 2.5.3’.4'.2'.2-Trichloroethane Trichloroethene (Trichloroethylene) m. 2009 Acrylamide Adducts Acrylamide Glycidamide Total and Speciated Arsenic Arsenic.4'-Tetrabromodiphenyl ether (BDE 47) 2.1.4’.2'.2'. 75 new chemicals are added for the 2003-2004 survey period and are listed in Table 1.5'-Tetrachlorobiphenyl (PCB 44) 2.5.4.4.2’.4'-Tetrabromodiphenyl ether (BDE 66) 2.5-Dimethylfuran Ethylbenzene Hexachloroethane Methyl-tert-butyl ether (MTBE) Nitrobenzene Styrene 1.2.2'.2-Dibromo-3-chloropropane (DBCP) Dibromomethane 1.2-bis[4-Hydroxyphenyl] propane) 4-tert-Octyl phenol (4-[1.4-Dichlorobenzene (p-Dichlorobenzene.

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

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

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

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

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. Fourth National Report on Human Exposure to Environmental Chemicals 7 . we have improved the procedure for estimating percentiles to better handle this situation. Taylor JK. Lewis Publishers. Quality Assurance of Chemical Measurements.Data Sources and Data Analysis Report. This improved procedure makes each repeated value unique by adding a unique negligibly small number to each repeated value. 1987. Therefore. Boca Raton (FL). Appendix A gives the details of the new procedure for estimating percentiles.

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

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

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

3 (55. 2005).4) 57.4 (53. and binding agents. 217 million pounds of acrylamide were produced commercially in the U. Smaller scale applications of polyacrylamides include additives to paperboard used for food packaging. Recently. pulp and paper production.0) 57.0-58.0 (53. or to glutathione conjugates (Calleman et al.2-114) 163 (147-191) 96. the main source of exposure is from the diet.1 (83.S.7-60. Survey Geometric mean (95% conf. EPA. smoking.6-104) 82.3) 63. widely distributed in tissues.3-2. Fennell et al.6-61. These estimated intakes are hundreds of times lower than occupational exposures.1) 101 (95. In 1997.2 (62. Tareke et al.6) 50. EPA reference dose of 0.5 (79. Elimination occurs mainly in the urine as mercapturic acid conjugates.9) 57.2 μg/kg/day (U.6) 71. In the general population. EPA. drinking water. and an average daily intake is estimated as 0.1) 53. 2005).S.0 (67. but are generally above the U.9-61. People may be exposed to acrylamide from foods. 1994). Foods such as french fries and potato chips can contain acrylamide at levels up to 100 times greater than levels found in cooked fish or poultry (DiNovi and Howard.8-55.5) 66.8 (52.2-77.3) 70. 2005. gels. such as potatoes and some grains.4 (59.7 (63.6 (51.0-104) 132 (115-151) 223 (194-243) 141 (120-152) 220 (189-237) 164 (147-191) 350 769 1889 2570 1523 3509 3592 03-04 03-04 03-04 61.6-65.4-83.0-108) 152 (139-175) 126 (111-142) 108 (86.0-49.9) 58.4-60. interval) 61.7) 75th 79. FAO/WHO.1) 46.9) 75. and well below doses known to cause nerve damage or carcinogenicity in animals.1-64.5 (44. as an absorbent in disposable diapers.7 (58. and peripheral neuropathy following chronic Acrylamide Geometric mean and selected percentiles of hemoglobin adduct concentrations (in pmol/g hemoglobin) for the U.S. mineral processing.2-70. 2005).9-105) 86.4) 57. FDA.4 (51. in some sealing grouts. Animal studies indicate that acrylamide is well absorbed. (NTP-CERHR.0 (69. Commercially. population from the National Health and Nutrition Examination Survey. acrylamide has produced upper airway irritation following inhalation of high levels.0 μg/kg for adults (FAO/ WHO.5 (52.4) 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. are heated at temperatures used for frying and baking.7-64.5-80.7) 54.4-89.0 (57.S. but can covalently bind to form adducts with proteins.2-93.2-59.6-75. 2005).2-91. In humans.4-60. 2004. Polyacrylamides are useful water-compatible polymers used in water treatment.. it was discovered that acrylamide is formed when starch-rich foods. 2005).7 (55. ocular and dermal irritation from direct contact with acrylamide containing materials. and in some cosmetics.5) 58.9 (54. and in the synthesis or compounding of dye materials.2) 57. Natural substances in the food are converted to acrylamide.4 (54. in permanent press fabrics.0-66.1-64.1-57. 2002).7) 58. and cosmetics (NTP-CERHR. glycidamide.4-76.6-108) 61.4) 100 (89.2-118) 98.6 (81. 2006.7 (65. 1990.0.8-57.S.8 (91.9 (69. and is either metabolized to the reactive epoxide.2-67.2 (58..3 (53. Acrylamide is not thought to accumulate in the body at environmental doses.1) 62.1 (47.2 (75.1 (73.6) 90th 141 (124-155) 03-04 03-04 03-04 03-04 03-04 03-04 03-04 59. see Data Analysis section) for Survey year 03-04 is 3.1-61.0-115) 156 (120-203) 146 (129-163) 149 (125-179) 218 (172-271) 197 (172-223) 1792 1874 2994 Limit of detection (LOD.Acrylamide Acrylamide CAS No.5-85.7) 96.4 (54. 2006). 79-06-1 General Information Acrylamide is a small organic molecule existing as a white crystalline powder in its pure state.1 (88. Estimated intakes in children are about twice that of adults (DiNovi and Howard.1) 55.3-71. acrylamide is synthesized and used in the production of polyacrylamide polymer.5 (74.6-66.9 (60.0) 85.2) 57. soil conditioners.7-64. although additional exposures from cosmetic products could add a similar amount (NTP-CERHR. Since acrylamide has limited volatility and high water solubility.9) 63. Fourth National Report on Human Exposure to Environmental Chemicals 11 .8 (57. and from dermal contact with products that contain residual acrylamide.3) 86..7) 73. environmental releases of acrylamide can enter aquatic systems and soils where it degrades within days and does not bioaccumulate (U.6) 90. 2004).8 (81.1 (52.6) 73.6 (56.9-52.

2003. and to increase DNA reactivity when glutathione availability is reduced (Klaunig et al. Schettgen et al.S.1) Selected percentiles ( 95% confidence interval) Sample 95th 167 (153-181) size 7278 Total Age group 3-5 years 6-11 years 12-19 years 20-59 years 60 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 59.5 (83. Survey Geometric mean (95% conf. dominant lethality)..1) 60. 2006) have been demonstrated after acrylamide dosing.1 (56.4) 46.4) 83.9 (57.9) 59.7 (61.. Puppel et al. glycidamide (NTP-CERHR.3 (56. scrotal. although different analytic methods can affect results.2-90. In addition.. Puppel et al.5 (56. 2005.7-62. uterine. 1997. and other sites) (FAO/WHO..9-77.2) 55. probably through its epoxide metabolite.5-66.6-64.0 (80.5) 75th 85.5 (42.7) 74. Adducts are formed when either acrylamide or glycidamide react to form a permanent covalent bond with hemoglobin in the blood. Animal studies have shown that acrylamide can cause nerve damage (neuropathy).epa.7-86.0) 118 (103-126) 121 (112-134) 113 (94. adrenal.4-65. 12 Fourth National Report on Human Exposure to Environmental Chemicals ..2 (72.3) 85. EPA.. 2004.9) 87. 2009). Hagmar et al.S. presynaptic nerve terminal binding (LoPachin. 2005.8 (51.5 (59.7 (57.. Glycidamide has been shown to react with DNA (Doerge et al.9) 65.9-62. fetal death. Glycidamide Geometric mean and selected percentiles of hemoglobin adduct concentrations (in pmol/g hemoglobin) for the U.3) 59. 2005.5-64.7) 61. 2005. 2005). male germinal cell injury. NTP-CERHR. EPA at: http://www.6-90.4 (61. gov/iris/ and from the Food and Agriculture Organization of the United Nations and WHO at: http://www. 2005. 2005.1-70.7) 60.2) 87. 1997.4 (57.. respectively) are markers of integrated acrylamide exposure over the preceding few months. 2006. 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. Vesper et al. 2005) and sperm DNA adducts (Xie et al. 2008).8-48. U. Acrylamide is clastogenic and can produce dominant lethal mutations. Maniere et al.8-61. and neuronal DNA reactivity (Doerge et al.9 (58. see Data Analysis section) for Survey year 03-04 is 4.1-62.0 (52.4-59. 2002.7 (84.0 (70.0-62. Biomonitoring Information Acrylamide and glycidamide hemoglobin adducts (AHA and GHA. Additional information is available from U.3-78.7 (87.1 (66.5) 87.9 (81. 2005. Vesper 2005) and smoking (Bergmark.9-64.4 (56.9-138) 143 (130-159) 96. Several of these studies have shown that smokers have adduct levels that are three to fourfold higher than non-smokers..5-92.. reproductive effects (reduced litter size.8) 60.1-60. 2005. Schettgen et al. 2004).5-94.4 (90.int/ ipcs/food/jecfa/summaries/summary_report_64_final.. 2005) have been demonstrated in animals.4-103) 79.4 (81. 2006)..9) 75. 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.. AHA levels have been shown to increase with dietary intake (Hagmar et al.1) 62.1 (57.0 (75.4) 53.8) 45.4 (51.pdf. 2005).. U.9-76.0-103) 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 64.1-56. Rice. most non-smokers had levels less than about 100 pmol/gram hemoglobin. 2005).2 (63.. thyroid.8-49.9-78.5) 90th 130 (120-141) 03-04 03-04 03-04 03-04 03-04 03-04 03-04 71.1 (82.1 (70. 2005.6 (90.2 (56.2) 65.0.who.4-98.. levels of AHA adducts decline but may remain detectable for several months (Hagmar et al.3) 59. 2006). to increase the unscheduled synthesis of DNA in tumor susceptible tissues (Klaunig et al.3) 59.. 2005). After exposure ceases.2-91.Acrylamide occupational exposures. Mucci et al. 2005.S. 2005. 2008).0) 94..1) 56.0-93. Axonal degeneration.7) 90.7-64.3-101) 95. altered gene expression in testicular tissues (Yang et al. population from the National Health and Nutrition Examination Survey..S. 2002. Klaunig et al.. IARC classifies acrylamide as probably carcinogenic to humans.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. Younger children may have slightly higher levels possibly due to increased intake of acrylamide-containing foods relative to body size (Dybing et al.2-68.5) 71.6-62. EPA. interval) 59.6 (66. 2001).8 (44. and cancer (mammary.

DNA adducts derived from administration of acrylamide and glycidamide to mice and rats. Spicer R. Perez et al.. Rome.. Adv Exp Med Biol 2005. Relationships between biomarkers of exposure and neurological effects in a group of workers exposed to acrylamide. Mucci LA. 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. da Costa GG. Food Chem.int/ipcs/ food/jecfa/summaries/summary_report_64_final. Malmberg B. Human exposure and internal dose assessments of acrylamide in food.. NIH Publication No. gov/~dms/acrydata. Scand J Work Environ Health 2001. Fennell TR. Toxicol Sci 2005.126(2):361-371. Granath F. Snyder RW. J Agric Food Chem 2008. symptoms of numbness or tingling in the extremities did not occur in exposed workers whose AHA levels were below 510 pmol/gram hemoglobin. References Bergmark E.Acrylamide In occupational settings. 2006.85:447-459. He F. Bruze M. Kamendulis LM. Twaddle NC. Available at URL: http://cerhr.fda. Kautiainen A. Hagmar et al. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Alexander J. AHA levels were several fold to several hundredfold higher than levels in non-exposed non-smokers (Bergmark et al. Churchwell MI. The Updated Exposure Assessment for Acrylamide. 2/3/09 Klaunig JE. morphological and molecular endpoints in animal models. Available at URL: http://www.561:21-37. July. Aprea P. Chem Res Toxicol 1997 Jan. 8-17 February 2005. 2004. Mutat Res 2005.580(1-2):157-165.Toxicol Appl Pharmacol 1994. 2005. Costa LG. McDaniel LP. Mechanisms of acrylamide induced rodent carcinogenesis. 1994). Osterman-Golkar S. Wirfalt E.niehs. LoPachin RM. In another study. Costa LG. and 39% of workers with levels above 1000 pmol/gram hemoglobin had these symptoms (Hagmar et al. CFSAN/Office of Plant and Dairy Foods.who. Tornqvist M. Bridson WE. Summer SCJ. Toxicol Appl Pharmacol 1993. Godard T. et al.pdf. Food and Drug Administration (FDA). Wu Y.pdf. 6013-6019. Guffroy M. 054472.43:365–410. Toxicol 2005.. et al. 2/3/09 Hagmar L. Center for the Evaluation of Risks to Human Reproduction (NTP-CERHR). 2009 Jan 8. Cheong HK. Monograph on the Potential Human Reproductive and Developmental Effects of Acrylamide. Rosen I.html#u1004. Duale N. 1993. Calleman CJ. Chem Res Toxicol 1990. et al.gov/chemicals/ acrylamide/Acrylamide_Monograph. Acrylamide neurotoxicity: neurological. Italy. Biomarkers of human exposure to acrylamide and relation to polymorphisms in metabolizing genes. Bergmark E. Andersen M.580(1-2):131-141.3:406-412. Becher G. 1999). Hemoglobin adducts of acrylamide and acrylonitrile in laboratory workers. Uncertainties. DiNovi M and Howard D. Farmer PB. Wilson KM. DNA damage and DNA adduct formation in rat tissues following oral administration of acrylamide.10(1):78-84. 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. Survey data on acrylamide in food: individual food products. Bjellaas T. Churchwell MI. Simultaneous analysis of hemoglobin adducts of acrylamide and Fourth National Report on Human Exposure to Environmental Chemicals 13 . Tornqvist M.580(1-2):119-129. 2001. Beland FA.cfsan. Laurentie M. Mutat Res 2005. April 13-15. Calleman CJ. Fennell TR. Available at URL: http://www. Tian G. 2004 Acrylamide in Food Workshop: Update Scientific Issues. 2/3/09 Perez HL. Mutat Res 2005. et al. Paulsson B.56. Health effects of occupational exposure to acrylamide using hemoglobin adducts as biomarkers of internal dose. Doerge DR. Axmon A.561:49-62. Toxicol Sci. [Epub ahead of print] Dybing E..27(4):219-226. Adv Exp Med Biol 2005. February. Differences in hemoglobin adduct levels of acrylamide in the general population with respect to dietary intake. Nordander C. 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. Burgess J. Chicago. National Toxicology Program. smokers and nonsmokers. and Research Strategies. Illinois. He F. Magnusson AL. Bergmark E. Calleman CJ. Bergmark E. Joint FAO/WHO Expert Committee on Food Additives. smoking habits and gender. Maniere I. Haugen M. Determination of hemoglobin adducts in humans occupationally exposed to acrylamide. et al. Acrylamide intake through diet and human cancer risk.120(1):45-54. Doerge DR. Hagmar L. Paulsen JE. 64th Meeting: Summary and Conclusions (FAO/WHO). Metabolism and hemoglobin adduct formation of acrylamide in humans. Yang JS. Acrylamide is metabolized to glycidamide in the rat: evidence from hemoglobin adduct formation. 2001). Zhang S.

1994. September. Drexler H.207(6):531-9. Integrated Risk Information System (IRIS). Gray JG. The carcinogenicity of acrylamide. Available at URL: http://www. Mutat Res 2005 Feb 7. U.txt. Toxicological effects of acrylamide on rat testicular gene expression profile. Han CH. U.htm. Meyers T. Automated method for measuring globin adducts of acrylamide and glycidamide at optimized Edman reaction conditions.206(1):9-14. Angerer J. Licea-Perez H. Reprod Toxicol 2005. Tjønneland A.epa. Liu K. Environmental Protection Agency (U. J Agric Food Chem 2008. Vesper HW. Adduction of biomacromolecules with acrylamide (AA) in mice at environmental dose levels studied by accelerator mass spectrometry. Rossbach B. a carcinogen formed in heated foodstuffs. Ingham L. Angerer J. Adv Exp Med Biol 2005. Washington (DC). Benetou V.S.gov/chemfact/s_acryla. Meyers T. Liu Y. Toxicol Lett 2002. Ospina M.19(4):527-34.S.S. Tornqvist M. Schettgen T. Chemical Summary for Acrylamide. 2/3/09 Vesper HW. Hallmans G. Cross-sectional study on acrylamide hemoglobin adducts in subpopulations from the European Prospective Investigation into Cancer and Nutrition (EPIC) Study.134(1-3):65-70. et al. Lee MH. Karlsson P. Rapid Commun Mass Spectrom 2006. Myers GL. Schettgen T. Environmental Protection Agency (U. Yang HJ. et al. Broding HC.163(2):101-8. Tjaden Z. Slimani N. Tareke E. J Agric Food Chem 2002. Fu D. acrylonitrile and acrylamide-biomarkers in occupational and environmental medicine. Choi JH. Kutting B.gov/iris/subst/0286. Letzel S. Agudo A.561:89-96. 2/3/09. Mutat Res 2005. Sun H. Pilot study on the impact of potato chips consumption on biomarkers of acrylamide exposure. A first approach to estimate the internal exposure to acrylamide in smoking and non-smoking adults from Germany. Smith A. Eriksson S.274(1):59-68. 14 Fourth National Report on Human Exposure to Environmental Chemicals . Vesper HW. EPA). Xie Q. Toxicol Lett 2006. Lee SH. Anal Biochem 1999. Puppel N. Fueller F. Weiss T. DNA strand breaking capacity of acrylamide and glycidamide in mammalian cells. Drexler H. Schettgen T. Jin Y. Chae C. propylene oxide. Han DU.epa.56(15):6046-53. EPA). Ospina M. revised 1/3/06. Hemoglobin adducts of ethylene oxide. Ding X. Rice JM.580(1-2):71-80.50(17):4998-5006. Rydberg P.S. Office of Pollution Prevention and Toxics. Determination of haemoglobin adducts of acrylamide and glycidamide in smoking and non-smoking persons of the general population. Drexler H.Acrylamide glycidamide by gas chromatography-mass spectrometry. Marko D. Int J Hyg Environ Health 2003. Int J Hyg Environ Health 2004.20(6):959-64. Acrylamide. Analysis of acrylamide. Available at URL: http://www. Angerer J.580(1-2):3-20.

83% of measurements had an LOD of 0.040-.360) .043-.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. producing roughly 1–2 mg of bioavailable nicotine per cigarette (Benowitz and Jacob.S.164 (.23 (1. and 17% had an LOD of 0.77 (2.42-4.740-1.54) 1.060 (<LOD-.68) .96 (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 .14-1.063) .190-.137 (.09-2.44) 2.01 (1.080-.163 (.060) .580 (.32-2.S.44 (1.180) .160) .96-4.770) . 2006).142-. Cigarettes contain about 1. 2004).084) .60-2.997-3.076-.53-4.073) < LOD .153-.50-1.201) .55 (1.54 (1.120 (.080 (.S.850 (.540-.015 ng/mL.086 (.800 (.220) .57) 2.505 (. and more than 50 compounds present in ETS are known or reasonably anticipated to be human carcinogens (NTP.320) .20-2.071) .015.78) 2.030 (.144 (.93) .19) .520 (.48-3.077) .900-1.14) .20) .09-3.55-2.21-1.05.17) .190-.92 (1.060 (.960-1.068) .068) .060-.130 (.30) 2.62) 2. ear problems.106-.930 (.670) .110-.32) 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.21-1. 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.145) .310-1.17 (1.26-1.50) 3.66-3.100-.110 (.140 (.53 (1.302) .68) 2.075 (.16) .260) 1.080-.04 (1.197) .950 (.790) . Survey Geometric mean (95% conf.63 (2.180) .14) .20 (.230 (.43 (1.94) 1.180) .175 (.580-1.164 (.220-.050-.120 (. acute respiratory infections.070) . 2004).47-3.480-.12 (1. stroke.060 (. and 03-04 are 0.35 (2.080-.198) * .160 (.070) 75th .910-1.124 (.76 (1.087) < LOD < LOD .167 (.137-.710 (.062 (.88 (1.058 (. The consequences of smoking and of using smokeless tobacco products are well known and include an increased risk for several types of cancer.080-.059-.054 (.110) .080) < LOD .730 (.052 (<LOD-.70-2.020-.053 (<LOD-.180) .99) 2.120 (.050) .09-3.77 (1.01) 3.120 (.150) .090-.30) * . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.18-3.20) 1.75) 1.163) .040-.120) .094) .510 (.20 (1. population from the National Health and Nutrition Examination Survey.54) size 5999 6819 6320 Total years 99-00 01-02** 03-04 50th .350 (.070) .02) 1.820) .84-3.190-.052 (<LOD-.660) .533-.230) .19) 1.066) . The smoke produced by burning tobacco contains at least 250 chemicals that are toxic or carcinogenic.120-.28) .12 (2.088-.506 (.45) 1.630 (.050 (.740-1.131 (.65 (1.148-.050 (<LOD-.600-1. ** In the 2001-2002 survey period.23 (2.44 (2.89) 1. Fourth National Report on Human Exposure to Environmental Chemicals 15 .625) .160) .400-.050) . and exacerbated asthma (U.85 (1. and 0.63-2.450-.Cotinine Cotinine CAS No. DHHS.66) 1.690 (.87-3. see Data Analysis section) for Survey years 99-00.180) .110 (.066-.188) .54 (1.060-.089) Age group 3-11 years 99-00 01-02** 03-04 .110-.077) .23-2.104-.40) .12) 1.39) 3.50-4.120-.630 (.040 (.070 (<LOD-.30) 2. and various other disorders (U.77 (1.15 (2.580) .480-1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.140-..160 (.310) .28-1.200) 1.111-.050 (<LOD-.621-1.080 (.840) 3.44) 2.00) 1.620 (.050-.234) .96) 2.216 (.05 ng/mL.080) < LOD < LOD .180 (.087 (.430-1.70) 2.180 (.990) .428-.770-1.108) * .726) .32-2.213) .220) .300) .187) .50 (1.22) 2.090-.860 (.920 (.540 (.500 (.15) 2.05) 1.68 (1.42 (1.050 (<LOD-.061) < LOD .350-.00) .030-.070-.115-.120 (.770) .312) .126) .066 (.310) 90th 1.17 (.047-.030-. acute respiratory illness.110-.19-2. Persons exposed to secondhand tobacco smoke (environmental tobacco smoke [ETS]) may have adverse health effects that include lung cancer and coronary heart disease.310-1.570-1.23 (.34 (1.990 (.48-2.140 (.88 (.160-. < LOD means less than the limit of detection.139) * .040 (.620-1.11) .95) 1.240 (.33-2.83-2.66 (1.060-.130) .950-1.110 (. Children exposed to ETS are at increased risk for sudden infant death syndrome.22) 2789 3152 2937 3210 3667 3383 Females Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 * .030-.060 (<LOD-.040 (.39 (1.047-. respectively. cardiovascular disease.193) . DHHS.02) 1.99) 2.62 (2.140-.410) .050 (<LOD-.350-. 1998).057-. which may vary for some chemicals by year and by individual sample.059-. maternal exposure during pregnancy can result in lower birth weight.160 (.470-.5% nicotine by weight (Kozlowski et al.570 (.090-.260-1.49) 1.308 (.12-4.110 (.087-.630 (.79) 3.210 (.150) .110 (.110) .071 (.280 (.49) 1.370-. emphysema.154-.21 (.02 (.81-2.38-2.

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

International Agency for Research on Cancer.S Department of Health and Human Services (U. Exposure of the U. Jarvis MJ. Biomonitoring data can also help scientists plan and conduct research about exposure to ETS and about its health effects. Health Effects of Exposure to Environmental Tobacco Smoke: The Report of the California Environmental Protection Agency. Current Intelligence Bulletin 54: Environmental tobacco smoke in the workplace. References Armitage AK.63:139-43. et al. Benowitz NL.114(6):853-858. The Health Consequences of Smoking: The Surgeon General’s Report—Executive Summary. Bernert JT. Benowitz NL. Atlanta (GA): 2005. Decrease in the prevalence of environmental tobacco smoke exposure in the home during the 1990s in families with children.S.gov/tcrb/monographs/10/. Centers for Disease Control. Racial/ethnic differences in serum cotinine levels among adult U. Filter ventilation and nicotine content of tobacco in cigarettes from Canada. Pirkle JL. Giovino GA.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. National Toxicology Program (NTP). Pirkle JL. Respiratory nicotine absorption in non-smoking females during passive smoking. Benowitz NL. Sweeney CT. Dollery CT. Brody DJ. Herrera B. DHHS).cancer.56:483-493.php. Modin G. National Center for Chronic Disease Prevention and Health Promotion. cigarette smokers: the Third National Health and Nutrition Examination Survey. Summary of Data Reported and Evaluation [online] 2004. Jacob P III. Houseman TH. Jacob III P. et al. Mehta NY. Department of Heath and Human Services. Am J Public Health 2004. the United Kingdom. 1999. Available at URL: http://monographs. Schober SE. Perez-Stable EJ. Herrera B. IARC Monogr Eval Carcinog Risks Hum.S.fr/ENG/Monographs/ allmonos90.niosh. Summary of Data Reported and Evaluation [online] 1986. Schwartz SS. In Report on Carcinogens.S.S. available at URL: http://mtn.S Department of Health and Human Services (U. IARC Monogr Eval Carcinog Risks Hum. J Pharmacol Exp Ther 1999.gov/library/ secondhandsmoke/.pdf.php. Environ Health Perspect 2006. Coordinating Center for Health Promotion. Kira S. Soliman S. Available at URL: http:// cancercontrol. Tobacco related exposures. The Health Consequences of Involuntary Exposure to Tobacco Smoke: A Report of the Surgeon General — Executive Summary. JAMA 1998. Turner DM. Tobacco Smoke and Involuntary Smoking. National Center for Fourth National Report on Human Exposure to Environmental Chemicals 17 . Metabolism of nicotine to cotinine studied by a dual stable isotope method. U. JAMA 1996.57(1):79115. 4/13/09 U. Brody DJ. Vol 83.nih. Strauss WJ. 4/13/09 Iwase A. [online]. Pechacek TF. Jacob P. Centers for Disease Control and Prevention. Bernert JT. Smoking and Tobacco Control Monograph 10 [online].S.pdf. 1999-2002. Available at URL: http://www. U. Ethnic differences in N-glucuronidation of nicotine and cotinine. Department of Heath and Human Services. 1991. DHHS).291(3):1196-1203. Curtin LR. Trends in the exposure of nonsmokers in the U. Tob Control 2006. Hukkanen J. population to environmental tobacco smoke: the Third National Health and Nutrition Examination Survey. Benowitz NL.gov/eid/rmca/critdocs/ criteriadoc/33. 4/13/09 International Agency for Research on Cancer. Epidemiol Rev 1996. June. Available at URL: http://monographs.cdc. Richter PA. Nicotine metabolism and intake in black and white smokers. Metabolism and disposition kinetics of nicotine. Centers for Disease Control and Prevention. Clin Pharmacol Ther 1994. 4/13/09 Perez-Stable EJ.280:135-140. iarc. Flegal KM. 2004. National Institute for Occupational Safety and Hygiene (NIOSH). Third National Report on Human Exposure to Environmental Chemicals. Warner K.niehs. and the United States. 11th ed. Aiba M. Sosnoff CS.fr/ENG/Monographs/allmonos90. Mowery PD. Pharmacol Rev 2005. 1988-1991. Pechacek TF. Coordinating Center for Health Promotion. Etzel RA. Pollack HA. Vogler GP. JAMA 1998. Fong I. Available at URL: http://ntp. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans.18:188-204.iarc.7:369-375.surgeongeneral. Tobacco Smoke. Maurer KR. Benowitz NL. population to secondhand smoke: 1988-2002.280:152-156. BMJ 1975. 1988-1991.275:1233-1240. Cotinine as a biomarker of environmental tobacco smoke exposure. Caudill SP. Kozlowski LT. U. Pickett MA.4:313-316. George CF.94(2):314-320. Giovino G.15:302-307. Caraballo R. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans.gov/ntp/roc/eleventh/profiles/ s176toba. 4/13/09 National Cancer Institute (NCI). Office on Smoking and Health [online] 2006. Smoke-free laws and secondhand smoke exposure in US nonsmoking adults. Vol 38. Tob Control 1998. 4/13/09 Centers for Disease Control and Prevention (CDC).S. Jacob P III.S. Lewis PJ. Absorption and metabolism of nicotine from cigarettes.

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

have been reported as result of self-poisoning by ingestion or excessive dermal application.130) < LOD .190) < LOD .210) 964 1191 1013 1344 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .130 (.100-. Neurological effects in humans.520) < LOD .110 (<LOD-. DEET is not genotoxic.EPA at: http://www. There are over 225 insect repellents brands containing DEET.160) < LOD . 2002). and it has not been rated by IARC or NTP with respect to human carcinogenicity.180) < LOD . < LOD means less than the limit of detection.120-.120-. Human health effects from DEET at low environmental doses or at biomonitored levels from low environmental exposures are unknown.180 (. 134-62-3 General Information N.S. Additional information is available from U.110 (.100-. People in outdoor occupations may apply DEET more frequently or use higher concentration formulations resulting in higher levels of exposure. After absorption. and they range in concentration from 4% to 100%.100-.130) < LOD .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 . DEET can be applied to clothing and the skin to repel biting insects. Urinary N. DEET is metabolized via hydroxylation and dealkylation pathways and eliminated in the urine within approximately 24 hours (Selim et al.epa.S.. 1998). 2005). EPA. which may vary for some chemicals by year and by individual sample.240) < LOD .270) 688 678 518 700 598 956 Limit of detection (LOD.110-.170 (.100-.1.130-.N. Its use is recommended for prevention of several vector-borne diseases.130 (.250) < LOD .110 (.100-..110-.110 (<LOD-.140) < LOD . General population exposure to DEET occurs from skin application and from inhalation of aerosol formulations. but higher DEET concentrations and different formulations may result in greater absorption (Sudakin and Trevathan.560) < LOD . DEET is not registered for use on agricultural commodities.N-Diethyl-meta-toluamide (DEET) CAS No.140 (.110 (.N-Diethyl-meta-toluamide (DEET) 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.140) < LOD . Fourth National Report on Human Exposure to Environmental Chemicals 19 .130-.140-.N-diethyl-meta-toluamide (DEET) is an insect repellent that was first marketed in 1957.gov/pesticides/. DEET is also used in combination with dermal sun screens (U.EPA. population from the National Health and Nutrition Examination Survey.N-Diethyl-meta-toluamide (DEET) N.130-. One survey detected DEET in 74% of sampled streams in the U..100 (<LOD-.130 (. (U.210 (. 1998).210) 480 580 672 829 825 1126 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . 2003).S. 1995. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.110 (. About 3-8% of dermally applied DEET is absorbed. (Kolpin et al. Survey Geometric mean (95% conf.S. Exposure can also occur from consuming food contaminated by DEET on hands or that was sprayed nearby. DEET is not a developmental or reproductive toxicant in animals (U.130-.EPA. including seizures and encephalopathy.180 (.220) size 1977 2535 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD 90th .S.S. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD . 2003).100-. DEET has low acute toxicity. Sudakin and Trevathan. Most reports of adverse effects from overexposure to DEET involve skin reactions (Bell et al.140) < LOD .449 and 0. 2002).170 (.150) < LOD .180 (.220 (.

200 (.640 (. Urinary DEET levels as high as 5. 2007).500 (. Urinary levels of DEET were characterized only at the 90th and 95th percentiles of the U.550) 688 678 518 699 598 956 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.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 .240-.370-.170-.300 (.270-.330 (.490) < LOD .N-Diethyl-meta-toluamide (DEET) Biomonitoring Information Urinary levels of DEET reflect recent exposure. 1992).240) < LOD .410 (.S. 20 Fourth National Report on Human Exposure to Environmental Chemicals .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 . In this survey period..250-. the limit of detection was lower than for the NHANES 1999-2000 survey period (CDC.N-Diethyl-meta-toluamide (DEET) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.330 (. 2005). 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.150-. DEET was detected in 10% of 60 Latino children in eastern North Carolina farm worker households (Arcury et al.270 (<LOD-.190 (.390-.150) < LOD .410-.350) < LOD .270) < LOD .130 (<LOD-.280-1. Urinary N.690 µg/L were measured in eight park employees who applied 71% DEET once a day (Smallwood et al. Finding a measurable amount of DEET in urine does not mean that the level of DEET causes an adverse health effect.280 (.190 (.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 .250) < LOD .230) < LOD .480 (.S. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.230-.230-.440) < LOD .140-.290-.500) 480 580 672 828 825 1126 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . representative subsamples from NHANES 2001-2002.630) < LOD .350-. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.N.190-.250 (.320) < LOD . interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD .410 (. population from the National Health and Nutrition Examination Survey.370) < LOD .320 (.350) < LOD ..270 (. Survey Geometric mean (95% conf.93) < LOD .190 (<LOD-.

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

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

nih. Rubin C. Pharmaceuticals.pdf .Scientific Committee on Toxicity. November 26. Serizawa S. 2/4/09 National Toxicology Program’s Report of the Endocrine Disruptors Low-Dose Peer Review (NTP). 2/4/09 National Toxicology Program Center for the Evaluation of Risks to Human Production (NTP-CERHR). Nippon Eiseigaku Zasshi 2004. Kim CS. and Hardy MP.nih. Available at URL: http://ecb. Bradley S. 2/4/09 European Commission.113(4):391-395. Yang M. U. and other organic wastewater contaminants in U. 2007. Environ Health Perspect 2008. Richter CA. Chung MK. Gender differences in the levels of bisphenol A metabolites in urine. Occup Environ Med 2002. Environ Health Perspect 2005. Human Health. Life Sci 2001. Arakawa C. Kiguchi M. Estimation of intake level of bisphenol A in Japanese pregnant women based on measurement of urinary excretion level of the metabolite. Ema M. Watanabe S. Endocrinology 2004.. Calafat AM.europa. Klinefelter GR. et al. In vitro and in vivo interactions of bisphenol A and its metabolite. Hara K. Research Triangle Park.145:592-603. 4. Brine DR. hormones..S. Urinary bisphenol A and plasma hormone concentrations in male workers exposed to bisphenol A diglycidyl ether and mixed organic solvents. Szigeti-Buck. Meyer MT. Shin HC. 2002. Wong LY. bisphenol A glucuronide.68(1):121-146.gov/ntp/htdocs/liason/ LowDosePeerFinalRpt. 2003. Hanaoka T. Park S. McConnell EE. DirectorateGeneral Health and Consumer Protection. Hum Ecol Risk Assess 2004. Exposure to bisphenol A from bis-glycidyl dimethacrylatebased dental sealants.59(9):625-628. Bisphenol A prevents the synaptogenic response to testosterone in the brain of adult male rats. with estrogen receptors alpha and beta. Available at URL: http://ntp. Munro IC. Caudill SP. Timms BG. Environ Sci Technol 2002. Ikka T. 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. Three-generation reproductive toxicity study of dietary bisphenol A in CD Sprague-Dawley rats. 32 Fourth National Report on Human Exposure to Environmental Chemicals .pdf. Twomey K.gov/chemicals/bisphenol/BPAFinalEPVF112607. Imai H. Leranth. Kuklenyik Z. Watanabe C. Zaugg SD. Reidy JA. Haighton LA. Han SS. Kim YH. Doull J. An evaluation of the possible carcinogenicity of bisphenol A to humans.137(3):353-362. C. et al. Matthews JB. Evaluation of developmental toxicity in rats exposed to the environmental estrogen bisphenol A during pregnancy. niehs.eu/ health/ph_risk/committees/sct/documents/out156_en. J Am Dent Assoc 2006. Available at URL: http://cerhr. National Institutes of Health. Department of Health and Human Services. Yoshinaga J. Lynch BS. Furukawa M.14(2):149-157. September. T. Barber LB. Kroes R. Bisphenol A. Hughes C. J Chromatogr B Analyt Technol Biomed Life Sci 2002. Urinary concentrations of bisphenol A and 4-nonylphenol in a human reference population.it/DOCUMENTS/ Existing-Chemicals/RISK_ASSESSMENT/SUMMARY/ bisphenolasum325. 2/4/09 Ouchi K. Belgium.10:875-921.59(4):403-408. Keimowitz AR. European Commission.35(2 Pt 1):238-254. Rhomberg et al. Joint Research Centre Institute of Health and Consumer Protection. Available at URL: http://ec. Reidy JA. Myers CB. May 22. Calafat AM. Toxicol Sci 2002. National Toxicology Program Center for the Evaluation of Risks to Human Production (NTP-CERHR).jrc. Regul Toxicol Pharmacol 2002. Italy. Fujii S. Pyo MY.J. Ecotoxicity and the Environment (CSTEE).S. streams. Koh WS. Kim JC. Exposure of the U. Available at URL: http://cerhr. 2/4/09 Fujimaki K. Kawamura N. 1999-2000: a national reconnaissance. Endocrinology 2008. Biochem Biophys Res Commun 2003. Rat two-generation reproductive toxicity study of bisphenol A. NTP-CERHR Panel Report on Reproductive and Developmental Toxicity of Bisphenol A. Cunha G.Environmental Phenols References Akingbemi BT. Han SY. Joskow R. Marr MC. Reprod Toxicol 2001. Zacharewski TR. Barton L. Ekong J. Needham LL.pdf. Barr DB. Chem Res Toxicol 2001.. Needham LL. Cohen JT. Estrogenic chemicals in plastic and oral contraceptives disrupt development of the fetal mouse prostate and urethra. Koulova AI. Furlong ET. Kolpin DW.312(2):441-448. vom Saal FS. niehs. Sottas CM. Barr JR. Proc Natl Acad Sci USA 2005. NTP-CERHR Panel Report on Reproductive and Developmental Toxicity of Bisphenol A.niehs. Ispra. Needham LL.S. Thurman EM. National Toxicology Program. Thomas BF. MacLusky. Gray GM. Howdeshell KL. Measurement of bisphenol A in human urine using liquid chromatography with multi-channel coulometric electrochemical detection. N. 2008. Weight of the evidence evaluation of low-dose reproductive and developmental effects of bisphenol A.102(19):7014-7019. NC.116(1):39-44.780(2):365-370.149:988-994. and Hajszan. population to bisphenol A and 4-tertiary-octylphenol: 2003-2004.gov/chemicals/bisphenol/bisphenol. Calafat AM.pdf . Brussels. 5: 505-523. Hlywka JJ. Tsugane S. et al.4’-Isopropylidenediphenol (Bisphenol-A) Summary Assessment Report.nih. August 2001. Cha SW.36(6):1202-1211. Harazono A. National Institute of Environmental Health Sciences.69(22):2611-2625.pdf. K. Tyl RW. Ye X.

Morgan MK. Food Chem Toxicol 2002.113(8):926-33.44(4):546-51. Low-dose in utero effects of xenoestrogens in mice and their relevance to humans: an analytical review of the literature. III. Colnot T. Welshons WV. Endocrine mechanisms mediating effects of bisphenol A at levels of human exposure. Sheldon LS. Witorsch RJ. Filser JG. Lordo RA. Large effects from small exposures.147(6 Suppl):S56-69. Vom Saal FS. Yang M. Fourth National Report on Human Exposure to Environmental Chemicals 33 . Nagel SC. and nonylphenol at home and daycare. Metabolism and kinetics of bisphenol A in humans at low doses following oral administration. Chuang JC. An extensive new literature concerning low-dose effects of bisphenol A shows the need for a new risk assessment. Kawamoto T. Csanady GA. Dekant W. Jang JY.Environmental Phenols Volkel W. An observational study of the potential exposures of preschool children to pentachlorophenol. Wilson NK. Biological monitoring of bisphenol a in a Korean population. Chang SS. Hughes C. Endocrinology 2006. bisphenol-A.40(7):905-12. Environ Health Perspect 2005.15:12811287. Chem Res Toxicol 2002. Kim SY. Arch Environ Contam Toxicol 2003. Lee SM.103(1):9-20. et al. vom Saal FS. Environ Res 2007.

did not bioaccumulate.70 (1. 140-66-9 General Information 4-tert-Octyphenol.400 (.60-3.50) .3-Tetramethylbutyl] phenol) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.600-1.400 (.80 (1. altered neonatal sexual development.500) . 4-octylphenol monoethoxylate was detected in 43.800-1.300 (<LOD-. Saito et al.. several European nations banned the use of alkylphenol ethoxylates in domestic detergents and other uses. The alkylphenol ethoxylates enter the environment through human use of products containing them.357 (. streams in 30 states (Kolpin et al.20-2.10 (.60-3.497) * .600) 1.20) 2.30 (1. Ying et al.300-.000 tons of alkylphenol ethoxylates were produced annually worldwide. impaired steroidogenesis.70 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.S.90) 2.600-1.g. and emulsifiers.70 (1.400) 1.268-. Blake and Boockfor.30) 90th 1. 1995.900 (. population from the National Health and Nutrition Examination Survey.60) . Katsuda et al.30) 2.389 (.300-.600) .00) 1229 1288 03-04 03-04 03-04 * .50) . interval) Selected percentiles ( 95% confidence interval) Sample 95th 2. orally administered 4-tert-octylphenol was well absorbed.30 (1.Environmental Phenols 4-tert-Octylphenol CAS No.5% of 139 U.600) .00 (. Bian et al.. < LOD means less than the limit of detection.600-1.30 (..20-2. to shorter chain alkylphenol ethoxylates. Alkylphenols also have been used as plasticizers and antioxidants in plastics and resins.10 (.200-. 2002). Less frequently.60-3.50) 1. 2004). During the 1980s and 1990s.60-3.30 (1. and impaired spermatogenesis (e. pesticides.274-.80) 2.20 (1. These high dose parenteral effects of 4-tert-octylphenol have included altered sex hormone levels and hypothalamicpituitary suppression.600-1.600-1.. fish) and drinking water. and through manufacturing waste streams (Warhurst.300 (<LOD-. is used to manufacture alkylphenol ethoxylates. Nonylphenol ethoxylates are more commonly used than octylphenol ethoxylates.60-3.500-1.50-2..20) 1.20-2. In rats.10-2. and some personal care products.30-2.60-3. 2000.90) 2. outdoor air may have detectable levels of 4-tert-octylphenol and 4-tert-octylphenol monoethoxylates.S.700-1. In the 1990s.500-1..80 (1. Survey Geometric mean (95% conf. which are anionic surfactants used in detergents.40 (1.50 (1. Indoor and to a lesser extent.20-2.500) .400 (.300 (<LOD-. and from contact with some personal care products and detergents.70 (1.477) .900 (. They are biodegraded to the corresponding alkylphenol (octylphenol or nonylphenol).g. see Data Analysis section) for Survey year 03-04 is 0.500) .900 (. Octylphenols and nonylphenols can also enter the environment directly from manufacturing waste streams.10) 2. Human exposure to alkylphenols and alkylphenol ethoxylates may occur through ingestion of contaminated foods (e. industrial cleaners.300 (<LOD-. and some of their degradation products are toxic to aquatic life..500 (. through sewage. over 500.20-2.40) 2. an alkylphenol.900 (. 2000. 1996).299-. Laws et al.507) * < LOD ..40) 2.3. testicular atrophy. Commercial formulations of alkylphenol ethoxylates usually contain a mixture of oligomers and isomers. and to alkylphenoxycarboxylates.20-2. 1997.369 (. 2002).50) 1. Human health effects from 4-tert-octylphenol or the corresponding octylphenol ethoxylates at low environmental doses or at biomonitored levels from low environmental exposures are unknown.50) 1.30 (1.1. and the polyethoxy chain may consist of up to 50 ethoxy units..30) 1.300 (<LOD-. In 1999-2000. including 4-tert-octylphenol.10) 1.50-3.40) * 03-04 03-04 03-04 . the various alkylphenols have also been used as emulsifiers and modifiers in paints. and was quickly eliminated from the blood (Certa et al.600-1. which may vary for some chemicals by year and by individual sample. altered estrus cycles and reproductive outcomes.10 (1.60) 1.200-. 2003. textiles.2. 34 Fourth National Report on Human Exposure to Environmental Chemicals .500) 75th .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 . leading to inhalation as another potential exposure route (Rudel et al.600) . Several alkylphenols. Urinary 4-tert-Octylphenol (4-[1.00 (. have demonstrated estrogenic effects particularly when injected at high doses in animals.60) 613 652 1092 Limit of detection (LOD.20) 314 715 1488 03-04 03-04 * * .40) 1. The alkylphenols can bioaccumulate in some fish.. 2006.00 (1.80 (1.40) 1. Disposition in humans has not been studied sufficiently.900 (.

62) .410 (.00) 2.730-1.03-6. 2004.1. 2000..530) .Environmental Phenols Myllymaki et al.500-1.17 (.10-2.00) 1. Nagao et al.08) 1. 2001).450) 1.337-.11) 2..270 (.460 (.59 (1. 4-tert-Octylphenol is not considered directly genotoxic.560) ..06 (2.25-2.67-2.276 (.450) .73) 2.40 (1.380 (<LOD-.54) * 03-04 03-04 03-04 .43) 1.29) 2.33) 3.270-. Calafat et al.85 (1.270 (. 1999).207-.41) . 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.22) . nonylphenol.890-2. population from the National Health and Nutrition Examination Survey.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 .280-.43-3.65-3.00) 2. Tyl et al.43) 1. Survey Geometric mean (95% conf.570) .62 (1.349) * < LOD .620) .24) 612 651 1091 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.78) 3.36-3.740 (.96-4. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.31-2.420) .3.62 (1.160-.64 (.470-1. It is unclear if estrogenic or other effects occur in animals through oral dosing. Urinary 4-tert-Octylphenol (4-[1.S. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.610) .11) 1. or their corresponding ethoxylates with respect to human carcinogenicity.770 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.300 (<LOD-.05-2.S.25) 90th 1.78) 1228 1286 03-04 03-04 03-04 * .470-1.540-1. IARC and NTP have not rated octylphenol.370 (<LOD-. Biomonitoring Information Urinary levels of 4-tert-octyphenol reflect recent exposure. In a small number of adult Japanese volunteers.11-2..384) * .550-1.470) 75th . (2008) showed that urinary levels of 4-tertoctyphenol were detectable in slightly greater than half of the participants of the U. at lower or environmentally relevant doses (Blake et al. Kawaguchi et al.00 (..76 (2.170-.199-. Sweeney et al. Fourth National Report on Human Exposure to Environmental Chemicals 35 .630-1.25) 2.81 (1.14) 314 713 1487 03-04 03-04 * * .15) 1.60 (1. 2004).740 (.18-4.320 (<LOD-. 2001.59) 1. Finding measurable amounts of 4-tert-octylphenol in the urine does not mean that the levels of 4-tert-octylphenol cause an adverse health effect.400) .269 (.435 (.260 (<LOD-.3-Tetramethylbutyl] phenol) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.50 (2.71) 2.910 (.40-4.02-4.640-1. the urinary concentrations of 4-tert-octyphenol were near or below the detection limit (Inoue et al.68) 2.03 (1. Yoshida et al. representative subsample of NHANES 2003-2004. 2005.68-2.33 (2.53-3.03 (1. 2003.20 (1.31 (1.78 (1.850 (.620-1..00 (.860 (.

Ito R. Boockfor FR. Camann DE. Taya K. Paranko J. Nicol L. prolactin. Saito Y. alkylphenols. Effects of 4-tert-octylphenol given in drinking water for 4 months on the male reproductive system of Fischer 344 rats. Reprod Toxicol 2001. Tyl RW. Cooper RL. Karjalainen M. Arch Toxicol 1996. Meyer MT. pesticides. Millette CF. Fail PA. Kawaguchi M.uk/resource/reports/ethoxylates_alkylphenols.207(1):59-68. Williams B. 2/4/09 Ying GG. Toppari J.44(8):1355-1361. testis size. J Chromatogr B Analyt Technol Biomed Life Sci 2004. Takai N. and sertoli cell number. hormones. Brine DR.foe.30(2 Pt 1):81-95. Toxicokinetics of p-tert-octylphenol in male Wistar rats. Kolpin DW. et al. streams. Pharmaceuticals. Biol Reprod 1997. Available at URL: http:// www. Yoshimura S. Effects of neonatal exposure to a high-dose p-tertoctylphenol on the male reproductive tract in rats. An environmental assessment of alkylphenol ethoxylates and alkylphenols. Inoue K.799(1):119-125. Environ Sci Technol 2003.28(3):215-226. Sakui N. Wiegand HJ. Nagao T. Certa H. and testosterone.co. Bodman GJ.15(6):683-692. bisphenol A and methoxychlor in rats. 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. Blake CA. Barber LB. Inoue K. Korn LR. Regul Toxicol Pharmacol 1999.14(5):325-332.S. Katsuda S.Environmental Phenols References Bian Q. Calafat AM. Maekawa A. Yoshida M. Horie M. and other organic wastewater contaminants in U. Maekawa A. Katsuda S. Kawaguchi M. Indoor air pollution by alkylphenols in Tokyo. Myllymaki SA. Environmental fate of alkylphenols and alkylphenol ethoxylates--a review.folliclestimulating hormone. Wang X. Chen J.pdf. Furlong ET.36(6):1202-1211. Yoshida M. Izumi S. Haavisto TE. Endocrinology 2000. Indoor Air 2004. Thurman EM. Exposure of the U. Taya K.71(1-2):112-122. Raychoudhury SS. Fedtke N. Reproductive effects in male and female rats from neonatal exposure to p-octylphenol. Watanabe G. Reidy JA. Boockfor FR. Kookana R. Phthalates. Anal Chim Acta 486:41-50. population to bisphenol A and 4-tertiary-octylphenol: 2003-2004. Laws SC. 36 Fourth National Report on Human Exposure to Environmental Chemicals . et al.S. Maternal exposure to octylphenol suppresses ovine fetal follicle-stimulating hormone secretion. Chronic administration of the environmental pollutant 4-tert-octylphenol to adult male rats interferes with the secretion of luteinizing hormone. Watanabe G. Seto H. Blake CA. 2003. Nair-Menon JU. Brody JG. Song L. Ye X. Nakagomi M.121(1):21-33.54(1):154-167. Ferrell JM. Needham LL. Spengler JD. Xu L. Seely JC. Reprod Toxicol 2004. Saito I. Okada F. Sweeney T. Toxicol Appl Pharmacol 2005. Toxicol Lett 2001. Toxicol Sci 2000.116(1):39-44. Roche JF. Infantile 4-tert-octylphenol exposure transiently inhibits rat ovarian steroidogenesis and steroidogenic acute regulatory protein (StAR) expression. Environ Sci Technol 2002. McCoy GL. Environ Health Perspect 2008.57(2):255-266. et al.18(1):43-51. Ono H.141(7):2667-2673. Muller AM. The toxic effects of 4-tert-octylphenol on the reproductive system of male rats. Estrogenic activity of octylphenol. Marr MC. Warhurst AM. Qian J. Makino T. et al. Takenaka A. Yoshimura Y. Carey SA. Toxicol Appl Pharmacol 2000. Myers CB. Food Chem Toxicol 2006. Rudel RA. Wong LY. nonylphenol. Environ Int 2002.37(20):4543-53. 1999-2000: a national reconnaissance. 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. Measurement of 4-nonylphenol and 4-tert-octylphenol in human urine by column-switching liquid chromatography-mass spectrometry. 1995. polybrominated diphenyl ethers.165(3):217-226. Onuki A. Brooks AN. Usumi K. Bolt HM. Zaugg SD. Two-generation reproduction study with para-tert-octylphenol in rats.

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

4) 7.8) 7.40-17.5-86.0-73.6-15.7) 123 (36. see Data Analysis section) for Survey year 03-04 is 2.3 (9.45 (5.70-16.1) 50.1) 9.20 (7.74 (5.48-10.0 (8.3-15.9 (11.4’-Trichloro-2’-hydroxyphenyl ether) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.4.50-10.10-9.7 (11.72-13.45-13.3 (8.45-10.6-65.0 (26.1) 9.4) 317 (231-433) 144 (96.90-10.6 (30.1) 7.3 (26.7 (14.9-61.0-15.5-14.7 (9.1) 14.2 (11.8-63.11-11.2-46.4) 51.0 (11. interval) 13.1) 9.0) 65.9) 8.0-213) 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 .2-58.0 (34.8) 9.3) 47.S.0-15.2) 13.2 (10. population from the National Health and Nutrition Examination Survey.48 (8. Survey Geometric mean (95% conf.89-11.1 (45.9) 7.3) 10.0 (36.5-250) 574 (461-716) 380 (258-430) 1229 1288 03-04 03-04 03-04 14.6) 31.21 (6.4.29-12.9-236) 193 (90.9 (33.4) 357 (225-456) 203 (87.3.7 (39.6) 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 9.4) 25.9 (50.3-31.0) 49.32-14.6) 10.9) 75th 47.60 (6.92-12.4-19.40-11.1) 11.7) 10.2 (37.8 (21.6-14.2-58.5 (11.2-14.5) 13.30-14.4) 73.6 (9.3) 6.6-111) 33.8-60.5) 11.16 (6.1-39.20-11.7) 292 (151-432) 132 (78.1 (15.2 (25.82 (8.4) 75th 43.8-127) 37. interval) 12.Environmental Phenols Urinary Triclosan (2.3-35.4) 90th 249 (188-304) 03-04 03-04 03-04 8.1) 13.2) 12.6 (10.6) 12.4’-Trichloro-2’-hydroxyphenyl ether) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.1 (8.43-13.20 (7. Survey Geometric mean (95% conf.5-341) 245 (163-334) 597 (372-992) 450 (254-750) 461 (383-527) 613 652 1092 Limit of detection (LOD.00 (4.8) 116 (39.20-13.20-10.4 (11.S.86-12.6-20.0) 9.54 (8.2 (13.4 (12.10) 84.6 (12.4 (32.5) 66. Urinary Triclosan (2.93 (7.1) 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 9.8-112) 30.3 (11. population from the National Health and Nutrition Examination Survey.0-19.3-67.50) 10.4-163) 304 (134-566) 261 (198-317) 157 (113-380) 655 (310-890) 472 (406-522) 314 715 1488 03-04 03-04 16.22-10.80 (5.7 (28.6-37.9 (8.6) 237 (175-294) 182 (138-217) 384 (294-506) 336 (225-480) 1228 1286 03-04 03-04 03-04 13.38-18.2) 9.6) 39.6) 90th 212 (172-241) 03-04 03-04 03-04 9.94 (7.60 (8.7-318) 224 (186-272) 236 (115-336) 356 (169-580) 385 (308-506) 314 713 1487 03-04 03-04 13.2 (27.6-14.5) 20.9) 32.8-85.00-8.18 (5.55 (4.8) 14.1) 9.4-18.4 (38.

Wong LY. Wigmore H. Levy SB.115:116-121. Environ Health Perspect 2008. and other organic wastewater contaminants in U. Calafat AM. Watanabe N. Kolpin DW. Aguera A. Br J Clin Pharmacol 1987.4’-trichloro-2’hydroxydiphenyl ether). 1999-2000: a national reconnaissance.24(3):209-218. Nagao Y. Shiratsuchi H. Windham G. Teitelbaum SL. Hernando MD. Fourth National Report on Human Exposure to Environmental Chemicals 39 . Anal Chim Acta 1004. Furia T.Environmental Phenols References Aiello AE. Chelimo C. Pinney SM. Ishibashi H. Reidy JA. and phenols in girls. Effects of nonylphenol and triclosan on production of plasma vitellogenin and testosterone in male South African clawed frogs (Xenopus laevis).524:241-247. IMS Ind Med Surg 1969. Britton JA. Ye X.50(1-5):153-156.69(20):1861-1873. et al. Wolff MS. Aquat Toxicol 2006. Pilot study of urinary biomarkers of phytoestrogens. Aranami K.S.66:1052-1056. Furlong ET. phthalates.7/2. Williams FM. Urinary concentrations of triclosan in the U. Sandborgh-Englund G. Ferrer I. Katsura E.S. Food Chem Toxicol 2000. hormones. et al. Veldhoen N. Evidence of 2. Zaugg SD. Gunderson MP. Hirano M. streams. Leonard PA. Odham G. Erratum in: Aquat Toxicol 2007. Chemosphere 2007. Gomez MJ. Pharmacokinetics of triclosan following oral ingestion in humans.80(3):217-227.36(6):1202-1211. Adolfsson-Erici M. Triclosan: applications and safety. Clapson DJ. Disposition and excretion of Irgasan DP300 and its chlorinated derivatives in mice. Kaneshima H. 4. Ekstrand J. et al. Benson WH. Ogawa H. Photolytic degradation of triclosan in freshwater and seawater. et al. Bodey GP. Developmental evaluation of a potential non-steroidal estrogen: triclosan.67(4):532-537. Bhargava HN. Kanetoshi A. Readman JW. Gilbert RJ. J Invest Dermatol 1976.38(2):64-71. Matsumura N. 4’-trichloro-2’-hydroxydiphenyl ether. The oral retention and antiplaque efficacy of triclosan in human volunteers. Skirrow RC. Mezcua M. Percutaneous penetration and dermal metabolism of triclosan (2.38(4):361370. The bactericidal agent triclosan modulates thyroid hormone-associated gene expression and disrupts postembryonic anuran development.4. Howes D.83(1):84. Hong HC. Okui T. Osachoff H.. Environ Health Perspect 2007. Lyman FL. population: 2003-2004. Ebersole R. J Toxicol Environ Health A 2006. Pharmaceuticals.23(5):579-583.28(9):1748-1751. Fernandez-Alba AR. Am J Infect Control 1996. Williams PE.8-dibenzodichloro-pdioxin as a photodegradation product of triclosan in water and wastewater samples. Barber LB. Foran CM. Meyer MT.116(3):303-307. Environ Sci Technol 2002. Randomized trial of a hexachlorophene preparation and P-300 bacteriostatic soaps. Biol Pharm Bull 2005. Bennett ER.17(5):637-644. Thurman EM. Mar Environ Res 2000. Toxicology of 2. Moss T.45 Suppl 2:S137-S147. Arch Environ Contam Toxicol 1988. Needham LL. Larson EL. Consumer antibacterial soaps: effective or just risky? Clin Infect Dis 2007.

980 (. After absorption.350 (. the elimination half-life may be a week or more (Uhl et al. bactericide.83 (2.350-1.32 (.76) .42) 973 1190 1021 1338 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .350) < LOD .64) 1.350-.58-2. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.30) 1. PCP is distributed to most tissues and is not extensively metabolized.350-. Effects including hyperthermia. has been restricted. air.350-.51) 1.09) . PCP use in the U.350 (.390 (.350 (.350-.350 (.650 (.53) 482 577 681 826 831 1125 99-00 01-02 99-00 01-02 * * * * .98 (1.10 (1. other polychlorinated benzenes. Human exposure to PCP has become less common.33-2.350) < LOD .350 (. 1986).45-2.350-.350 (.10) 1.76) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * . PCP cannot be used on wood in residential or agricultural buildings. hypertension.42) 696 680 521 696 603 951 Limit of detection (LOD.350-.5.60) 1.94 (1.78) 1.630 (. population from the National Health and Nutrition Examination Survey. ingestion of contaminated food or water.350 (.58-2.65 (.350-.350-.350) < LOD .350 (. utility poles and fence posts). see Data Analysis section) for Survey years 99-00 and 01-02 are 0.350 (. Acute.350-..48-2.01 (<LOD-1.40 (.350-.94 (1. which may vary for some chemicals by year and by individual sample.350-.00 (. and dermal contact with PCP-treated products.00) 2. PCP is degraded by sunlight and metabolized rapidly by microorganisms.350-1.47-3.350 (.18 (<LOD-1.350) < LOD .30 (1. herbicide. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.350-. To-Figueras et al. mollusicide.960) 1.350 (.75) 2.62 (.990 (<LOD-2. In the environment. 40 Fourth National Report on Human Exposure to Environmental Chemicals .350) < LOD .510-5.350 (. Kohli et al. are eliminated in the urine.00) 1.650) 1.660 (.350 (.10) 1. and metabolic acidosis were observed in CAS No.08-3.590-1.530) 1.350) < LOD .80) . PCP is eliminated over a few days (Braun et al.350) < LOD . and possibly of lindane (IPCS. and it is used primarily as a preservative for wood to be used outdoors (e. 1976.30) .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 .67) 1.350 (. The parent compound and conjugates.350-.37) .350 (.350-2. PCP has been detected in soils.350-1.350) < LOD .S.350-2. 2002.S.350) < LOD .54-2.65 (.g.70) 2.48 (.350-.350-. algaecide and insecticide.770 (. so it is relatively non-persistent. Human health effects from PCP at low environmental doses or at biomonitored levels from low environmental exposures are unknown.350) < LOD .350) . with repeated or chronic exposure.350-. 87-86-5 Also a Metabolite of Several Organochlorine Insecticides General Information Pentachlorophenol (PCP) and its sodium salt were once widely used as a fungicide.04) 1.510-3. 1979).00) 1..73 (1.. Since 1984.90) 1.350) < LOD . After a single dose.350 (. < LOD means less than the limit of detection.350-2.90) 2. high dose exposure to PCP can induce a hypermetabolic state and excessive heat production as a result of uncoupling mitochondrial oxidative phosphorylation.350) < LOD .350) < LOD .350 (.350 (. PCP also may be eliminated in urine as a metabolite of hexachlorobenzene.350-.Fungicides Pentachlorophenol inhale it or absorb it through exposed skin.30 (.350) < LOD ..350 (.350) < LOD .30) 1.10 (<LOD-1.350-. water and sediments because of the large amounts that were produced and used historically.350 (. 1997).680-1.70) .350-.50) 1.23 (.33) .860-2.350-1.890-1. and animals.890 (.350) < LOD < LOD 75th .10 (. plants. PCP is absorbed rapidly and well by all exposure routes.350) < LOD .390 (.25 and 0.47-5.90 (1. Workers who manufacture or apply PCP may Urinary Pentachlorophenol Also a Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.60) 1.350) 90th .350-.350-.. General population exposure to PCP may occur by inhalation of contaminated air. along with small amounts of tetrachlorohydroquinone and conjugates.91 (1.990-2.850-2.350 (.350-2. Survey Geometric mean (95% conf.350-.76) 1.500-2.37 (.480-2.350-2.30 (.

29-3.35-2.320) < LOD .560) < LOD .83 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.730) < LOD .250 (. children in the 1980’s.epa. respectively) (Becker et al.40-2.430-.92) 1. the 95th percentile of urinary PCP levels was about fiftyfold higher than that for 6-11 year olds in NHANES 2001-2002 (Hill et al. IARC has determined that pentachlorophenol is possibly carcinogenic to humans.67-3. 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.S.95) 3.18 (1.25 (1.26 (1.19) 2.320) < LOD .55) 973 1190 1021 1337 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .52 (<LOD-1.75) 1. Among adults in the NHANES 1999-2000 subsample..420) < LOD ..800) < LOD 1. EPA at: http://www.35) 1.gov/ pesticides/ and from ATSDR at: http://www.atsdr.400 (.310) < LOD .360 (.220-. carcinogenic.30) 1. 2004.360-.800-1.S.570 (.18) .290) < LOD .30 (. Pentachlorophenol is not mutagenic or teratogenic.320) < LOD < LOD 75th .16-1.350) < LOD .590-1..560) < LOD .00-1.84 (1.79) 1. 1991).19) 2.300 (.52 (<LOD-1.21-2.67 (1. urinary PCP levels at the 95th percentile were approximately fivefold lower than 95th percentile values measured in a nonrandom subsample from NHANES III (1988-1994) participants (Hill et al.67 (1.. and the FDA has established a standard for bottled water.380-.html.16 (.40) 1.440 (.S.25-2.760 (. 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.06-3.780) < LOD .25-2.290-. 2003).52) 1.40) 1.52 (1. Survey Geometric mean (95% conf.08 and 5.900-1.650 (.34 (.830) < LOD . More information about external exposure (i.90) 1.Fungicides adults and children severely exposed to PCP through ingestion.67 (1. environmental levels) and health effects is available from the U.94-3.84-4. EPA has developed standards for PCP in drinking water and the environment.510-.56) 1.330-.10-2.cdc.500-...610 (.21 (.69 (1. Death can result from seizures and cardiovascular collapse.99) 482 577 681 825 831 1125 99-00 01-02 99-00 01-02 * * * * .950-1.82) 1.240-.40) 1.910-1.06 (.75 (<LOD-2.13 (.26 (1.35) 1.25) 1. 1989).55) 1.00) 1.270-.84) 1.25 (1.09-1.9 mg/L.67-3.11) 2.590) < LOD .630 (..67 (1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1. Urinary PCP levels at the 95th percentile in this Report are approximately half the corresponding 95th percentile values found in German adults evaluated in 1998 (Becker et al.950-1. The U.370 (.950-1.78) 1.500 (. van Raaij et al.06) 1.320 (.35-2.300 (.57 (1.260 (.40) 1.30) 1.510-.82 (1.19 (1.850 (.57 (. inhalation.500-1.19) 2. In a small sample of U. Urinary levels of pentachlorophenol in the general population are far below (hundreds of times lower than) urine levels reported for workplace exposure to PCP or among people living in PCP-treated log homes (Cline et al.30-2.250 (. In NHANES 2001-2002 subsamples.09 (<LOD-2.470 (.51) 1.94 (1. Fourth National Report on Human Exposure to Environmental Chemicals 41 .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 .94 (1.78) 1.6 and 14. 1989).490) < LOD .710-1.270-.S.00-1. the median and 95th percentile urinary PCP levels were approximately three times lower than comparable values in German adults (2. or skin absorption.310-.430) < LOD . respectively) (Seifert et al. 1995). population from the National Health and Nutrition Examination Survey.75) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .EPA.650) 90th 1.650 (. OSHA has established an occupational standard.0 mg/L.40) 1.67 (1.e.10 (1.920 (. 2003).990 (.73 (1.560-.48-2.08) 696 680 521 695 603 951 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.220-. chronically administered high doses of PCP were hepatotoxic.280) < LOD .25-1.S.780-1.580-. and adversely affected thyroid function (U.290-.36) .300 (.340-.gov/ toxpro2.67-2..700-2. 2000). In animals.

Environmental Protection Agency (U. Bailey SL. Needham LL. Seifert B. Pesticide residues in food-2002-Joint FAO/WHO meeting on pesticide residues. van den Berg KJ.18:475-481. Barrot C. U. J Expo Anal Environ Epidemiol 2000. 206:15-24. 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.4:289296. et al. Dev Toxicol Environ Sci 1979.54(3):203-208. Smith SJ. To-Figueras J. Otero R. Effects of hexachlorobenzene and its metabolites pentachlorophenol and tetrachlorohydroquinone on serum thyroid hormone levels in rats.105(1):78-83. Schmid P. Notten WR. To T. Head SL. Pentachlorophenol measurements in body fluids of people in log homes and workplaces. Bragt PC. Safe A. Baker S. Int J Hyg Environ Health 2003. International Programme on Chemical Safety (IPCS). Fast DM. Helm D. r e g u l a t i o n s . Environ Health Perspect 1997. Seiwert M.Fungicides Finding a measurable amount of PCP in urine does not mean that the level of PCP causes an adverse health effect. Shealy DB. Metabolism of hexachlorobenzene in humans: association between serum levels and urinary metabolites in a highly exposed population. Cline RE. PCP: Human Risk Characterization [online]. Pesticide residues in urine of adults living in the United States: reference range concentrations. The metabolism/ pharmacokinetics of pentachlorophenol in man and a comparison with the rat and monkey. Schulz C. The German Environmental Survey 1990/1992 (GerES II): reference concentrations of selected environmental pollutants in blood. Arch Toxicol 1986.18(4):469-474.org/documents/jmpr/jmpmono/2002pr08. urine.71:99108. drinking water and indoor air. Schlatter C. EPA). Phillips DL. Uhl S. hair. Santiago-Silva M. Can J Biochem 1976. Gregg M. 2002. Available at URL: h t t p : / / w w w. Braun WH. Arch Environ Contam Toxicol 1989.S.10:552-65. Hill RH Jr. 4/21/09 Kohli J. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children. Hill RH Jr. Seiwert M. The metabolism of higher chlorinated benzene isomers. et al. htm. Jones D. Chenoweth MB. Krause C. Blau GE. Seifert B. available at URL: http://www. Holler JS. Becker K. Environ Res 1995.inchem. house dust. Needham LL. Hill RH. Rodamilans M. 11/30/2004. Kaus S. Schulz C. et al. 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. References Becker K. Sala M. Toxicology 1991: 67(1):107-16.58:182-186. 4/21/09 van Raaij JA. Engel R.S. Pharmacokinetics of pentachlorophenol in man. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. 42 Fourth National Report on Human Exposure to Environmental Chemicals . Biomonitoring data can also help scientists plan and conduct research about PCP exposure and health effects. Lindane. Arch Environ Contam Toxicol 1989.

850 (.30) < LOD 1.40-5.497 (.60 (1.450 (<LOD-. 2002.85) 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 .10) .50) < LOD .80) 1.860 (.600) < LOD 1.09) 2. inhalational.600) < LOD .00-2. it was used in home sanitizers for surfaces.76) 1.632) Selected percentiles ( 95% confidence interval) Sample 95th 2.520 (.490 (<LOD-..370-. OPP is still used as a disinfectant fungicide for industrial applications. Cnubben et al.10) 1.3 and 0.EPA.50 (1.60-3.10 (1.50-4. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. sodium ortho-phenylphenate (SOPP).610 (.20-2.370-.780) < LOD .740 (.820 (.550-1.567 (.03) 1.450 (<LOD-.10-2.410-.S. 2006).34) 1. and it is eliminated rapidly from the body as OPP glucuronide and sulfate conjugates (Bartels et al.950) < LOD . OPP is efficiently absorbed from the gastrointestinal tract and through the skin. 2006).498 (.30 (1.22 (.890 (.890 (.50) < LOD .40 (.350-1.836) * .30-2.40-7.80-3..50 (1.640) < LOD .20) < LOD 2.20 (.390-.00) < LOD .600-1.610-1. in paints.30) 1.600) < LOD 75th . fungicides.10) 1.570-1.830 (.17 (. and sanitizers.91) 973 1190 1018 1339 99-00 01-02 99-00 01-02 99-00 01-02 .90 (1.970 (.580-1.90) 1.92 (.28-3.20 (1.690) < LOD . Fourth National Report on Human Exposure to Environmental Chemicals 43 . small amounts of OPP have been measured in human adipose tissue (Onstot and Stanley.50) < LOD .349-.509 (.552 (.560-8.433-.33 (. 1989).402-.10-1. 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.621) * .50) 1.750-2. Human health effects from OPP at low environmental doses or at biomonitored levels from low environmental exposures are unknown.60-2. Both have been used in agriculture to control fungal and bacterial growth on stored crops.50 (1.30-7.00 (1.00) .696) * . Survey Geometric mean (95% conf. 90-43-7 General Information Ortho-phenylphenol (OPP.389-. Both chemicals degrade within hours to weeks in the environment (U. or 2-phenylphenol) and its water-soluble salt. In the past.22) 2. OPP is considered to be moderately toxic after acute oral doses in animal studies. on ornamental plants and turfs.420 (<LOD-. or apply these chemicals may be more highly exposed than the general population. < LOD means less than the limit of detection.370-.30) < LOD 90th 1. OPP was detected in 40 of 60 different canned beers at concentrations in the low parts per billion (Coelhan et al. Most agricultural food applications have been revoked.480-1. OPP is volatile. leaving the chemical residue OPP.636) * .28 (. which may vary for some chemicals by year and by individual sample.770 (. formulate.10) . whereas SOPP is not volatile and is more water soluble. Workers who manufacture.61) 2. such as fruits and vegetables.493 (.S.508 (.450 (<LOD-.27 (.02) 1.770 (.790) 2.630) < LOD .20) 2.742) * .50-2.600-1.570-2. EPA.90 (1.20 (1.23) 695 680 520 695 603 953 Limit of detection (LOD.40-5. SOPP is applied topically to the crop and then rinsed off.386-.07 (.500-2.90) .90) .00) .3.570-.710) 3.50-3. General population exposure can occur via dermal.Fungicides ortho-Phenylphenol CAS No. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.490 (<LOD-. Available evidence suggests that OPP does not accumulate in the body.00 (1.80 (2.50) . or oral routes from residential use and by ingesting treated food or food that was in contact with treated surfaces or equipment.570 (.890) 1..00 (1.19 (. are antimicrobial agents used as bacteriostats.10 (1. Estimated human intakes have been below recommended intake limits (U. Timchalk et al.88) 1.30) < LOD .60 (1.760-2.20-3.540-2.EPA.670) 2.490 (<LOD-.880-2. population from the National Health and Nutrition Examination Survey.389-.470 (<LOD-. and it has limited water solubility.930 (.645) * .60 (1.85) 2. and as a wood preservative. 1998).600-1.800-3.466 (.624) * .590-2.S. but OPP and SOPP are still used on pears and citrus (U.860) * 99-00 01-02 99-00 01-02 99-00 01-02 .690-1.80) 1. 2006).00 (1. however.10) 2.496 (.90) 2.490 (<LOD-.600) < LOD .710-2.14 (<LOD-3. interval) .40-2.20) < LOD 1. 1998.840-1.23) 480 577 681 827 830 1125 99-00 01-02 99-00 01-02 . 2006).S.364-.10) .638) * .570 (.490 (<LOD-.

656) * .385 (.560) < LOD 75th .410 (<LOD-.96 (1.93) . but no neurologic.860 (. Survey Geometric mean (95% conf.496 (.51-3.88-4.91) 695 680 520 694 603 953 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.470) < LOD .510 (<LOD-.96 (1.640-1.38) 1.18) 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.810-1.09-3.12) < LOD 1.420 (<LOD-.270-.690 (.514 (.410 (<LOD-. Additional information is available from U.43) 3. population from the National Health and Nutrition Examination Survey.900) < LOD . 1999.75 (1. Murata et al. Nakagawa et al.86 (1.560-2.750 (. reproductive. Volunteers exposed to 0. 2005.00 (.550) < LOD .480-. 1993.4 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.59) 1. Kwok et al.38-3.06-4.40-13.670 (.00 (1.558) Selected percentiles ( 95% confidence interval) Sample 95th 2. 2005)..96) 1.343 (.460-.26) 1. OPP was not found to be mutagenic.12-2.666) * .600-1.84 (1.508) * . 1984. leading to production of two metabolites. 2000.650-1.248-.11 (.43-2. 44 Fourth National Report on Human Exposure to Environmental Chemicals . Dermally applied OPP was not carcinogenic in a 2-year experimental study in animals (NTP.EPA 2006). 1997.568) * .53) 1. and it has classified OPP as not classifiable with respect to human carcinogenicity.900-1.453 (. Urinary ortho-Phenylphenol (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.510-.990) < LOD . population in the subsamples from NHANES 1999-2000 and 2001-2002 (CDC.11) < LOD 90th 1. or. U. Biomonitoring studies on levels of OPP provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of OPP than are found in the general population.13) 1. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects..59) .EPA at: http:// www.33-2..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 . interval) .46) < LOD 1.02 (. Bomhard et al.455-. Smith et al.08-1.950) < LOD .43 (1.840 (. CDC.06 (1.S.4) 3. 1998.S.620-1.Fungicides anemia. 1992.epa.09-6.580) < LOD .89 (1. OPP or SOPP produced carcinomas of the bladder only after phase II detoxification pathways were saturated.17) * 99-00 01-02 99-00 01-02 99-00 01-02 .21 (.04-4.58) 2. Pathak and Roy.S.69 (1.360 (<LOD-. Detectable levels were seen in over half the U.44 (1.329-.93) .gov/pesticides/.750 (.47) .25-6.580-1.29) 1.382 (.750-2.. 2002.810) < LOD .670) < LOD .20) < LOD 3.29) 1.880-1. by possible genotoxic mechanisms (Hagiwara et al.470 (<LOD-.291-. U.550-.980 (..78 (2..420 (<LOD-..403-.07) 2.24-2. In high dose animal studies.62) .550 (.11) 4.21) 1..61 (1.27) < LOD .32) 3. 1999.570) < LOD 1.08) 1. less likely.620-1.500) < LOD .940-2.24-2..75 (1.05-2.61 (2.791) * .980 (<LOD-1.311-.28 (<LOD-4. 1984. 2002.61 (.52 (.97 (2.91 (1.08-2. ortho-phenylhydroquinone and ortho-phenylbenzoquinone. Brusick.670 (.0) 1.610) < LOD 1.320 (<LOD-.43-2.32) 1.21-2.860 (.353-.74 (1. 2002).780 (.96-4.970) 1.590) * .780-14..17 (.17 (.770-2.910 (<LOD-1.380 (. 1986). Finding a measurable amount of OPP in urine does not mean that the level of OPP causes an adverse health effect.11-1.30) 480 577 681 826 830 1125 99-00 01-02 99-00 01-02 .800-1.33) .06-5.28 (2.17) 2.38) 973 1190 1018 1338 99-00 01-02 99-00 01-02 99-00 01-02 .11 (.93) 1.31) < LOD .440 (.361-. Biomonitoring Information Urinary OPP levels reflect recent exposure.910-1.EPA 2006). Zhao et al.93 (1.473) * .444 (. 2005).484) * .64 (2.910 (.S.09 (1.301-. IARC has classified SOPP as a possible human carcinogen.38) 2.S. These metabolites may induce carcinogenicity via nongenotoxic regenerative hyperplasia of the bladder (Appel. Ito et al.81) 1. or developmental toxicity was observed (Bomhard et al.01) 1.

Turteltaub KW. Hirose M. Xenobiotica 1998. Elliott GR. Centers for Disease Control and Prevention (CDC). Coelhan M. et al.20(5):851-857. Drugs. food additives and natural products as promoters in rat urinary bladder carcinogenesis.nih. Long-term toxicity and carcinogenicity study of sodium o-phenylphenate in B6C3F1 mice.28(6):579594.Fungicides References Appel KE. Narang A. July 28. Moore GA. Tayama S. Toxicol Appl Pharmacol 1998. Pathak DN. 2005. Eastmond DA. Detection and characterization of DNA adducts formed from metabolites of the fungicide ortho-phenylphenol.54(16):5731-5735. Bartels MJ.. Reregistration Eligibility Decision (RED) for 2-phenylphenol and salts (Orthophenylphenol or OPP). Sangha G.286(2):309-319. Shirai T.niehs. Analysis of genotoxicity and the carcinogenic mode of action for ortho-phenylphenol. Roy D. Sangha GK.S. The pharmacokinetics and metabolism of 14C/13C-labeled ortho-phenylphenol formation following dermal application to human volunteers. 1989.45(5):460-481. 4/13/09 Onstot JD. Hagiwara A. Moriya K. Roberts AL.EPA).159(1):18-24. EPA-560/5-89-003. Bartels MJ. O-phenylphenol and its sodium and potassium salts: a toxicological assessment. Imaida K.S. Bartels MJ. Brusick D. Determination and levels of the biocide ortho-phenylphenol in canned beers from different countries.43(7):14311437. Moldeus P. Zhao S. Arch Toxicol 2000. Fukushima S. Gierthy J. NTP Technical report on the toxicology and carcinogenesis studies of ortho-phenylphenol (CAS No. In vivo genotoxicity of sodium orthophenylphenol: phenylbenzoquinone is one of the DNA-binding metabolite(s) of sodium ortho-phenylphenol. Environ Mol Mutagen 2005. Inoue S. Christenson WR. Environmental Protection Agency (U. Regul Toxicol Pharmacol 2002. Oxidative damage to cellular and isolated DNA by metabolites of a fungicide orthophenylphenol. Determination of orthophenylphenol in human urine by gas chromatography-mass spectrometry. EPA 739 R-06004. Bromig KH. Leser KH. J Chromatogr B Biomed Sci Appl 1997. Toxicol Appl Pharmacol 1999. Bormett GA. Kawanishi S. Bomhard EM. Buchholz BA. Ito N.gov/oppsrrd1/REDs/ phenylphenol_red.17(8):411-417. 2006. Mendrala AL. Stanley JS. Brendler-Schwaab SY. Richter M. J Agric Food Chem 2006. Selim S. Meuling WJ. Third National Report on Human Exposure to Environmental Chemicals.35(2 Pt 1):198-208. Bartels MJ. Nakagawa Y. St John MK. The carcinogenicity of the biocide ortho-phenylphenol. Crit Rev Toxicol 2002.(56):399-407. Mutat Res 1993. Cnubben NH. Office of Toxic Substances.50(11):3351-3358. Cano M. Fourth National Report on Human Exposure to Environmental Chemicals 45 . Carcinogenesis 1999. U. Identification of SARA compounds in adipose tissue.pdf.S.pdf.32(6):551-625.S. IARC Sci Publ 1984. Herbold BA. Timchalk C. Dose-dependent binding of ortho-phenylphenol to protein but not DNA in the urinary bladder of male F344 rats. Ito N. Atlanta (GA). J Agric Food Chem 2002. Smith RA. Relationship between metabolism and cytotoxicity of ortho-phenylphenol in isolated rat hepatocytes. Biochem Pharmacol 1992. Hum Exp Toxicol 1998. McNett DA. U. van de Sandt JJ.gov/ntp/htdocs/LT_ rpts/tr301.epa. Comparative metabolism of orthophenylphenol in mouse. Available at URL: http://www. March 1986. National Toxicology Program (NTP). Hakkert BC. Eadon G. Comparative in vitro-in vivo percutaneous penetration of the fungicide ortho-phenylphenol.22(10):809-814. Environmental Protection Agency (U.703(12):97-104. Freyberger A. Timchalk C. Fukushima S. 90-43-7) in Swiss CD-1 mice (dermal studies). Hagiwara A. Urinary physiologic and chemical metabolic effects on the urothelial cytotoxicity and potential DNA adducts of o-phenylphenol in male rats. Brzak KA. Vogel JS. Murata M. Arnold LL. rat and man.74(2):61-71. EPA). 4/9/09. Christenson WR. Food Chem Toxicol 1984. Shibata M.150(2):402-413. Kwok ES. Glas K. et al. Available at URL: http://ntp.

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

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

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

EPA 738-R-00-009. Striley CA. Coleman S.248(2-3):123-133. EPA). Fourth National Report on Human Exposure to Environmental Chemicals 49 .S. 5/30/06. EPA). J Agri Food Chem 1989. Hum Exp Toxicol 1996.108(12):1151-1157. Chem Res Toxicol 1998.cornell. Olsson AO. Ward EM. pages 3682-3690. Hladik ML.html.S. Casida JE. Barr JR. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. 2000. Federal Register: January 24. Thurman EM. Number 15.15(9):702-735. Alavanja MC. Report of the Food Quality Protection Act (FQPA) Tolerance Reassessment Progress and Risk Management Decision (TRED) for Acetochlor. Heederik D. Wratten SJ. Andrews HF. Environ Health Perspect 2003. Barr DB. 2005. Green T.39(17):6561-6574. Third National Report on Human Exposure to Environmental Chemicals. Deddens JA.Herbicides References Ashby J.gov/oppsrrd1/reregistration/REDs/acetochlor_tred.S. Tinwell H.37(4):10881093. Finding minimal herbicide concentrations in ground water? Try looking for their degradates. Wilson AG. J Expo Anal Environ Epidemiol 2005. Kolpin DW. Environ Health Perspect 2000. et al. Evaluation of the potential carcinogenicity and genetic toxicity to humans of the herbicide acetochlor. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. Linderman R.11(4):353359. Feil VJ. U.edu/profiles/herbgrowthreg/24-d-butylate/acetochlor/acetochlor_pet_100.S.24(10):1003-1012. and other herbicides in rivers. Reynolds SJ.111(5):749-756. epa. Hines CJ. Lefevre PA. Hodgson E. Roberts AL. Jefferies PR. Burkhardt MR. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns.248(2-3):115-122. Kinney PL. et al. Comparative metabolism of chloroacetamide herbicides and selected metabolites in human and rat liver microsomes. Whyatt RM. Davison KL. Battaglin WA. Sci Total Environ 2000. reservoirs and ground water in the Midwestern United States. Sanderson WT. Camann DE. Atlanta (GA). Acetochlor (Harness) Pesticide Petition Filing 1/00. Linhart SM. Kier L. J Expo Sci Environ Epidemiol 2007. Environ Sci Technol 2005. Volume 65. Hsiao JJ.pdf. Rose RL. March 2006. Environmental Protection Agency (U. imidazolinone. Dialkylquinonimines validated as in vivo metabolites of alachlor. Available at URL(non U. Available at URL: http://www. Occurrence of sulfonylurea. Comparative metabolism and elimination of acetanilide compounds by rat.cce. Identification of human urinary metabolites of acetochlor in exposed herbicide applicators by high performance liquid chromatography-tandem mass spectrometry.17(6):559-566. Barr DB. Feng PCC.S.15(6):500-508. Centers for Disease Control and Prevention (CDC). and metolachlor herbicides in rats. Furlong ET. acetochlor. Curwin BD.EPA): http://pmep. Hein MJ. Quistad GB. Larsen GL. 5/30/06 U. Environmental Protection Agency (U. Xenobiotica 1994. Sci Total Environ 2000. Barr DB. Bravo R. Peter CJ. et al. sulfonamide. 1998.

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

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

usgs. DNA adduct formation by alachlor metabolites. sulfonamide. Brown MA. Environmental Protection Agency (U. et al. Kier LD. Geneva.S.org/documents/pds/pds/pest86_e.248(2-3):123-133. Sacramento.43(25):2087-94. Available at URL: http:// www. acetochlor. Tolos W. WHO/ FAO Data Sheets on Pesticides. Finding minimal herbicide concentrations in ground water? Try looking for their degradates. EPA). Barr JR. Biagini R. Alachlor in Drinking-water. Lau H. and metolachlor herbicides in rats.11(4):353359. MacKenzie B. Circular 1291. Jefferies PR. Third National Report on Human Exposure to Environmental Chemicals.44(18):1325. Sci Total Environ 2000. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. Hill AB. Available at URL: http://water. 1997.int/water_sanitation_health/dwq/chemicals/en/alachlor. Davison KL.S. 1992-2001.395(2-3):159-171. Larsen GL. Hladik ML. Quantitative assessment of the mutagenic potential of environmental degradative products of alachlor. Thurman EM. Hill RH Jr. Biological monitoring of commercial pesticide applicators for urine metabolites of the herbicide alachlor. World Health Organization. December 1998. Sci Total Environ 2000. Background document for development of WHO Guidelines for Drinking-water Quality. Mutat Res. U. Martens MA. Camann DE. Centers for Disease Control and Prevention (CDC). Casida JE. Dialkylquinoneimine metabolites of chloroacetanilide herbicides induce sister chromatid exchanges in cultured human lymphocytes. Whyatt RM. Peter CJ. No. Casida JE. The Quality of Our Nation’s Waters Pesticides in the Nation’s Streams and Ground Water. Henningsen G. imidazolinone. Thelin GP.43(9):2504-2512. Hines CJ. Gilliom RJ). Sanderson WT. revised February 15.inchem. Environ Health Perspect 2003. 86. 2/27/09 Jefferies PR. 1999. Andrews HF. 2007. Casida JE.56(9):883-889. Am Ind Hyg Assoc J 1995. Occurrence of sulfonylurea.248(2-3):115-122.htm.epa.pdf. Kinney PL. Furlong ET. Brown KK. Geological Survey (USGS). Environ Sci Technol 2005. Feng PCC.37(4):10881093.pdf. World Health Organization (WHO). Bull Environ Contam Toxicol 1996. Striley CA.S. Kolpin DW.php. An evaluation of the carcinogenic potential of the herbicide alachlor to man. Life Sci 1988. who. Hines CJ. 2003.Herbicides References Battaglin WA.39(17):6561-6574. Thake DC. et al. Ann Occup Hyg 2003. Available at URL: http://www. Identification of a major human urinary metabolite of alachlor by LC-MS/MS. Heydens WF. Hsiao JJ. International Programme on Chemical Safety (IPCS). Water-Resources Investigations Report: Distribution of Major Herbicides in Ground Water of the United States Water Resource Investigations Report No. Burkhardt MR. Linhart SM.47(6):503-517. ALACHLOR. Quistad GB. Wilson AG. Supplemental Technical Information (available on-line only). Clark JM. Available at URL: http://www. Barr DB.56(6):853-859.gov/nawqa/pnsp/pubs/circ1291/ supporting_info. reservoirs and ground water in the Midwestern United States. J Agri Food Chem 1989. Dialkylquinonimines validated as in vivo metabolites of alachlor. Roberts AL. J Ag Food Chem 1995. Feil VJ. 98-4245 (by Barbash JE. Wratten SJ. Chem Res Toxicol 1998. 1996. 4/2/09 U. March 2006. 1999. Atlanta (GA). Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models.111(5):749-756.gov/oppsrrd1/ REDs/0063. 1998. 2/27/00 52 Fourth National Report on Human Exposure to Environmental Chemicals . Erratum in: Life Sci 1989. 2/27/09 U. EPA 738R-98-020. Tessier DM. Biagini RE. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor.S. Xenobiotica 1994. Deddens JA. Geological Survey (USGS).24(10):1003-1012. 2005. Quistad GB. Reregistration Eligibility Decision (RED) Alachlor.18(6):363-391. Shealy DB. and other herbicides in rivers. Kolpin DW. Kimmel EC. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. California. Driskell WJ. Hull RD. Shoemaker DA. Comparative metabolism and elimination of acetanilide compounds by rat. Hum Exp Toxicol.

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

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

inchem. Stoker TE. Biagini RE. Vonk A. Determination of atrazine metabolites in human urine: Fourth National Report on Human Exposure to Environmental Chemicals 55 . Pubertal development in female Wistar rats following exposure to propazine and atrazine biotransformation by-products. Stoker TE. Sanderson WT. No. Curwin BD. Gillis JH.76(1):190-200. The effects of atrazine on female wistar rats: an evaluation of the protocol for assessing pubertal development and thyroid function. Clayton CA. Lucas AD.. J Toxicol Environ Health 1994.htm. Environ Health Perspect 2007. Geneva.64(9):672-678. 3/11/09 Laws SC. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa.53(2):297-307. 2001). Blewett C. Cooper RL.Herbicides Biomonitoring Information Urinary levels of atrazine mercapturate reflect recent exposure. J Toxicol Environ Health 1994. Short-term effects of chlorotriazines on estrus in female Sprague-Dawley and Fischer 344 rats. Simpkins JW. Steroids 1999. 1999) and 83 Minnesota children with multiple urine collections during 1997 (Adgate et al. 2007).61(4):331-355. Atrazine disrupts the hypothalamic control of pituitary-ovarian function. Shoemaker DA. Available at URL: http:// www. Fleenor-Heyser DG. 1993). diamino-S-chlorotriazine and hydroxyatrazine. Deddens JA. 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. Hines CJ. Stoker TE.atsdr. In a study of 60 farm worker children. Eldridge JC. Wetzel LT. Gillis JH.2 μg/L in 15 farmers studied several days after spraying the pesticide (Curwin et al.47(6):503-517. Noriega N.. et al. et al. Through immunoassay atrazine equivalents (detected mostly as atrazine mercapturate). Barr DB. Carr WC Jr. 2005).58(2):366-376. Jones AD.. Goldman JM.cdc. Pfeifer KF. Barr DB. 2001 [online]. Short-term effects of chlorotriazines on estrus in female Sprague-Dawley and Fischer 344 rats. Pest Manag Sci 2005. Reynolds SJ. Barr DB. 2005).. Agency for Toxic Substances and Disease Registry (ATSDR). Wetzel LT. Cottica D. Lioy PJ. Ferrell JM. Ferioli A. In the NHANES 2001-2002 subsample. Schmid J. Grzywacz JG. 82. Goodrow MH.. demasculinized frogs after exposure to the herbicide atrazine at low ecologically relevant doses. 3/11/09 Arcury TA.43(2):155-167. Mendoza M. levels of atrazine mercapturate were generally not detectable (CDC. Toxicol Lett 1993. 2000). 2003. Tapia J. Striley CA. Catenacci G. Collins A.gov/toxprofiles/tp153.99(8):5476-5480. Quandt SA. Eberly LE. Stuart AA. Bradway DE. Proc Natl Acad Sci USA 2002. Freeman NC. Eldridge JC. Sanborn JR. The mammary tumor response in triazine-treated female rats: a thresholdmediated interaction with strain and species-specific reproductive senescence. 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. Ferrell JM. Aldous CN. the urinary geometric mean levels for herbicide applicators in Ohio and Wisconsin were about 6 μg/L (Hines et al. ATRAZINE. Biological monitoring of human exposure to atrazine. atrazine mercapturate was infrequently detected at the detection limit of < 1 μg/L. Toxicological profile for atrazine. Breckenridge CB. 2005. Maroni M. Saiz SG.. Hein MJ.109(6):583-590. et al.115(8):1254-1260. Extrom PC. Lee M. The geometric mean of urinary atrazine mercapturate was 1. Available at URL: http://www. atrazine was detected in only four children (Arcury et al. Heederik D. Bersani M. Finding measurable amounts of atrazine mercapturate in urine does not mean that the levels of atrazine mercapturate cause an adverse health effect. 1996.43(2):155-167. et al. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample.30(2):244-247. Tyrey L. WHO/ FAO Data Sheets on Pesticides. Toxicol Sci 2000. Environ Health Perspect 2001. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. et al. Determination of urinary residue levels of the N-dealkyl metabolites of triazine herbicides. Pesticide urinary metabolite levels of children in eastern North Carolina farmworker households. J Agric Food Chem 1982. Chen H. Centers for Disease Control and Prevention (CDC). Gammon DW.15(6):500-508. Brown KK. Cooper RL. urinary concentrations ranged from 5-1756 μg/L (Lucas et al. Perry et al.html. et al. International Programme on Chemical Safety (IPCS). Laws SC. Hayes TB. Ann Occup Hyg 2003. J Expo Anal Environ Epidemiol 2005. Atlanta (GA). Cooper RL. Toxicol Sci 2003. McElroy WK. Barbieri F. Seiber JN.. A risk assessment of atrazine use in California: human health and ecological aspects.org/documents/pds/pds/pest82_e. In a small number of field workers. Toxicol Sci 2000.69(2):217-222. Moseman RF. Hermaphroditic. In small studies of Maryland residents in 19951996 (MacIntosh et al. Stevens JT. References Adgate JL. World Health Organization.

Environmental Protection Agency (U.php. Guidici DL.58(1):50-59. 4/2/09 56 Fourth National Report on Human Exposure to Environmental Chemicals . 1992-2001.S. Boerma J. J Expo Anal Environ Epidemiol 1999. Singzoni B.S. The Quality of Our Nation’s Waters. Office of Prevention.S.27(6):599612. Needham LL. Laws SC.6(1):107-116. Toxicol Sci 2000. Toxicol Appl Pharmacol 2002.Herbicides development of a biomarker of exposure. Perry M.gov/nawqa/pnsp/pubs/ circ1291/supporting_info. Breckenridge CB. Kastl PE. van den Berg M. Case No. Delzell E. The effects of atrazine metabolites on puberty and thyroid function in the male Wistar rat. Hammerstrom KA. Pesticides and Toxic Substances. 0062.67(2):198-206. Fenton SE. EPA). A risk characterization for atrazine: oncogenicity profile. Urinary biomarkers of atrazine exposure among farm pesticide applicators. 2003b. Cooper RL. Exposure parameters necessary for delayed puberty and mammary gland development in LongEvans rats exposed in utero to atrazine.10(7):479. Lansbergen GW. Ann Epidemiol 2000. EPA Office of Pesticide Programs. Stoker TE. May 2003a. A longitudinal investigation of selected pesticide metabolites in urine. Wood C.S. MacIntosh DL. Christiani D. Toxicology 1990.9(5):494-501. Geological Survey (USGS). 2007. Pesticides in the Nation’s Streams and Ground Water.56(2):69-109.61(1):27-40.gov/scipoly/sap/meetings/2003/june/ finaljune2002telconfreport. The effect of atrazine on puberty in male Wistar rats: an evaluation in the protocol for the assessment of pubertal development and thyroid function. Wetzel L.pdf.S. Chem Res Toxicol 1993.epa. Langvardt PW. Induction and inhibition of aromatase (CYP19) activity by various classes of pesticides in H295R human adrenocortical carcinoma cells. Toxicol Sci 2002. EPA). Dagenhart D. Tortorelli J. U. Guidici DL. Cooper RL. Sanderson JT. A review of epidemiologic studies of triazine herbicides and cancer. Environmental Protection Agency (U. White paper on potential developmental effects of atrazine on amphibians. Rayner JL. Determination of the effect of tridiphane on the pharmacokinetics of [14C]-atrazine following oral administration to male Fischer 344 rats. Available at URL: http://www. 3/11/09 U. Available at URL: http://www. Ryan PB. Circular 1291.usgs. March 2006. Supplemental Technical Information (available on-line only).182(1):44-54. Stevens JT. Washington (DC).gov/oppsrrd1/REDs/ atrazine_ired. Toxicol Appl Pharmacol 2004. J Toxicol Environ Health A 1999.195(1):23-34.pdf. Crit Rev Toxicol 1997. revised February 15. Dryzga MD. Laws SC.epa. Osborne DW. Sathiakumar N. Available at URL: http://water. Stoker TE. 6/1/09 U. Interim Reregistration Eligibility Decision For Atrazine. Timchalk C. Environmental Fate and Effects Division.

43) 1.230 (<LOD-.32 (1.910) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD . Recent estimates of chronic intakes of 2. although dermal exposure may be significant for herbicide manufacturing plant workers exposed to high concentrations of 2.610 (. 2.05-2.490 (. population from the National Health and Nutrition Examination Survey. and it is often mixed with other chlorophenoxy acid herbicides (such as dicamba.10) < LOD 1. myotonia. Intentional overdoses and unintentional high dose exposures to chlorophenoxy acid herbicides have resulted in weakness. it acts as a plant growth hormone..2.S. As much as 62 million pounds of 2.22) < LOD . At low levels.420-.27 (1. It is not well absorbed through the skin.610-. 1977). 2007). and mecoprop). with a half-life of several days to several weeks.24 (.21) 1.760 (.690 (.EPA.420) < LOD .310 (. the chlorophenoxy herbicide 2. General population exposure to 2.400) < LOD .4-D or exposed for prolonged periods.210 (<LOD-.320) 90th . by direct contact with agricultural and residential areas after applications. 2004).16) < LOD . It was first registered with U.930-1.4-D is rapidly absorbed via oral and inhalation routes.890) < LOD . but at higher levels they are herbicidal. headache.910) < LOD .60) 1. Once absorbed. hypotension.730 (. It is poorly bound in soils. in 2001 (U. nausea. 94-75-7 General Information Widely used throughout the United States.690 (.4-Dichlorophenoxyacetic Acid CAS No.4-D can be applied either as an aqueous salt or as oil-soluble esters. 2. 1974.70) 1. Sauerhoff et al.680-1.S.350) < LOD < LOD < LOD .4-D has low acute toxicity.4-dichlorophenoxyacetic acid (2.80) 1.330 (.540-. 4-D. Kohli et al.10 (<LOD-1.EPA. abdominal pain.670-1.960-1.230-.210-.4-D have been below recommended intake limits (U.250 (<LOD-..550-1.690-1.02-1.4-Dichlorophenoxyacetic acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.690 (.30 (<LOD-2. Fourth National Report on Human Exposure to Environmental Chemicals 57 .08) < LOD .952 and 0.490) < LOD < LOD < LOD .S.4-D at low environmental doses or at biomonitored levels from low environmental exposures are unknown.51 (1.. these herbicides can enhance plant growth.13) < LOD .27 (. Acid and salt forms are much less toxic to fish and aquatic invertebrates than the ester forms.EPA in 1948. Survey Geometric mean (95% conf. 1989.07 (.S.10 (<LOD-1. Similar to other chlorophenoxy herbicides. MCPA.66) < LOD 1. 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. and by consuming food or drinking water contaminated with 2.4-D is eliminated mostly unchanged in the urine with an elimination half-life ranging from 10 to 33 hours (Arnold et al. < LOD means less than the limit of detection.560-. It is rarely detected in ground waters (USGS.4-D were used in the U.660) 1.260 (<LOD-.4-D may occur during residential applications.910) 1.03) 695 659 520 668 589 892 Limit of detection (LOD. dizziness.49) 477 546 677 797 823 1070 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD .930 (. 2.370-.27-2. and aquatic environments.20 (<LOD-1.740 (. 2. 2005).410) < LOD . agricultural. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.48) < LOD 1.4-D) controls broadleaf weeds in residential.810-1.S.250 (<LOD-.40) 1. Human health effects from 2.310) < LOD .20 (.55 (1.Herbicides 2. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 1. and delayed Urinary 2.37) 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 .890 (.22) 962 1135 1015 1278 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .00-2.560-1.440-1. renal and hepatic injury.

05) .670 (.890) < LOD 1.810-1.480 (. Hill et al.39) < LOD 1..580-.4-D had urinary levels several hundred to several thousand times higher than the 95th percentiles of the NHANES subsamples (CDC.EPA.780) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD . IPCS.73) .7.590 (<LOD-1.Herbicides neuropathy (Bradberry et al..560-.56) . adrenals and gonads (NTP.08 (. thyroid.340-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.380 (<LOD-. Pearce and McLean. liver. 1989).270 (<LOD-.700 (. The 95th percentiles of the NHANES 1999-2000 and 2001-2002 subsamples were roughly similar to the 95th percentile values reported in a nonrandom subsample from NHANES III (1988-1994) (CDC. 2001. IPCS. 1994).S. U.390) < LOD < LOD < LOD .330-.980) < LOD 1.3.920) < LOD 1. in small samples of children (Hill et al.19) .660) < LOD .850) < LOD .13 (. Epidemiological studies have reported associations of several types of cancer. 2003. myotonia.32 (<LOD-2..8-tetrachlorodibenzo-pdioxin) (Garabrant and Philbert.4-Dichlorophenoxyacetic acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.380 (<LOD-.660 (.S. 2004).680) < LOD . such as soft tissue sarcoma and non-Hodgkin’s lymphoma.670 (. Kolmodin-Hedman and Erne. U.990-1.16) 1. 2005).17 (..41 (1. 2005).S. or teratogenic effects in chronic rodent studies (Charles et al. Post-application levels in farmers and home gardeners were dependent on Urinary 2.26) 962 1135 1015 1277 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD ..epa.27-1.270-.590 (<LOD-1.S.4-D does not have significant reproductive. 2006. In previous samples of the U. CDC.890-1.670 (<LOD-1. Biomonitoring Information Urinary levels of 2... 2000).4-D production plant workers and a few forestry workers spraying 2.08 (. urinary 2.780 (. population (Hill et al..640 (. IPCS.440 (. 2005). 2005. Survey Geometric mean (95% conf.EPA. 1996.810-1.380) < LOD . 1996. 2. 1985.26) 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 . Acute high doses administered to laboratory animals produced ataxia. population from the National Health and Nutrition Examination Survey.S.720 (.24) 1. Frank et al.610-.490 (.gov/pesticides/. U.570) < LOD .410) < LOD 1.780) . Additional information is available from U. IARC considers the chlorophenoxyacetic acids group of chemicals as possibly carcinogenic to humans.13 (. 1980. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 1.4-D was not found to be genotoxic or carcinogenic in animal studies (Garabrant and Philbert..14 (..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.340 (.40) 695 659 520 667 589 892 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. developmental.930-1. It is unclear whether these associations are related to the chlorophenoxy herbicides. with the exposure to chlorophenoxy herbicides as defoliants or contaminated herbicides.4-D reflect recent exposure.4-D levels were detectable in less than a quarter of the individuals studied.520-. IOM. 2. 1992). other exposures. 1996.08 (.740 (.35) < LOD .EPA at: http://www. 2002.350 (<LOD-. U.380-.4-D are eye irritants. and of adults and children (Baker et al. or to contaminants in the herbicide formulations (specifically 2.470) < LOD . Average post-application urinary levels of 2. 2005.410 (<LOD-.780-1. eyes. The acid and salt forms of 2.620-. 2005.790) < LOD .29) 477 546 677 796 823 1070 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD .820-1. Kutz et al. and evidence of histological injury to the kidneys.EPA.790) 1. 2002. 58 Fourth National Report on Human Exposure to Environmental Chemicals .560-.550-. 1995). Knopp et al.S.410) < LOD < LOD < LOD .S. 1995.610-. 2.410) 90th . 2005. 2005).EPA 2005).

4:318-321. Developmental toxicity studies in rats and rabbits on 2. Fast DM. Baker BA.4-D and 2.4:427-435. et al. Campbell RA. Occup Environ Med 1994. Carter-Pokras OD. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Quantification of selected pesticide metabolites in human urine using isotope dilution high-performance liquid chromatography/ tandem mass spectrometry. 2003. Solomon KR.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. van Ravenzwaay B.4 dichlorophenoxyacetic acid (2. To T. TOX-63 Peroxisone Project (2.4-D than levels found in the general population. Third National Report on Human Exposure to Environmental Chemicals. Available at URL: http:// www.4-dichlorophenoxyacetic acid and its forms.15(6):500-508.Herbicides the time since application. In farm families.inchem. Curwin BD..27(1):23-38. Kutz FW. The pharmacokinetics of chlorinated phenoxy acid herbicides: a literature. Scand J Work Environ Health 2005. Frank R.nap. Tandon JS. 2005). J Expo Anal Environ Epidemiol 2000. Committee to Review the Health Effects in Vietnam Veterans of Exposure to Herbicides (Fourth Biennial Update. Beasley VR. Shealy DB. Survival and Growth Curves from NTP Toxicity Studies. J Environ Sci Health B 1992. the number of acres to which it was applied (Curwin et al.4-dichlorophenoxyacetic acid in the chemical industry: results of a five year biological monitoring study.71(2):99-108. J Expo Anal Environ Epidemiol 2005 Nov.4-dichlorophenoxyacetic acid (2. Kolmodin-Hedman B.4-D). 2006. Board on Health Promotion and Disease Prevention. Assessment of exposure to 2. Baker SE. Updated March 7. Sanderson WT.niehs. Stephenson GR.4:97-100. 3/17/09 Fourth National Report on Human Exposure to Environmental Chemicals 59 . Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. Barr DB.60(1):121-131. Murphy RS. J Toxicol Environ Health 1992.10(6 Pt 2):789-798. Hill RH Jr. Veterans and Agent Orange: update 2002. Arch Environ Contam Toxicol 1985.. cfm?objectid=06FF8DA6-E5A1-90CD-3F26562CEC5CDDE5.51(3):152-159. Finding a measurable amount of 2.. Chapman P. Environ Res 1995. Pesticide residues in urine of adults living in the United States: reference range concentrations.php?record_id=10603. Head SL. Biomonitoring for farm families in the farm family exposure study. 3/17/09 Institute of Medicine (IOM). Xenobiotica 1974. Arch Toxicol Suppl 1980. Toxicol Sci 2001. 2. Cole DC. Arnold EK.4-D): exposure and urinary excretion.31 Suppl 1:90-97. Washington (DC): National Academies Press. Needham LL. Needham LL. Harris et al. Bailey SL. Holler JS. Exposure of homeowners and bystanders to 2. 2005 Charles JM.4-D.4-Dichlorophenoxyacetic Acid). Tables.18(4):469-474. Hill RH Jr.31 Suppl 1:98-104. Sircar KP. Ritter L.edu/catalog. Sirons G J. Bus JS. Mandel et al. Gregg M. Brody D.nih.5-T). TOX-63: TOXICITY REPORT CURVES. Biomonitoring studies of 2. Baker S. 1992). Pesticides residues in food: 1996 evaluations Part II Toxicology. Hein MJ.4. Dhar MM.gov/index. Cook BT. 2005. Philbert MA. and the use of protective clothing or equipment (Arbuckle et al. Arch Environ Contam Toxicol 1989. et al. Mandel JS. Crit Rev Toxicol 2002. Acquavella JF. 914.37(2):277-291.4-D were highest in the farmers who applied the 2. Erne K.4-dichlorophenoxyacetic acid (2. Driskell WJ. National Toxicology Program (NTP).S.4-D in urine does not mean that the level of the 2. general population. Selected pesticide residues and metabolites in urine from a survey of the U. Ripley BD. Absorption and excretion of 2.4-dichlorophenoxyacetic acid in man. geometric mean urinary levels of 2. Gupta BN. Vet Hum Toxicol 1989. Alexander BH. Dichlorophenoxyacetic acid. 3/17/09 Knopp D. Heederik D. Scand J Work Environ Health 2005. Review of 2. Harris SA. International Programme on Chemical Safety-INCHEM (IPCS).. Atlanta (GA). Honeycutt R.31(2):121-125. Biomonitoring of herbicides in Ontario farm applicators. Available at URL: http:// www. et al. Estimation of occupational exposure to phenoxy acids (2. Centers for Disease Control and Prevention (CDC). Khanna RN. Garabrant DH.32(4):233-257.4-. 2005).4-D will result in an adverse health effect. Hanley TR Jr. the amount of pesticide applied. References Arbuckle TE. Forestry workers involved in aerial application of 2. Available at URL: http://ntp. Beeson MD.4-D) epidemiology and toxicology. 2005. Barr DB. Wilson RD. Reynolds SJ. Smith SJ.htm.org/documents/jmpr/jmpmono/v96pr04. Kohli JD. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children. other family members had levels ranging only slightly higher than the 95th percentile levels in NHANES 1999-2000 and 2001-2002 subsamples (CDC.

Blau GE. The fate of 2. 4/2/09 U.S. 1992-2001. 2.S. Available at URL: http://www.gov/oppsrrd1/ REDs/factsheets/24d_fs. 60 Fourth National Report on Human Exposure to Environmental Chemicals .htm. Braun WH. Environmental Protection Agency (U. Pesticide industry sales and usage .EPA).S. EPA 738 F-05-002. June 2005. S.php.4-D) following oral administration to man. Toxicology 1977. March 2006. Office of Prevention Pesticides and Toxic Substances. Pesticides in the Nation’s Streams and Ground Water.S. Environmental Protection Agency (U.epa. Geological Survey (USGS). Circular 1291. 2004.8:3-1U. 3/17/09. 2007.4-D RED Facts.4-dichlorophenoxyacetic acid (2.pdf.2000 and 2001 market estimates. revised February 15. The Quality of Our Nation’s Waters. Gehring PJ.epa.Herbicides Sauerhoff MW. 3/17/09 U. Washington (DC): U. gov/oppbead1/pestsales/01pestsales/market_estimates2001. Available at URL: http://water.EPA. Available at URL: http://www.gov/nawqa/pnsp/pubs/ circ1291/supporting_info.EPA).S.usgs. Supplemental Technical Information (available on-line only). May.

WHO. 2007.. USGS. though the 95th percentile for males was 0. Kolpin et al. EPA at: http://www.. and on non-crop land for general weed control. Metolachlor is well absorbed dermally. Davison et al. 1999. 2007.gov/pesticides/. 2000. Hladik et al. 1995. whereas 60% of applicators had detectable amounts.EPA. and convulsions were observed at lethal doses in animal studies. including corn.. NTP and IARC do not have ratings regarding human carcinogenicity. Biomonitoring studies on levels of metolachlor mercapturate provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels metolachlor than are found in the general population. Occasionally in the past.2% of a small reference population had detectable metolachlor equivalents by immunoassay in their urine.S. WHO. U. Hines et al.200 μg/L (CDC. EPA. sorghum and other crops. 2005).S. 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. The geometric mean metolachlor mercapturate was 4. Fourth National Report on Human Exposure to Environmental Chemicals 61 . Salivation. so applicators.. 2005.Herbicides Metolachlor available from U.S.EPA considers metolachlor to be a possible human carcinogen.EPA. and it was not mutagenic in mammalian cells (U. Additional information is Urinary levels of metolachlor mercapturate reflect recent exposure. 2003). Metolachlor did not show developmental or reproductive toxicity in chronic animal studies. Metolachlor has low potential for acute toxicity (U. It is absorbed by plants and inhibits plant protein synthesis. Feng and Wratten.. Human health effects from metolachlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown. formulators. In animals.S. 1995). Urinary levels of metolachlor mercapturate were generally not detectable in the NHANES 2001-2002 subsample. 2003). This metabolite is not a marker of exposure to either plant metabolites or environmental degradates of metolachlor which can be present in the environment. (2003) showed that 2.epa. 1995). 51218-45-2 General Information Metolachlor is a chloroacetanilide type herbicide that is applied for preemergent control of grasses and broadleaf weeds on agricultural crop land. but another metabolic pathway can produce 2-methyl-6-ethylaniline and its reactive metabolite which may account for observed effects (Coleman et al. mercapturate conjugates were the predominant metabolites. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 1998). Metolachlor or its degradates can leach from soils and have been detected in watersheds of agricultural land. lacrimation. 2005). Gilliom. People exposed to metolachlor will excrete metolachlor mercapturate in their urine. metolachlor levels in water have exceeded lifetime human health advisory levels (U.. 2003).EPA.S.S. and field workers may have significant exposures via this route. General population exposure may occur through the consumption of contaminated food or drinking water. soybeans.. 1994. in both ground and surface waters (Battaglin et al. metolachlor was quickly absorbed after dermal or oral doses. 1989.7 μg/L in the urine of farmers after they had sprayed metolachlor (Curwin et al. In animal studies. 1995). Jefferies et al. 2000. Finding measurable amounts of metolachlor mercapturate in the urine does not mean that the levels of metolachlor mercapturate cause an adverse health effect. Metolachlor shows little potential to bioaccumulate but is moderately toxic to fish. and eliminated in urine and feces over two to three days (WHO. Biomonitoring Information CAS No. Estimated human intakes have been below recommended limits (U.

220) < LOD 1192 1346 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . 62 Fourth National Report on Human Exposure to Environmental Chemicals .200 (<LOD-.S. Survey Geometric mean (95% conf.740) 679 700 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.200 (<LOD-. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2538 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 580 831 1127 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD . which may vary for some chemicals by year and by individual sample.Herbicides Urinary Metolachlor mercapturate Metabolite of Metolachlor Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.2. Urinary Metolachlor mercapturate (creatinine corrected) Metabolite of Metolachlor Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. < LOD means less than the limit of detection. interval) Selected percentiles ( 95% confidence interval) 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 .240) 679 701 957 Limit of detection (LOD.440 (<LOD-. population from the National Health and Nutrition Examination Survey. see Data Analysis section) for Survey year 01-02 is 0.670 (<LOD-.500) < LOD 1192 1345 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. population from the National Health and Nutrition Examination Survey.S. Survey Geometric mean (95% conf.

Feil VJ.S. Furlong ET. Third National Report on Human Exposure to Environmental Chemicals. Background document for development of WHO Guidelines for Drinking-water Quality. 3/26/09 U.111(5):749-756. EPA 738R-95-006. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. Kolpin DW. Rose RL.pdf 3/30/09 Hines CJ. imidazolinone.15(6):500-508. Sci Total Environ 2000. et al. Burkhardt MR. Casida JE.usgs. acetochlor.pdf. Finding minimal herbicide concentrations in ground water? Try looking for their degradates. reservoirs and ground water in the Midwestern United States. Geological Survey (USGS). Gilliom RJ). Pesticides in U. U.html. Available at URL: http://www. Gillion. Atlanta (GA). J Agri Food Chem 1989. Linhart SM. Jefferies PR. Hsiao JJ. 98-4245 (by Barbash JE.248(2-3):123-133. Curwin BD.usgs. Thelin GP. Biagini RE. Chem Res Toxicol 1998.39(17):6561-6574. Thurman EM. Reynolds SJ. 2007.ESTfeature_gilliom. Hein MJ. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. Hodgson E.php. March 2006. Supplemental Technical Information (available on-line only). streams and groundwater.int/water_sanitation_health/dwq/chemicals/ metolachlor. Kolpin DW.47(6):503-517. Environ Health Perspect 2003. Available at URL: http://water. Comparative metabolism of chloroacetamide herbicides and selected metabolites in human and rat liver microsomes. Water-Resources Investigations Report: Distribution of Major Herbicides in Ground Water of the United States Water Resource Investigations Report No. Peter CJ. et al. Coleman S. Davison KL. Shoemaker DA.who. Available at URL: http://water.24(10):1003-1012.S. Quistad GB.11(4):353359. Hladik ML.41:3409-3414.S. Centers for Disease Control and Prevention (CDC). Geological Survey (USGS). Circular 1291. Linderman R. 1999. Brown KK. Heederik D. Kinney PL. Striley CA. Wratten SJ. 2005. Barr DB. Sacramento.pdf. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns.Herbicides References Battaglin WA. Occurrence of sulfonylurea. J Expo Anal Environ Epidemiol 2005. Environ Sci Technol 2005. Ann Occup Hyg 2003. Deddens JA.gov/nawqa/pnsp/pubs/circ1291/ supporting_info. Environmental Protection Agency (U.108(12):1151-1157.gov/oppsrrd1/ REDs/0001. The Quality of Our Nation’s Waters Pesticides in the Nation’s Streams and Ground Water.248(2-3):115-122. 1992-2001.37(4):10881093. Environ Health Perspect 2000. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. sulfonamide. usgs. April 1995. Roberts AL. revised February 15. Environ Sci Technol 2007. Available at URL: http://www. Xenobiotica 1994.S. Available at URL: http://water. Comparative metabolism and elimination of acetanilide compounds by rat. 4/2/09 U. Larsen GL. Camann DE. Alavanja MC. Barr JR. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. 3/27/09 Fourth National Report on Human Exposure to Environmental Chemicals 63 . Dialkylquinonimines validated as in vivo metabolites of alachlor.gov/nawqa/ pnsp/pubs/wrir984245/text. Sci Total Environ 2000. and metolachlor herbicides in rats. Sanderson WT. Reregistration Eligibility Decision (RED) Metolachlor. 2003. 1998. California. Barr DB. EPA). 6/1/09 Whyatt RM. Ward EM.gov/nawqa/pnsp/pubs/files/051507.S. R. Feng PCC. World Health Organization (WHO). Metolachlor in Drinkingwater. Andrews HF.epa. and other herbicides in rivers.

these herbicides can enhance plant growth. it is not well absorbed through the skin.4-D were used as defoliants in the Vietnam War (e.. 2. < LOD means less than the limit of detection.4. 1974).5-T. Ester forms of 2.3. but higher levels are herbicidal. Although 2. abdominal pain. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1814 2538 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 430 580 618 831 766 1127 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 891 1192 923 1346 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 652 679 483 701 531 957 Limit of detection (LOD.4.4. Given the commercial unavailability of 2. 1992). such as soft tissue sarcoma and non-Hodgkin’s lymphoma.4.5-trichlorophenol and other degradates. At low levels. with an elimination half-life of approximately 19 hours (Arnold et al.5-T (Holson et al.4.5-T has been rarely detected in ground waters (USGS. Mohammad and St. which may vary for some chemicals by year and by individual sample..S. renal and hepatic injury.5-Trichlorophenoxyacetic acid (2. myotonia. Human health effects from 2.4. Teratogenic and developmental effects have been reported in studies of multiple rodent strains treated with high doses of technical grade 2. ranging from several weeks to many months.4.5-T in soil varies with conditions. and delayed neuropathy (Bradberry et al. Nelson et al.4.1.2 and 0. and concern about contamination with 2. 2.4. 2.4.5-T use as a herbicide in 1985. 2007). Omer.8-tetrachlorodibenzo-p-dioxin (TCDD) led to the discontinuation of 2. headache. Intentional overdoses and unintentional high dose occupational exposures to chlorophenoxy acid herbicides have resulted in weakness.. The half-life of 2. hypotension.Herbicides 2. 64 Fourth National Report on Human Exposure to Environmental Chemicals .4..5-Trichlorophenoxyacetic acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. 2004). see Data Analysis section) for Survey years 99-00 and 01-02 are 1. Chlorophenoxy herbicides act as plant growth hormones. with the exposure to chlorophenoxy herbicides as defoliants Urinary 2.. Survey Geometric mean (95% conf. the general population is unlikely to be exposed to it. 1992.g.4.5-Trichlorophenoxyacetic Acid CAS No. nausea. dizziness.4.5-T is eliminated mostly unchanged in the urine.5-T) is a chlorophenoxy acid herbicide that is no longer registered for use in the United States. 1986.4.5-T was once applied as either an aqueous salt or as an oil-soluble ester.4.. 93-76-5 General Information 2. Agent Orange). Once absorbed into the body. Kohli et al.5-T at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 1989. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 2. population from the National Health and Nutrition Examination Survey. Epidemiological studies have reported associations of several types of cancer.5-T degrades to 2.5T is rapidly absorbed via oral and inhalation routes.7.4.5-T and 2.

2002.5-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.EPA.3.5-T itself is not mutagenic. It is unclear whether these associations are related to the chlorophenoxy herbicides. IPCS.4.000 times higher than the detection limit for the NHANES 2001-2002 data (Kolmodin-Hedman and Erne. urinary levels of 2. In the NHANES 1999-2000 and 2001-2002 subsamples (CDC. Biomonitoring studies on 2.5-T reflect recent exposure. Urinary 2.4. 2004). Survey Geometric mean (95% conf.. 2005).4.5-T also were below the limit of detection (Kutz et al. population from the National Health and Nutrition Examination Survey. Fourth National Report on Human Exposure to Environmental Chemicals 65 .S. Finding a measurable amount of 2.gov/pesticides/. Additional information is available from U. Pearce and McLean. 2005.5-T than levels found in the general population. Biomonitoring Information Urinary levels of 2.EPA at: http://www. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.4.4. other exposures. U. 2. 1996.5-T measured after a day of exposure in a few asymptomatic herbicide applicators were 35.Herbicides or contaminated herbicides.4.5-T does not mean that the level will result in an adverse health effect.8-tetrachlorodibenzop-dioxin) (Garabrant and Philbert. Mean urinary levels of 2. 2003. similar to results of NHANES II (19761980).S. 1992). 1980).4. IOM.epa.4.4.S.7.5-T were generally below the limit of detection. in which urinary levels of 2. or to contaminants in the herbicide formulations (specifically 2. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1814 2537 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 430 580 618 830 766 1127 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 891 1192 923 1345 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 652 679 483 700 531 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.5-Trichlorophenoxyacetic acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. IARC considers the chlorophenoxyacetic acids group of chemicals as possibly carcinogenic to humans.

Pesticides residues in food: 1996 evaluations Part II Toxicology. 914. Vet Hum Toxicol 1989. Board on Health Promotion and Disease Prevention. Developmental toxicity of 2.pdf. Crit Rev Toxicol 2002. Sheehan DM. Khanna RN.4. et al. Gaines TB.31(2):121-125.4. Veterans and Agent Orange: update 2002. LaBorde JB. Holson JF. et al. Erne K. Multireplicated dose-response studies in four inbred strains and one outbred stock of mice.EPA).EPA.8(5):551-60.19(2):286-297.S. I. 2005.5-T).4. McCallum WF. Poisoning due to chlorophenoxy herbicides.19(2):298-306. Mohammad FK.edu/catalog. 3/17/09 Institute of Medicine (IOM). 210:250-255. Third National Report on Human Exposure to Environmental Chemicals. Holson JF.4. Beasley VR. Murphy RS. Gupta BN. Proudfoot AT. gov/oppbead1/pestsales/01pestsales/market_estimates2001. Philbert MA. Nelson CJ. Tandon JS.4-D/2.4.2000 and 2001 market estimates. International Programme on Chemical Safety-INCHEM (IPCS). Sircar KP.4-dichlorophenoxyacetic acid (2. Washington (DC): National Academies Press. Committee to Review the Health Effects in Vietnam Veterans of Exposure to Herbicides (Fourth Biennial Update. Dhar MM. Estimation of occupational exposure to phenoxy acids (2. Agricultural exposures and non-Hodgkin’s lymphoma. Gaylor DW. Gaines TB. May. Centers for Disease Control and Prevention (CDC). Atlanta (GA).epa. II. Brody D. Developmental toxicity of 2.5-T).4. 3/17/09 Kohli JD. LaBorde JB.Herbicides References Arnold EK. Behavioral and developmental effects in rats following in utero exposure to 2.5-trichlorophenoxy acetic acid in man. Available at URL: http:// www.S. J Toxicol Environ Health 1992.4-D) epidemiology and toxicology.php?record_id=10603. Carter-Pokras OD. Office of Prevention Pesticides and Toxic Substances. 2003. Garabrant DH.5-trichlorophenoxyacetic acid (2. Arch Toxicol Suppl 1980. Vale JA.5-T). Bradberry SM. 3/17/09 66 Fourth National Report on Human Exposure to Environmental Chemicals . Dichlorophenoxyacetic acid. 2. Multireplicated dose-response studies with technical and analytical grades of 2. The pharmacokinetics of chlorinated phenoxy acid herbicides: a literature. Cook BT. Scand J Work Environ Health 2005. St Omer VE.31 Suppl 1:1825. Available at URL: http://www. Toxicol Rev 2004. Neurobehav Toxicol Teratol 1986.32(4):233-257. Fundam Appl Toxicol 1992. S.37(2):277-91. Selected pesticide residues and metabolites in urine from a survey of the U. U.S.4:318-21. Pesticide industry sales and usage . Wolff GL. McLean D.4.4-D and 2. Kolmodin-Hedman B. Review of 2. Kutz FW.inchem. general population. Washington (DC): U.5-T in four-way outcross mice. Nelson CJ. Fundam Appl Toxicol 1992. Pearce N.23(2):65-73. Absorption and excretion of 2.org/documents/jmpr/jmpmono/v96pr04. Environmental Protection Agency (U.htm.5-trichlorophenoxyacetic acid (2. discussion 5-7. Arch Int Pharmacodyn Ther 1974.4. 2004.5-t mixture.4-. Available at URL: http:// www.nap.

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

Carbamate Insecticides

Carbofuran

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

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

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

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

Selected percentiles
( 95% confidence interval)

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

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

years 99-00 01-02

50th < LOD < LOD < LOD < LOD

75th < LOD < LOD

90th

* *

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

* * * * * *

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

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

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

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

482 578 681 827 831 1125

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

* * * *

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

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

973 1190 1021 1340

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

* * * * * *

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

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

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

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

696 680 521 696 603 953

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

68

Fourth National Report on Human Exposure to Environmental Chemicals

Carbamate Insecticides

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

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

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

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

Selected percentiles
( 95% confidence interval)

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

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

years 99-00 01-02

50th < LOD < LOD < LOD < LOD

75th < LOD < LOD

90th

* *

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

* * * * * *

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

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

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

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

482 578 681 826 831 1125

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

* * * *

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

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

973 1190 1021 1339

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

* * * * * *

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

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

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

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

696 680 521 695 603 953

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

Fourth National Report on Human Exposure to Environmental Chemicals

69

Carbamate Insecticides

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

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Carbamate Insecticides

Propoxur

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

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

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Carbamate Insecticides

Urinary 2-Isopropoxyphenol
Metabolite of Propoxur

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

Selected percentiles
( 95% confidence interval)

Sample 95th < LOD < LOD size 1917 2503

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

years 99-00 01-02

50th < LOD < LOD < LOD < LOD

75th < LOD < LOD

90th

* *

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

* * * * * *

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

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

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

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

456 574 655 820 806 1109

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

* * * *

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

936 1178 981 1325

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

* * * * * *

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

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

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

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

664 677 500 696 585 931

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

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Fourth National Report on Human Exposure to Environmental Chemicals

Carbamate Insecticides

Urinary 2-Isopropoxyphenol (creatinine corrected)
Metabolite of Propoxur

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

Selected percentiles
( 95% confidence interval)

Sample 95th < LOD < LOD size 1917 2502

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

years 99-00 01-02

50th < LOD < LOD < LOD < LOD

75th < LOD < LOD

90th

* *

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

* * * * * *

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

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

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

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

456 574 655 819 806 1109

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

* * * *

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

936 1178 981 1324

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

* * * * * *

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

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

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

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

664 677 500 695 585 931

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

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Carbamate Insecticides

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

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Fourth National Report on Human Exposure to Environmental Chemicals

Organochlorine Pesticides

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

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

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

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

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

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

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

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

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

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Organochlorine Pesticides

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

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Fourth National Report on Human Exposure to Environmental Chemicals

Organochlorine Pesticides

Aldrin

CAS No. 309-00-02

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

Dieldrin

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

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

Selected percentiles
( 95% confidence interval)

Sample 95th < LOD < LOD size 2275 1946

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

years 01-02 03-04

50th < LOD < LOD < LOD < LOD

75th < LOD < LOD

90th

* *

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

* * * *

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

756 588 1519 1358

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

* * * *

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

1057 946 1218 1000

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

* * * * * *

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

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

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

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

559 456 512 485 1045 881

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

Fourth National Report on Human Exposure to Environmental Chemicals

77

2000). 1991). 2005). Serum dieldrin levels at the 95th percentile in NHANES 2001-2002 and 2003-2004 subsamples were approximately ten times lower than the corresponding percentile measured in NHANES II (1976-1980). 1989).e.. dieldrin at higher doses caused irritability. 1995). IARC has determined that aldrin and dieldrin are not classifiable with regard to human carcinogenicity.cdc. 2004). EPA has established environmental standards for aldrin and dieldrin. Survey Geometric mean (95% conf. in which only 10. In samples obtained between 1973 and 1991 from Norwegian women. 1987). serum aldrin levels were below the limit of detection. environmental levels) and health effects is available from ATSDR at: http://www. population from the National Health and Nutrition Examination Survey. 2000). 1998) and behavioral changes (Carlson and Rosellini. Information about external exposure (i.. 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.gov/toxpro2. similar to results in a subsample of NHANES II (19761980) (Stehr-Green. and seizures.. Levels of aldrin also were not detectable in 1996-1997 pooled samples from New Zealand adults (Bates et al. Studies done in vitro showed that dieldrin binds to estrogen receptors (Soto et al.. Kanthasamy et al. Epidemiologic and animal studies have not conclusively associated dieldrin exposure with risk for developing Parkinson’s disease (Corrigan et al.S.6% of the subsample had dieldrin levels above the limit of detection (Stehr-Green 1989). which may vary for some chemicals by year and by individual sample. the offspring had altered CNS neurotransmitter levels (Sanchez-Ramos et al. When fed to experimental animals. 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.. tremors.. nausea. OSHA has established workplace exposure standards for aldrin and dieldrin.atsdr. the median serum dieldrin level was generally similar to the 90th percentile for females in this Report (Ward et al.... The U. 2004). seizures (Smith.. and the FDA monitors foods for pesticide residues. 2000. 2005. In a study of pesticide applicators with occupational exposure to aldrin. 78 Fourth National Report on Human Exposure to Environmental Chemicals .. 1998). both aldrin and dieldrin caused liver enlargement and liver tumors.S. and occasionally.html. 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. but no estrogenic effect was noted in a study that used cultured cells (Tully et al. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 2275 1946 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 03-04 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 756 588 1519 1358 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1057 946 1218 1000 01-02 03-04 01-02 03-04 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 559 456 512 485 1045 881 < LOD means less than the limit of detection for the lipid adjusted serum level. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Li et al. Biomonitoring Information In the NHANES 2001-2002 and 2003-2004 subsamples.Organochlorine Pesticides twitching. vomiting. When dieldrin was fed to pregnant rodents.

090-.9 (12.6-24.8-25.6 (15.6-33.0) < LOD 9.090 (<LOD-.4) 95th 20.110 (.202) 539 456 484 487 980 885 < LOD means less than the limit of detection for the lipid adjusted serum level.109-.30 (8.130-.0) 21.3 (19.S.110 (.10 (<LOD-16.6-24.124) .2) 15.147) 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 .3 (13.00 (8.080-.8 (9.100-.1 (13.70 (7.054-.0 (10.30 (8.109 (.089 (.098 (.110 (.048 (<LOD-.40-9.139 (.130) .00-14.147 (.117) < LOD .120 (.103 (.8-24.9 (14.4-18.4) 20.190) .8) 15.2-15.4) 21.0 (11.80-9. Fourth National Report on Human Exposure to Environmental Chemicals 79 .113 (.5-15.0) 19.1) < LOD 9.100 (.064 (.130) .9-22. which may vary for some chemicals by year and by individual sample.108-.054-.9 (13.140 (.138) .080 (.1-24.1) 20.5) 21.060) .8-17.083-.070-.140-.063-.1-18.7-22.102 (. which may vary for some chemicals by year and by individual sample.8-19. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.055 (.130) .7-19.077 (.6) 19.8) 14.120 (.073-.1-16. 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 .100-.3 (18.S.4) 539 456 484 487 980 885 Limits of detection (LOD.9-23.242) .6 (14.4-17.1 (18.158) .160 (. see Data Analysis section) for survey years 01-02 and 03-04 are 10.130-.8 (11.120) .4 (12.100) .090-.80 (<LOD-10.101) .2) Sample size 2159 1952 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD 10.180) .4) < LOD < LOD 16.177) Sample size 2159 1952 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD .139 (.4) 19.8-17.50) 15.4) 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 8.6 (15.3-21.059 (.3 (14.086-.160) .5) 15.1-19.120-.7 (<LOD-15.0 (10.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.109-.8 (18.7) 716 587 1443 1365 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD 9.6) 9.7) 15.138 (.8) < LOD 8.110-.2) 14.062 (.8. population from the National Health and Nutrition Examination Survey.088-.150 (.075) < LOD .056-.2) 11.4) 14.5-17.1) 15.0-21.0 (15.062 (.090 (.5-17. Survey years 01-02 03-04 Geometric mean (95% conf.180) .5 and 7.3 (18.120 (.112) 95th .190) .5) 19.084-. population from the National Health and Nutrition Examination Survey.049-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.1) 14.90) 90th 15.110) .130 (.116) .064) 90th .053 (<LOD-.077-.1) 15.5 (<LOD-11.096-.4 (12.170) .60-10. 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.160 (.9 (13.090-.103 (.100) .140) .069) < LOD < LOD .070) .6) 16.054-.058) < LOD .7 (14.149) . < LOD means less than the limit of detection. 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 9.0-25.7 (15.130-.9 (12.080) .50 (8.093) .112-.110) .5 (16.40-10.2) 12.182) 716 587 1443 1365 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD .070 (<LOD-. Survey years 01-02 03-04 Geometric mean (95% conf.9-38.80-10.1) 13.062-.100-.1) 10.150 (.

bioaccumulation.inchem. Revised Feb. Jr and Laws ER. Stehr-Green.27:405-421. J Toxicol Environ Health 1989. Finley B. Kitzazwa M. 4/21/09 Jorgenson JL.54:1431-1443. Shore RF. et al. 4/21/09 Hoyer AP. Pesticides in the Nation’s Stream and Ground Water.cfsan. Available at URL: http://www. Dieldrin-induced neurotoxicity: relevance to Parkinson’s disease pathogenesis. Anantharam V. Frey JM. New York.352:1816-1820.150:263-271. Roy ML.9:1357-1367. References Agency for Toxic Substances and Disease Registry (ATSDR). Six high-priority organochlorine pesticides. No:429-436.47:1059-1087. Chapin RE. 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. Grandjean P. Needham LL. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Priestly BG. David VL. J Toxicol Environ Health. 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.59:229-234. 1992-2001. Edwards JW. Kanthasamy AG. Mann D. Mumtaz MM. Evaluation of epidemiologic and animal data associating pesticides with Parkinson’s disease. Aldrin and dieldrin: A review of research on their production environmental deposition and fate. Sanchez-Ramos J. Handbook of Pesticide Toxicology. Toxicol Lett 1992. September 2002. Song S. Vol. Cox. Available at URL: http://www. Ginsburg KS. Inc.htm.cdc.fda. Aldrin and Dieldrin [online]. Facca A. 731-915. plasma dieldrin.org/documents/ehc/ ehc/ehc91. In Hayes WJ. Wienburg CL. Environ Health Perspect 1995. Organochlorine exposure and risk of breast cancer. Garrett N. Serum organochlorine levels and breast cancer: a nested case-control study of Norwegian women. Lancet 1998. et al. Narahashi T. Mink PJ. Smith AG. are nonestrogenic in transfected HeLa cells. Chlorinated Hydrocarbon Insecticides. J Occup Environ Med 2005. Eds. and epidemiology in the United States. Exp Neurol 1998. Grajewski B. Chung KL. and lymphocyte sister chromatid exchange. International Programme on Chemical Safety (IPCS). Chemosphere 2004. Patterson DG Jr. Exposure to low doses of the environmental chemical dieldrin causes behavioral deficits in animals prevented from coping with stress. Available at URL: http://www. Environ Health Perspect 2001.html. Turner W. Environmental Health Criteria 91. Reprod Toxicol 2000. Sonnenschein C. 2007 [online].gov/ circ/2005/1291/. Kanthasamy A. Organochlorine insecticides in substantia nigra in Parkinson’s disease.64-65 Spec. Jorgensen T. toxicology. Brock JW. 6/1/09 Ward EM. Buckland SJ. Hartvig HB.91(1):122-126. Demographic and seasonal influences on human serum pesticide residue levels. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. PA.66(4):229-234. 15. Fernandez MG. Ellis H. Sodium and GABA-activated channels as the targets of pyrethroids and cyclodienes. Part A 2000. Jr. The E-SCREEN assay as a tool to identify estrogens: an update on estrogenic environmental pollutants. August 2008. United States Geological Survey (USGS).gov/~dms/ pesrpts. Psychopharmacology (Berl) 1987.gov/toxprofiles/ tp1. Andersen A. Cancer Epidemiol Biomarkers Prev 2000.14:95-102. Available at URL: http://pubs. Toxicity of dieldrin for dopaminergic neurons in mesencephalic cultures. Tully DB. 4/21/09 Bates MN. Li AA. 80 Fourth National Report on Human Exposure to Environmental Chemicals . Neurotoxicol 2005. Rosellini RA. Int Arch Occup Environ Health 1994. Teta MJ. McIntosh LJ.usgs. Basit A.html. 1989. pp. Effect of occupational exposure to aldrin on urinary D-glucaric acid. Olea N. Carlson JN.atsdr.26:701-719. Daniel SE. VT. Corrigan FM. Patterson DG Jr. 1991. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. Serrano FO.103(Suppl 7):113-122. 2 Classes of Pesticides. Schulte P. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Academic Press. Toxicological profile for aldrin/dieldrin [online]. Food and Drug Administration (FDA).109(Supp1):113-139. either singly or in combination. Soto AM.Organochlorine Pesticides in the NHANES 2001-2002 and 2003-2004 subsamples (Edwards and Priestly 1994).

1 (<LOD-12.5 (41. 2007).6 (25.8-73.2) < LOD 11. Heptachlor was used as a soil and seed treatment and for termite control in and around buildings until 1988.10-11.3) 10. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.2-28.8-20.9 (11.6 (43.4 (22.7) 9.0 (32.9) 37.2 (37.89-10. As a result of the manufacturing process.2 (39..6 (16.0) 27.5-47.7 (43.1) * 11.4 (30.20-10. Survey Geometric mean (95% conf.2-49. 1994).5 (33.1 (15.1 (11.1 (<LOD-12.8 (10.70 (<LOD-10. and dairy products are the usual sources of exposure to these chemicals in the general population.1-15. and 03-04 are 14.2-49.1 (27. Fourth National Report on Human Exposure to Environmental Chemicals 81 .2) 36.0-67.9) 23. 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.5) < LOD < LOD < LOD < LOD 13.9 (15.20 (<LOD-11.1) 22.5.2-56.0-61. Consequently.9 (29.5 (31.9) 17. 10.9 (21.6-45.5-13.0) 41.0) 20.9) 31.1) 30. Chlordane is not currently produced or used in the U.3 (27.6) 36.3 (<LOD-19.7) 19. fish.6) 48. buildings.1) * 11.8 (18.0-33.2) 33. Technical grade chlordane had contained 7% trans-nonachlor.8-33.7 (34.5-43.1-50.4 (31.8) 27.5) < LOD < LOD 9.8-31.9) 36.3 (25.6-24.7-39.37 (8.8 (42.6) 20.3-24.2) * 12.3) 37.1-25.9-40. foods high in fat such as meat.7-56.8 (40.0 (16.2 (28.4-45.3 (28.1 (17. 76-44-8 General Information Chlordane and heptachlor are structurally related organochlorine pesticides and were used in the U.0) 37.63 (8.6-24.1 (44.8) 663 752 595 998 1497 1383 20 years and older Gender Males 99-00 01-02 03-04 * 11.2) 37.9 (26.0) 31.0) 21.20-11.0 (37.6) 9.9) 13.0) 75th 20.5) 37.1) 16.6) 39. lawns.10-18.8) 52.8 (17.69-10.2 (21.9 (18.0 (<LOD-12.3) 18.9) 39.2-21.0-25.1-65.9 (26.4) 22.3 (20.9) 10.8 (17.6-12.1 (<LOD-12.8-33.4) < LOD < LOD < LOD 23.S.5 (8. 01-02.7 (10.5-32.2 (36.4) 18.9) 23.3-45.90 (8.6) 9.2) 22.5) 628 557 462 350 501 493 559 1031 898 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.4-21.5) 44.1) 30.2 (10.5) 21.5-41.1 (25.6-18.5-42.8) 52.9 (11. population from the National Health and Nutrition Examination Survey.74 (<LOD-10.6) 8.1 (16.6) 49.9-21. respectively. heptachlor use has been limited to treatment of fire ants near power transformers.Organochlorine Pesticides Chlordane CAS No.5) 10.7 (32.5 (34.3-45. from the early 1950’s until the mid-1980’s.4 (10. 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.3 (26.6 (9.3) 41.7 (<LOD-13.6 (9.9-42.1) 90th 34.5 (<LOD-12.1-51.0-13. Until 1988.7-25. chlordane was used to kill termites and other insects on agricultural crops.9) 11. Since 1992.0 (26.1 (20.2) < LOD 11.7) 42.0 (20. and in soil.9 (15.5-65.9-21.5) 38.7-70.S.4) 12.4-14.5-40.4) 39.6) 11. 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.4 (30.6-53.7) 35.2) 46.4 (<LOD-12.8-43.4) 29. which may vary for some chemicals by year and by individual sample.8) 53.2 (9.1 (40.7 (19.9 (31.5-44.5) 9.7 (17. 2007).8) size 1661 2249 1978 Total years 99-00 01-02 03-04 50th < LOD 11. and 7.2) 34.6) 23.8 (10.9-38.7) 28.5-38. 57-74-9 Heptachlor CAS No.0-12.4-51.82-11.4) 37.5) 793 1049 963 868 1200 1015 Females 99-00 01-02 03-04 Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * 11.3 (11.10 (8.6) < LOD 11.S.6) 48. in addition to trace amounts of numerous other related compounds (ATSDR.36-11. 1994.3) 10.8-32.3) 18. Heptachlor and chlordane and their metabolites bioaccumulate in fatty animal tissues.5) 56.8.4 (35.8) 44.9) 47.1-25.8) 18.1-19.7-14.7 (42.7) 31. < LOD means less than the limit of detection.7) 19.3-49.7 (<LOD-32.7 (34. Both of these chemicals and their metabolites can cross the placenta and are excreted into breast milk.3-43. see Data Analysis section) for Survey years 99-00.2-26.1) < LOD < LOD < LOD < LOD < LOD 8.4-40.8-23.8-61.3 (21.7-12.4) < LOD 11.9) 11.8-42.9 (36. interval) Selected percentiles ( 95% confidence interval) Sample 95th 44.9 (17. the technical grade product of each chemical contains 10%-20% of the other chemical.2 (41.1) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * 12.3 (9.0-18.3-32.5.30-11.

380) . In laboratory animal studies.079) .071 (.258-.066 (.160) . 2002.140 (.064) < LOD .310 (.100-.210 (.077) .180-.280) .120-.290-..269 (.115-.063-.210 (.150 (.061-. 1977b.104) .130) .560) . Le Marchand et al.063 (.203-.208 (.100 (.204 (.070 (. which may vary for some chemicals by year and by individual sample.130) .170) .300) .190-.049 (<LOD-.180-.165-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.270 (.140 (.150 (.271 (.280 (.290) .260 (.083 (.450) .230-.300) .058-.120 (.160 (.080) .330 (.130 (.083) .080 (.213) * . 1986).240 (. 2007.220-.063 (.082 (.130-.149 (.300) .080) .062) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * .053-.320 (. population from the National Health and Nutrition Examination Survey.360) .110-. FDA established allowable residues of chlordane.189 (.120-. No clear evidence of excessive cancer rates was demonstrated in human epidemiologic studies (ATSDR. characterized by seizures and paralysis.063) .240) . IARC considers chlordane and heptachlor as possibly carcinogenic to humans.320 (.110 (<LOD-. and the U.370 (. and breast milk is a major excretion route in lactating women. Chronic feeding studies with either chlordane or heptachlor have demonstrated reduced fertility.055-.250 (.170) .270 (.180) .320 (.370 (.440) .091) . and inhalation exposure.130-.400) . 1981).190-.270 (.063 (.067 (.140-.130-.136) .070) . and NIOSH and ACGIH have recommended workplace exposure levels for each pesticide.077) .350) . Information Serum Oxychlordane (whole weight) Metabolite of Chlordane Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U.070 (<LOD-.076) < LOD .260-.075 (.066-. Elimination of all these chemicals from the body occurs over months to years.080) . 82 Fourth National Report on Human Exposure to Environmental Chemicals .148-.400) .250-.200 (.080 (. Rogan.160) .057 (.168-.077) . Acute.199-.S.286 (.300 (.087-.057) * .050-. Epidemiologic studies have not demonstrated teratogenic or developmental effects (Baker et al.258 (. IARC.148) .065-.260 (.320 (.146) . 1986).310) .073) < LOD < LOD < LOD < LOD .240-.216-.090-.048-.230 (.290-.100-. Takahashi et al.280-.280-.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 * * * * . high doses of either chlordane or heptachlor block inhibitory neurotransmitters and result in central nervous system toxicity.Organochlorine Pesticides (Dallaire et al.070-. 1977a.190-.070-. 2001.069 (<LOD-.128 (. Chlordane is metabolized primarily to oxychlordane and to a lesser extent.227) < LOD .058-.057-.340) .066 (<LOD-.300) . 1991.250 (.053-.S.119 (.310-.. Survey Geometric mean (95% conf.126) .350 (.320) .290 (..160) .302) .062) < LOD . 1996.253-. Chlordane and heptachlor are absorbed after oral.063 (.063) * . Smith. 2007).140) .146) < LOD < LOD .170) .115 (.207) .126 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th .070-.070 (<LOD-. The U.070) < LOD < LOD < LOD < LOD < LOD .350 (.100 (<LOD-.056 (.430) .090) .130-. Subtle neurodevelopmental effects have been observed rodents after prenatal exposure to heptachlor (IPCS.210-.348) .200-.133) 90th .280 (. dermal.073 (.240-. Shindell and Ulrich.070 (<LOD-.373) .286 (.090) .207 (.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.108-. EPA has established environmental criteria for chlordane and heptachlor.050 (<LOD-.291) size 1661 2249 1978 Total years 99-00 01-02 03-04 50th < LOD .066-.077) .200-. heptachlor.320) 663 752 595 998 1497 1383 20 years and older Gender Males 99-00 01-02 03-04 * .068) . Human health effects from either chlordane or heptachlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown.130 (.S. neonatal mortality. 2006).300-.315 (.280-.223) .170) .510) .047 (<LOD-.245-.106-.150-.068-.074-. chronic doses of heptachlor have produced liver enlargement and injury.370 (.130-.112 (.340) .130 (.200-.225 (.231) . OSHA has established occupational exposure criteria.260 (.189-.068) 75th . and alterations in immune function of offspring.079) < LOD < LOD < LOD . and heptachlor epoxide in foods and bottled water.230 (.. 1991).150 (.320) .220-.150) .140-. to heptachlor.310) .410) .290-. both chlordane and heptachlor induced hepatic cytochrome P450 enzymes and increased the incidence of liver tumors (NTP.450) .170-.140 (.058 (.230-.220 (. The major metabolite of heptachlor is heptachlor epoxide.120-.310) .104-.060 (<LOD-.287) .242-.170) .140 (.070 (<LOD-.230) .230-.246-.092) .180) .430) . which is also persistent in the body (ATSDR.290) .

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

8) 14.4 (<LOD-54. < LOD means less than the limit of detection.2-27.3) 18.3 (13.8) 14.4 (11.0-16.3) 23.1) 20.3) 27.7 (13.2-16. 01-02.2 (18.8) 13.6 (13.8-46.8) 20.7 (10.3) 18.S.2 (<LOD-25.2) 15.1 (19.4 (<LOD-19.3) 16.6-21.4 (15.5 (18.8) 19.50) < LOD < LOD < LOD 17.9-29.8 (13.6 (16.0) size 1589 2259 1963 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th 90th 15.9-25.8-24.4) 21. 10. interval) Selected percentiles ( 95% confidence interval) Sample 95th 24.0-19.2 (<LOD-16.8 (15.8.6 (14.0) 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 13.5) < LOD 14.5. and 03-04 are 14.8 (13.5) 19.6 (<LOD-27.5 (<LOD-21.4 (11.5 (11.8) 13.6 (8.8-24.9) * * * 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 8.1-15.2-27.0-17. * 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.20 (<LOD-9.6 (12.0-54.1) 13.5 (<LOD-32.1-38.0-17.40) 15.6.8) 15.7-25.9 (15.4) 18. see Data Analysis section) for Survey years 99-00.9-23.1 (16. Survey Geometric mean (95% conf.6 (11.3) 10.2) 20.10-13.1-29.7-18.7 (16.1-16.5 (11.8 (18.5) 598 553 460 336 503 490 539 1041 888 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.2 (<LOD-62.Organochlorine Pesticides Serum Heptachlor epoxide (lipid adjusted) Metabolite of Heptachlor Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U.6) < LOD < LOD < LOD 27.6-17. 84 Fourth National Report on Human Exposure to Environmental Chemicals . population from the National Health and Nutrition Examination Survey.6) 13.9-29.8) 16.8 (<LOD-23.2) 26. and 7.1) 23.8 (18.5 (10.8-24.6 (16.5) 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 7.2-17.0 (15.7-19.3) 18.3 (<LOD-25.3) 22.9 (12.8) 21.9) 15.9-16.6) 14.0 (11.6) 22.0) 13.3-18.2) 13.90 (<LOD-9.8-23. respectively.8) 19.

108) .170 (<LOD-.170 (.130) .180) . interval) Selected percentiles ( 95% confidence interval) Sample 95th . Fourth National Report on Human Exposure to Environmental Chemicals 85 .090 (.170 (.200) .090-.076-.180 (<LOD-.082-.110 (.180) .220) .170) .310) .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 .170 (.101 (.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.135 (.090-.090-.120 (<LOD-.270) .113-.100 (.161) size 1589 2259 1963 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th 90th .140) . which may vary for some chemicals by year and by individual sample.101 (.190 (.120-.130-.S.067-.069 (.130-.055 (<LOD-.104) .110 (<LOD-.100 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.190) .090-.057 (<LOD-.110-.130-.094 (.094 (.380) .135 (.180) .110) .077-.170) .071-.100 (.170) .074-.128 (.110) .180) .133 (.130-.190) .310) .100-. Survey Geometric mean (95% conf.106-.190) .108-.120 (<LOD-.096 (.173) 638 741 592 951 1518 1371 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .090-.120) .200) .180 (.063) < LOD < LOD < LOD .150 (<LOD-.150 (.150 (.070-.107-.100 (.130 (<LOD-.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.110 (.149) .063) .077-.110-.098 (.100 (<LOD-.053-.200 (.117) .120) .126 (.090 (<LOD-.113) .097) < LOD .100-.087 (.120 (.157) . population from the National Health and Nutrition Examination Survey.116) < LOD < LOD < LOD .240) .111-.130 (.111) .140) .140-.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 .130) .110 (<LOD-.090-.

1-16.2 (64.2) 19.Organochlorine Pesticides Serum trans-Nonachlor (lipid adjusted) Metabolite of Chlordane Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U.7 (59.2-37.8 (15.6) 25.1) 78. and 7.6) 56.0 (16.0) 40.0-113) 68.9 (15.6 (32. respectively.8-110) 59.5 (15.1) 18.3) 32.6 (50.0) 75th 31.1-22.5 (25.6-66.5) 35.5.8 (26.4 (30.2 (60. see Data Analysis section) for Survey years 99-00.8 (13.5-111) 68.8-19.3-21.2 (19.1 (17.3 (49.0-38.2-18.2) < LOD 10.4-22.4-62.1) 17.3-58.0) 18.7-160) 86. which may vary for some chemicals by year and by individual sample.7) 15.2 (14.9 (15.5-17.8 (19.5-95.9-69.8-19.3-74.3) 32.7-113) 68.1-28.86-13.4) 48.1) 17.5) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * 20.8 (26.4) 19.3-86.9 (51.5 (45.6) 82.7) 52.1 (22.0-68.7 (13.9 (29.5-87.8 (26. 01-02.4) 20.8 (11.7-29.1) 17.5) 9.0-20.9) 14.4-35.9 (<LOD-14.0-93.9-20.2-18.1-20.8 (30.0 (62.8) 19.0 (42.7 (11.9) 14.3) 650 558 457 404 514 486 722 1052 889 Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 03-04 Limit of detection (LOD.1) 62.6 (15.4-52.2-21.8 (71.4 (45.7-21.8 (28.8 (<LOD-20.0 (15.5-36.5) 14.9) 922 1062 955 1011 1224 1000 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 * 11.9-45.6 (52.2 (15.5) 36.0 (16.7) 35.9-65.7-38.8 (42.0-143) 112 (68.6) 10.7 (18.3-39.0) 33.2 (14.0 (14.4 (16.3) 15.9-58.1) 14.2) 30.3) 19.3) 16.2) 59.5-20.7 (28.5 (44.0-23.1) 17.0 (42.8) 80.0 (13.1) 16.3 (45.0 (60.7) 73.8-77.70 (<LOD-12.8-67.8) 51.7 (16.6 (57.7-77.3) 30.1) 17.8 (12.3-30.7) 14.9 (36.6-88.1 (10. Survey Geometric mean (95% conf.8-79.4 (12.4 (11.6 (56.5) 48. population from the National Health and Nutrition Examination Survey.9-22.0-123) 74.8-21.4) 107 (84.3 (58.9 (28.7 (59.2-88.9 (16.10 (<LOD-11.6) 56.3) 18.6) 60.1-55.1-34.6) 84.2 (59.3) 30.7-32.0-59.2 (25.5-69.3-57.0) Selected percentiles ( 95% confidence interval) Sample 95th 79.5.7) 78.3 (17.2 (7.7-20.1 (48.1 (47.5) 30.4-23.4) 16.5 (13.6-20.1-34.3 (16.7 (30.4-67.3) 25.0-24.6) 13.7) 59.5) 78.5) 90th 55.7-17.9-40.0) 13.1) 17.3) 36.7-23. 10.3-32.7-22.6) 34.2 (36.8.2) 20.6 (12.7 (35.1-16.3 (14.8-41.0 (29.6 (56.2) 17.3) size 1933 2286 1955 Total years 99-00 01-02 03-04 50th 17.9 (19.0 (13.2) 34.9) 51.7 (74.8 (45.5) 19.4 (28.6) 54.0-37.7-18.4 (67.6 (<LOD-14.1) 78.0 (15.0) 664 758 589 1269 1528 1366 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 17.8 (49.4-18.5) 14.9 (66. and 03-04 are 14. interval) 18.5) 26.2-23.6-82.0) < LOD < LOD 8.1-51.4) 55.9 (51.1 (41.0-93.8-16.0-23.7) 17.9 (47.7) 28.8-90.7) 78.9) < LOD < LOD < LOD 20.7) 56.8 (16.6-22.5-19.3 (14.5) 20.7-34.8 (17.6-54.8-90.5 (15.1) 17.3-50.1 (65.6 (16.S.2) 39. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.9) 51.9-64.0 (19.1) 30. < LOD means less than the limit of detection.2 (27.6-19.4) 59.1-18.2-17.4-36.3 (56. 86 Fourth National Report on Human Exposure to Environmental Chemicals .8-16.9-35.5) 22.8) 47.1) 32.1) 31.7-35.1) 18.1-126) 67.9-89.8 (28.3) 18.0) 49.0 (48.0-22.9-65.2 (26.8 (28.8-129) 74.8 (13.0) 19.9-36.5) 77.2-16.

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

et al.cdc. Ayotte P. Natl Cancer Inst Carcinog Tech Rep Ser 1977b. Stehr-Green P. Dewailly E. Evaluation of human exposure to the heptachlor epoxide contamination of milk in Hawaii. gov/toxprofiles/tp12. Circumpolar maternal blood contaminant survey. Academic Press. 2006. Muckle G. 1963-1967.gov/ntp/ htdocs/LT_rpts/tr009. 6/1/09 Rogan WJ. Arch Pediatr Adolesc Med 1996. 2001. Toxicological profile for heptachlor and heptachlor epoxide [online]. Wong L.28:497501. Gilman A. Environ Health Perspect 2003. Organochloride pesticide residues in human milk in Hawaii. 731-915.41:145–148. Odland JO. Hawaii Med J 1991. Hertz-Picciotto I.gov/toxprofiles/tp31. Bull Environ Contam Toxicol 1981:27:506-511. Sci Tot Environ 2006. J Occup Med 1986.84:151-161. May 1994. Baker DB. Trends in birth defects for a Hawaiian population exposed to heptachlor and for the United States. Jr and Laws ER. Lawrence River (Quebec. 1986. National Toxicology Program (NTP). Covaci A. et al.pdf. Keller JA. August 2007.html. 4/21/09 Agency for Toxic Substances and Disease Registry (ATSDR). LeMarchand L.org/ documents/cicads/cicads/cicad70. Determinants of serum polychlorinated biphenyls and organochlorine pesticides measured in women from the child health and development study cohort. Darnerud PO.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Handbook of Pesticide Toxicology. Estimation of Human Exposure to Heptachlor Epoxide and Related Pesticides in Hawaii. 1979-1980. Mortality of workers employed in the manufacture of chlordane: an update. Environ Res 2000. 79.pdf.150:981-990.niehs. Loo S.atsdr. Bjerselius R. Chashchin V.9:1-109. Chlorinated Hydrocarbon Insecticides.8:1-123.nih. Senie R. Kolonel LN. 4/21/09 James RA. A Report to the Hawaii Heptachlor Research and Education Foundation. Available at URL: http://ntp. Takei G. Temporal trends of organochlorine concentrations in umbilical cord blood of newborns from the lower north shore of the St. Hansen JC. KalubaSkotarczak A. Shindell S and Ulrich S. 1991 pp. et al. Bioassay of chlordane for possible carcinogenicity.inchem. Lulek J. Atuma S. Arch Environ Health. Tartter P. An evaluation of serum pesticide residue levels and liver function in persons exposed to dairy products contaminated with heptachlor. Inc. Chlordane and heptachlor [online]. Eds. Vol. Siegel BZ. Organochlorines in Swedish women: determinants of serum concentrations. Jr.50(3):108-118. Dewailly E. 4/21/09 Dallaire F.htm.259(3):374-377.html. Wolff MS. Pollutants in breast milk. 4/21/09 Baker DB. JAMA 1988. Available at URL: http://www. Berkowitz GS. Aune M. Available at URL: http://www. Poland. organochlorine pesticides and polybrominated diphenyl ethers in human umbilical cord serum. Saidein D. Wohlleb JC.110(8):835-838. Laliberte C.atsdr. 6/1/09 National Toxicology Program (NTP). 1993. Barker J. maternal serum and milk from Wielkopolska region. Smith AG. Environ Health Perspect 2002.gov/ntp/ htdocs/LT_rpts/tr008. Concise International Chemical Assessment Document 70 Heptachlor [online]. In Hayes WJ. Available at URL: http://ntp. Vol.org/documents/iarc/ vol79/79-12. Glynn AW. Bioassay of heptachlor for possible carcinogenicity. Voorspoels S. Sci Total Environ 2004.org/site/foundation/ research/projects2.inchem. Available at URL: http://www. Granath F. Bleiweiss IJ.htm.Summaries & Evaluations.330:55-70. 9/25/07 International Programme in Chemical Safety (IPCS). New York. Brower S. International Agency for Research on Cancer (IARC). 1994-1997 organochlorine compounds. Dendle WH. Canada). 88 Fourth National Report on Human Exposure to Environmental Chemicals .110:617-624. et al.html.111:349355. Willman E. Distribution of polychlorinated biphenyls. Drews K. Natl Cancer Inst Carcinog Tech Rep Ser 1977a.cdc. Van Oostdam JC. Charles MJ. Environ Health Perspect 2002. Available at URL: http://www. Jaraczewska K.heptachlor. Takahashi W.niehs. Royce W. Available at URL: http://www.nih.372:20-31. Head SL. Toxicological profile for chlordane [online]. Organochlorine exposures and breast cancer risk in New York City women. 2 Classes of Pesticides. International Agency for Research on Cancer (IARC) .

when virtually all use of it was banned. inhalation.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.Organochlorine Pesticides Dichlorodiphenyltrichloroethane (DDT) CAS No.2-dichloroethenylidene)-bis[4-chlorobenzene] (DDE) and 1.0-15.8. It is still used in some countries. It was produced and used in the U.90 (<LOD-12.6 (31.8-26. food.0-37. and 03-04 are 20.8) 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. continues to be the primary source of DDT exposure.1) 31.9) < LOD < LOD 9.5 (14.10 (<LOD-12.2 (11. 01-02. Survey Geometric mean (95% conf. Smith. p. and 7.3 (<LOD-21.6 (22.6 (25.S. resulting in fetal exposure.3) 22. 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. These chemicals are highly persistent in soil.5 (23.8) 15.0 (18.9 (21. sediments. and trace amounts of several related compounds.3 (27. after World War II until 1972.8-23.0-155) 83.0) 26.7) 12. DDT and DDE can cross the placenta.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. and water. particularly for endemic vector and malaria control.9 (10.0-27. DDT was used at one time as a treatment for head and body lice.S. depending on conditions.0) 40. as well as in plant and animal tissues. 1991). DDT and DDE are distributed to all body tissues with the highest concentrations found in adipose tissues (ATSDR. 1991).1 (33.9) 29.2) 155 (59.00 (<LOD-10.6-33. or dermal exposure. Both Serum p. which may vary for some chemicals by year and by individual sample. although DDT and DDE intakes have decreased over time (FDA.1’-(2. < LOD means less than the limit of detection.p’-DDD (4% or less).2) < LOD < LOD 9. air.9) 17.6 (<LOD-25. Fourth National Report on Human Exposure to Environmental Chemicals 89 .4) < LOD < LOD < LOD 61.1 (23. see Data Analysis section) for Survey years 99-00.2-95. particularly meat.8-39. population from the National Health and Nutrition Examination Survey.p’-DDT (65%-80%).p’-DDT (15%-21%). population.1-71.2 (<LOD-40.10-13.7-16.4) < LOD 17.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.9) 14.7) 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. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.3) 21.5) < LOD < LOD 9.8) 30. In the general U.7 (19.5) 23.0) 19. which is a mixture containing p.1 (<LOD-39.0 (10.7 (15. DDT can be absorbed after ingestion.2-65.6 (9. 17.2-bis(p-chlorophenyl) ethane (DDD).5 (23.0) 20.9 (<LOD-20.4 (23.3-16.3 (<LOD-31. respectively.8-17.9 (10.1-27.0-53.4.5-54. The biodegradation half-life of DDT in soil varies from 2 to 15 years. 2008.6) 635 566 461 356 514 490 564 1061 890 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.2) 30.3) 21. interval) Selected percentiles ( 95% confidence interval) Sample 95th 28. In the body. fish.1’-dichloro-(2. o. DDT usually refers to the technical product. 1988).5) 25.50-11. 2002.5 (15.3-590) 293 (104-541) 48.0 (21.9 (10. DDT is converted to DDE and several other metabolites. Only a small proportion of DDT is metabolized and excreted (Smith.0 (18.3-236) 24.5-36. and dairy products.70 (8.3) 28.9-34.S. Food imported from countries that still use DDT may contain the chemical or its residues. DDT is converted in the environment to other more stable chemical forms.0-35.7) < LOD 18.8) 36.7. including 1. Gunderson.9-28.

530 (. Animal studies reported reduced fertility.061) < LOD < LOD < LOD .130 (<LOD-.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.343) < LOD .059-.180) .078-.180-.. overt signs of acute human toxicity include vomiting.200 (.p’-DDD and p.240 (.105-.34) . Jusko et al.. 2004. Several reviews of cancer epidemiologic studies have concluded that a link between DDT and breast cancer is inconclusive (Beard. 2001). 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. accidental exposures.180) .530) .180 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 1997). 2006. 2002. DDT may bind to estrogen receptors (Chen et al. 1956).150) . Gladen and Rogan. dioxins and furans).01) .. Snedeker.114-.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 . 2002. 2001). Epidemiologic studies of children with environmental exposure to DDT and DDE have not demonstrated neurologic or developmental abnormalities (Gladen et al. although the risk for preterm delivery may be related to maternal DDE levels (Longnecker et al.170) .095) < LOD .160-.150-.201 (.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. 1996).420) .150 (<LOD-.140) .26) 1. polychlorinated biphenyls. 2006). 2000.330-4.075) 1.. Gray et al.167) size 1679 2305 1965 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * * .051 (<LOD-.230) .140-... Studies of DDT exposure and pancreatic cancer. and duration of lactation.106) < LOD < LOD .220) .080-.400 (. 2006.071-.. resulting in exposure to nursing infants (Rogan. and seizures.180 (. 2001). Reproductive effects in humans affecting birth weight.150-.400) .106) . Calle et al..074-.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 ..00 (.079) < LOD < LOD . reproductive organ abnormalities.p’-DDE can produce anti-androgenic effects (Gray et al. Human health effects from DDT at low environmental doses or at biomonitored levels from low environmental exposures are unknown.065-.260) . population from the National Health and Nutrition Examination Survey.084 (.078 (. premature delivery. and altered behavior after neonatal exposure (Eriksson and Talts.098-. It is difficult to attribute outcomes in human studies solely to DDT because of potential co-exposure to other persistent organohalogen chemicals (e. In high dose.142 (. 2006.290) .068-.130 (<LOD-.132-.170 (. Hayes et al. which may vary for some chemicals by year and by individual sample. 2006). 1998).143) < LOD < LOD . In laboratory animals..190 (.069) . interval) Selected percentiles ( 95% confidence interval) Sample 95th . other organochlorines.128 (.250 (.150 (<LOD-.064 (..086 (.240) .190-1.g.048 (<LOD-.S.146 (.120 (<LOD-.106-.054-. fertility. have not been consistently demonstrated (Beard.313 (. 2002.108 (.120-.203) . Beard.189-.170-.130-.62 (. 1995. 2002. both DDT and DDE may induce specific cytochrome P450 isozymes (Nims et al.230) . 90 Fourth National Report on Human Exposure to Environmental Chemicals . 2001).250-1.130 (<LOD-.112 (.Organochlorine Pesticides chemicals are excreted in breast milk.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 .570-4.087 (.063 (<LOD-. Longnecker et al. 2006). Survey Geometric mean (95% conf.627) . Mariussen and Fonnum. tremor. and o.. lung cancer.146 (.00) . and leukemia have also been inconclusive (ADSDR.190 (.071 (. Jusko et al.220) . A workplace standard for DDT has been established by Serum p.

html. for males and females in the NHANES 19992000 subsample (Pavuk et al. Smith. population from the National Health and Nutrition Examination Survey. and 03-04 are 18. compared to levels observed in this Report (Anderson et al.gov/ pestcides/ and from ATSDR at: http://www. respectively. Heudorf et al. 1989). 2004). Survey Geometric mean (95% conf.7-129) 297 (256-344) 338 (303-376) 268 (217-332) 108 (97.6. Link 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. IARC classifies DDT (p. environmental levels) and health effects is available from the U. 1998. population declined by about fivefold to tenfold.. 1991). Stehr-Green.S. 2002. 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. mean serum levels of DDT and DDE in the U. 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.cdc. Declining DDE levels over time have also been observed in the German population.p’-DDT) as a possible human carcinogen.8. 2003)...epa.. 2003. More information about external exposure (i.atsdr.3. 8. so serum DDE levels may be an indicator of historic exposure and may be higher than DDT levels in the same person. Since the 1970’s.S.. Compared to females in the NHANES 1999-2000 subsample.gov/ toxpro2.Organochlorine Pesticides OSHA and a guidance established by ACGIH. In a population-based sample of men and women from eastern Slovakia. NTP considers DDT as being reasonably anticipated to be a human carcinogen. 2005)..6 (81. mean DDE levels were about fivefold higher among women of southern Spain exposed by virtue of Serum p. 01-02.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. In general. see Data Analysis section) for Survey years 99-00.. and the most recent median levels for German adults and children are similar to levels in this Report (Becker et al.S..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. 2004). 2002.7-119) 113 (100-140) 93. Biomonitoring Information DDE persists in the body longer than DDT.e. the lipid-adjusted geometric mean levels of DDT and DDE were each fivefold to tenfold higher than the 95th percentile and geometric mean levels. and 7. EPA at: http://www. levels of DDT and DDE increase as a person ages as a result of cumulative exposure (ATSDR. respectively. Fourth National Report on Human Exposure to Environmental Chemicals 91 .

57 (3.62-6.54 (1.46 (1.623 (.68 (2.52-6.6 (9.1 (8.Organochlorine Pesticides nearby agriculture (Botella et al.37-16.71 (5.29 (1.53-15.91-2. In the NHANES 1999-2000.34) 2.4 (12.78 (4.8) 15.30-1.520 (.79) 4.71) 12.51-49.54-7.07 (5.860 ng/L) and DDE (about 14.890-1.68-4.0) size 1964 2298 1956 Total years 99-00 01-02 03-04 50th 1. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.76) 1.81-5.34) 6.79) Selected percentiles ( 95% confidence interval) Sample 95th 11.1) 12.00-1. 1989).6) 9.500-.70-3.38 (1.646) .21) 3.46 (1.30-1.49 (1.36-11.01-11.47) 3.7-20.43-4.7-48.18 (6.13 (1.69) 4.6 (17.51-8.3) 13.611-1.35) 1.66-2.39) 1.63 (1.0 (9.59 (4.3 (8.24) 1.92 (3.66) 3.75) 1.963-1.76) 1.26-10.66-4.18-4.57) 2.97 (3.994-2. A small study of Indian men with background exposure reported mean serum DDT and DDE levels that were around fiftyfold higher than the 95th percentile for DDT and tenfold to twentyfold higher than the geometric mean DDE levels among males in this Report (Bhatnagar et al.46-2.6) 9.10-1.870 (.39-1.71 (6.30 (1.590 (.39 (3. 1991). less than one percent had detectable serum levels of o.385-.56-3.81) 11.06) 3.57-3.85 (1.557) 1..59 (1.84 (3.63-15.1) 7.8) 686 758 588 1278 1540 1368 20 years and older Gender Males 99-00 01-02 03-04 1.25) 8.65) 1.2 (9. which is similar to the overall geometric mean of 260 ng/g lipid in the NHANES 1999-2000 subsample (Bloom et al.600) .28) 1.53) 1.92 (3. 1971).87-16.56-6. or p.90-8.23 (7.55-9.456 (.12 (6.6) 13.01-5.97-4.6 (7.40-4.61 (1.22-1.65 (1.9-38.72) 1. 2005).p’-DDT (Stehr-Green.05) 1.02) 1.27-1.3) 16.50 (2. population from the National Health and Nutrition Examination Survey.71) 32.01) 1.18-3.93 (7.30 (1.726) .9-17.5) 7.49) 8..05 (3.51-15.54) 8.34-3.14-9.59) 6.796 (.2 (19.50-17.63 (1.S.5) 5.8 (14.430-. Workers involved in production or application of DDT developed neurologic abnormalities associated with blood levels around 100-300 mg/L.51) 3.02-8.87 (5.p’-DDT.83 (1.57-2.47 (1.36-1.00 (6.4) 13. Finding a measurable amount of p.06) 1.91) 3.8 (9.22 (7.96) 1.76-3.49 (6.88 (2.965-1.59 (1.07) 1.5) 16.10-5.04 (6.6 (8.36) 3. 309 versus 268 ng/g lipid.9 (15.14) 2.5) 22.32 (1.4-19.52 (1.56) 2.85-4.66) 4.04-1.80) 1.37-10.64) 3.20 (.3-43.561 (.07) 1.10) .4) 9.8 (13.66) 1.19-14.p’-DDE in serum does not mean that the level of the chemical causes an adverse health effect. Serum p.32-9.48-4.490 ng/L) were found many years ago in a study of pesticide workers in Argentina (Radomski et al.01-1.2 (9.635) 1.16-1.82) 1.69 (1.26-2.70) 1.18-1.18) 1.45 (1.57 (1.41 (1.3) 937 1069 955 1027 1229 1001 Females 99-00 01-02 03-04 Race/ethnicity Mexican Americans 99-00 01-02 03-04 3.60-13.77 (1.26 (1..3) 10.75) 6.77 (1.48 (6.2) 19.52 (3.6) 8. High mean levels of whole blood DDT (about 3.49 (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.32) 1.488-..13) 4.69 (2. 2001-2002 and 2003-2004 subsamples.61-2.25 (1.17-3.63 (6.32-1.22) .36-2.40-8.92) 1.33-1.75 (4.09-1.76 (2.00) 7.03-1.9 (26.516 (.03-4. 2004).11 (2.64-2.34 (7.534-.8 (13.43-8.66-17.1) 40.27) 3.25) 1.1 (9.81-18.01-15.2-32.44) 1.81 (7.4) 14.69) 8.01-11.69 (.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.39-2.0 (12.85-10.p’-DDT.79) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 .8-90.10) 2.9) 7.37-1.34-11.0) 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 .53 (2.01) 1.80 (2.99) 1.2 (6.26) 3.25-16.15-4.6) 9. interval) 1.00 (.36 (3.31-2.51 (1.58) 75th 3. serum levels of o.7 (8.24 (1.14-1.18-1.820-1.57 (1.4 (8. Consumers of Great Lakes sport fish had mean serum DDE levels that were only slightly higher than nonconsumers.01-1.7) 9.12 (.91 (6.37-4.58) 1.51) 1.32 (1.75) 2.43 (5.57-13.81 (1.32-1.45 (1.7) 13.21) 90th 7.7-19.37 (1.96) .14 (1.40-4.19) 4. 2004).80) 3.56-2.72) 1.41-12.730) . considerably higher than levels in this Report (Smith.53) 7.55 (2.02 (2.40 (3.43-4.66) 1.84-3.25 (.680-1.13-2.0) 2.6) 12.16 (2.17 (3. In a subsample of NHANES II (19761980) participants.91-3.12-1.14) 2.3 (9.25-14.68) 2.9) 5.6) 9.75 (8. o.p’-DDT were below the limits of detection.419-.31 (1.82 (1.58) 1.80) 1.11-1.90) 22.6) 11.24-17.88-35.38 (1.5) 10.2) 26.31-12.59) 3.7) 16. Survey Geometric mean (95% conf.

S.8. see Data Analysis section) for Survey years 99-00. respectively. 17.p'-Dichlorodiphenyltrichloroethane (lipid adjusted) Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U. and 7. Survey Geometric mean (95% conf. and 03-04 are 20. which may vary for some chemicals by year and by individual sample. 01-02.4. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD < LOD size 1669 2279 1946 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD < LOD 90th * * * Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 667 756 588 1002 1523 1358 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 796 1059 949 873 1220 997 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 632 565 458 354 507 486 560 1045 880 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.Organochlorine Pesticides Serum o. < LOD means less than the limit of detection. population from the National Health and Nutrition Examination Survey.7. Fourth National Report on Human Exposure to Environmental Chemicals 93 .

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

96:34-40. Levels of DDT. et al. Bates MN. et al. Kashyap R. et al. Beard J.fda. Am J Epidemiol 2002. Saiyed HN. Biochem Pharmacol 1997. Chemosphere 2004. Schulz C. Drexler H. Transcriptional activation of the human estrogen receptor by DDT isomers and metabolites in yeast and MCF-7 cells.1-dichloro2. Zaidi SS. Garrett N. et al. Gabrio T. Buckland SJ.162:890-897. Chen CW. Calle EE. Bloom MS. Rogan WJ. September 2002. and HCB residues in human blood in Ahmedabad.85:504508. and polythelia among male offspring.html. Epidemiology 2006. 4/21/09 Gladen BC.2-bi(p-chlorophenyl)ethylene and risk of cryptorchidism. Needham LL. Patterson DG Jr. Seiwert M. Aune M. Swanson MK. Bhatnagar VK.cdc. Olson JR. Current internal exposure to pesticides in children and adolescents in Germany: blood plasma levels of pentachlorophenol (PCP).358:110-114. Talts U. Int J Hyg Environ Health 2003. lindane (g-HCH). Gunderson EL. Needham LL.58:1185-1201.53(8):1161-1172. Kaus S. Brock JW. Neurotoxicol 2000. Greenfield TA.111:349355. Charles MJ. Environ Res 2004. Effects of environmental antiandrogens on reproductive development in experimental animals. Hum Reprod Updat 2001. Food and Drug Administration (FDA). Association between maternal serum concentration of the DDT metabolite DDE and preterm and small-for-gestational-age babies at birth. Prenatal DDT exposure in relation to anthropometric and pubertal measures in adolescent males. Davis MD. Environ Health Perspect 1998. Darnerud PO. Klebanoff MA.155(4):313-322. et al. HCH. Longnecker MP. Klebanoff MA. Granath F.106(5):279-289. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Lepom P. Toxicological profile for DDT.205:297-308. Willman EJ. J Assoc Off Anal Chem 1988. Maternal DDT exposures in relation to fetal and 5-year growth. Glynn AW. Profiles of ortho-polychlorinated biphenyl congeners. Falk C. Cerrillo I. Longnecker MP. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. Furr J. Zhou H. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. Olson J. 4/21/09 Anderson HA. Hurd C. Environ Res 2005. et al.52:301-309. DDT and human health. Organochlorines and breast cancer risk. Herrman T. Brock JW. CA Cancer J Clin 2002. hypospadias. dietary intakes of pesticides. India. Atuma S. Notides AC. Exposure of women to organochlorine pesticides in Southern Spain. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Botella B. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003.17(6):692-700. Link B. Ostby J. dichlorodiphenyldichloroethylene.7(3):248-264. Moysich KB. Available at URL: http://www. Hanrahan L. and Mirex among male Lake Ontario sportfish consumers: the New York State Angler cohort study. Parks L. and DDD [online].54:1431-1443. Ellis H. Cueto C. et al. Gladen BC.cfsan.html. Gray LE Jr. Chemosphere 2005. Katz SH. Barr DB. Angerer J. Neonatal exposure to neurotoxic pesticides increases adult susceptibility: a review of current findings. Henley SJ. Heudorf U. JAMA 1956. Olea-Serrano MF.71(6):1200-1209. April 1982 to 1984.gov/ toxprofiles/tp35. Klebanoff MA. Vorojeikina DP. Am J Public Health 1995. and dichloro(diphenyl)ethylene (DDE). Hediger ML. a biostable metabolite of dichloro(diphenyl)trichloroethane (DDT). Int J Hyg Environ Health 2002. Durham WF. and other chemicals. DDE and shortened duration of lactation in a northern Mexican town. Krause C. et al. The Great Lakes Consortium. Organochlorines in Swedish women: determinants of serum concentrations. Lambright C. Vena JE. Eriksson P. Koepsell TD. Thun MJ. et al. Bull Environ Contam Toxicol 2004.112(17):1761-1767. Becker K. Arnold SF. Savitz DA. Available at URL: http://www. Bjerselius R. Environ Health Perspect 2004. selected elements. Gray KA. August 2008. Crespo J.97(2):178192.21(1-2)37-48. Olea N. Needham LL. Fourth National Report on Human Exposure to Environmental Chemicals 95 . Frumkin H. Jr.355:7889. Paepke O. Baker RJ. Lancet 2001. Hayes WJ. Burse VW. Jusko TA. FDA total diet study. Wolf CJ.gov/~dms/ pesrpts. Biomonitoring of persistent organochlorine pesticides. Maternal serum level of 1. Zhou H.atsdr. Rivas A. hexachlorobenzene. Kulkarni PK. The effect of known repeated oral doses of chlorophenothane (DDT) in man. DDE. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population.72:261265.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Sci Tot Environ 2006. Piechotowski I. Jr.206:485-491. Zoellner I. Environ Health Perspect 2003..

Blood levels of organochlorine pesticides in Argentina: occupationally and nonoccupationally exposed adults. Environ Health Perspect 2001. Comparative pharmacodynamics of CYP2B induction by DDT. Rogan WJ. Reddy AB. Fox S. Lynch CF. DDE. Pollutants in breast milk. DDE. Smith AG. Radomski JL. Chlorinated Hydrocarbon Insecticides. Thomas PE. J Toxicol Environ Health 1989. and DDD in male rat liver and cultured rat hepatocytes. et al. Handbook of Pesticide Toxicology. Crit Rev Toxicol 2006. Vol. Snedeker SM. Rey AA. Environmental exposure to PCBs and cancer incidence in eastern Slovakia.Organochlorine Pesticides Mariussen E. Jones CR. Inc. Nims R. children and newborn infants. PA. Jr. Academic Press. Pavuk M. Chovancova J.27:405-421.150:981-990. Pesticides and breast cancer risk: a review of DDT.20(2):186-193. Petrik J. Chemosphere 2004.53:455-477.36:253-589. Astolfi E. Eds. et al. and dieldrin. Arch Pediatr Adolesc Med 1996.54:1509-520. New York. Schecter A. Cerhan JR. 96 Fourth National Report on Human Exposure to Environmental Chemicals . 2 Classes of Pesticides. Fonnum F. Toxicol Appl Pharmacol 1971. 731-915. Lubet R. Neurochemical targets and behavioral effects of organohalogen compounds: an update. Stehr-Green. Demographic and seasonal influences on human serum pesticide residue levels. 1991 pp. J Toxicol Environ Health Part A 1998. Deichmann WB.109:35-47. In Hayes WJ. Jr and Laws ER.

S. Endrin has been detected in soils. 1992. Ketoendrin is a major photodegradation product (IPCS. Survey Geometric mean (95% conf.S. 1979..30 (<LOD-6.40) < LOD 547 433 487 446 1000 831 Limit of detection (LOD.Organochlorine Pesticides Endrin CAS No. 1981). Kavlock et al.60 (5. see Data Analysis section) for Survey years 01-02 and 03-04 are 5.40) < 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 5.30) < LOD 5. manufactured. Endrin was used as an insecticide. fatty infiltration..S. and occasionally at low levels in sediment and surface waters. High doses produced renal tubular necrosis and diffuse kidney degeneration in animals. Skeletal abnormalities and cleft palate in the offspring were associated with endrin when it was fed to pregnant laboratory rodents (Chernoff et al. EPA.20 (<LOD-5.S. total diet surveys (FDA. Human health effects from endrin at low environmental doses or at biomonitored levels from low environmental exposures are unknown. Depending on soil conditions. population from the National Health and Nutrition Examination Survey. or from contact with contaminated soils and sediments in areas where endrin was applied. interval) Selected percentiles ( 95% confidence interval) Sample 95th 5. endrin is converted rapidly to its major metabolite. have been cancelled by the U. Further conversion occurs to 12-ketoendrin and various conjugated metabolites which are excreted in urine and feces. largely the result of historical agricultural application or run off from contaminated soils (ATSDR. 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.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. General population exposure can occur after ingestion of endrin residues on food items imported from countries where endrin is still used. 1992). unless the dose is high and the exposure is very recent. All uses of the pesticide in the U.40-5. 72-20-8 General Information Endrin. characterized by generalized seizures in previously healthy persons occurred in Pakistan when sugar contaminated with endrin was ingested (Rowley et al. a stereoisomer of dieldrin. inhalation or dermal exposure routes. An epidemic of acute endrin poisoning. Over time. Endrin was not widely used as a termiticide. which may vary for some chemicals by year and by individual sample.S. 2008). < LOD means less than the limit of detection. and inflammation (Smith. IPCS. 1991). rodenticide and avicide. 1992). 1987). endrin has been detected with declining frequency in U.8. or discarded. At high doses. 1996. 1992). Because it is metabolized so rapidly.10 (<LOD-5. Endrin is absorbed rapidly after ingestion. Smith.. endrin blocks inhibitory neurotransmitters in the central nervous system resulting in excitation and seizures (Narahashi et al. is no longer manufactured in the U. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. unlike aldrin and dieldrin.09 and 7. Fourth National Report on Human Exposure to Environmental Chemicals 97 .10 (<LOD-5..50) < LOD 5. anti-12hydroxyendrin. In the body.20 (<LOD-5. Hepatic effects of endrin exposure have included necrosis. Endrin does not accumulate in body tissues (IPCS.50) < LOD < LOD < LOD 5. endrin usually is not detected in serum of exposed individuals. endrin can persist for years. 1991).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 5.40 (<LOD-6.

Finding a measurable amount of endrin in serum does not mean that the level of endrin causes an adverse health effect.html.020 (<LOD-. population from the National Health and Nutrition Examination Survey. Workplace exposure standards for endrin have been established by OSHA. and the FDA monitors foods for pesticide residues. with the highest value 6. This finding is consistent with other general population studies (Bates et al.020 (<LOD-.020) < LOD .gov/toxpro2. which may vary for some chemicals by year and by individual sample.020 (<LOD-..S.020) < LOD 547 433 487 446 1000 831 < LOD means less than the limit of detection for the lipid adjusted serum level.S.24 ng/mL (about 6..e. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Information about external exposure (i. Ward et al. 98 Fourth National Report on Human Exposure to Environmental Chemicals .020) < LOD < LOD < LOD 730 539 1457 1286 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . Serum Endrin (whole weight) Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U.020 (<LOD-. Biomonitoring Information In the NHANES 2001-2002 and 2003-2004 subsamples.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 . Survey Geometric mean (95% conf.020 (. 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. EPA has established environmental standards for endrin.020 (<LOD-. IARC has determined that endrin is not classifiable with regard to human carcinogenicity. serum levels of endrin were below the limit of detection. 2000).020) < LOD < LOD < LOD 1022 885 1165 940 01-02 03-04 01-02 03-04 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD ..020 (<LOD-.cdc.atsdr.. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.Organochlorine Pesticides The U. environmental levels) and health effects of endrin is available from ATSDR at: http://www. In a small study of Spanish women hospitalized for elective surgery.020) < LOD < LOD < LOD .020-. endrin was detected in 9% of serum samples. 2004.24 ng/g of serum) (Botella et al.020) < LOD . interval) Selected percentiles ( 95% confidence interval) Sample 95th . 2004).

cdc. Patterson DG Jr.9:1357-136. Convulsions caused by endrin poisoning in Pakistan.inchem. Exposure of women to organochlorine pesticides in Southern Spain. Chlorinated Hydrocarbon Insecticides. New York. Chemosphere 2004.cfsan. Olea-Serrano MF. Hardjotanojo W.64-65 Spec. Ginsburg KS. Burse VW. Turner W. Fetotoxic effects of prenatal exposure in hamsters. Sodium and GABA-activated channels as the targets of pyrethroids and cyclodienes. Frey JM. et al. pp. Eds. Rowley DL. Pediatrics 1987. et al. Roy ML. 4/21/09 International Programme on Chemical Safety (IPCS).gov/~dms/ pesrpts. Toxicological profile for endrin [online]. 4/21/09 Bates MN. Grajewski B. Whitehouse DA. Needham LL. Liddle J. Rivas A. Perinatal toxicity of endrin in rodents. Available at URL: http://www. Academic Press. Cancer Epidemiol Biomarkers Prev 2000. 2 Classes of Pesticides. Schulte P.atsdr. Gray LE. Andersen A. No:429-436. Patterson DG Jr.54:1431-1443. Narahashi T.fda.21:141-150.96:34-40. Chernoff H. August 1996. Food and Drug Administration (FDA). Gray JA. Toxicol Lett 1992. Endrin [online]. 4/21/09 Kavlock RJ. Available at URL: http://www. Rogers E. et al. Toxicology 1979. Sokal D. Jr and Laws ER. Environ Res 2004. Kavlock RJ. August 2008. Available at URL: http://www. Cerrillo I.htm.gov/toxprofiles/tp89. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Crespo J. Serum organochlorine levels and breast cancer: a nested case-control study of Norwegian women. II. Hanisch RC. Hanisch RC.html.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Gray LE. Saleem M. Ellis H. In Hayes WJ. 731-915. Buckland SJ. et al. Smith AG. 1992. Ward EM. Chernoff N. Garrett N. Olea N. Perinatal toxicity of endrin in rodents. Environmental Health Criteria 130. Fourth National Report on Human Exposure to Environmental Chemicals 99 . Botella B. Fetotoxic effects of prenatal exposure in rats and mice.html.org/documents/ehc/ehc/ ehc130. 1991.79(6):928-934. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. I. Vol. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. Rab MA.13:155-165. Toxicology 1981. Jr. Gray J. Handbook of Pesticide Toxicology. Inc.

8 (15. HCB is well absorbed after oral administration.3 (20.3) * * 15.0) < LOD < LOD 15. It is a persistent chemical and bioaccumulates in both aquatic and terrestrial food chains (ATSDR.6) < LOD < LOD 24.4) < LOD < LOD 22.5-TCP) and 2.0-19.9-20. < LOD means less than the limit of detection. see Data Analysis section) for Survey years 99-00.4) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * 13.1) < LOD < LOD 15.9 (25.6-33. Urinary metabolites include pentachlorophenol (PCP).9) < LOD < LOD 19.8 (26.4 (11. and sediment (Barber et al.4.5 (13.6-32. water. and foods with a high fat content. and 7. 1988).4. and accumulates in fatty tissues where it persists for years.7 (15.0-28.5-trichlorophenol (2. 118-74-1 General Information Hexachlorobenzene (HCB) was used from the 1930’s to the 1970’s in the U.7) < LOD < LOD 75th < LOD < LOD 90th * * 15. primarily as a fungicide and seed treatment until the U.6) < LOD < LOD 26.2 (14.0) * * 15.4 (22. 01-02.4) < LOD < LOD 33.8) size 1702 2277 1961 Total years 99-00 01-02 03-04 50th < LOD < LOD 14.4) < LOD < LOD 23..9-17.7-15.6-TCP) (To-Figueras et al. respectively.3 (12. Although it is not manufactured as an end-product in the U.5-14.2-15. 2005).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 * * 14.2-31.3) < LOD < LOD 20.6 (21..0.6) < LOD < LOD 14.4) < LOD < LOD 14. * Not calculated: proportion of results below limit of detection was too high to provide a valid result..6-19.7) < LOD < LOD 24. distributes widely throughout the body.1 (17.2) < LOD < LOD 13.Organochlorine Pesticides Hexachlorobenzene CAS No. population from the National Health and Nutrition Examination Survey.4.9) < LOD < LOD 20. 2008. these metabolites can also be produced after exposure to other chlorinated compounds (Kohli et al.6 (23.7-26. Gunderson.S.8 (22.0 (14.6-44.9) < LOD < LOD 28..2 (14.6 (24.7-21.7) * * 14.9) < LOD < LOD 16.9) 19.2 (17.4 (18.7-29. and 03-04 are 118.9) < LOD < LOD 20.7-16.3 (22.4.5-14.0) < LOD < LOD 15.3) < LOD < LOD 29.9-24. and has been detected in soil. 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.3 (22.7 (27. air. 2002).0 (25.8) < LOD < LOD 27.4.1 (14.5) < LOD < LOD 18. 2. 1976).S.4-16.2) < LOD < LOD 29.9-15.7-16. which may vary for some chemicals by year and by individual sample.3-20.6) < LOD < LOD 26.9-30. or game taken from areas with HCB contamination.4 (18.5 (13.9-32.3) 24.3-22.3 (16. Survey Geometric mean (95% conf.7-22. 100 Fourth National Report on Human Exposure to Environmental Chemicals .9 (23.0) < LOD < LOD 24.8-15.8) 583 554 460 350 511 488 636 1052 888 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.5-18.4-15.4) < LOD < LOD 18.0-16.6-26.0-25.1 (14. 31.8.5-15. wildfowl.9 (14. The general population may be exposed to HCB through diet. HCB may be created as either a byproduct or an impurity in the manufacturing process for certain chemicals and pesticides.7 (19.S.5-15.4) < LOD < LOD 19.0 (18. The FDA dietary surveys have shown that over time.2-15.1-16.1-20.5-33.1) * * 15.3 (14.7) 807 1058 957 895 1219 1004 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * 16.5 (14. breast milk is an additional route of elimination in nursing women. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD 28.7 (15. 1997).2 (24. EPA cancelled its use in 1984. particularly by consuming fish.1 (13. HCB is slowly metabolized. and elimination occurs by renal and fecal routes.6-trichlorophenol (2.S.9) < LOD < LOD 15.9 (25.7-30.2 (13. Workers in chemical manufacturing industries may be exposed to HCB via inhalation or dermal pathways. Hexachlorobenzene has entered the environment as a result of industrial activities and pesticide applications.6) < LOD < LOD 25. HCB has been detected in fewer foods since the 1980s (FDA.3-26.0 (18. Therefore.

Chronic feeding studies in animals have demonstrated kidney injury.089-.099) < LOD < LOD .203) < LOD < LOD .113-.102 (. and NTP classifies hexachlorobenzene as reasonably anticipated to be a human carcinogen.118) < LOD < LOD .104 (.099) < LOD < LOD .cdc. 1982. More information about external exposure (i. HCB interferes with normal heme synthesis.135-. Infants were exposed transplacentally and through breast milk. and the FDA has established a bottled water standard for HCB. and liver and thyroid cancers (ATSDR.169-. Fourth National Report on Human Exposure to Environmental Chemicals 101 .092 (..147-.107-.123 (. The U.171 (.196) < LOD < LOD .155) < LOD < LOD .163) < LOD < LOD .atsdr.095-. reproductive and developmental toxicities.156 (.100) < LOD < LOD .190 (.118-.e.126) .123 (.111-.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 * * . which is manifested by increased deltaaminolevulinic acid synthase activity and decreased uroporphyrinogen decarboxylase activity.092 (.095 (. and many died before 2 years of age (Peters et al.148-. immunologic abnormalities.094 (.083) < LOD < LOD . as well as hypertrichosis. a consequence of these heme abnormalities is a condition known as acquired porphyria cutanea tarda.epa.085) * * .145-.072-.186 (.129) < LOD < LOD .091-. Schmid.088-. environmental levels) and health effects is available from the U.132) < LOD < LOD .157-.090 (.089-. 2002).090 (.127-. anorexia. 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. Survey Geometric mean (95% conf.064 (.179 (.111) < LOD < LOD . and weakness.069) < LOD < LOD .099) < LOD < LOD .163-. IARC classifies hexachlorobenzene as possibly carcinogenic to humans.. Human health effects from HCB at low environmental doses or at biomonitored levels from low environmental exposures are unknown.098 (.097) .145-. ACGIH has developed workplace exposure limits for HCB.078 (.092-.088-.130) < LOD < LOD .147 (.097 (.094) < LOD < LOD .S. Biomonitoring Information Serum concentrations reflect the body burden of HCB. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD .079 (.157 (.S.167 (. acute doses produce central nervous system depression and seizures.107) < LOD < LOD .086) < LOD < LOD .062-.114-.html.176-.gov/toxpro2.081-.102) < LOD < LOD .060-.121 (. 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.122) < LOD < LOD .081 (.173) < LOD < LOD .085-. In humans.090 (.175) < LOD < LOD .082-.203) < LOD < LOD .114-. EPA at: http://www.Organochlorine Pesticides chemical.167) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * . 1960). population from the National Health and Nutrition Examination Survey.160 (. arthritis.073-.095 (.120 (.123 (.178-. which may vary for some chemicals by year and by individual sample.095) * * .088-.090-.191 (.S. This condition.258) < LOD < LOD .212) size 1702 2277 1961 Total years 99-00 01-02 03-04 50th < LOD < LOD .092 (.143-.115 (.097) < LOD < LOD .118-.141) < LOD < LOD .069) * * .223) 591 747 588 1111 1530 1373 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * .095) < LOD < LOD 75th < LOD < LOD 90th * * .109) * * . thyromegaly.176) < LOD < LOD .159-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.086-.086-.225 (.163 (.065 (.077-. EPA has established a drinking water standard. With chronic exposure.125 (.182 (.174-.140 (.152) < LOD < LOD .087 (.gov/pesticides/ and from ATSDR at: http://www.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. very high.

et al. Cripps DJ. Otero R.111:349355. distribution. Link et al. 4/21/09 Barber JL. Bjerselius R. Epidemiology of hexachlorobenzene-induced porphyria in Turkey: clinical and laboratory follow-up after 25 years.77:173182. Reference values updated. IARC Sci Publ 1986. but overall. As a result of the lower limit of detection in NHANES 2003-2004. Lecha M. Hexachlorobenzene in the global environment: emissions. HCB levels were directly related to age.cfsan. Darnerud PO.110(8):835-838. 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.349:144. and the geometric mean concentration of HCB in whole blood was 0. Available at URL: http://www. 2005. Can J Biochem 1976.. Peters HA. Biomonitoring of persistent organochlorine pesticides. than the limits of detection (on a whole weight basis) in NHANES 19992000 and 2001-2002 (Herrero et al. Food and Drug Administration (FDA). Jones D. Jones KC. J Assoc Off Anal Chem 1988. levels. Atuma S. 2002. van Wijk D. et al. In a representative sample of the 1998 German adult population. Dewailly E. Seiwert M. Gabrio T. Bryan GT.. Factors predicting organochlorine pesticide levels in pregnant Latina women living in a United States agricultural area. Sala M. 2005). Hexachlorobenzene content in human whole blood and adipose tissue: experiences in environmental specimen banking. Aune M. FDA total diet study. Dallaire F. Ozalla D. trends and processes. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Biol Neonate 2002.. 2002). respectively. Paepke O.. Schwartz JM.fda. Dogramaci I. et al. 2002) and among children (Link et al. however. Santiago-Silva M. References Agency for Toxic Substances and Disease Registry (ATSDR). and other chemicals. Canada).9% of participants had quantifiable levels (Stehr-Green.atsdr. Finding a measurable amount of hexachlorobenzene in serum does not mean that the level of the hexachlorobenzene causes an adverse health effect. Environ Health Perspect 2003. declines in background HCB levels ranging from around 50%90% have been documented in studies using cord blood (Dallaire et al. Muller C. lower than the limit of detection (on a lipid adjusted basis) in NHANES 1999-2000 and 20012002. 1999). August 2008. Temporal trends of organochlorine concentrations in umbilical cord blood of newborns from the lower north shore of the St. dietary intakes of pesticides. 1986.html. Zoellner I.. Chemosphere 2005. 1989). Agerelated increases of HCB in body fat and serum have been consistently noted in general population studies (Becker et al.. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. selected elements. Schulz C. Granath F.gov/~dms/ pesrpts. 2002. Lackmann GM. Gocmen A. Sweetman AJ. Organochlorines in Swedish women: determinants of serum concentrations.Organochlorine Pesticides in the NHANES 1999-2000 and 2001-2002 subsamples. 2002. Over the past two decades. Herrman T. Gunderson EL. J Exp Sci Environ Epidemiol 2007. Muckle G. Lackmann.gov/ toxprofiles/tp90. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Urinary porphyrin excretion in a human population highly exposed to hexachlorobenzene.. Eskenazi B. Polychlorinated biphenyls and hexachlorobenzene in full-term neonates.135(4):400404. The metabolism of higher chlorinated benzene isomers.39(12):744-749.. more HCB levels were quantified. Sci Tot Environ 2005. Bertram et al. Becker K. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003.. Toxicological profile for hexachlorobenzene update [online]. Residency near industrial or agricultural areas has been associated with higher serum HCB levels (Barber et al. factory workers chronically exposed to HCB and residents near the factory had serum HCB levels that were 150 to 50 times higher. Bradman et al. Holland NT. Arch Neurol 1982.. Herrero C. Krause C. In Spain. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Piechotowski I. Fenster L. Link B. Lepom P. Safe A. HCB detection in serum also was proportional to age. et al. Kaus S.. 4/21/09 Glynn AW.58:1185-1201. Available at URL: http://www. only 4. 2005).html. In the 1976-1980 NHANES subsample. April 1982 to 1984. Arch Dermatol 1999. 2006).81(2):82-85. 2002.205:297-308.71(6):1200-1209.54(3):203-208. Kohli J. but approximately five times higher than the overall geometric mean level in 2003-2004 (Becker et al.cdc.44 mg/L. Int J Hyg Environ Health 2002. 102 Fourth National Report on Human Exposure to Environmental Chemicals .17:388–399. 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. Kemper FH. Bradman A. Glynn et al. 2003). September 2002. Lawrence River (Quebec. Barr DB. Bertram HP. Laliberte C. Ayotte P. Environ Health Perspect 2002. Lackman.

Organochlorine Pesticides Schmid R. Cutaneous porphyria in Turkey. To-Figueras J. Barrot C. Demographic and seasonal influences on human serum pesticide residue levels.105(1):78-83. Rodamilans M.27:405-421.263:397-398. et al. Metabolism of hexachlorobenzene in humans: association between serum levels and urinary metabolites in a highly exposed population. Environ Health Perspect 1997. Otero R. Stehr-Green. N Engl J Med 1960. Fourth National Report on Human Exposure to Environmental Chemicals 103 . J Toxicol Environ Health 1989. Sala M. Santiago-Silva M. PA.

1-16.6 (40.80 (<LOD-14.1-32. See the section “What’s New” at the beginning of this Report for details. and 7.8-68.7 (29. and 03-04 are 9.7) 32.7 (<LOD-16. < LOD means less than the limit of detection.9) Selected percentiles ( 95% confidence interval) Total * * 50th < LOD < LOD < LOD 75th 19. Lindane (1%) lotion and shampoo are available by prescription for singleuse application to treat human scabies and head lice.7-96.0) 8.3 (13.6-135) 69. commonly known as lindane.5) 14.3) 14.2 (48.2-55.45) < LOD Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 99-00 01-02** 03-04 16.6-42.9-81. containing about 64% alpha and 10%-15% gamma isomers. and have been used either as fungicides or to synthesize other chemicals.2 (31.4-111) 84.6 (33.1-27.5) 90th 42.5528.8 (23.30-11.7) 56. 58-89-9 General Information Hexachlorocyclohexane (HCH). 2005).5 (14.1 (16.2) 9. water.4) 21.4) 51.S.7 (13.0) 17.0) 7.7) 27.7 (35.5) 16.5-123) 49.1 (27.7 (25.5) 632 563 460 403 513 487 702 1051 887 Non-Hispanic blacks Non-Hispanic whites Limits of detection (LOD.3) 34.8) 39.70 (6. 6.S. and delta.36.9 (32.9 (62.04-10.6) 36.68 (<LOD-10.1 (12. can be used as an insecticide and has been used to kill soil-dwelling and plant-eating insects. so they can accumulate in fatty tissues of animals.1 (11.4) 901 1067 952 992 1224 1007 Females 11. particularly alpha and gamma have been detected widely in air.6) 18.4 (50. The other isomers can be formed during the synthesis of lindane. As pesticide applications of HCH were increasingly restricted or eliminated. HCH isomers are lipophilic.8) 12.61-12.0) 41.0) 71.0-23.2-87. However.9 (26.6-89.0-111) 70.87 (9.0 (<LOD-12.6) 16.7) 97.7 (53.5) 22.1 (21.5-29.6-47.89 (<LOD-9.1 (9.8) * * * * * * 15.1-49.6-62.0-20. 104 Fourth National Report on Human Exposure to Environmental Chemicals .7-166) 70.70-19.76.5 (8.6) 47.9 (30.5 (43. It is no longer produced or sold in the U.1-36.9-24.4 (52.9-51.5) 40.6) 50.2 (50.4-50.5 (11.3) 51.6-14.8 (64.1-37.2-52.6-37.3) 25.20-16.1-32.2) 142 (99.1 (18.5 (16.7 (30.7 (62.9-21.6 (22. The gamma isomer.5) 29. environmental levels declined.2 (9.8-16.0 (14.2 (18.1 (30.2-46.8 (21.6) 653 758 589 1240 1533 1370 20 years and older 10.1 (9.7-20.8) 95th 68.7) < LOD < LOD < LOD < LOD < LOD < LOD 37. interval) 9.9) 15.9 (50.4 (8. and sediment as a result of historic production and use. respectively. In 2006.0 (33.70 (8. formerly referred to as benzene hexachloride. HCH isomers.5 (37.7) 18. HCH does not bioaccumulate to an appreciable extent in plants (ATSDR.1) 31.9) 45.0-21.2-98.80 (6.Organochlorine Pesticides Hexachlorocyclohexane CAS No.7-69.9-178) 48.8-54.9-14.8) 7.8) 27. General population Serum beta-Hexachlorocyclohexane (lipid adjusted) Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U.4) 10.S.90) 7.2) 36.6-18.7) 73. gamma.2) 62.70-12.2-42. Survey years 99-00 01-02** 03-04 Geometric mean (95% conf.8-87.8 (33.0) 35.0 (35.0 (8.7-69.5 (24.3-56.8 (32.6 (10.90-8.4-73.66-12.2) 13. Lindane has a half-life of about two weeks in soils and water.3 (26. population from the National Health and Nutrition Examination Survey.9) 81.8) 52.7-26.3-38.50) 8.9 (9.5) 67. soil.8-19.1-15.56-12.2-22.6-20.4) 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 21.5) 11.43 (<LOD-9. exists in several isomeric forms.8) < LOD 10.9 (40.2 (34.6) 35.0-34. 319-85-7 gamma-Hexachlorocyclohexane CAS No.4) 11.4 (11.7) 10. **In survey period 2001-2002.09) < LOD Gender Males 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD 14.2-67. 01-02.2-20.46-11.1) 13.9) 17.1) 12. Technical grade HCH is a mixture of all four isomers.3) 37.8.7-96.0-70.9 (11.4) < LOD 9.4 (12.0 (37. each result has been multiplied by 1.90-8. see Data Analysis section) for survey years 99-00. which may vary for some chemicals by year and by individual sample.4) 44.4 (16.0-70.1) 71. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. beta.2 (29.7) 10.6 (17.4) < LOD < LOD < LOD 46.3 (42.8 (17.0 (19.8-199) 134 (85.7) 23.8 (9. EPA cancelled agricultural uses of lindane (ATSDR.1) 12.60-13.4-45. the U.2-17.3-85. 2005). including alpha.4) 27.3 (62.3 (42. 608-73-1 beta-Hexachlorocyclohexane CAS No.6 (16.8 (10.9-56.

from 6% of samples in 1982-1984 to 2% in 1994 (FDA.710) .320 (.078 (.480 (.250) .220) .125) < LOD < LOD < LOD . HCH isomers are absorbed after inhalation.068-.680) .305) .220-. and memory loss (Nigam et al.222 (.280-.380 (. interval) .083 (. Acute high doses of lindane after ingestion or excessive skin application of the 1% lotion have produced seizures in humans.470) .092 (. ataxia. paresthesias.144 (.110) . See the section “What’s New” at the beginning of this Report for details.191-.086) < LOD < LOD < LOD < LOD < LOD < LOD .290 (.067 (.308-.690) .340-. which may vary for some chemicals by year and by individual sample.062 (.580 (.103 (.150) .270 (. The U. the serum half-life was about 20 hours among children (Ginsburg et al.570 (.331 (.254) 95th .081-.130-.139 (.059-.281 (. FDA pesticide monitoring program has shown a temporal decline in the detection of lindane.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. or dermal exposure.400) .083) .210-.234 (.170-. 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. 1977).056-.250 (.090-.120-. 2008.420-.521 (.070-.090 (.100) .480) .5528.100-.330 (.096) .290) .160) .050 (.191-. each result has been multiplied by 1.460) .124-.210) .620-1.119) .294-.070 (. HCH crosses the placenta and is also excreted in breast milk (Radomski et al.070 (.118-.050-.100-.077) < LOD .103-.620) .287 (.410-.340) .442 (.S.064 (.120) .560 (.080-.370-.Organochlorine Pesticides exposure to HCH is through the diet.360) .240-.310 (. Survey years 99-00 01-02** 03-04 Geometric mean (95% conf.100 (.120-.090 (.050-.814) .220 (. HCH isomers are metabolized to chlorophenol metabolites that are excreted in the urine (Angerer et al. Distribution is mainly to fatty tissues.300-. Pesticide applicators or agricultural workers could be exposed to HCH by inhalation and dermal pathways.050 (<LOD-.290 (.120 (.410 (.360-.260) . resulting in a half-life of about seven years..140) .250 (. Acute high dose toxicity in rodents affects the central nervous system producing decreased activity.120 (.118 (.058 (<LOD-.072 (.180-.069) . 1983).080 (.089-.057-. hepatic enzyme induction.290 (.173-.050-.100) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.37) 1. Workers who directly handled HCH have complained of headache.510) .091) .310) .120 (.170-.160-.450 (.450-.098 (.32) . 1971.100-.240 (. Fourth National Report on Human Exposure to Environmental Chemicals 105 .840) . U. Human health effects from HCH isomers at low environmental doses or at biomonitored levels from low environmental exposures are unknown.382-.412 (.150 (.090 (. Rogan.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 .280-.051-.077) < LOD .140 (.058) < LOD Gender Males 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD .066) Selected percentiles ( 95% confidence interval) Total * * 50th < LOD < LOD < LOD 75th . and nephropathy developed (IPCS.190-1.. for lindane.410) .404) .080 (. After dermal application of lindane 1% lotion. 1996.190) .297-.210 (.220-.210 (.230-.065 (.167 (.290) .600) . EPA has established a drinking water standard.120) .070) .175 (.400) ..260) . ingestion.120-.470 (. 1986).S. tremors.070-.661) 901 1067 952 992 1224 1007 Females .057 (<LOD-.200-.250 (.040-. and FDA has established a bottled water standard and food residue tolerances for lindane.130) .150-.060) .048 (<LOD-.200 (.089) .057) < LOD Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 99-00 01-02** 03-04 . 2002).050-.372 (.214) .. **In survey period 2001-2002.480 (.580-1.200-.057-.244-.146-.410) .050) . Gunderson 1988).01 (.065 (.460 (.190) .260-.190-.130 (.450) .140) .131-.103) 90th .700) .250-.910 (.110) .073-. and seizures.05) .350) .221-.250-. 1981).050 (.080) .310) .080-.319) . probably by blocking inhibitory neurotransmitters in the central nervous system.390-.110-. respectively. OSHA and ACGIH have established workplace standards and guidelines.501) .150) . When animals were chronically fed lindane at high doses.080) * * * * * * .350 (.047-.216 (.050 (<LOD-.080-.390 (.587) 653 758 589 1240 1533 1370 20 years and older . enlarged livers. Saxena et al.051 (<LOD-.062 (. population from the National Health and Nutrition Examination Survey.174) .070-.110) .360 (.056-.140) .160 (.064) .330-.100 (.S.560) . The beta isomer accumulates in fatty tissues and is metabolized more slowly.067) ..

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

. Finding a measurable amount of HCH isomers in serum does not mean that the level of HCH isomers causes an adverse health effect.. 1998). * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 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. 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. in this Report (Nigam et al. 2005).. 2003). In a small study of adults who consumed sport fish from the Great Lakes. 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. Radomski et al. 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. 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).Organochlorine Pesticides 2001-2002 survey period (Link et al. 1986.S. respectively. the median beta-HCH levels were similar or slightly higher than the 95th percentile in this Report (Anderson et al.. Fourth National Report on Human Exposure to Environmental Chemicals 107 . Survey Geometric mean (95% conf. which may vary for some chemicals by year and by individual sample. population from the National Health and Nutrition Examination Survey.

The Great Lakes Consortium. Piechotowski I. Buckland SJ. Botella B.120:1-82. Needham LL. Bhargava AK. Metabolism of gammahexachlorocyclohexane in man.57(4):315-320. gov/toxprofiles/tp43. Toxicol Appl Pharmacol 1971. Becker K. Rogan WJ. Biomonitoring of persistent organochlorine pesticides. VI. Ellis H. et al. Nigam SK. J Toxicol Environ Health 1989. Rev Environ Contam Toxicol 1991. Reisch JS. Schulz C. Herrman T.27:405-421. Demographic and seasonal influences on human serum pesticide residue levels. Olea-Serrano MF. available at URL: http://www. org/documents/jmpr/jmpmono/2002pr08. Sturgeon SR.html. Exposure of women to organochlorine pesticides in Southern Spain. Rey AA.106(5):279-289.54:1431-1443. et al. 4/21/09 Anderson HA.48:127-134. Lowry W.71(6):1200-1209. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Placental transfer of pesticides in humans. Crespo J. FDA total diet study. and other chemicals.9(4):417-424. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Serum concentrations of organochlorine compounds and endometrial cancer risk (United States). Glynn AW.inchem. Angerer J. Environ Health Perspect 1998. Absorption of lindane (g benzene hexachloride) in infants and children. Visweswariah K. Bai KM. Int J Hyg Environ Health 2002. Krause C. Falk C.html. 108 Fourth National Report on Human Exposure to Environmental Chemicals . Paepke O. Available at URL: http://www.58:1185-1201. Bull Environ Contam Toxicol 2004.atsdr. selected elements. Environ Res 2004. Saxena MC.cdc. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. Blood levels of organochlorine pesticides in Argentina: occupationally and nonoccupationally exposed adults. Raju GS. Siddiqui MKJ. Occupational exposure to hexachlorocyclohexane. Serum hexachlorocyclohexane residues in workers engaged at a HCH manufacturing plant. dietary intakes of pesticides. Lepom P. J Pediatr 1977. Needham LL. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. International Programme on Chemical Safety (IPCS). August 2008. Int Arch Occup Environ Health 1983. Pollutants in breast milk. PA. et al.gov/~dms/pesrpts. Bhatnagar VK. Gabrio T. Kutty D. Organochlorines in Swedish women: determinants of serum concentrations. and HCB residues in human blood in Ahmedabad. August 2005. Saiyed HN. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. children and newborn infants. Stehr-Green.cfsan. et al.htm. FDA Pesticide Program Residue Monitoring 1993-2006 [online].fda. et al. Int Arch Occup Environ Health 1986. Toxicological profile for hexachlorocyclohexanes update [online]. Bates MN. Seiwert M.20(2):186-193. 2002. Bjerselius R.111:349355. Heinrich R. Garrett N. Link B. Needham LL. Kulkarni PK. Granath F. Astolfi E. et al.52(1):59-67. April 1982 to 1984. Deichmann WB. Pesticide residues in food-2002-Joint FAO/WHO meeting on pesticide residues. Olea N. Levels of DDT. Potischman N. Environ Health Perspect 2003. Darnerud PO. 4/21/09 Ginsburg CM. et al. HCH. Chemosphere 2005. Aune M.72:261265.205:297-308. Cancer Causes and Control 1998. Karnik AB. Organochlorine pesticides and polychlorinated biphenyls in human adipose tissue. Gunderson EL. Rivas A. Available at URL: http://www. Olson J. Kashyap R. Kaus S. Atuma S. Bottimore DP.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Burse VW. Brinton LA. 4/21/09 Kutz FW. Rothman N. Zoellner I. Brock JW. Krishna Murti CR. Radomski JL. Wood PH. Hanrahan L. Chemosphere 2004. India. Zaidi SS. Maass R.150:981-990. Patterson DG Jr. Arch Toxicol 1981. Cerrillo I.91:998-1000. Arch Pediatr Adolesc Med 1996. J Assoc Off Anal Chem 1988. Majumder SK.96:34-4Food and Drug Administration (FDA). Lindane.

6-305) 15.2 (7.7 (12.6) size 1853 2257 1951 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th 15. Mirex contamination of Lake Ontario and adjacent waterways has been well documented (ATSDR. 01-02.0 (14.S. and foods. Mirex can cross the placenta and be excreted in breast milk.S. water. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. disposal. it is a highly persistent chemical in the environment.S.90-29. 1995). Mirex has been detected in air. mirex was detected in human adipose samples. and 03-04 are 14.S. aquatic organisms.8.2-230) 13.3-225) 15. which may vary for some chemicals by year and by individual sample.70 (<LOD-15.8) < LOD 15.0 (<LOD-108) < LOD < LOD 50. where it was applied directly to soil and by aerial spraying.7 (<LOD-47. 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. In studies conducted in the 1970’s and 1980’s.40 (<LOD-13. Some states and the U.6) < LOD < LOD < LOD < LOD 71. sediments.7) < LOD 66. resulting in exposure to newborns and nursing infants.. 1991). 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. after which it is widely distributed in the body and stored in fat.70-24.0-374) 11.6 (<LOD-108) 9. especially those from persons living in the southeastern U.6 (<LOD-23.5-425) 40. Mirex is absorbed through the skin and from the gastrointestinal tract. soil. Occupational exposure is limited to workers at sites where mirex contamination is present.. Mirex is not metabolized in the body.6 (<LOD-31. 2385-85-5 General Information Mirex has not been produced or used in the U. EPA have issued public health advisories or warnings that fish from contaminated lakes and rivers may contain mirex.1 (<LOD-65. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 57. < LOD means less than the limit of detection.Organochlorine Pesticides Mirex CAS No.6. respectively. Mirex binds strongly to soil. Fourth National Report on Human Exposure to Environmental Chemicals 109 . see Data Analysis section) for Survey years 99-00.10-37. and 7.1) 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 16.4) < LOD 63.3 (15. since 1977.8 (12.1 (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 13.7) 8.5 (<LOD-115) 153 (30.8 (<LOD-73.2) 51.6) 9. 1985. animals.4) < LOD 15.5 (<LOD-42.4-230) 18.1 (<LOD-104) < LOD < LOD < LOD < LOD 39.4 (8.5. (Kutz et al. where it has a half-life of 12 years.4) 617 548 459 398 500 484 688 1049 884 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. or pesticide application.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 19.0 (12. population from the National Health and Nutrition Examination Survey.5-291) 11. Ingested mirex that is not absorbed is eliminated in the feces within about 48 hours. Formerly.5-82.1 (13.70-40.10 (<LOD-15.5 (9.S.3) < LOD < LOD < LOD < LOD < LOD < LOD < LOD 15. Survey Geometric mean (95% conf.3 (15. its major uses were as a flame retardant additive and as a pesticide to kill fire ants and yellow jackets in the southeastern U. 10.

S.92) .106) < LOD .170) 887 1052 949 966 1205 1002 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .055-.090 (<LOD-.090 (<LOD-. 1989).08 (.8.430 (. 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.. serum mirex levels were generally below the limits of detection (Stehr-Green.410 (.059 (<LOD-. Inuit mothers from three Arctic areas had geometric mean serum mirex levels that were threefold to sevenfold higher than nonInuit mother from other Arctic regions.240) < LOD < LOD < LOD < LOD < LOD < LOD < LOD .gov/toxpro2.110 (<LOD-. IARC classifies mirex as possibly carcinogenic to humans. and NTP classifies mirex as reasonably anticipated to be a human carcinogen.Organochlorine Pesticides exposures are unknown.100 (<LOD-.635) < LOD .html.090-1.077 (<LOD-.080-1.7 ng/g of lipid.02) . The U.73) . 1991).310 (.064 (<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.268) < LOD .370 (. and the FDA monitors foods for pesticide residue and has established an action level for mirex in fish tissue.79) . EPA has established environmental standards for mirex. 2004). More information about external exposure (i.053-. 2005). * Not calculated: proportion of results below limit of detection was too high to provide a valid result. In samples obtained between 1994 and 1997.084) * * * 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 .090-1.470) . which may vary for some chemicals by year and by individual sample. 2001-2002. environmental levels) and health effects is available from the ATSDR at: http://www.79) . reproductive toxicity included decreased fertility and testicular damage.690) .41) . The geometric mean mirex levels of the Inuit mothers were 8. Laboratory animals fed high doses developed liver enlargement and liver tumors.450) 1.102) < LOD < LOD < LOD < LOD .112 (.510) < LOD < LOD .070-1. Smith.100 (<LOD-.052-. 7.220 (<LOD-. developmental abnormalities including cataracts and edema in the offspring have been reported (ATSDR..256 (.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.470 (.106 (.079 (<LOD-.093 (. Survey Geometric mean (95% conf. as well as in a subsample of NHANES II (1976-1980) participants.090 (<LOD-.054 (<LOD-.062-.470) .140 (<LOD-.080-1.atsdr. Finding a measurable amount of mirex in serum does not mean that the level of mirex causes an adverse health Serum Mirex (whole weight) Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U.170) < LOD . interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD .450 (.S.089-.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 . 1995.220) . and 2003-2004 subsamples. population from the National Health and Nutrition Examination Survey.610) < LOD < LOD < LOD < LOD . In addition. and 4..e.108 (.cdc.37) .090-1.170) size 1853 2257 1951 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .170-3. Biomonitoring Information In the NHANES 1999-2000. 110 Fourth National Report on Human Exposure to Environmental Chemicals .

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

50-25.940-3. interval) Selected percentiles ( 95% confidence interval) Sample 95th 16.8) 21.0 (4.30-44. Trichlorophenols have been detected in fish taken from waters near waste water treatment and industrial discharges (ATSDR.0 (4.0) < LOD 21.9 and 0.30) < LOD < LOD < LOD < LOD < LOD 1.60-18. may occur by inhalation or dermal routes.7.0) < LOD 5. 2.8-tetrachlorodibenzo-p-dioxin occurs during the synthesis of 2. usually at herbicide production or waste incineration facilities.00 (2.0) < LOD 5.0) 2.50 (.27) 482 570 681 815 831 1112 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD 1.60 (.4.0 (5.00-3.71 (<LOD-8. 112 Fourth National Report on Human Exposure to Environmental Chemicals .30-27.5-TCP) and 2.40 (2.20 (4. EPA.4. soils.50 (1. however. are metabolites of several organochlorine chemicals. and sediments.80-41.00-3.S.40 (2. Formation of 2. surface water.19 (<LOD-6.00-8.80 (1.27) size 1994 2497 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD 75th 1.4. 2. Occupational exposures.57 (<LOD-15. Exposure to trichlorophenols also may result from metabolism of lindane. Trichlorophenols are no longer manufactured commercially.0) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 1. Survey Geometric mean (95% conf. and polychlorinated benzenes (Kohil et al.6-TCP was also used as a wood preservative and may still be used in production of some fungicides (ATSDR.40 (1.03) 9. Such workers would probably Urinary 2.30-3.50-63.40 (1.9 (<LOD-121) 9.90-33.4.20-71. hexachlorobenzene. Both chemicals have been detected in air. other organochlorines.40 (2.4.00 (3.40-18.6-TCP were used as intermediates in the production of certain pesticides.30) < LOD 4.10-3.0) < LOD 5.3.4.0) 2.0) 2.4.0) 2.0) 2.40) < LOD 6.5-Trichlorophenol CAS No. 88-06-2 Metabolites of Organochlorine Pesticides and Other Environmental Chemicals General Information The chlorophenols. public drinking water systems did not detect 2.40 (2.50 (2.20-36.5-Trichlorophenol Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.30 (.60) < LOD 8. 2006).72) < LOD 1.0) 14. 2. * 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 (4.40 (.0) 5.980-3.63) 18.42 (<LOD-12.6-trichlorophenol (2. including hexachlorobenzene and hexachlorocyclohexanes.920-3.80) < LOD 1.0 (3. but they may be produced as by-products during manufacturing of other chlorinated aromatic compounds.4. < LOD means less than the limit of detection.S.0) 2.20) < LOD 1.50) < LOD 1.5-trichlorophenol. 95-95-4 2.20) < LOD 5.0 (8. recent sampling of U.71 (<LOD-8.50-16.4.40 (.4.40-11.60 (4.30-40.0) < LOD 11.60-8.60 (2.900-2.6-TCP in any of the samples (U.7) 24.30-11.42 (<LOD-8. Historically.S.9.Organochlorine Pesticides 2.980-3.5-trichlorophenol (2.0) < LOD 11.0) < LOD 973 1178 1021 1319 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * . 1999)..40) < LOD 1. Small amounts of trichlorophenols also can be produced during combustion of natural materials and the chlorination of drinking water or waste water that contains phenols.6-TCP).4.40) < LOD 4.20) < LOD 90th 5.5TCP and 2.6-Trichlorophenol CAS No. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. Environmental sources of these compounds include industrial discharges or run off from pesticide facilities or disposal sites. General population exposure may occur by ingesting contaminated food or water and by inhaling contaminated air. population from the National Health and Nutrition Examination Survey. 1999).80 (2. 1976).31 (<LOD-9.950 (<LOD-1.0 (3.30-27.4.27) 696 661 521 696 603 939 Limit of detection (LOD.30-27.

in addition to dioxins. the 95th percentile urinary 2.31) < LOD 2.46 (1. 1995) were similar.24) < LOD 6.. 2003).5-TCP nor 2.4. NTP classifies 2.3 mg/L in a nonrandom subsample from NHANES III (Hill et al.16 (.95 (3.4.6-TCP had increased rates of hepatic tumors.11) 482 570 681 814 831 1112 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD 1.. but almost twenty times higher than 95th percentile values reported in German adults aged 18-69 years (Becker et al.2) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 2. and lymphomas.75 (<LOD-6.4.24) < LOD 5.28-25.60-3.5-TCP among adults in this Report and in a nonrandom subsample from NHANES III (Hill et al.88-16.93-11. Urinary 2.79-4.49 (1..86 (3.8) 4.68 (<LOD-8.. environmental levels) and health effects is available from ATSDR at: http://www.19-12. At lower doses.980 (<LOD-1.81 (<LOD-9.6) 4. which includes trichlorophenols. the 95th percentile urinary 2.24-11.2) < LOD 5.02-3..4. Survey Geometric mean (95% conf.820-2. More information about external exposure (i.6-TCP at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 1989).75 (3. Neither 2. urinary 2.6-TCP levels at the 95th percentile were up to eight times higher than 3.2 (2.4. population from the National Health and Nutrition Examination Survey.4) 5. interval) Selected percentiles ( 95% confidence interval) Sample 95th 11.11) 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 2.6) 4.36 (1.5-TCP and limited for 2.S.5-TCP or 2.4.55 (4.69-18.13-13.44 (1. leukemias.6-TCP as reasonably anticipated to be a human carcinogen.5) 11.8 (5. furans. was similar to the corresponding percentile for 6-11 year olds in NHANES 1999-2000 (Hill et al. Human health effects from 2.5-Trichlorophenol (creatinine corrected) Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.4) < LOD 3.2) 2.53-3.6-TCP.e.80 (1.16) < LOD 90th 5.4 (6.4.1 (<LOD-58.6-TCP were developmental or reproductive toxicants in animals (ATSDR 1999).7 (4.78-19. In the same 2-6 year old children.20-6.html. as being possibly carcinogenic to humans.29 (1.00-29. animals showed hepatocellular abnormalities. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.05-8. 2003.9 (5.24) < LOD 1.Organochlorine Pesticides be exposed to mixtures of chlorophenols.37-11.78) < LOD 1. Among 6-11 year old children in NHANES 1999-2000.920-2.53-3.83-12.37) 696 661 521 695 603 939 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.3) < LOD 973 1178 1021 1318 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .0 mg/L.57 (<LOD-7. 1995) and up to 19 times higher than the 95th percentile value of 1.4) < LOD 3.atsdr.05-17.82 (<LOD-32.78 (3.43 (2.68-4.32) < LOD 4.44 (.3 mg/L reported in German adults aged 18-69 years (Becker et al.4. Biomonitoring Information In the NHANES 1999-2000 and 2001-2002 subsamples.6) 4.4.3 (5. IARC considers the experimental evidence for animal carcinogenicity inadequate for 2..33) < LOD < LOD < LOD < LOD < LOD 2.gov/toxpro2.4.90 (4..00-19.cdc.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. However. 2004).0) 7.47-8.37) 16. 7..17) 9.. Fourth National Report on Human Exposure to Environmental Chemicals 113 .27-17.5) < LOD 12. and other chlorinated compounds.15) < LOD 2.02) < LOD 7.50) < LOD 2.67 (1.00) < LOD 4. recent small studies have not demonstrated increased exposure to trichlorophenols in workers who dredged contaminated soils or incinerated waste materials (Agramunt et al.9) 12.57 (<LOD-7.24 (3. Laboratory animals chronically fed high doses of 2.62-20. The 95th percentiles for 2.73 (<LOD-8.1) 2.5-TCP. 1989).69 (2.8) < LOD 9.64 (4.57 (3.19-4. 2003).4.4.74) 11.67 (1. IARC classifies combined exposures to polychlorophenols.4.43) < LOD 12. Radon et al.

0) 19.26 (2.30-2.90) 2.30) 4.7 (13.89 (3.54) 6.7) 21. 114 Fourth National Report on Human Exposure to Environmental Chemicals .3 (11.5-TCP and to the median 2.85) * 3.46-3.80 (3.0-54.59-6.80-20. similar to the limit of detection for this Report (Anderson et al.60) 6.3) 23.0) 14.0) 13. for males in NHANES 19992002 (Agramunt et al.53) 4.45 (5. the median urinary 2.0) 15.0) 10.60-21.0) 7.28) 24.80-25.8 (9. Biomonitoring studies on levels of 2.0) 11.20-6.0 (13.36 mg/g creatinine. 1991).0-44.0 (12.1 (8.0) 13.4. Urinary 2.20-23.40 (2.40-4.70-6.6-TCP in urine does not mean that the level of 2.60) < LOD 5.8-15. Finding a measurable amount of 2.7 (9.3 (11.0 (8.69 (3.4.2 (14.5-TCP or 2.4.0) 11..52-3.06) * 2. Urinary 2.3. was about six times lower than the median urinary levels for males in this Report (Radon et al.10) 6.74-3.0 (20.6-TCP exposure and health effects.0 (9.85 (2.0 (4..35-3.6 (12.66 (8.67) 4.91-4..00 (2.6-TCP were monitored in a group of hazardous waste incinerator workers from 19992002.14 (2.80-7.60 (3.0 and 1.9) 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 2.40-7. see Data Analysis section) for Survey years 99-00 and 01-02 are 1. which may vary for some chemicals by year and by individual sample.48-26.0) 14.6 (11.09) 15.67-12.6-TCP provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of 2.0 (15.4.4.90 (4.2) 481 574 678 820 830 1109 99-00 01-02 99-00 01-02 2.7 mg/L.5-TCP and 2.2) 12.40) 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.95-6.59) 4.98-7.9) 694 677 519 696 602 931 Limit of detection (LOD.95) 3.0-50.4.2) 25.90 (3. respectively. 2003).0-37.6) 21.0-38.0 (8.70) 5.10-3.00 (4.4.24 (2.4.4-17.31) * 2. 2004).56 (3.40 (2.7-16. Survey Geometric mean (95% conf.5-TCP or 2.45) < LOD 11.50-5.2-0.6-19.20 (3.0) 19.0 (7.01-6.63) 90th 15.4.0 (6. Biomonitoring data will also help scientists plan and conduct research about 2.70-3.30-33.6TCP values.0 (14.23) 2.40) 2.10 (5.6-TCP (0.95 (4.75 (8.4.55-3.9 (13.0) 9.40-2.73-9.0-41. interval) 2.0) 10.74 (2.1) 16.4.8) 18.3-17.00-4.0) 13.5-46.70) 1.84) 2.92 (2.5-TCP level of 0.0 (20.70 (2.70 (2. Sawmill workers exposed to chlorophenol wood preservatives had urinary 2.78 (2.52 (2.0) 7.20) 4.8-24.04) 2.8-13.4.40-2.6 mg/g creatinine) and 2.0) 6.5-TCP or 2.98-11.89-6.Organochlorine Pesticides A small study of adults who ate Great Lakes sport fish reported a mean urine 2.6) 970 1178 1019 1325 99-00 01-02 99-00 01-02 99-00 01-02 2.45-9. In harbor workers exposed to chlorophenol-contaminated river silt.4.32) * 3.80-6.0-38.65) 15.33-4.6-TCP level.0 (11.76) 3.80 (2.0) 12.4.0 (14.51-12.20 (3.90-8.6TCP causes an adverse health effect.28) * 2.00 (1.6-TCP than are found in the general population.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.49 (6.18) Selected percentiles ( 95% confidence interval) Sample 95th 25.4 (17.9) 13.78 (2.36-5.10-3.5-TCP (0.8) 32.1-25.65 (5.3) 20.60-37.40-14.10) 2.36 (1.10-2.4 (10.32-4.87-14.4 (9.23) 3.70) 5.44) 75th 4.18-3.45 (2.0-18.32) 3.60-3.7) 33.0) 17.99) 6.09-7.80 (2.4.4. population from the National Health and Nutrition Examination Survey.9 (11.58-3.02) 2.0-43.53) 2.20-3.6-Trichlorophenol Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.25-11.58 (1.0 (6.0) 13.70-6.0 (6.1 (10. 1998).5-TCP and 2.00-21.23-2.0-68.80) 1.0 (15.40-32.79 (5.12) 2.40) 4.30-2.0 (16.30-11.4.4 (8.3) 37.6) 26.40) 3.S.68 (<LOD-2.47 (3.0 (14.60 (2.7) * 99-00 01-02 99-00 01-02 99-00 01-02 4.0) 17. < LOD means less than the limit of detection.0) 9. Mean values of 2.70) 3.3-26..60 (3.72-10.5-TCP or 2. 0.57 (<LOD-2.50 (2.31 (3.4.5 mg/g creatinine) were similar to the limit of detection for 2.4.7-3.6-17.08 (2.07 (<LOD-3.4.6-22.

78) 2.38) 22.2 (12.38 (2.1 (13.41 (3.40 (2.9 (9.22 (1.70-9.2 (13.6) 8.1) 14.8 (7.43 (<LOD-2. population from the National Health and Nutrition Examination Survey.68) 2.1) 694 677 519 695 602 931 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.51 (2.6 (9.49) 4.6 (9.10 (6.4) 9.0 (9.56) < LOD 11.76) 2.63) * 4.87 (3.19-5.63-13.05 (3.33-2.3) 8.63) 4.23 (1.50-8.5-28.53 (3.40 (7. interval) 2.26-13.04-16.6) 12.15 (6.58 (4.4) 8.6 (6.78) 90th 12.05 (6.Organochlorine Pesticides Urinary 2.81) 2.13 (1.10-9.06) 4.99-2.3-37.83-5.6 (5.46-14.88) 4.68) 2.0) 8.2 (7.5) 11.00) 4.20-2.9 (9. Fourth National Report on Human Exposure to Environmental Chemicals 115 .65) 2.88 (2.14-2.9) 8.9) 8.90) 2.33) * 2.3-23.4 (11.25 (3.51-21.77-4.56 (7.91 (3.56-5.28-4.00 (2.51) 18.1-32.73-22.41-6.88) 5.7 (14. Survey Geometric mean (95% conf.26 (6.25 (3.62-15.88) * 2.87-6.88-7.65-2.53) * 2.59 (2.00 (3.18-4.6) size 1989 2502 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th 2.1 (8.01 (3.92) 4.76) 4.09-3.95-2.5) 9.75) 75th 4.98 (1.5 (10.4) 4.53-11.8) 11.0 (11.88) 1.47-5.25-2.78 (2.9) 481 574 678 819 830 1109 99-00 01-02 99-00 01-02 2.63 (2.22-9.1) 11.02) 3.06) 11.76-8.5) 8.14-13.8 (8.9) 19.43-7.49-3.52 (3.7) 6.18-2.17) 13.63-15.9) 7.7-36.98) 10.42 (2.87) 2.63 (<LOD-2.6-31.0) 10.5) 12.6) 970 1178 1019 1324 99-00 01-02 99-00 01-02 99-00 01-02 2.83 (3.4.13-6.33 (7.5) 11.67-17.82-2.23) 4.21-11.22-2.04-2.6-Trichlorophenol (creatinine corrected) Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.1-21.08-2.96) < LOD 4.82 (8.35 (3.02 (1.42) 2.87) * 2.87-7.82 (3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.30-2.0 (6.5 (8.27-9.91-2.8) 21.6 (10.66-4.72-16.52) 2.73) 5.15 (1.32 (2.4 (12.65-21.8) 19.91 (7.29 (6.3 (9.60-2.11) 10.83-6.65) 18.44 (3.48-2.50 (2.88) 4.2 (8.2) 19.06-2.90 (1.83-6.89) 10.94-13.25-17.53) 4.52 (5.60 (4.38 (4.22 (<LOD-2.89-2.22 (3.26) * 99-00 01-02 99-00 01-02 99-00 01-02 4.5 (7.24 (1.9-64.6) 13.33 (1.76) 1.6 (22.32-19.82) 2.72) 32.17-4.8) 12.77) 2.00) 4.S.10) 4.7) 25.54 (2.79-17.38-5.55-2.43 (2.29-4.29-4.25-15.17) 2.9-32.16-10.9-29.71 (3.9-34.81) Selected percentiles ( 95% confidence interval) Sample 95th 21.6 (12.81-9.52) 2.

206:15-24. Chlorophenol exposure in harbor workers exposed to river silt aerosols. July 1999.106(5):279-289. Kaus S. Head SL. Needham LL. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. Burse VW. Urinary excretion of chlorinated phenols in saw-mill workers. Smith SJ. Bailey SL. Kohli J. Fast DM. Can J Biochem 1976. Hanrahan L. Falk C.146:83-91. S. Szadkowski D. Becker K. Monitoring internal exposure to metals and organic substances in workers at a hazardous waste incinerator after 3 years of operation. Arch Environ Contam Toxicol 1989. Holler JS. Needham LL. Toxicological profile for chlorophenols [online]. U. et al. Jones D. html. Jarvisalo J.54(3):203-208. Olson J. Shealy DB. Pekari K. Environmental Protection Agency (U. Pesticide residues in urine of adults living in the United States: reference range concentrations. December 2006 Draft. Int J Hyg Environ Health 2003. The Great Lakes Consortium.gov/safewater/ccl/pdfs/reg_determine2/report_ ccl2-reg2_ucmr1_occurrencereport. 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]. Gregg M.epa.gov/toxprofiles/tp107. Am J Ind Med 2004.71:99108.63:57-62. Available at URL: http://www. Wegner R. Corbella J. Environ Res 1995. Environ Health Perspect 1998.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). et al. Domingo A. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children. Aitio A. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population.pdf.18(4):469-474. Seiwert M.cdc. Hill RH Jr. Baur X. Lindroos L. To T. Available at URL: http://www. Luotamo M. Radon K. Safe A.atsdr.EPA). Anderson HA. 5/19/09 116 Fourth National Report on Human Exposure to Environmental Chemicals . Schulz C. Domingo JL. Int Arch Occup Environ Health 1991. The metabolism of higher chlorinated benzene isomers. Hill RH Jr. Seifert B. et al. Baker S. Toxicol Lett 2003.45:440-445. Heinrich-Ramm R.S. 4/21/09 Agramunt MC. Poschadel B.

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

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

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

02) 4.599-1.740-2.0) 6.80) 2.43-12.34-7.10 (.54 (3.56 (4.717-1.490-2.74 (8.2) 672 678 473 509 696 578 595 948 752 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.20-30.81) 11.58) Selected percentiles ( 95% confidence interval) Total * * 50th 1.0 (6.08-2.81) 1.30-4.90) 2.32 (.0) 9.50-5.4 (7.05-7.60 (5.44 (2. which may vary for some chemicals by year and by individual sample.7 (12.63) 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.8) 19.13 (2. 01-02.00) 3.02-5.52) 6.10-7.290 (<LOD-.20-4.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.620-1.27-15.98-12.10 (2.0) 10.20-7.1.1-17.42) .12-19.S.50 (.70-14.61) 4.0 (7.21 (.48-7.00-12. see Data Analysis section) for Survey years 99-00.22 (.2.42-3. respectively.1) 10.89) 9.80) 4.33-18.4 (7.750-1.20 (.90) 3.0) 10.2 (7.38-5.14) * * .35-12.58 (5.954 (.5 (8.80) 3.08 (<LOD-2.579-1.79-7.71-9.600 (<LOD-1.39 (8.51) 2.71 (2.2) 16.60-11.780) < LOD 3.60-25. 120 Fourth National Report on Human Exposure to Environmental Chemicals .0) 11.93 (4.13 (2.840-1.50 (2.955 (.68-7.55-8.80 (2.58 (2.40-11.6) 18.9) 14.70-11.9 (8.3) 17. and 0.40-14.0) 11.0 (8.1 (10.40-1.2 (7.8-32.20 (.810-1.80-22.2) 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 1.40-16.26-8.34-3.00 (4.82-12. < LOD means less than the limit of detection.981 (.35-11.5) 15.10 (2.8 (14.4 (9.2 (9.2) 16.8 (12.60-18.0 (8.29) * * 1.58 (3.00 (5.00-12.0) 11.1 (9.0) 6.670-1.91) 4.94) * * .00 (1.00-7.39 (3.00-27.860-2.0) 20.98-5.76 (2.70 (2.30 (2.80) .56-13.4) 18.0) 12.28) 1.10) < LOD < LOD 4.7 (14.67) 3.97) 8.30 (4.80-24.30 (2.623-1. interval) 1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.890 (<LOD-2.16 (2.07-10.2 (9.40-19. population from the National Health and Nutrition Examination Survey.44-38.00) 3.26-6.0) 10.0) 15.10 (.80 (4.70) < LOD < LOD 75th 3.2 (7.53) 4. 0.2) 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 1.9) 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 1.70-23.2 (14.4 (9.20 (.0) 11.56 (1.8 (8.20 (.26 (5.80) 2.0 (7.0) 10.19) 9.7) 11.0 (7. and 03-04 are 0.12) 4.50) 2.8) 7.86 (1.2 (11.4) 20.57-7.66) * * 1.27-3.0 (8.93-24.16) 4.1) 95th 13.80) 11.55-6.0 (6.90-5.0) 5.5-16.3-15.85 (3.0 (4.3) 14.0 (5.90-4.2-20.4) 17.8) 11.17-3.15) 14.44-3.2.290 (<LOD-1.52) * * 1.8) 7.5 (11.70) .80) 2.08-15.35-16.9) 8.5) 20.60 (1.70-19.47) * * 1.80-4.5-17.97) 90th 7.99 (5.52-11.1-23.6) 7.0-28.36-4.70 (4.0) 7.1) 13.90 (1.21) 9.0) 5.757-2.80) .94) 3.73) * * .9-18.830 (<LOD-3.50-36.530 (<LOD-2.40-5.50 (4.0) 6.45 (2.61 (3.60) .81) 11.13-2.40 (.56 (6.0) 5.46) 10.23-5.758-1.83 (5.0 (9.37 (3.95) 5.32) 1.20 (2.86-15.0 (12.79 (5.3) 16.82) 10.0-27.0 (7.70) < LOD < LOD 1.96-3.00-19.30-6.15-12.01) * * 1.11 (.700-1.04) < LOD 1.0) 10.60) < LOD < LOD 4.2) 14.2 (14.970-2.47) 5.33 (5.10) < LOD .8 (9.0 (9.03 (.00-27.72) 5.74 (8.

855 (.74) 90th 7.41-12.2) 8.98 (3.82-6.574-1.82-14.05) .42) 12.95 (3.1 (8.54-4.5-13.58) * * 1.40 (3.883 (.440 (<LOD-2.7) 5.960 (.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.00-19.94 (2.28 (5.93-5.00-13.2) 7.89-3.7) 12.40-5.55-20. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.40-14.54-2.540-1.23 (4.37-5.03) 2.5-32.75-7.2) 5.90-5.05 (.43 (.73 (1.27) < LOD 2.94 (4.750 (<LOD-1.1 (6.84 (5.78 (2.620-1.87 (3.11-6.8) 8.61 (1.95) 2.2) 13.26) * * .03 (7.84) 7.19 (4.45-5.10 (3.818 (.09) 2.566-1.890 (<LOD-1.82-26.28) 10.88-10.780 (<LOD-1.81-5.98) .68) < LOD < LOD 3.92-2.860 (.9 (9.533-1.5) 12.34 (6.56) .69) 4.10-13.830-1.94-10.5) 11.88-15.98-5.90-8.40) 4.S.02-14.1-15.15-10.773-1.72) 11.03) 2.0) 6.28-9.9 (5.04 (1.924 (.37) 9.6) 8.7 (9.60) * * .47 (3.2) 5.4) 13.46) 2.1) Sample size 1949 2519 1928 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.93-9.66-15.67) 4.5) 7.54-15.3) 15.560-1.09 (.62) .71-2.83 (7.35 (1.47) * * .61-13.9) 16.04-6.29) * * .34 (6.53) 9.0) 7.93) 9.4) 4.9-28.34) * * .38) .9 (9.6 (9.7 (10.00 (4.79-9.03-6.8) 6.43 (3.09-11.650-1. population from the National Health and Nutrition Examination Survey.13) 4.06-2.35) < LOD < LOD 3.67-19.31-14.89) * * 1.69) 2.66 (2.8) 12.870-2.56-13.07 (.54-11.3) 12.37 (4.52) 4.890 (<LOD-1.94-23.61 (1.1) 4.920 (.4) 4.996 (.94-22.820 (.6) 11.7) 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 .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 1.60) 2.87 (1.66-34.74) 4.75 (7.94-9.3) 5.02 (2.98) 9.633-1.21-23.03 (2.7) 18.00-17.608-1.57 (4.24-3.80 (6.18 (.36) * * 1.88) 2.1) 4.5 (4.01-2.79-3.932 (.2) 9.2 (8.69-10.43) 2.40-3.4 (4.1 (10.23) 4.45-11.34) < LOD < LOD .8) 7.14 (3.71) 10.32-12.6) 13.1 (9.69 (4.47 (3.790 (.40-12.9) 11.9) 12.85 (6.66 (5.81 (1.75 (3.02-2.8) 16.98) .7 (8.75) 14.5) 8.30) 2.57) 4.1 (7.75) 2.47 (1.20-8.85) 2.47) 2.1 (11.5-16.37 (5.87-5.29 (2.56) 4.51-5.61-29.56) 7.549-1.8 (10.66 (1.62-5.2) 95th 12.67) 1.80) 9.92-5.54) .28 (4. Fourth National Report on Human Exposure to Environmental Chemicals 121 .68-4.570-1.31 (3.76) < LOD . interval) .6) 9.510-1.57 (6.38 (1.960 (<LOD-2.40-28.44 (2.500-1.5) 7.41) Selected percentiles ( 95% confidence interval) Total * * 50th .5-20.0 (8.2 (6.64-5.37-3.40) < LOD < LOD 75th 2.7) 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.3) 16.83) 8.60-9. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.50) 7.25) 6.00 (4.42 (3.57-10.77 (6.430-1.39 (2.2 (10.25) < LOD .02 (7.900 (.4 (9.45-5.28 (2.41) .00) 8.80 (2.76-4.98-22.88 (5.710 (<LOD-1.53 (6.82-14.30 (1.53-11.05 (1.46-5.6 (10.80 (7.

58 (1.80) 5.3 (9.3 (6.970 (<LOD-2.45 (3.35) 4.14 (6.0) 12.90) 4.80-21.37 (3.8) 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 1.790 (<LOD-1.0) 14.8-17.80 (2.70-9.7 (10.7) 14.90 (1.78) 5.00) 7.2) 14.4-17.6 (10.6-19.00-18.20) 3.20) .41) 3.10 (<LOD-1.1 (10.0) 19.0-24.50) 3.75 (3.0 (10.80) .0 (7.12 (4.7) 15.5) 21.00) 8.5-26.00) 3.3) 20.00-4.0-24.0) 6.0 (15.90 (6.15-6.20-8.73) 7.00-18.10 (.0 (13.90-15.95 (5.39-13.50) 5.95-9.60 (6.7) 16.35 (6.3 (11.670 (<LOD-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.41-5.20) 3.34-10.670 (<LOD-1.74) * * * * * 1.31) 1.51) < LOD 1.10-4.90 (2.10-15.2 (7.5.0) 9.35-3.80) .82) 8.0 (10.3) 8.7) 10.580-2.50-4.8 (12.0) 12.90 (6.15-2.70) 2.24-5.46-28.6) 14.90) 8.1 (10.1) 11. respectively.95 (2. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th .80 (2.7 (11.5. population from the National Health and Nutrition Examination Survey.16-1.40 (2.0) 11.00 (.3 (9.9-14.34-5.90 (5.9-17.3) 22.31-12.62-17. < LOD means less than the limit of detection.81-6.00) 3.1-23.66) 4.3 (12.0) 13.86-10.61 (3.34-3.27) 9.92-17. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.3) 10.99 (3.04 (3.70 (8.80-14.20-4.9 (12.8) 8.50) .60 (5.80-4.96) 3.6) 11.70-8.00-16.0) 7.90 (2.97-4.8) 9.0) 18.0) 9.30) < LOD < LOD 4.8-20.3 (7.22 (6.60) < LOD < LOD 2.67-10.67) 4.670 (<LOD-1.20 (<LOD-2.4 (10.0 (9.98-9.18) * * * * * * * * 1.4) 11. see Data Analysis section) for Survey years 99-00.910 (<LOD-2. which may vary for some chemicals by year and by individual sample.42 (1.90-31.20-18.0-33.90 (6.6) 18.80-3.00) < LOD .27 (3.90-15.84-4.2 (9.4) 672 678 498 509 695 579 595 948 757 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.6 (10.88) 10.31-7.47-6.92) 9.3) 14.00-4.9) 16.90 (6.90 (2.70 (1.9-15.67) 3.30) 3.7) 22.24 (2.10) 6.0) 11.22-12.61-32.80-6.8-20.80-8.80-12.9) 10. 122 Fourth National Report on Human Exposure to Environmental Chemicals .7-19.5) 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 * * * * * * .9) 95th 14.4 (14.0 (8.0-29.37) 2.80 (5.90-9.22 (6.5 (8.5 (9.52 (6.0) 12.28 (7.4 (10.10-10.30) < LOD < LOD . 01-02.00-9.670 (<LOD-1.30) 3.50-5.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. and 0.70-5.75 (2.66-13.72) 2.77-3.0 (5.9) 9.77-14.89) 2.29-4.4) 7.0) 14.22) 8.740 (<LOD-1.0) 13.27) .27 (7.34 (6.8 (12.70-9.49-4.680 (<LOD-1.29) < LOD < LOD < LOD < LOD 3.89 (2.0-19.58.40 (2.6-41.8-21.17 (7.9 (7.650-1.27) 4.64) 10.6) 952 1187 946 997 1332 1019 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * 1.6) 14.0 (9.53 (3. 0.63-14.11-6.0) 23.60 (2.01 (2.25 (2.39 (5.33-11.7-21. and 03-04 are 0.18 (3.46-4.96) 90th 7.06 (2.88) 3.0 (14.30) 8.59-3.40) < LOD < LOD 75th 2.S.5 (8.

9) 19.88-7.55) .03 (2.29 (2.6) 14.4-16.3) 9.6) Sample size 1949 2518 1962 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.4) 16.63 (2.00 (5.4) 9.890-2.78 (4.27) * * * * * * * * 1.68) .16 (3.59-3.96-11.70-2.940) < LOD < LOD 1.67 (1.92 (5.64-11.3-17.0 (13.0) 14.6 (13.6 (11.80) 3.93-10.00 (2.530-1.07 (5. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.32-8.850 (<LOD-1.8 (10.4) 6.75-3.7) 14.0 (11.29 (5.06 (<LOD-1.38) 1.28-12.2) 12.2) 12.2) 12.37-5.620 (<LOD-.29-2.00) 2.3-34.6) 12.3 (7.48 (2.5) 8.5 (15.09-11.14 (2.0 (10.00) 8.5 (10.69-11.690 (.05-3.6 (13.77 (2.74-19.96-10.30) 7.2-15.01-5.54) 9.07-3.78 (6.2) 10.8) 16.6) 7.0-21.6 (12.50-17.38 (1.83 (7.07) 2.12 (7.85-17.54-5.91-9.950) .77) 3.23-3.30) 8.93 (2.78) 4.4) 15.6 (10.99) 2.1 (8.8 (8.39-17.7) 12.7) 14.7-23.4-15.42) 7. Fourth National Report on Human Exposure to Environmental Chemicals 123 .00 (<LOD-1.11 (5.89-13.79-9.9 (9.3) 6. population from the National Health and Nutrition Examination Survey.4-18.5 (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.53-8.27) < LOD .95) 90th 8.38 (2.9-25.86) 9.45) 6.86-3.70-35.28) 6.51-10.2) 16.27) 1.7 (10.2-30.9 (9.73 (5.09-11.89-3.34-18.25 (4.33-10.12) < LOD < LOD 4.2 (9.973 (.04) 9.5 (11.7-19.3) 8.89 (3.27) 5.85-8.5) 10.79-6.910 (<LOD-1.03 (6.61 (2.51-7.6-19.20-3.38 (.38-13.4) 7.99 (4.44-6.42-19.27-13.43 (2.68-19.95 (2.760 (<LOD-1.75-3.21-21.55 (2.2) 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.21) * * * * * 1.590 (<LOD-.89-3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.2) 19.78-10.89) 5.9-17.810 (<LOD-1.920 (<LOD-1.00 (3.87 (3.0 (8.3) 12.91) 3.82-8.19) 3.8) 11.2 (9.97-4.1) 13.7) 15.5) 13.780-1.92) 3.07) 2.93 (<LOD-2.47-9.00 (<LOD-1.88 (1.41 (7.97) < LOD .1 (13.89-10.82-11.45) 3.55) 16.18) 2.1) 10.5 (8.6) 6.86 (3.30) 2.6) 13.4) 7.28 (1.58 (4.34) < LOD < LOD < LOD < LOD 3.81 (7.36 (2.72-4.15 (1.74-4.3-17.06) .11-3.67 (7.2) 15.0-19.83 (6.30-5.71 (1.42) 8.89 (2.15) < LOD < LOD 75th 2.25-9.68-4.6) 471 576 310 664 821 715 814 1121 937 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * .95) 3.54 (7.6) 952 1187 945 997 1331 1017 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * .7 (8.7 (10.2) 8.02-4.72) 4.6 (11.16-14.33) 3.37) 3.8) 14.1 (19.00 (7.94 (5.1) 20.71) < LOD < LOD 2.32) 2.93 (6.4 (11.S.63 (6.3-15.03) 3.6) 95th 16.50 (6.3-21.9) 16.5-17.29) 3.5) 22.94-14.4-16.9 (9.52-3.7) 9.68-10.77 (2.4) 7.7 (11.

20) 1.760 (.29-2.00-2.49) .390-.00) 1.22 (1.00-4.89) 1.48 (1.30 (.580-.17) 1.17-4.49) 2.500 (<LOD-.20 (1.42-2.16) 2.98-3.01) .30) 4.930) 1.720 (.89) 672 678 478 509 695 553 595 948 745 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.990-1.60) 3.303-.94 (3.749 (.79) .87-3.83) .73-5.89-6.83) 2.01-3.26 (2.20) 2.425 (.960) .16-3.74-5.20-2.710 (. respectively.90-4.10-1.83) 1.910 (.20-1.22-3.90) 3.46-3.860) < LOD < LOD .910-1.05-3.89) .45 (2.31) 2.45 (1.690 (.27 (2.60 (2.58 (1.388-.22-8.700) .59-2.459 (.30 (.759) * .618) * .95) 2.880) < LOD 75th .16) 1.70-2.60-4.720-1.240 (<LOD-.359-.31-3.505 (.380-.S.400) .910) 1.83 (2. see Data Analysis section) for Survey years 99-00.41-5.03) 1.76 (1.50 (1.20 (1.79) .20) 3.680-1.73 (2.30-3.70-7.960-1.74) 3.34) 2.600 (<LOD-.570 (<LOD-.20) 2.390-.50 (1.750-1.34) 2.540 (.73 (1.949) .08 (2.86) 3.05-2.740 (.490 (<LOD-.590-.210 (<LOD-.50) 1.46 (2.64 (1.41 (2. and 0.45-4.45 (1. 01-02.790 (.840 (.80) 2.70 (1.580-1.560-.440-.15) 2.50-2.780 (.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Diethylthiophosphate (DETP) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.700) .77 (1.70 (1.10) 1.80) 5.18 (1.585) * * .930) < LOD .32 (1.90) 2.75 (2.382-.1.740-.21) 3.800 (.690-.14-1.48 (2.80 (2.467 (.570-1.63 (1.95 (2.91) 2.33-2.32-1.65 (2.50 (1.40 (1.26) .01-1.39) 2.09.780 (.61 (1.930-1.30-3.20-2.690) .09 (.55 (3.90 (1. which may vary for some chemicals by year and by individual sample.10) 3.980) 1.13) .77-2.17) 1.30 (1.460-.592-.810) .00) 2.453 (.11-3.336-.592) * .570 (.50 (1.00 (1.60) 2.59-6.970) 1.80) 3.69-4.710 (.29) 1. < LOD means less than the limit of detection.20) 3.50-2.380-.88) 1.20-3.592) * 50th .10-1.96-5.68-5.160 (<LOD-.75-2.50 (1.14 (1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.04) .90) 2.08 (2.80) 3.353-.820 (.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 * .11-3.80 (1.960 (.940) < LOD .280-.570 (<LOD-.80) 2.449 (.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 * .31-3.657) * * .30) 1.350-.18 (.670) .201-.455 (.950) 90th 1.2.10) 1.22-3.89) 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 * .780) .30-1.570 (.710) .587) * * .54-2.94) .620-1.350-.70 (1.57 (2.46 (1.96-3.15) 2.35) 1.20) 1.343 (.10) 1. population from the National Health and Nutrition Examination Survey.19-1.22-2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.20 (1.930 (.820 (.31) 95th 2.86 (1.54 (2.04) 1.95-5.94 (2.550 (.46) 1.20 (2.78) .600-1.54) . 124 Fourth National Report on Human Exposure to Environmental Chemicals .550 (.570) * .76-6.450 (<LOD-.970) .740 (.340-.730) .457 (.740-1.880 (.57 (1.260 (<LOD-.750) 1.25-1.38) 1.597) * .27 (3.97 (2.40 (1.30) 2.549 (.850) < LOD .83 (2.30 (.600-.398-.80) 3.830 (. interval) Selected percentiles ( 95% confidence interval) Total * .13) 2. 0.37-2.47) 2.960) 1.510 (<LOD-.98 (2.720-1.32) 3.960) .650-.584) .23-3.510 (.680-1.690-1.880) < LOD .380) .36-4.47 (1. and 03-04 are 0.30) 4.98) .

377-.550-.390-1.07) 5.08-2.348-.75) 6.515) * * .380-.49-4.67) 1.44-2.250 (<LOD-.91 (1.24) 4.280 (<LOD-.76) 1.95) 1.22) 1.43) 2.66) .38 (2.84-6.550-1.17-2.67-3.136-.04-5.22-3.560 (.28 (1.02-3.03-1.440-1.990-1.234 (.490 (.00-1.08-3.38-3.22 (2.22) .19 (1.05-4.79) 1.60) .509 (.800-1.73 (2.57-2.42 (.00 (3.32) 5.22-2.11) 1.80) 471 575 296 664 821 689 814 1122 918 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * .305 (.840) 1.99) 1.23) 2.550) .72) 1.372 (.05-2.55-3.850) 1.253-.07-2.720-1.05 (1.06) 4.75 (2.57 (1.61-3.92-8. population from the National Health and Nutrition Examination Survey.310 (<LOD-.380) .560-.97 (1.23) 3.590) * 50th .07 (.90) 2.33 (1.500-.82) 2.70 (2.84 (2.320-.800) < LOD .97) 1.448 (.58) 3.660-.485) * * .67) .77-3.840) 1.700 (.60 (2.880) 1.23) 2.520-.42-6.270-.16) 1.11 (.43) 2.510 (.32-1.79 (1.14 (2.920) .870) .33) .790) .550-.00-3.72) 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 * .08-3.750 (.710 (.370-.03-2.07) 1.270 (<LOD-.17) 2.69 (1.400-1.87 (2.630) * .69 (3.739) * .39 (1.250 (<LOD-.09) .940-1.530 (.710 (.580-.02-6.742) * * .70 (3.22) 4. interval) Selected percentiles ( 95% confidence interval) Total * .760) < LOD 75th .63 (1.310 (<LOD-.670 (.80) 2.645) .72 (1.16-2.47-4.04-1.380-1.460 (.06-2.78) 3.330 (<LOD-.52) 3.72-4.25-3.31-1.32 (.930-1.61-3.34 (1.470) .820) .285-.08-3.510-.590-1.453 (.32) 1.740) .42) .520 (.64 (2.71) .460-1.730) .43 (1.830 (.50 (1.690) < LOD < LOD .22-3.08-3.760) .07-3.580) .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.71 (1.180 (<LOD-.20) 1.42-8.99) 2.830) 90th 1.480) .700 (.403) .08) 1.08-2.680 (.60) 1.92 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.97 (1.900) 1.750 (.53) .82 (2.60 (1.62 (2.270-.55 (1. Fourth National Report on Human Exposure to Environmental Chemicals 125 .700 (.870 (.92) 3.02-3.640 (.71) 2.58-6.840) .597) * .45 (1.49 (1.08 (2.300-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.330-.300 (<LOD-.57-4.18-2.98) 1.412-.23) 1.471-.310-.393 (.61) 2.17) 2.740) < LOD 1.81) 2.89 (1.320-.230 (<LOD-.66 (2.94) .16-1.57 (3.07) 1.390) .540-.97) 2.08) 2.980-1.77 (3.950-2.480-1.47 (1.10) 2.38 (1.75 (1.820) 1.47 (1.73-3.58 (1.44) 2.447 (.77-4.552 (.75-3.30-2.11-2.580 (.41 (.65) 2.510 (.29-4.640 (.20-7.88) .688) * .52 (1.13 (1.08-2.98) 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 * .88 (1.444-.50) 1.318-.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.36) 3.23 (.640 (.591 (.05) < LOD .45 (2.67 (1.30) 3.790 (.910) < LOD .20-2.39) 2.32) 2.67 (1.460) .400) .04) 95th 2.470 (<LOD-.07) 1.720 (.43) 1.89-3.61 (3.72 (2.350) .335-.590 (.535 (.08 (.62 (1.368) * .05) 1.64 (2.560-.S.710 (.

8) 39. see Data Analysis section) for Survey years 99-00.48-2.5-40.35-6.0-62.0 (25.9) 17.8 (22.1-47.0 (20.3 (12.20) 1.0) 15.0) 3.58-2.0-39.70) 1.70 (7.48) 5.0 (38.0) 20.0-41.05) * 2.40-16. < LOD means less than the limit of detection.60 (2.1) 18.71 (4.0) 28.85) * 2.6 (15.4-76.75-14.10 (1.92) * 2.70-6.29) 2.0 (26.4 (10.0 (38.1-40.30) 11.10-13. and 0.0-110) 34.59 (1.0 (38.23-2.41) 1.43-7.44) 2.1) 140 (46.2-80.44) 3.77) 38.0-53. which may vary for some chemicals by year and by individual sample.70 (.70 (1.0) Sample size 1948 2518 1965 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 2.41 (1.49-2. respectively.61-2.86 (1.0) 16.1 (25.83 (3.8) 671 678 498 509 695 579 595 947 757 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.82 (1.00-24.4) 38. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.18.05) 1.530-4.7 (12.0 (38.0 (8.79-2.0 (13.0-52.18) 14.2-33.0 (33.2) 16.33 (5.53) 40.0) 32.470 (<LOD-1.6-54.2-27.9 (19.53) 1.04) 3.0) 3.58) 16.0-62. interval) 1.6-27.9-21.0 (24.21 (1.7-22.41) 1.20 (2.71) 5.87-7.6 (11. population from the National Health and Nutrition Examination Survey.06 (1.99 (2.78 (1.3) 31.3 (23.42) 1.64-8.98 (1. 0.2-26.7) 47.5) 30.0) 28.80-18.23) 9.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.2-47.04 (<LOD-2.26 (.0) 4.32 (2.5 (24.14) 5.63-6.8) 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 1.86-3.0) 3.1) 95th 48.54 (1.0-230) 35.81-3.6) 52.0) 42.71-2.9 (27.830-4.91 (4.21 (4.9-51.0) 45.2-62.0) 8.8) 32.9) 48.0) 4.45) 2.5.41) 5.10-4.0) 17.2 (19.1) 38.3) 28.0) 19.90-8.0-47.16) * 1.0) 4.12 (3.10) 39.16) 2.72 (1.10 (1.0-260) 34.59 (1.70 (1.88) 3.10) .90 (1. 01-02.80) 90th 38.0-29.53 (1.1 (25.0 (8.25-3.0-58.40) < LOD 2.600-2.0) 6.3) 33.0 (38.0) 33.6 (9.0 (19.88) 1.10 (1.0-31.0) 15.0) 18. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.13 (1.19-2.74-2.12) 1.97) 6.0) 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 2.5-74.09 (4.80) 1.65 (4.0) 17.690-3.1 (26.23-2.0) 30.3 (24.1-25.40) < LOD 1.0-41.70) 5.18) 20.4-22.57-2.2-39.3 (10.2-27.02 (2.6-45.48-2.83 (1.0 (7.66-5.3 (12.50 (2.9 (19.0 (40.40) 50th 2.9) 18.610 (<LOD-1.1 (11.7 (12.8) 41.50-20.30) 4.27-6.78) 9.0 (38.1-19.0-110) 42.21 (3.93-3.36-2.77 (1.0 (32.81-2.40-4.0-50.90 (1. 126 Fourth National Report on Human Exposure to Environmental Chemicals .26) 75th 11.0-92.0) 20.54 (3.8-21.13) 12.11) 2.83-2.06) * 2.70-17.4 (15.1 (22.67 (1.79 (2.7) 20.95 (5.83-2.94 (1.0 (11.11 (4.0-41.2 (12.0) 5.76 (2.6 (26.80-2.7 (28.50-5.830-3.92-5.96) 5.0-53.46-2.S.10 (7.9) 38.8) 62.80) .0-58.31-6.19) 2.46 (.76 (2.0 (37.46-6.41-4.70) 1.5) 69.98) * 2.6-22.90) 11.69) 2.0-49.00 (.13 (1.0-39.9 (10.8 (26.5-20.53) * 2.0-43.9 (23.5-45.0 (6.80) < LOD 1.2) 31.4.79 (1.60) < LOD 1.61 (1.10 (1.4) 19.0 (21.85 (1.0) 16.64-3.8 (12.44-7.0 (8.50-7.4 (19.0) 31.3 (14.0) 13.18) 6.8 (12.1-20.17-2.50-17.04-8.7-41.29-4.0 (20.20-4. and 03-04 are 0.57-2.0) 3.0 (38.1 (10.07-5.30-14.29-9.0 (17.52 (4.5-27.0-69.00 (.30 (.8-24.3) 38.05-3.50-2.1) 38.660-2.1-46.3) 26.45) 2.44) Selected percentiles ( 95% confidence interval) Total * 2.

0) 30.44) 9.27) 50th 2.06) 75th 9.88 (4.5) 70.2-34.00) 1.9 (26.82 (2.28 (1.7 (18.2) 4.0) 25.9 (19.26-2.1) 13.23) 37.69-18.54-2.08) 1.7 (24.1) 13.00 (4.870-3.70 (1.2-28.17-3. Fourth National Report on Human Exposure to Environmental Chemicals 127 .0) 48.8-45.6 (7.14-8.9) 54.1 (50.18-1.2 (22.59-15.06) 1.1 (25.4) 14.17) 2.8) 32.0-40.70-4.75) * 1.47 (1.82) 1.83) .8-34.4-39.11-2.16 (1.64 (1.18) * 2.5 (8.670-1.07) 9.4) 12.40 (5.9-18.9) 3.5-36.96-16.7-37.3) 28.27) 10.7-109) 22.62 (2.59-2.7 (10. population from the National Health and Nutrition Examination Survey.51) .3) 13.2) 671 678 497 509 694 578 595 947 756 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.43-12.22 (2.0-118) 29.0) 3.3-42.38-1.46-6.2) 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 2.19) 5.99-4.25-3.66 (1.35) 1.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.6-38.35 (2.6) 112 (40.9 (10.0 (23.2 (15.33-5.58-2.7-47.9-41.86) * 2.33) 1.5 (15.5-43.71 (1.860 (<LOD-1.60) 4.7-20.26-4.12) 3.3 (10.66) 8.9) 24.15 (.91-2.16 (1.0-71.71) 8.95-16.4-21.37 (1.84-13.2 (8.6) 19.1 (34.37-2.19-14. interval) 1.5 (15.95) 90th 32.7-19.97 (1.6-49.2) 33.16 (1.00) 6.7-38.57 (6.2 (16.22-3.6-32.40 (2.47-17.7) 34.899-2.71-2.870-3.91 (6.69-5.41 (2.19 (1.61-2.56) 1.2) 13.22-2.1) 25.67 (1.36) 10.9) 12.61 (1.3-22.66 (1.80-8.1) 52.6) 3.4 (5.0) 13.68) 47.09 (5.9 (13.890-4.2) 13.9) 24.38 (3.93) 5.33) < LOD 1.3 (9.46-22. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.38) 5.94) 19.7) 23.75 (1.14 (.2) 41.7 (11.4 (12.40-4.3-19.1-22.0) 47.6) 11.27-3.21 (4.2-70.7) 66.6-51.7 (18.3 (8.67-16.45-1.8) 11.9-37.28) 1.31) 2.48) 1.1 (39.7) 30.90 (.5) 27.75-6.02 (.5 (34.2-38.00-16.7) 95th 51.43-2.32-3.72) 2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.06) 1.36 (4.68 (1.02) 1.0 (23.23) < LOD 2.9-36.8-26.01 (.06-1.51) < LOD 1.58-17.4-67.23-1.2-47.8-43.0 (14.22 (.32 (3.16-2.9 (7.96) 2.57) 4.02) * 1.6) 3.5 (17.54-15.5 (6.1 (33.67 (1.52-4.1-60.5 (13.9 (39.2 (21.60 (.1) 27.4 (11.07-2.0-70.33) 2.88 (1.46-5.03-2.9-95.750 (<LOD-1.0 (32.4) 12.67-3.4 (21.0 (25.6) 23.4 (19.61-22.35) .18) 3.94-20.39 (1.7) 26.4 (9.80 (1.0 (6.2) 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 1.07-2.8) 31.12 (1.1) 36.5-190) 30.53) 1.5-97.46) 1.76-2.7) 61.83 (.8) 15.88 (4.5 (41.8) 23.0 (39.4) 3.3-27.9-52.11) < LOD 1.38-5.95-16.56 (2.34) * 1.1 (12.6) 7.48 (4.95 (2.45 (1.1) 27.43) * 2.1) 15.6 (24.75 (1.20-5.7) 15.2) 36.0) 10.36-13.6 (11.680-4.7-43.S.59-2.0) 952 1187 945 996 1330 1017 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.88 (1.870-3.888-1.40-7.3 (10.8 (7.4-34.4 (25.86) * 3.9) 3.47 (3.0 (17.79 (2.24 (1.79-17.1) 25.63-5.8) 3.20) Selected percentiles ( 95% confidence interval) Total * 1.2 (9.4 (25.03) 1.94) 1.1) 17.8-37.3 (20.19-6.52 (1.1-63.30) 28.4-71.0 (19.19) 5.50 (2.27 (6.08 (1.62) 4.29-5.55 (2.50-5.930 (<LOD-1.6 (27.

530-.320 (.460 (.650) . 128 Fourth National Report on Human Exposure to Environmental Chemicals .610 (.990) .270 (.450 (.320-.450 (.090 (<LOD-.310) < LOD < LOD < LOD < LOD .140-.310 (.630 (.05.30) .540) .820 (.30) .600 (.10) .630 (. 0.42) .870 (.410) < LOD < LOD < LOD < LOD .310 (.200) < LOD < LOD .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 * * * * * * .190 (.830 (.700-1.610 (.32) .350) < LOD < LOD < LOD < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.120-.210 (.830 (.640-1.230) . see Data Analysis section) for Survey years 99-00.440-1.640) .540 (<LOD-.720 (.510-1.430 (.36) .680-1.090 (<LOD-.40) . population from the National Health and Nutrition Examination Survey.150) .140) .171) * * .310) < LOD < LOD < LOD < LOD .410-.860) .720-1.470-1.610-1.220 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.610-.680 (.330-.13) .00) .680-1.180) .360-.560 (.140-.30) .990 (.150 (<LOD-.090 (<LOD-.850) < LOD .540) 672 678 498 509 694 579 595 947 757 Non-Hispanic blacks .400-.60) 1.1.S.1.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.740) < LOD .130) .130-. and 0.650) . 01-02.120 (<LOD-.42) .870 (.820 (.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 * * * * * * * * * .380-.860-1.850 (.380-.830) < LOD .117 (. and 03-04 are 0.10) .540) .03) .130-.210 (.390) < LOD < LOD .20) .850 (.370-.130-.260 (.410-. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th 75th .660 (. respectively.120-.290) < LOD < LOD < LOD < LOD Non-Hispanic whites Limit of detection (LOD.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 .870) < LOD .420-.450 (.760) < LOD .690-1.100 (.720) .110-.470 (.640) .900 (.300-1.080 (<LOD-.570) .162) * * * * * .840) .780) < LOD 1.300-.730-.650-1.380-. < LOD means less than the limit of detection.130) .290) < LOD < LOD < LOD < LOD .290) < LOD < LOD < LOD < LOD 90th .680) .099-.650-1.290 (<LOD-.310-.160) .940 (.240 (<LOD-.700-1.090 (<LOD-.130 (.700-1.650 (.050-.140-.170-.870 (.550) .640 (.160-.410-1.230-.10 (.990) .700-1.160) .190 (.490 (.730) .12 (.930 (.870 (.090 (<LOD-.770) < LOD 95th .360-. which may vary for some chemicals by year and by individual sample.390 (.10) .15) .620 (.560 (.430-.280) < LOD < LOD < LOD < LOD .58) .770 (.090 (<LOD-.460-.870 (.220 (<LOD-.350) .840) .080 (<LOD-.830) .084-.370-.190 (.

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.700 (.800-1.520) 672 678 497 509 693 578 595 947 756 Non-Hispanic blacks .080 (.990) .380-1.03 (.320 (<LOD-.62) 1.810 (.36 (1.050 (<LOD-.440 (.260-.140-.450 (.720 (.120) .140) .330-.580 (.140-.260) .870) .390-.300 (.110) .540) .580 (.400) .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 * * * * * * .78) .650-1.210 (.19 (.440-1.170) < LOD < LOD .02) .570 (.360-.730 (.060-.380 (.890 (.080) .070 (<LOD-.230 (<LOD-.14) 1.670-1.110) .080 (<LOD-.057-.940) .880 (.410 (.220) < LOD < LOD < LOD < LOD .730) .330 (.650) < LOD .29 (.220 (.300-.400 (<LOD-.270) < LOD < LOD < LOD < LOD .03 (. Fourth National Report on Human Exposure to Environmental Chemicals 129 .470 (<LOD-.60) .640-1.370 (<LOD-.940) .230-.330-.500-1.300-.330-.500 (<LOD-.520-.090 (<LOD-.570-.330 (.070 (<LOD-.560 (.860-2.084-.S.540 (.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 .170 (.970) .660-1.580-1.24 (.780) < LOD 1.100-.310) < LOD < LOD < LOD < LOD .860 (.670 (.140-.740 (.116 (.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 * * * * * * * * * . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.600) .410-.67) .310) < LOD < LOD < LOD < LOD Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.110) .150-.140-.00) < LOD .161) * * .990) .380-.500) .09) .580) .880-1.410-.24) .200 (.38) 1.110) .140-.230) < LOD < LOD < LOD < LOD .110-.540 (.780 (.700 (.240-.730) .610-1.860 (.550 (.850 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th 75th .460 (.190 (.730) .700) .740) < LOD 1.280) < LOD < LOD < LOD < LOD . population from the National Health and Nutrition Examination Survey.86) .190 (.01 (.111) * * * * * .760) .200 (.960) .02-1.070 (<LOD-.12) < LOD .360 (.170 (.720 (.250-.700-1.58) 1.100 (<LOD-.580) < LOD .510-.410) .86) .360-.710-1.03) .340-.390-.20) 1.750) < LOD 95th .070 (<LOD-.360) < LOD < LOD < LOD < LOD .380-.120) .450) .090 (.180-.03 (.380-.410 (.570-1.410) < LOD < LOD .490-1.600-1.550 (.43) .190-.66) 1.270 (.670 (.290) < LOD < LOD < LOD < LOD 90th .

40-7.87) 5.890 (.90 (1.0) 2.45 (2.80 (4.90) .S.52) 5.6) 672 678 498 509 695 552 595 947 752 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. 0.20-4.20 (1.00-17.28) 1.740 (.800) 90th 13.0) 4.380-.0 (17.83) 2.0) 5.16) 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 .21-3.510-.87) 12. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th 2.67 (1.960 (.60) 1.38-3.0-40.10 (3.42) .24-7.0) 5.20 (1.07-3.0) 3. which may vary for some chemicals by year and by individual sample.425-1.07-3.49) 17.0) 4.0) 2.730 (. respectively.840-3.99) 19. < LOD means less than the limit of detection.6) 5.3) 952 1187 935 997 1331 995 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * .400-1.14) .42) 2.690 (.900 (.20-17.11) 13.0 (13.05-3.0 (7.08.0) 5. and 03-04 are 0.11) .97) 20.00) . and 0.97) 20.21) 3.30 (.30-7.62-8.90) .0 (16.40-20.53-7.36-3.20) < LOD < LOD < LOD < LOD < LOD 1.910) 2.86) 4.88-3.0 (3.12) * * * * * * * * .0-38.40-8.370-.46 (1.0) 5.15) 19.74 (3.99 (1.870) < LOD < LOD .0-40.31-10. see Data Analysis section) for Survey years 99-00.480-.210-1.250 (<LOD-.48 (2.43-4. population from the National Health and Nutrition Examination Survey.00) 1.03 (.600 (.67 (2.610 (.0-44.10-9.94-3.35) 11.360-1.0) 2.62) 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 * * * * * * .10 (3.14-5.1.07 (3.00-17.30 (1.30) 95th 19.05 (2.18) 1.840 (.36-3.85-3.0-38.96 (1.70) 2.70-3.55-4.90-37.50) .90-28.07 (1.32 (1.0-38.80) < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 4.40) 2.50) 2.99) 11.83-3.35) 5.07 (3.720) 2.28) .47 (3.0 (4.0 (5.26 (2.39) .07) 1.770) 2.770 (<LOD-1.60) .830 (.0) 2. 01-02. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.40) 1.55-8.30 (2.70-7.750-1.90-20.40 (1.15) 14.0) 7.1.70-17.68) 2.63 (3.750-2.00) .74) 5.52 (1.110 (<LOD-.40 (1.48) 13.13 (3.70-50.67) .0) 2.350-.51 (2.800-4.94-8.0 (5.70-30.0 (4.82-4.61 (1.30-3.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.10 (.260-.691 (.850) 16.90-9.0 (17.39 (2.53) 20.620-1.960 (<LOD-1.0) 2.83-3.35-10.29-10.580 (.65) 1.30) .0 (17.0 (5.51-8.0 (17.30-6.00 (.330 (<LOD-1.05 (3.10-3.23-6.76 (1.12-1.37) .66) 4.00 (1.840 (<LOD-1.0 (5.90) .640 (.53 (2.880) 5.610) < LOD < LOD < LOD < LOD < LOD 2.63) 32.640 (.800) 17.0) 4.32-9.40-4.590 (.190-1.170-1.01) 5.350-.11 (1.0 (17.33 (4.90 (2.49 (1.0) 2.49 (1.30 (1.30 (1.0-39.59-5.31) .080-1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.94 (1. 130 Fourth National Report on Human Exposure to Environmental Chemicals .0 (5.52 (1.20-4.0) 4.0 (6.14) 2.28-9.10-3.

430 (<LOD-.10-3.860-2.96-25.48 (4.S.48-42.17) 5.4) 2.7) 4.730-3.02) .1 (5.14-6.650) 90th 10.25-9.340-.150 (<LOD-.82-11.55) 21.50) .47-10.53) 27.940-4.40) 1.5) 2.57-40.850-3.5 (11.1) 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 * * * * * * .0) 4.7) 5.57) 1.40 (.8 (20.79 (.86) .29-4.270 (<LOD-.51-4.370 (.85 (1.55) 21.56) .890 (.1 (7.33-4.04 (1.7) 6.840-3.12 (4.55 (3.60 (1.830-3.47) 5.02 (.47-10.830 (.8) 2.03) 2.7) 3.450 (.33-3.40-12.970-3.69) 2.91-4.748 (.18) 1.37) 4.5-40.33-5.33 (3.580) 1.35 (.83-11.64) 30.06 (.540 (.630-1.31) .740-1.88-3.31) .71 (.22) 2.6) 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 * * * * * * * * * .44-11.430) 1.50 (2.820 (.5) 2.8) 7.31-7.24) 3.1) 2.0 (9. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.75) 5.39) 20.74 (2.340 (.59 (1.250 (<LOD-.15) 9.85-3.50 (4.57) 8.83 (4.770) .8) 7.240-.260-.22-27.41 (4.260-.500 (.11-5.5 (9.02 (1.370) < LOD < LOD < LOD < LOD < LOD 1.07 (2. population from the National Health and Nutrition Examination Survey.580 (.41) 18.18) 95th 21.05) .320-1.474-1.3) 2.0 (4.790) 11.9) 5.690-5.77 (.27 (2.12-4.48-7.270-.340-.590) 2.2 (8.8) 1.820) .69-7.33 (1.25-38.560 (.13 (2.960 (.18) * * * * * * * * .7 (6.620-3.28-6.11) .660) < LOD < LOD .790 (.50) 11.40-2.14 (1.23-7.5) 7.07-21.80) 3.470 (.360 (.89 (2.4-34.780-4.10) 2.710 (<LOD-1.390-.92 (2.310-.84) 9.370-1.580-1.04-16.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.67) 2.4 (4.540-1.61) Sample size 1949 2517 1927 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .56 (1.7 (12.67 (2.8-33.81-17.30 (4.88 (2.66-47.62 (1.21-3.32-6.73 (4.96-8.64-4.00-19.38 (2.52 (.90-6.36 (.00) .71 (2.43) .97) .51-44.2-38.03) 16. Fourth National Report on Human Exposure to Environmental Chemicals 131 .10 (2.700) < LOD < LOD < LOD < LOD < LOD 1.340-.330-1.01 (1.8) 2.86 (3.670 (.800-2.88 (.190-1.32) 9.8) 4.88) 17.65 (2.31-18.45 (1.53) .17 (1.700) 6.580) 16.67) 1.25 (1.02-4.96) 2.08) .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.62-17.57 (.49-2.5 (8.47) .9 (11.80 (.3) 3.29 (4.98 (4.44) .600 (<LOD-1.60) < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 4.9) 6. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th 1.930) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.56) 2.67-6.650 (.91) 2.09-3.

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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. Lancet. Lasarev M. vibration sense and tremor among South African farm workers.332(1-3):71-80. Claypoole K. Ames RG. van der Hoek W. and spatial learning in monkeys and rats. Lambert WE. Schenker M. low-level organophosphate exposure on delayed recall. Rohlman D. Frasca G. S. J Toxicol Environ Health A 2005. Stark A.30(2):98-103. Variation in organophosphate pesticide metabolites in urine of children living in agricultural communities. Organophosphate pesticide exposure and neurobehavioral performance in agricultural and non-agricultural Hispanic workers. Washington (DC): U. Jenkins B. National Academy of Sciences. Lewis JA. discrimination. Rothlein J. Am J Public Health 1994. 2004. Ruberu DK. Salvini S. Biological monitoring of organophosphate pesticides in preschool children in an agricultural community in Thailand. Mounce LM. The Pesticide Health Effects Study Group. Chronic central nervous system effects of acute organophosphate pesticide intoxication. Masala G. et al. The presence of dialkylphosphates in fresh fruit juices: implication for organophosphorus pesticide exposure and risk assessments. and cholinesterase status of date dusters and harvesters in California. Available at URL: http://books. gov/oppbead1/pestsales/01pestsales/market_estimates2001.58(11):702710. Rothlein J. Keefe TJ. Scand J Work Environ Health 1998. Narang A. Available at URL: http://www. Gladstone EA. Russo J. Pedersen L. Myers JE. Occup Environ Med 2001. O’Malley M. 1/12/09 Peiris-John RJ. Savage EP.345(8958):11351139. Caltabiano LM. Neurotoxicology 2005. Takamiya K. Smit LA. Weerasekera G. Occup Environ Med 1995. London L. Neurotoxicity among pesticide applicators exposed to organophosphates. Environmental Protection Agency (U. Seiber J. Marshall E.114(5):691-696. Pesticides in the Diets of Infants and Children. McCauley L.php?record_id=2126&page=1.52(10):648-653. Arch Environ Health 1988. Neuropsychological effects of long-term exposure to organophosphates in sheep dip. Environ Health Perspect 2005. Hansen S. Buccafusco JJ. May. metabolite clearance. Environ Health Perspect 2006. A behavioral evaluation of pest control workers with short-term.113(4):504-508. Effects of chronic. Dinoff TM.338(8761):223-227. Weisskopf C. Lancet 1995. Bradman A. EPA). Occupational exposure to organophosphate pesticides: a neurobehavioral study. Saieva C. Bull Environ Contam Toxicol 1994. Robson MG.2000 and 2001 market estimates. Keifer M. et al. Irish RM. Office of Prevention Pesticides and Toxic Substances.edu/ openbook. Pilkington A. Buchanan D. Berry H. Johnson C.24(1):18-29. Bravo R.S. J Occup Environ Med 2002.12(2):134-141. Steenland K. Lasarev M.43(1):38-45. Tumino R. Malathion deposition. et al. Barr DB. Nell V.pdf. Stokes L.20(2):115-22. National Research Council (NRC). Rosenstock L. Gillham R. Prendergast MA. Kidd M. Monitoring of urinary alkyl phosphates in pestcontrol operators exposed to various organophosphorus insecticides. Calvert IA. Levy LS.68(3):209-227 Maizlish N. Hore P. Thompson ML. Int J Occup Environ Health 2006. Santana J. Petchuay C. Scherer J.26(2):199-209. 1991. Muniz J. Fourth National Report on Human Exposure to Environmental Chemicals 133 . Arch Environ Health 1975. U.52(2):190-195. Effects of occupational exposure to organophosphate pesticides on nerve and neuromuscular function.12(2):153-172. Wickremasinghe AR. Jamal GA.44(4):352-357.epa.84(5):731-736. Pesticide industry sales and usage . Twenty-four-hour urinary excretion of ten pesticide metabolites in healthy adults in two different areas of Italy (Florence and Ragusa). 1993 [online]. Spurgeon A. Aprea C.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Krieger RI. Chrislip D. low-level exposure to the organophosphate diazinon. Beach J. Terry AV Jr. 4/7/09 Young JG. Samuels S. Arch Environ Contam Toxicol 2000. Am J Ind Med 1987.nap. et al. Muniz J. Washington (DC). Effects of long-term organophosphate exposures on neurological symptoms. Vitayavirasak B. Burcar PJ. Sci Total Environ 2004. Heaton RK. Visuthismajarn P. Rodnitzky RL. McConnell R.S. Chronic neurological sequelae to organophosphate pesticide poisoning. Association between in utero organophosphate pesticide exposure and abnormal reflexes in neonates.38(4):546-563. Stephens R. EPA. Neurotoxicol Teratol 1998. Lu C. Phillips J. Daniell WE. et al. Chronic neurological sequelae of acute organophosphate pesticide poisoning. Eskenazi B.

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

7-23.05-5.44 (3.50 (2. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.60-3.S.5 (8.89 (2.10 (3.97) 2.10-17.40 (5.63 (1.02 (7.S. but can be detected in streams receiving runoff from application sites.24-3. USGS.0) 12.90-7.44-5.70-15.0 (13.67 (1. staying bound to soil particles.4 and 0. applied to structures to kill termites.90-4.99-4.20) 2.17 (1.57 (2.8) 10.51 (1.14) Selected percentiles ( 95% confidence interval) Sample 95th 10.3) 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 1.28-3. Survey Geometric mean (95% conf.09 (3.81-2.30-11. 5598-13-0 General Information The chemical 3.77 (1.92 (1. and on plants for days to several weeks.62-2. Estimated intakes from diet and water have not exceeded recommended intake limits. It also has been applied directly on animals to kill mites. and sprayed to kill mosquitoes.25) 1.90) 3. Exposure can also result from contact with contaminated surfaces. For instance.20-3.47-11.55-5.67 (2.20-16.90 (2.0 (7.95 (4.79-2.28) 2.2 (10.68 (7.50-4.10) 2.40-2.4) 481 573 681 823 832 1113 99-00 01-02 99-00 01-02 1.34) 1. 1999.31-2. Chlorpyrifos is very toxic to fish and aquatic invertebrates and shows modest degrees of bioconcentration. and inhalation routes. Approximately 80.60 (5.20) 4.05) 1.4 (9.60) 5.3) 8.70 (1.50 (1.0) 10.13 (1.70-5.71 (1.Organophosphorus Insecticides: Specific Metabolites Chlorpyrifos CAS No.39) 4.50-2.31-2.50-2.64) 3.7) 8.000 pounds are used per year.9-18.50-14.9 (7.9 (10.0) 7.8-15.0) 18.47-13. 2921-88-2 Chlorpyrifos-methyl CAS No.40-26.0) 12.67 (2.83) 1. After 2001.24-1.02 (1.74-9.37 (4.2) 972 1183 1022 1326 99-00 01-02 99-00 01-02 99-00 01-02 1.30-12.66-15.80 (7.90 (1.52-12. interval) 1.03) 99-00 01-02 99-00 01-02 99-00 01-02 2.89-2.0) 10.80) 1.77) 1.35) 1.80 (1.29) 90th 7.3 (11.0) 12.13-3.59) 2.84) 1.94 (4.90-8.5-24.63 (8. It has low leachability.00-8.0 (7.51) 1.68-2.10 (1.0 (7.70-17.97) 4.97-7.72-4.90) 7. 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.50-4.50 (2.21) 3.10 (4.4 (10. Approximately 21-24 million pounds per year were used domestically from 1987-1998.04-10.30-1.80) 4.90-2.61 (1.86) 4.0) 8. Chlorpyrifos is not well absorbed through the skin but dermal exposure can be significant when other routes of exposure are low.3 (8.97) 7.90 (1.40) 2.44-2.20-14.53 (1.6-Trichloro-2-pyridinol Metabolite of Chlorpyrifos and Chlorpyrifos-methyl Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.5) 7.00-24.0 (9. Chlorpyrifos is Urinary 3.4. 2002).20 (4.30) 5.0) 14. population from the National Health and Nutrition Examination Survey.29-1.77-6.20) 10.0) 12.40-13.61-7.60 (4.30) 4.S.52-2.30) 4.90 (3.97) 2.20) 2. chlorpyrifos was no longer registered for indoor residential uses in the United States.36 (4. air.77-15.40 (5. and dust.0) 9.30-2.02) 1.and post-construction structural applications for termite control were to be phased out by 2005 (U.50 (2.8) 9.60-3. dermal.7) 9.61) 75th 3. Inhalational and dermal routes of exposure are important in pesticide formulators and applicators.6) 7.25) 3.EPA.80-8.70-11.39-2.00) 3.3 (10.91 (1.30-9.00) 2. pre.6-trichloro-2-pyridinol (TCPy) is a metabolite of chlorpyrifos and chlorpyrifos-methyl.27 (7.10 (5.78 (7.60-4.15 (1.70 (1.80) 2.30-5.87-6.76 (1. chlorpyrifos and TCPy were detected in all indoor air and dust samples (Morgan et al.16) 2.30 (2.47-9.00) 1.9) 11.22) 2.19 (1.37) 5.40 (6.43-2.45 (1.43-2.20 (2.04-10.37 (1.7) 13.4 (8.71 (2.03) 1.76 (1.70) 1.9) 697 660 521 701 602 947 Limit of detection (LOD.72) 2.46-2.1) 5.80) 12.30 (4. 2002).5.50 (1.91) 16.50-8.30 (2..5. Chlorpyrifos is a broad spectrum organophosphorus insecticide that has been widely used to control insects on food crops such as corn.32) 2.70-16.59-2. in 142 urban homes and preschools in North Carolina. Chlorpyrifos-methyl is an organophosphorus insecticide also used in agriculture and not registered for residential use.0 (7.40-10.0) 8.60 (2.0 (7.20-11.01) 1.38 (3.0) 6.96) 3.80-10.20-2.0) 11.74 (1. Fourth National Report on Human Exposure to Environmental Chemicals 135 .4-15.0) 10.90 (6.26) 7.95) 7.35) 2.20-4. Chlorpyrifos is degraded in agricultural soils with a half-life of several months.98-15.60-2.47) 1. The general population may be exposed to chlorpyrifos via oral.9 (9. 2005).71 (6. and is infrequently detected in ground water (IPCS.50-5.47 (4.09 (2.22 (1.51-2. 2007).63 (2.0) 12.10) 6.19-3.88 (1.0-28.66-4.1-16.0) 15.0 (10.EPA.32-1.40) 9.

24-4.1 (10.11 (2. Roy et al.56 (1.06 (1..24-24. and behavior may occur at systemically nontoxic doses or at doses of chlorpyrifos that do not result in cholinergic signs (Aldridge et al.91) 2.80-4.88-9. Howard et al.EPA.17-4.12-1.71 (1.88-8.85 (2.46 (2. Chlorpyrifos and chlorpyrifos-methyl both demonstrate moderate acute toxicity in animal studies. These organophosphorus insecticides share a mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system. In addition to being a metabolite of chlorpyrifos and chlorpyrifos-methyl in the body. resulting in excess acetylcholine at nerve terminals.24) 75th 2.7) 697 660 521 700 602 947 136 Fourth National Report on Human Exposure to Environmental Chemicals .85) 1. the detection of TCPy in a person’s urine may reflect exposure to the environmental degradates.83-11. Thus.90-9.3) 8.56) 5.69 (1.49-2.85) Selected percentiles ( 95% confidence interval) Sample 95th 8.24 (1.39) 6.33) 2.31-1.42 (5.64-7.60 (1.30-1.3) 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 1.83) 1.3 (7. weakness.16) 6. Based on animal data and human cholinesterase monitoring during occupational exposure. phosphorothioates such as chlorpyrifos are metabolically activated to the “oxon” form which has greater toxicity than the parent insecticide.71) 3.55 (4.72-2.88 (1.43 (4.05-8.35) 1.91) 1.91) 10. The metabolite TCPy does not inhibit acetylcholinesterase enzymes.44 (5.12-3. cholinergic effects. ubiquitous lowlevel environmental exposures in humans would not be expected to result in inhibition of cholinesterase activity.16 (4.38) 3.36) 1.39-1. chronic exposure to chlorpyrifos may be associated with slight alterations in some components of neurophysiologic testing (Steenland et al.45-1.62-7.83-2.70-4.81 (3. Recent in vitro and in vivo animal studies suggest that effects on neuronal morphogenesis.44 (6.48 (1.28) 2.11-9..94-12.09 (1.63-2.19-2.23) 14.44 (1.80-6.66 (1.86 (1.79-13.93 (2.22) 1.84-6.09-3.06-4.54) 5.99-8.2) 6.. In pesticide applicators.940-1.80-11. 2006a.92) 3.39 (4..76 (2.32) 1.58 (4.56 (4.45 (1. Ricceri et al.77) 1. interval) 1.97 (3.6) 9. Survey Geometric mean (95% conf.98 (7.82) 8.28) 2.96) 3.03) 1..94-14.1-38.97) 3.97 (2. paralysis. 2000).22-6.4) 4. and seizures.88-8.42-2. 2006.33 (1.57-2.14-8.59) 3.78 (1.41 (1.73 (1. 2005.58) 1.62) 1.42 (6.43-10.29 (3.75 (1.26-14.88) 6. Betancourt et al.25-1.74) 1.66-11.21-6.47 (5.72) 1.48 (2.05) 3.97) 3.0) 10.88 (1.93) 5.80) 3.55) 1.88-10.7) 7. 2005.63 (5.15 (4.57) 2.31-4.59-2.57) 9. Urinary 3.8) 972 1183 1022 1325 99-00 01-02 99-00 01-02 99-00 01-02 1.12) 1.00 (7.20-1.92-2.46 (1.00) 1.19-1. 2002).05-1.64-2.02) 7.64 (1.76 (3.1 (7.37 (1.24-5.44 (5.0) 481 573 681 822 832 1113 99-00 01-02 99-00 01-02 1.47 (1.06 (5.39 (2.20 (2.44 (1.52 (5.01) 3.93 (1.53-5.49 (1.72) 2.6-Trichloro-2-pyridinol (creatinine corrected) Metabolite of Chlorpyrifos and Chlorpyrifos-methyl Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.49-2.58) 5.00-8.0) 6.44-6.00-13.53 (2.27-7. TCPy can also occur in the environment from the breakdown of the parent compounds.33 (5.49-2.8) 9.09-2.5) 5. 2006b).3) 8.85) 4.66) 1..47-2.5 (6. 2005.35-1.99) 1.24) 5.54 (2.07) 5.. 2006.91-4.24-1.87-3.09-1.21-1. Chlorpyrifos is eliminated from the body primarily in the urine with a half-life of approximately 27 hours (Nolan et al.91 (3.08) 6. and producing acute symptoms such as nausea.95 (3.05-4.51 (1.07) 1.89) 4.14) 1.01) 3. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”).01) 1.6) 10.33 (.31) 1.68) 1.02 (5..58-5.1-21.11 (2.57-2.S.35) 2.17-4.97-3.33-7.63 (4.0) 12.58 (1.22 (4.30-4. Once absorbed.9 (12. Overt cholinergic toxicity from chlorpyrifos has been described following suicidal ingestion and unintentional high level occupational exposure.95 (1.81) 2.19) 3. neurotransmission. TCPy is more persistent in the environment than chlorpyrifos itself (U.47 (1.25-12.86 (3.0) 16.91 (4.56) 2. 1984).98 (6.27-1.23-1.. Slotkin et al.60-3.56-2.82 (3.50 (4.2 (7. population from the National Health and Nutrition Examination Survey.93 (4. Human health effects from chlorpyrifos or chlorpyrifosmethyl at low environmental doses or at biomonitored levels from low environmental exposures are unknown.19) 6.55 (1.92 (1.3) 9.5.85-4. vomiting.40) 1.93) 2. Metabolic hydrolysis leads to the formation of TCPy. and other metabolites.22 (6.91-13.68) 6.05-3.82 (2.65-11.82-4.75) 6. 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.65-15.01) 99-00 01-02 99-00 01-02 99-00 01-02 3.11) 7.25-11.58 (1.91) 1.S.34-1.85 (3.86 (1.62) 90th 5.Organophosphorus Insecticides: Specific Metabolites rapidly absorbed following ingestion.

2005..92(2):500-506.S.. 2005).EPA. Of 482 pregnant women living in an agricultural community. representative subsample of NHANES 19992000 (CDC. 2006) and episodically many times higher for pesticide applicators than median levels from NHANES 1999-2000 (CDC.gov/toxpro2. et al.. Lotti A.S... 2005). Measurements of urinary TCPy in single spot urine collections show variability over time in environmentally exposed individuals and are poorly correlated between collections. 1999). 2005). 2000). 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. et al. 2005). MacIntosh et al.gov/pesticides/. Koch et al. Following crack-and-crevice application of chlorpyrifos in their homes. the weighted population mean of TCPy measurements was approximately three times higher (Adgate.e. 2005) appear roughly similar to values reported for a nonrandom subsample of NHANES III (1988-1994) participants (Hill et al. Alterations in central nervous system serotonergic and dopaminergic synaptic activity in adulthood after prenatal or neonatal chlorpyrifos exposure.113(8):1027-1031. Burgess SC.82(2):305-312.cdc. Barr DB. Fourth National Report on Human Exposure to Environmental Chemicals 137 .5.6-trichloro-2-pyridinol in the Italian population—validation of analytical method and preliminary results (multicentric study).S. Betta A. Effect of developmental exposure to chlorpyrifos on the expression of neurotrophin growth factors and cell-specific markers in neonatal rat brain. 2003.. 2001). Giordani B. Eberly LE. 1992.63(3):218220. Other small studies of environmentally-exposed persons have shown a high frequency of detecting low levels of TCPy... Barisano A. (1999) reported mean urinary TCPy levels in a sample of Maryland adults that were about three times higher than adults in the U.. 2005. Aldridge JE. Toxicol Sci 2006. 76% had detectable levels of TCPy and levels were similar to those reported for NHANES 1999-2000 (Eskenazi et al. CDC. U. Some reproductive and teratogenic effects in animal testing were only observed at high doses of chlorpyrifos that caused overt maternal toxicity. Slotkin TA. Replacing conventional diets with organic diets in 23 children led to about a fourfold decrease in urinary levels of chlorpyrifos. Curwin et al..Reference values of urinary 3. Lioy PJ. Chlorpyrifos exposure and biological monitoring among manufacturing workers. 2005). Carr RL. In Minnesota and South Carolina farmers who used chlorpyrifos. median urinary levels on the conventional diet were several fold higher than those in the NHANES 1999-2000 subsample (Lu et al.. Haidar S. 2004). urinary TCPy levels averaged about sixfold higher than those in the NHANES 1999-2000 subsample (Mandel et al. Environ Health Perspect 2001. Freeman NC. subsamples of NHANES 1999-2000 and 2001-2002 (CDC. but levels were roughly four to six times higher than the geometric means in the U. Biomonitoring Information Urinary TCPy levels reflect recent exposure. Additional information about external exposure (i.Organophosphorus Insecticides: Specific Metabolites 2004. 2001) and Italy (Aprea et al. Whyatt et al. Levels of TCPy in the U. 1995) and were similar to levels reported in studies of healthy adults in Germany (Koch et al.. 2005). Garabrant D. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Berent S. EPA at: http://www.atsdr. 2001) than the corresponding values reported for the group aged 6-11 years from the NHANES 1999-2000 subsample (CDC.epa. Perera et al. Meyer A. Catenacci G.html and from U. Estimation of dose or intake based on the urinary excretion of TCPy indicates that environmental doses are generally below recommended limits (Hore et al. Urinary levels of TCPy have been found to be hundredsfold higher for chlorpyrifos manufacturing workers (Burns et al. J AOAC Int 1999. et al. Chlorpyrifos is not considered to be mutagenic or carcinogenic (NTP. 2005. Clayton CA. In a probability-based sample of 102 Minnesota children aged 3-13 years. References Adgate JL.S. urinary TCPy levels in children were reported not to have increased (Hore et al. Occup Environ Med 2006.... 2006). 2002). Seidler FJ. Chlorpyrifos levels in house dust and hand rinses did not correlate with levels of TCPy in urine (Lioy et al. environmental levels) and health effects is available from ATSDR at: http://www. Aprea C. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample. 2004). Magnaghi S. population (CDC.. 2007).S. Albers JW. the geometric mean urinary TCPy levels were similar in parents and children. In Iowa farm families using several different pesticides. but not chlorpyrifos. Environ Health Perspect 2005.109(6):583-590. Burns CJ. Finding a measurable amount of TCPy in urine does not mean that the level will result in an adverse health effect. Betancourt AM. suggesting changing low-level exposure and variance in collection timing with respect to exposure (Meeker 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. Hines CJ. Ann Occup Hyg 2007.S. Tate CA.6-trichloro-2-pyridinol. Baker BA. Brain Res Dev Brain Res 2005. Neurologic function among termiticide applicators exposed to chlorpyrifos. EPA).niehs. Reid TM. Barr DB. 2921-882. et al. Ryde IT. J Expo Anal Environ Epidemiol 2000.15(4):297-309.6-trichloro 2-pyridinol in their everyday environments. Hammerstrom KA. Environ Health Perspect 2006b. J Expo Anal Environ Epidemiol 2005. Bravo R. Barr DB. Weltzien E. Comparative developmental neurotoxicity of organophosphate insecticides: effects on brain development are separable from systemic toxicity. Zhang J. J Expo Anal Environ Epidemiol 2005. Kinney P. Curwin BD. et al. gov/ntpweb/index. Slotkin TA. Urinary pesticide concentrations among children.nih. et al. National Toxicology Program (NTP). 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Toxicol Appl Pharmacol 1984. Hardt J. Saunders JH. et al. Levin ED. 2005. Freeman N. Bailey SL. 1992.htm. Sharma V. Third National Report on Human Exposure to Environmental Chemicals. chlorpyrifos. Eskenazi B. Yang D. Robertson GL. Sheldon LS. Scand J Work Environ Health 2005. Int J Hyg Environ Health 2001. et al. Available at URL: http://ntp. Jewell NP. Head SL. Lorenzini P. Acquavella JF. Irish R. Lu C. Steenland K. Striley C. Pellizzari E. Available at URL: http://www. Seidler FJ.71:99108.31 Suppl 1:98-104. Bennett DH. Edwards RD. Bruun D.108(4):293-300. Kromhout H. Chuang JC. mothers and fathers living in farm and non-farm households in Iowa. Jones PA. U. Capone F. et al. Quantitative morphological assessment reveals neuronal and glial deficits in hippocampus after a brief subtoxic exposure to chlorpyrifos in neonatal rats. et al. Mandel JS. Effects of transplacental exposure to environmental pollution on birth outcomes in a multiethnic population. EPA 738-R- 138 Fourth National Report on Human Exposure to Environmental Chemicals . Rauh V. Temporal variability of urinary levels of nonpersistent insecticides in adult men. Morgan MK. Environ Res 1995. Environ Health Perspect 2004.114(5):746-751. Environ Health Perspect 2000. Developmental neurotoxicity of organophosphorous pesticides: fetal and neonatal exposure to chlorpyrifos alters sex specific behaviors at adulthood in mice. Bucelli R. Hein MJ. Chrislip DW. Environ Health Perspect 2006a.15(3):271-281. February 5. Bravo R.204(2-3):175-180. Fenske RA. Alexander BH. Slotkin TA. Executive summary of safety and toxicity information. et al.113(2):211-219. Gregg M. Gurunathan S.10(4):327-340. House dust levels of selected insecticides and a herbicide measured by the EL and LWW samplers and comparisons to hand rinses and urine metabolites.Organophosphorus Insecticides: Specific Metabolites Centers for Disease Control and Prevention (CDC). Ryan L. Rick DL. Ryan PB. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population.5. Dick RB. Levin ED.114(2):260-263.inchem.111(2):201-205. Ricceri L.73:8-15.51(1):53-65. Ozkaynak H. Biomonitoring for farm families in the farm family exposure study.155(1):71-80. et al. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides.

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

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

see Data Analysis section) for Survey year 01-02 is 0. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.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 . Survey Geometric mean (95% conf.2. population from the National Health and Nutrition Examination Survey.S.200 (<LOD-.200 (<LOD-.670 (<LOD-1.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. < LOD means less than the limit of detection.380 (<LOD-. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2481 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . Survey Geometric mean (95% conf. Urinary 3-Chloro-7-hydroxy-4-methyl-2H-chromen-2-one/ol (creatinine corrected) Metabolite of Coumaphos Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.S.270) < LOD 659 701 920 Limit of detection (LOD. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.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 . Fourth National Report on Human Exposure to Environmental Chemicals 141 . population from the National Health and Nutrition Examination Survey. which may vary for some chemicals by year and by individual sample.560) < LOD 659 700 920 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2480 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .

Comparative organophosphate-induced effects observed in adult and neonatal Sprague-Dawley rats during the conduct of multigeneration toxicity studies. EPA 738-R-00-010.pdf.epa. Eigenberg DA. Anal Bioanal Chem 2003. Olsson AO. Available at URL: http://www. Sadowski MA. Reregistration eligibility decision (RED) addendum and FPQA tolerance reassessment progress report: Coumaphos. Reprod Toxicol 1998. U.S. Centers for Disease Control and Prevention (CDC). Atlanta (GA). 2005.12(6):619-645. Freshwater KJ. September 2000. Nguyen JV. Barr DB.Organophosphorus Insecticides: Specific Metabolites References Astroff AB.S. Environmental Protection Agency (U. Third National Report on Human Exposure to Environmental Chemicals.gov/oppsrrd1/ REDs/0018tred.376(6):808-815. EPA). 1/14/09 142 Fourth National Report on Human Exposure to Environmental Chemicals . A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine.

USGS. Once absorbed. 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. Metabolic hydrolysis leads to the formation of 2-isopropyl4-methyl-6-hydroxypyrimidine. diazinon produced wild bird kills before use restrictions were in place. Prior to 2000.2 and 0. Experimental diazinon exposure in people has demonstrated its rapid elimination into urine. It is toxic to birds.05) < LOD < LOD 644 678 484 700 554 956 Limit of detection (LOD.S. and particularly when it was ingested in granular form. see Data Analysis section) for Survey years 99-00 and 01-02 are 7. 2007). vegetable. 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. an organophosphorus insecticide that is used to control insects on nuts. Survey Geometric mean (95% conf. since 2004. Estimated intakes from diet and water do not exceed recommended intake limits (U.49 (<LOD-2.11) < LOD < LOD < LOD < LOD 454 580 632 829 756 1126 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 894 1191 948 1344 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1. It has been infrequently detected in general groundwater sampling but has been detected in streams receiving runoff from application sites (IPCS. population from the National Health and Nutrition Examination Survey. in some pest strips. and other metabolites. 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.45 (<LOD-3. seed and foliar applications are planned to be phased out (U. Most granular formulations.EPA. 2004). but these uses have been phased out. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 1998). 1998.S. Fourth National Report on Human Exposure to Environmental Chemicals 143 . but is rapidly absorbed orally (IPCS.7. < LOD means less than the limit of detection. fruits.Organophosphorus Insecticides: Specific Metabolites Diazinon CAS No. It is also used for cattle ear tag applications to control flies and ticks and. Fish and aquatic invertebrates show modest degrees of bioconcentration and are very sensitive to toxic effects. Before these restrictions. about 13 million pounds of diazinon were used annually on agricultural sites in the United States. 2004). Diazinon is biologically and chemically degraded in soils with a half-life of about a few weeks. Diazinon is not well-absorbed through the skin. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”). phosphorothioates such as diazinon are metabolically activated to the “oxon” form which has greater toxicity. 333-41-5 General Information The chemical 2-isopropyl-4-methyl-6-hydroxypyrimidine is a metabolite of diazinon.EPA. in the past. diazinon cannot be sold for residential use.S. which may vary for some chemicals by year and by individual sample. and forage crops. aerial. diazinon was widely used in residential and garden application. Inhalational and dermal routes of exposure can be significant for pesticide applicators.

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

Dumas P. Pewnim T. Pesticides in the Nation’s Streams and Ground Water. Alteration of mice L-tryptophan metabolism by the organophosphorous acid triester diazinon. 4/7/09 Lu C.. urinary 2-isopropyl-4-methyl-6hydroxypyrimidine was detected in less than 14% of multiple samples collected during varied diets (Lu et al. Environmental Health Criteria 198. 1992-2001. 2006). Centers for Disease Control and Prevention (CDC). Effects of chronic intake of diazinon on blood and brain monoamines and amino acids. Toepel K.S.Organophosphorus Insecticides: Specific Metabolites 2005). Quantification of selected pesticide metabolites in human urine using isotope dilution high-performance liquid chromatography/ tandem mass spectrometry. 1998. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine.50(5):505-515.37(4):501-507. Irish R.134(1-3):105-113.9(2):117-131. (2003) found that 2-isopropyl4-methyl-6-hydroxypyrimidine was detectable in 96% and 58% of the subjects.pdf. Drug Chem Toxicol 1986. Available at URL: http://www.S. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides.org/documents/ehc/ehc/ehc198. The Quality of Our Nation’s Waters. Baker SE. References Anthony J. Environmental Protection Agency (U. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Liu F. Atlanta (GA). Barr DB. revised February 15. Diazinon. Kruse RL. 2005. Ann Occup Hyg 2006. J Expo Anal Environ Epidemiol 2000.gov/ oppsrrd1/REDs/diazinon_ired. Banister EW. Needham LL. In 54 Canadian greenhouse workers. Semen quality in relation to biomarkers of pesticide exposure. 6/1/09 Fourth National Report on Human Exposure to Environmental Chemicals 145 . Bravo R. Interim reregistration eligibility decision (IRED. Bouchard M. Available at URL: http://www. et al. Environ Health Perspect 2003. Drobnis EZ. Swan SH. 1/14/09 U. Study for Future Families Research Group. Driskell WJ. EPA 738-R-04-006. Nguyen JV.114(2):260-263. International Programme on Chemical Safety-INCHEM (IPCS). 2007 [online].inchem. Jones K. Bull Environ Contam Toxicol 1986. Anal Bioanal Chem 2003. Cocker J. Environ Health Perspect 2006.376(6):808-815. EPA). Garfitt SJ. Noisel N. Effect of sublethal levels of diazinon: histopathology of liver.S. Exposure to the organophosphate diazinon: data from a human volunteer study with oral and dermal doses. Biological monitoring of exposure to organophosphorus insecticides in a group of horticultural greenhouse workers. Biochem Pharmacol 1992. Available at URL: http://pubs. Seifert J. May 2004.111(12):1478-1484. Third National Report on Human Exposure to Environmental Chemicals. Fenske RA. Geological Survey (USGS). Oloffs PC. 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. Mason HJ. Barr DB. In 23 children.epa.10(6 Pt 2):789-798. Banister E. Oloffs PC. Barr DB. Toxicol Lett 2002. urinary 2-isopropyl-4-methyl-6-hydroxypyrimidine levels were below the limit of detection (Bouchard et al. March 2006. Olsson AO.. Rajendra W.usgs. Carrier G. Brunet RC. Sadowski MA.htm. Swan et al. Beeson MD. Barr DB. U. Diazinon. Redmon JB. 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. In a small number of men visiting fertility clinics in Missouri and Minnesota. 2006).gov/circ/2005/1291/.44(11):2243-2250.

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

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

73(1):182-94. et al. Comparison of organophosphorus pesticide metabolite levels in single and multiple daily urine samples collected from preschool children in Washington State.S. Dumoulin MJ. Petitti D. Sharma GD. U.74(2):following table of contents. The Quality of Our Nation’s Waters. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. 2007 [online]. Malathion deposition. Krieger RI. Bouchard M. Available at URL: http://www. Am J Epidemiol 1990. Geological Survey (USGS). Irish R. Toxicol Sci 2003 May. 6/1/09 148 Fourth National Report on Human Exposure to Environmental Chemicals . Environmental Protection Agency (U. Flessel P. Environ Health Perspect 2001.S. In vitro studies on the genotoxicity of the organophosphorus insecticide malathion and its two analogues. Eberly LE. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population. Bradman A. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample. Carrier G. Hertz-Picciotto I. Goldhaber M. J Expo Anal Environ Epidemiol 2005. Pesticides residues in food: 2003 FAO/WHO Meeting on Pesticide Residues. Am J Public Health 1987. Environ Health Perspect 2004. Malathion (addendum). Bravo R. Prasad SB.S. Harris JA. Hammerstrom KA.112(10):1116-1124. Available at URL: http://www. Centers for Disease Control and Prevention (CDC). Grether JK.inchem. revised February 15. Pluth JM. J Expo Anal Environ Epidemiol 1999. Cancer Res 1996. Ryan PB. Genotoxic effects of malathion: an organophosphorus insecticide using three mammalian bioassays in vivo. March 2006. Eskenazi B. Arch Environ Contam Toxicol 2000.gov/circ/2005/1291/.514(1-2):223231. Harley K. Albertini RJ.9(5):494-501.77:1009-1010. htm. Hooper K. Giri S. Lu C. Swan SH. EPA 738-R06-030. Available at URL: http://pubs. Szyfter K. Curl CL. 4/7/09 Kissel JC.org/documents/jmpr/jmpmono/v2003pr06.epa. Nicklas JA. Giri A.109(6):583-590. et al. Genetic toxicity of malathion: a review. Barr DB. Lioy PJ. Barr DB. Freeman NC. Dinoff TM. Weltzien E. Trzeciak A. Lu C. Jewell NP. Blasiak J. Pesticides in the Nation’s Streams and Ground Water. EPA).132(4):794-795.445(2):275-283. International Programme on Chemical Safety-INCHEM (IPCS). Reregistration eligibility decision (RED) Malathion. and cholinesterase status of date dusters and harvesters in California. July 2006.22(1):7-17. Barr DB. Mutat Res 2002. A toxicokinetic model of malathion and its metabolites as a tool to assess human exposure and risk through measurements of urinary biomarkers. 2005.usgs. Environ Mol Mutagen 1993. Jaloszynski P.114(2):260-263. O’Neill JP. Fenske RA. A longitudinal investigation of selected pesticide metabolites in urine. Environ Health Perspect 2006. metabolite clearance. 1992-2001. Third National Report on Human Exposure to Environmental Chemicals. MacIntosh DL. Clayton CA.38(4):546-553.gov/oppsrrd1/REDs/ malathion_red. Reproductive outcome in women exposed to malathion. Quintana PJ.56(10):2393-2399. Brunet RC. Needham LL. Samuel O. Rappaport E.15(2):164-171.pdf. Atlanta (GA). Increased frequency of specific genomic deletions resulting from in vitro malathion exposure. Kizer KW: Exposure to aerial malathion application and the occurrence of congenital anomalies and low birthweight. Neutra R.Organophosphorus Insecticides: Specific Metabolites References Adgate JL. 6/1/09 U. Barr DB. Toepel K. et al. Griffith W. Thomas D. Gosselin NH. Mutat Res 1999. Kedan G. Erratum in: Toxicol Sci 2003 Aug.

32-1.20 (<LOD-2.30-5. ethyl parathion.74) 5. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.40) 2.00 (2.12) < LOD < LOD 1.700 (<LOD-.10-11.92-2.10) 22.92) 5.57) 1.89 (2.33 (1. was once a restricted-use insecticide with limited applications on certain agricultural crops.20-5.298-00-0 Ethyl Parathion CAS No.0) 3.49 (1.50) 2.26 (1.850) < LOD .09-1. and eliminated rapidly from the body after absorption (Kramer et al. interval) Selected percentiles ( 95% confidence interval) Sample 95th 5.01) 4. 56-38-2 General Information Para-nitrophenol is a metabolite of the insecticides methyl parathion. In the 1990s.90-9.45) 5. Methyl parathion is not registered for residential use in the United States.47) 2.20 (2.. < LOD means less than the limit of detection.40-3. peak domestic use was as high as 5-6 million pounds per year.60-36.790 (<LOD-.80 (1.940 (<LOD-2.40-4.22-3. pulmonary. which may vary for some chemicals by year and by individual sample.32-1.30 (1. Many previous registered agricultural uses of methyl parathion have been cancelled (U.50-9.02-6.70-6.30 (2.730 (<LOD-.70 (3.10) 4.60-24.50 (2.0) 3.32-3.33) 2.300-. first registered in 1948. phosphorothioates such as methyl and ethyl parathion are metabolically activated to the “oxon” forms which have greater toxicity than the parent insecticides. 1977).70-6. Once absorbed.69 (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 1.80 (2.85 (2. on cereal grains.10 (3.70-6.18-3.50) 3.28 (1. Methyl parathion has low water solubility.50 (1.0) 3.24) 479 565 680 813 830 1099 99-00 01-02 99-00 01-02 * * * * < LOD .50) 3.10-1.910) < LOD < LOD < LOD 1. 2003).66 (2.80 (2. more slowly absorbed through the skin. fish. In animal studies.50-14.71) 971 1164 1018 1313 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .01-4.37-2.45 (1. Fourth National Report on Human Exposure to Environmental Chemicals 149 .60) 1.70-3.71 (2.0) 2.67 (1.41-4..36-1.770 (. all registered uses were voluntarily cancelled (U.62 (1.70-3. O-ethyl-O-(4-nitrophenyl) phenylphosphonothioate. Ethyl parathion.00) 3.60-19.71 (3.1..13-1.61) < LOD 1. Estimated intakes from diet and drinking water have been below recommended limits.91-3.32 (1.70 (2. 2002.70 (2.58) 3. Metabolism of ethyl or methyl parathion leads to the formation of paranitrophenol.70 (<LOD-3.0) 3.46 (3. and to a lesser extent.15-3.860 (<LOD-1.67) < LOD 1. and aquatic invertebrates.910) < LOD .50 (1.70 (2.02) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .37-4.21 (2. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Urinary para-Nitrophenol Metabolite of Ethyl Parathion.05) 4.0) 3. Methyl parathion use is highly restricted.27) 2.40) 1. 2000).40-4.10 (<LOD-6.910) < LOD < LOD .21-1. and oral routes can occur in pesticide and agricultural workers (Muttray et al.Organophosphorus Insecticides: Specific Metabolites Methyl Parathion CAS No.10 (3.50 (1.60-5.50 (2. population from the National Health and Nutrition Examination Survey. binds tightly to soils resulting in low leachability.S.44) 2.70) 2. Methyl Parathion.40) 4. Ethyl and methyl parathion are infrequently detected in groundwater sampling (USGS.19 (.90-11.61) < LOD 1.990-1. Morgan et al. and has a short half-life in soils and on plants.69) 4.90 (1.70) 2.28-4.01) 695 660 518 679 603 941 Limit of detection (LOD.00 (2.50) 1.80) 2.28 (1.48) 90th 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.30-16.20) 5.40 (1.EPA.0) 4.EPA. 2006).11-4.8 and 0.34 (3.37-4.70) 2. Survey Geometric mean (95% conf.60 (4. Given its limited use.79) 4.72 (3. 2007). and Nitrobenzene Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.11) 2. Both are toxic to birds.16) < LOD 1. with limited applications in agriculture. but by 2003. Increased risk of exposure via dermal.37) 2. It had been applied to cotton. the potential for human exposure to either ethyl or methyl parathion through the diet or drinking water is low. and of the chemical nitrobenzene.0 (3.50 (1.30-3.57-4.S. methyl parathion was rapidly absorbed after ingestion.S.

but lists ethyl parathion as a possible human carcinogen.78 (2. does not inhibit acetylcholinesterase enzymes.20) . Overt cholinergic toxicity and death from methyl and ethyl parathion have been described following suicidal ingestion.970 (.57-2.980 (.60 (1. Zurich et al.25 (2.720 (<LOD-.39 (1.77-7.93 (2.78-2.71 (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 .70) 3..01 (2. 2006. 1990.430 (.80 (1.38-3.00) 2.20 (3. 2006.11-4.92 (2.Organophosphorus Insecticides: Specific Metabolites Metabolites”).55 (<LOD-3.67 (3. 2005.48-4.43) 4. The metabolite.16-4. and producing acute symptoms such as nausea. resulting in excess acetylcholine at nerve terminals.23) 1. Survey Geometric mean (95% conf.840 (.21-21.79) 1.83 (1.15) 3. and other metabolites.08-3.29) 1.79 (1.29) 2.94-47.30) 3.00 (1.720-1.10 (1. ethyl parathion.55) 2.33) 479 565 680 812 830 1099 99-00 01-02 99-00 01-02 * * * * < LOD . 1995).03) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .S.690-1. accidental exposure.33-3. paranitrophenol.14-3. Thus.98-7.500) < LOD < LOD . 1991).60-2. 150 Fourth National Report on Human Exposure to Environmental Chemicals .04 (2. Human health effects from parathion or ethyl parathion at low environmental doses or at biomonitored levels from low environmental exposures are unknown.EPA considers methyl parathion unlikely to be carcinogenic to humans.870) < LOD .97 (2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.26) 17.82) < LOD .7) 3.09) 2..540) < LOD . 2004). and other organophosphorus insecticides share a common mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system.37-1.82 (2.07) 2.88) 1.310-.epa.97-10.78) 2.17-4.44-3.31) < LOD .3) 2.07 (1. Slotkin et al.800-1.91 (1.44-3..11) 1.78-2.80 (1. In large doses. 2003.35-3.97 (<LOD-4.08) < LOD .20) 3.59 (1.2) 2.90 (1. 1978.880 (.05) 4.. Methyl parathion is not considered genotoxic.1) 2. retinal atrophy and sciatic nerve degeneration have also been observed (IPCS.67-2.41-2.35-3.76-14. methyl parathion.html and from U. Parathion and methyl parathion have high acute toxicity in animal testing. gov/toxpro2. EPA at: http://www.56-2.930 (. or generally to have reproductive toxicity at doses below those causing acetylcholinesterase inhibition in most animal studies (IPCS.950) < LOD .71) 1.39) 1. environmental levels) and health effects is available from ATSDR at: http://www.e.57) 6.680 (<LOD-1. paralysis.atsdr.94-4. and seizures. WHO..4 (3. and unintentional acute or chronic high-level occupational exposure (Hill et al.91) 1.06) 971 1164 1018 1312 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .17) .73 (1.440 (<LOD-.88 (1.30-1.850-1.25) 1. Methyl Parathion.95) 1.370 (<LOD-. population from the National Health and Nutrition Examination Survey.400 (<LOD-. 2004). and Nitrobenzene Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U..940 (<LOD-1.790-1.. interval) Selected percentiles ( 95% confidence interval) Sample 95th 4.15-10. In addition to being a metabolite of methyl and ethyl parathion.45) 695 660 518 678 603 941 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. vomiting.S.01 (. Jaga and Dharmani.61) 4. cholinergic effects.29 (2. At high animal doses of methyl parathion.730-1.89 (2. Lores et al.33-6.00 (1.01-3. gov/pesticides/.970 (.04) 1.08 (1.31-3.84) 3.790-.33-3. the detection of para-nitrophenol in a person’s urine may also reflect exposure to the environmental degradate. U.S.13-12.640) < LOD < LOD 1.10) 90th 2.86 (2.96 (1.2) 2. teratogenic. Recent in vitro and in vivo animal studies suggest that parathion may have additional neuronal and glial cell effects at lower doses (Guizzetti et al..60) 2. IARC does not consider ethyl parathion and methyl parathion classifiable as human carcinogens.cdc.21) 1.9) 1.57-7.530) < LOD < LOD < LOD .87 (1. Urinary para-Nitrophenol (creatinine corrected) Metabolite of Ethyl Parathion. Orsorio et al. Additional information about external exposure (i.830-1.930 (. para-nitrophenol can also occur in the environment from the breakdown of the parent these organophosphorus pesticides and from nitrobenzene.89 (2.26 (1.13) 4. Karanth and Pope et al. weakness.72-2. 1995.96 (1.

Barr DB. Lewalter J. Hryhorczuk DO. a range of values several hundred times higher than levels found in the U. Environ Res 1995. Parathion-Methyl (addendum). Comparison of organophosphorus pesticide metabolite levels in single and multiple daily urine samples collected from preschool children in Washington State. Karanth S. 4/7/09 Jaga K.org/documents/jmpr/jmpmono/v95pr14. Head SL. Effect of organophosphorus insecticides and their metabolites on astroglial cell proliferation. Baker S. end-of-shift urinary para-nitrophenol levels ranged from 190 to 410 µg/ gram of creatinine (Leng and Lewalter. Environ Health Perspect 2002. general population (CDC. et al.9:311-320. Weltzien E.. Chicago area methyl parathion response. Guizzetti M. Laboratory investigation of a poisoning epidemic in Sierra Leone. Kramer RE. Rev Environ Health 2006. 2003) and in 482 pregnant females from an agricultural region of California (Eskenazi et al. Pharmacokinetics of methyl parathion: a comparison following single intravenous. J Biomed Sci 2002. oral or dermal administration. Cline RE. Clark JM.5 mg (500 µg)/g creatinine for workers at the end of shift. Methyl parathion: an organophosphate insecticide not quite forgotten.inchem.25(5):599-606.. Harley K. Wellman SE. Kedan G.110 Suppl 6:1085-1091. 2005. Moseman RF.15(2):164-171. Hill RH Jr. Turner WE. Griffith W. J Anal Toxicol 1990.Organophosphorus Insecticides: Specific Metabolites Biomonitoring Information Urinary levels of para-nitrophenol reflect recent exposure. Rockhold RW. Lores EM. Arch Environ Health 1978. Pesticide workers may have much higher levels following pesticide applications. 2002).33(5):270-276. Alley CC. Shealy DB. Baker RC. Centers for Disease Control and Prevention (CDC). population (Olsson et al. Lin LI. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.. 2005. Environ Health Perspect 2004. Giordano G.71:99108. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population. Needham LL.S.112(10):1116-1124. Curl CL. 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. Finding a measurable amount of para-nitrophenol in urine does not mean that the level will result in an adverse health effect. McCann et al. Neurotoxicol Teratol 2003. DiPietro E. Bailey SL. J Expo Anal Environ Epidemiol 2005. CDC. Baker SE. Urinary excretion of paranitrophenol and alkyl phosphates following ingestion of methyl or ethyl parathion by human subjects. et al. Pope C.htm. Jewell NP. ACGIH recommends a BEI of 0. 1995. McClure PC. Hill RH Jr. Atlanta (GA). Available at URL: http:// www. Barr DB. International Programme on Chemical Safety-INCHEM (IPCS). Leng G.. 2004). 2002. 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. Fourth National Report on Human Exposure to Environmental Chemicals 151 . Moomey CM. Dharmani C. Bradman A. Hetzler HL. 1995). 2005. 1999). Third National Report on Human Exposure to Environmental Chemicals. Measurement of p-nitrophenol in the urine of residents whose homes were contaminated with methyl parathion. References Barr DB. et al. Pathak S. and many residents were symptomatic (Barr et al.S. Environ Health Perspect 2002. In a study of workers who handle parathion. Morgan DP. Pesticide residues in urine of adults living in the United States: reference range concentrations...14(4):213-216. et al. Toxicology 2005.21(1):5767. Kissel JC. Occup Environ Med 1999. 2005).56(7):449553. Arch Environ Contam Toxicol 1977. Role of individual susceptibility in risk assessment of pesticides.6(2-3):159-173.215(3):182-190. Head SL. Slach EF.. 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. Bradway DE. McCann KG. et al. Eskenazi B. Gregg M. Runkle KD. Barr JR.110 Suppl 6:1075-1078. Organophosphorus pesticide poisonings in humans: determination of residues and metabolites in tissues and urine. Lu C. Hill et al. 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. Rubin et al. Barr DB. 2005). Costa LG. and levels were similar or slightly lower that those in a small convenience sample of the U. Ashley DL. 2002. Age-related effects of chlorpyrifos and parathion on acetylcholine synthesis in rat striatum.

Esteban E. Environmental Protection Agency (U. Pesticides in the Nation’s Streams and Ground Water.pdf.epa. pdf. Toxicol Lett 2006.D. Rosenberg J. Ethyl parathion.S. Barr DB. Yacovac R. Hill G.epa. Olsson AO. Monnet-Tschudi F. Available at URL: http://www. Investigation of a fatality among parathion applicators in California. Schilter B.pdf. 2007 [online]. Levin ED. Available at URL: http://pubs. R. EPA). Available at URL: http://www. 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. Dunlop B. May 2003. Case No.201(2):97-104. Slotkin TA.20(4):533-546. 1995-1996. Sadowski MA. Backer G. Rubin C. Tate CA. EPA-738-FOO-009. 0153.E. Assessment of human exposure and human health effects after indoor application of methyl parathion in Lorain County. External and internal exposure of wine growers spraying methyl parathion.114(10):1542-1546. Nguyen JV.usgs. Hill RH Jr. Ohio. et al. EPA). Interim reregistration eligibility decision (IRED) for Methyl Parathion.376(6):808-815. Ryde IT. The Quality of Our Nation’s Waters.Organophosphorus Insecticides: Specific Metabolites Muttray A.who.gov/oppsrrd1/REDs/factsheets/0155fct. September 2000. Involvement of glial cells in the neurotoxicity of parathion and chlorpyrifos. Available at URL: http://www. March 2006. 1/12/07 U.110 Suppl 6:1047-1051. Environ Health Perspect 2006. Osorio AM. Toxicol Appl Pharmacol 2004. Facts.162(2-3):219-224. U. Ames RG.04/106. Mengle DC. Methyl parathion in drinking water. Environmental Protection Agency (U. revised February 15. Seidler FJ. Geological Survey (USGS). Costa LG. 5/19/09 Zurich MG.S. Kieszak S.S. 152 Fourth National Report on Human Exposure to Environmental Chemicals . Letzel S.S.S. Environ Health Perspect 2002.gov/circ/2005/1291/. Honegger P. WHO/SDE/WSH/03. 2004. 1/14/09 U. 6/1/09 World Health Organization (WHO). Anal Bioanal Chem 2003. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine. Am J Ind Med 1991.int/water_sanitation_health/dwq/chemicals/ methylparathion. 1992-2001. Jung D.

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

700-. interval) Selected percentiles ( 95% confidence interval) Sample 95th .210-. Survey Geometric mean (95% conf.820) < LOD < LOD .08) 1165 1316 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .740 (. 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. population from the National Health and Nutrition Examination Survey.21) < LOD .760 (<LOD-.680 (<LOD-.670 (<LOD-1. interval) Selected percentiles ( 95% confidence interval) Sample 95th .17 (.460) 1165 1316 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .07) . which may vary for some chemicals by year and by individual sample.930) size 2481 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD .850 (.200-.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 .740-1.64) .210-1.780 (.300-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.500 (.840 (.31) .94) .880) 567 810 1104 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD .55) .670) 567 810 1104 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD .Organophosphorus Insecticides: Specific Metabolites Urinary 2-(Diethylamino)-6-methylpyrimidin-4-ol/one Metabolite of Pirimiphos-methyl Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.580-1.430 (<LOD-.410 (<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.840) 669 687 929 Limit of detection (LOD.780 (<LOD-1.700-1.470 (.950) < LOD < LOD 1.00) 669 687 929 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.27) . 154 Fourth National Report on Human Exposure to Environmental Chemicals . Survey Geometric mean (95% conf.S.250 (<LOD-.2. see Data Analysis section) for Survey year 01-02 is 0.S. < LOD means less than the limit of detection.780 (.780 (<LOD-1.610 (<LOD-1.15) < LOD .210 (<LOD-.

fda.epa. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine. Pesticides residues in food: 1992 evaluations Part II Toxicology. 1/14/09 Fourth National Report on Human Exposure to Environmental Chemicals 155 . Available at URL: http://www.htm. U.inchem. Food and Drug Administration (FDA). 2535. EPA). Total Diet Study: Summary of Residues Found Ordered by Pesticide. Sadowski MA. Available at URL: http://www. 850. 4/7/09 International Programme on Chemical Safety-INCHEM (IPCS). Pirimiphos-methyl. cfsan. July 2006. gov/oppsrrd1/REDs/pirimiphos-methyl_ired.S. Environmental Protection Agency (U. Finalization of interim registration eligibility decision for pirimiphos-methyl. Case No.pdf. 2005. 4/7/09 Olsson AO.Organophosphorus Insecticides: Specific Metabolites References Centers for Disease Control and Prevention (CDC). June 2003.376(6):808-815. Nguyen JV.S. Third National Report on Human Exposure to Environmental Chemicals.gov/~acrobat/tds1byps.pdf. Anal Bioanal Chem 2003. org/documents/jmpr/jmpmono/v92pr16. Available at URL: http://www. Market Baskets 91-3-01-4. Atlanta (GA). Barr DB.

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

choreoathetosis. Garey J. Kuhn K. Agrawal AK.. Go et al. 2006). Idel H. et al. Ose K.gov/toxprofiles/ tp155. Int J Hyg Environ Health 2002. the pyrethroids are not considered genotoxic in in vitro testing or carcinogenic in animal testing (WHO. Wolff MS. on immature and adult mice: changes in behavioral and muscarinic receptor variables.gov/pesticides/ and from ATSDR at: http://www. Garey J. Hu JY. [Effects of fenvalerate on reproductive and endocrine systems of male rats] Zhonghua Nan Ke Xue 2002. Fredriksson A. 2005). Lewalter J. salivation. fenvalerate. Additional information about pesticides is available from U. Zhao RC. Lack of (anti-) androgenic or estrogenic effects of three pyrethroids (esfenvalerate.62:101-108. Ray et al. Miller GW. cdc. Assessing estrogenic activity of pyrethroid insecticides using in vitro combination assays.300(3):161-165. Yang J. Toxicol Appl Pharmacol 2006. Idel H. Kim IY.211(3):188-197. Garey and Wolff. Lee SJ.. Go V.35(2 Pt 1):227-237. 2005). Estrogenic and antiprogestagenic activities of pyrethroid insecticides. Leng G. In developing rodents. Eriksson and Fredriksson. Kuhn KH. 2005). Shukla Y. et al. Kamita Y. hypersensitivity. 1999. cyfluthrin was the most frequent pyrethroid associated with symptomatic effects (irritant respiratory and dermal effects.23(6):665-673.205(6):459-472. Elwan et al. References Agency for Toxic Substances and Disease Registry (ATSDR). Human cases of systemic poisoning are rare and usually result from accidental exposure or intentional ingestion of pyrethroid insecticides. Indoor pyrethroid exposure in homes with woollen textile floor coverings.27(12):1273-1283. IARC considers deltamethrin and permethrin as not classifiable as to their human carcinogenicity. McCarthy AR. neurochemical changes in cholinergic.1/15/09 Aziz MH. Levsen K. Kim TS. Kunimatsu et al. tremor..atsdr.. Ranft U. Neurotoxic effects of two different pyrethroids. 2002. Adhami VM. Kang IH. Seth PK. motor activity. Wang SL. Neurotoxicol Teratol 2001.. Shin JH. Available from URL: http://www. 2003. 2001. Behavioral and endocrine changes induced by perinatal fenvalerate exposure in female rats. Leng G. paresthesias) reported in agricultural workers from 1996 to 2002 (Spencer and O’Malley. Shaw IC. J Reprod Dev 2004. Bull Environ Contam Toxicol 1999. et al. Bernardi MM. Generally. Thomson BM. and seizures (ATSDR. Lazarini CA. 2006. Chen JH. 2003. 2006.27(4):609-614. Berger-Preiss E.. Kim HS. bioallethrin and deltamethrin. J Environ Monit 2006. Transient dermal paresthesias have been reported among pesticide applicators after direct contact with certain types of pyrethroid pesticides. 2004. Signs and symptoms of acute pyrethroid poisoning after massive ingestions include agitation.251(3):855-859. Hu et al. 2002). Eriksson P. Varoli FM. Sunami O. Moniz AC..atsdr. Florio JC. 2001. Fourth National Report on Human Exposure to Environmental Chemicals 157 . Wolff MS.. Soderlund et al. McCarthy et al. and catecholaminergic pathways and behavioral changes have been demonstrated at subacute and subchronic doses for some pyrethroid pesticides (Aziz et al. Elwan MA.cdc. Estrogenic potential of certain pyrethroid compounds in the MCF-7 human breast carcinoma cell line.gov/toxpro2.. September 2003. Regul Toxicol Pharmacol 2002. though a few pyrethroid pesticides and some metabolites have shown weak or inconsistent estrogenic effects on standardized assays (ATSDR. 2005). Pyrethroid pesticide-induced alterations in dopamine transporter function.8(1):18-21. 2000. Caudle WM.8(1):197-202.50(2):245-255. Kunimatsu T. et al. Kim et al.. dopaminergic. Yamada T. Toxicological profile for pyrethrins and pyrethroids. Wieseler B. The pyrethroids in general use are not considered teratogenic or to have significant reproductive toxicity (ATSDR.107(3):173-177. Human doseexcretion studies with the pyrethroid insecticide cyfluthrin: urinary metabolite profile following inhalation. Salzgeber SA. Song L. and permethrin) in the Hershberger and uterotrophic assays. Richardson JR. Guillot TS. Abell AD.S. Environ Health Perspect 1999. Leng G. Leng A. Spinosa HS. Effects of prenatal exposure to deltamethrin on forced swimming behavior. Estrogenicity of pyrethroid insecticide metabolites. In California. Lemonica IP. 2003. Neurodevelopmental consequences of gestational exposure (GD14-GD20) to low dose deltamethrin in rats.. Bernardi MM. Neurosci Lett 2001.108(1):78-85. EPA at: http://www. 2003.html.html. WHO.. Okuno Y. Toxicokinetics of pyrethroids in humans: consequences for biological monitoring.. Pauluhn J. Biochem Biophys Res Commun 1998. Xenobiotica 1997. Toxicol Appl Pharmacol 1991. 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. Lazarini et al. Cruz-Casallas PE. Sugiri D. Neurotoxicol Teratol 2005. Shafer. epa. Pogo BG. 1998. 2002).Pyrethroid Pesticides and other ion channels may also explain some pyrethroid effects. 1991. and striatal dopamine levels in male and female rats. Moniz et al. Concomitant exposure to organophosphorus insecticides may increase pyrethroid toxicity by slowing metabolic clearance of the pyrethroid.

gov/ circ/2005/1291/. U. Piccirillo VJ. Reregistration Eligibility Decision for Cypermethrin. Environmental Protection Agency (U. 2007.186:57-72. Revised February 25. June 2006a. Shafer TJ. 5/26/09 Woollen BH. Pyrethroid insecticides: poisoning syndromes. 5/26/09 158 Fourth National Report on Human Exposure to Environmental Chemicals .epa.usgs. Environmental Protection Agency (U. Geological Survey (USGS). sumithrin synthetic pyrethroids for mosquito control.htm.S. resmethrin.pdf. Soderlund DM.int/hq/2005/WHO_ CDS_WHOPES_GCDPP_2005. Xenobiotica 1992. Forshaw PJ. Toxicology 2002.who.38:95-101. EPA). Available at URL: http://www.S.S. March 2006. 19962002. June 2006b.22(8):983-991. Pesticides in the Nation’s Streams and Ground Water. 5/26/09 U. EPA).epa. synergies. 5/26/09 U. Environ Health Perspect 2005. et al. Developmental neurotoxicity of pyrethroid insecticides: critical review and future research needs. Permethrin Facts (Reregistration Eligibility Decision Fact Sheet).113(2):123-136.10.S. and therapy. Mechanisms of pyrethroid neurotoxicity: implications for cumulative risk assessment. EPA). Environmental Protection Agency (U.S. Mullin LS. Sargent D. Sheets LP.gov/pesticides/ health/mosquitoes/pyrethroids4mosquitoes. J Toxicol Clin Toxicol 2000.171:3-59. Spencer J. Pyrethroid illnesses in California. pdf. Safety of pyrethroids for public health use. World Health Organization (WHO). 2005. 1992–2001.S. Available at URL: http://pubs. O’Malley M. 5/26/09 U. Rev Environ Contam Toxicol 2006. Available at URL: http://www. Available at URL: http://whqlibdoc. Laird WJ.Pyrethroid Pesticides Ray DE. Marsh JR. Available at URL: http://www. April 2002. Meyer DA. Pesticide and Evaluation Scheme. Permethrin.gov/oppsrrd1/REDs/ factsheets/permethrin_fs.epa.S. Clark JM.htm. Lesser JE.gov/oppsrrd1/REDs/cypermethrin_red. Crofton KM. The metabolism of cypermethrin in man: differences in urinary metabolite profiles following oral and dermal administration.

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

* Not calculated: proportion of results below limit of detection was too high to provide a valid result.2.2 and 0. < LOD means less than the limit of detection. 160 Fourth National Report on Human Exposure to Environmental Chemicals . Survey Geometric mean (95% conf.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. which may vary for some chemicals by year and by individual sample. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. 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. population from the National Health and Nutrition Examination Survey.

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

Int J Hyg Environ Health 2006. Int Arch Occup Environ Health 2004. Hoppe HW. Pyrethroid illnesses in California. Spencer J. Atlanta (GA). Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides.206(2):85-92. et al. Seiwert M.209(3):221-233. Heudorf U. Angerer J. Ranft U. Heudorf U. Arch Environ Contam Toxicol 2004. Schulz C.209(3):293-299. J Expo Anal Environ Epidemiol 2003. Kolossa-Gehring M. Sugiri D. 19962002. Int J Hyg Environ Health 2006. 162 Fourth National Report on Human Exposure to Environmental Chemicals . Isotope dilution highperformance liquid chromatography-tandem mass spectrometry method for quantifying urinary metabolites of synthetic pyrethroid insecticides. Hadnagy W. Butte W. Angerer J. 2005. Berger-Preiss E. Rev Environ Contam Toxicol 2006.13(2):112-119.186:57-72. Becker K. Bernard CE. Krieger RI.77(1):67-72.46(3):281-288. Olsson AO. Ball M. Environ Health Perspect 2001. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine. Heudorf U. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. O’Malley M. Leng G. Drexler H. Idel H. Williams RL.Pyrethroid Pesticides References Baker SE. Third National Report on Human Exposure to Environmental Chemicals. Angerer J. Barr DB. Int J Hyg Environ Health 2003. Angerer J. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Centers for Disease Control and Prevention (CDC).109(3):213-217. Human exposure to indoor residential cyfluthrin residues during a structured activity program.

transcypermethrin and trans-cyfluthrin.340) . and trans-cyfluthrin.43) .300-.220-.2dimethylcyclopropane carboxylic acid in urine not only reflects the metabolic transformation of any of the three pesticides. the presence of trans-3-(2.110-.1 and 0.640 (. and ciscyfluthrin.460-. Biomonitoring Information Urinary levels of cis.900 (.730 (.670-1.and trans-isomers.or trans-3-(2.280 (.250-.580-1.68359-37-5 Cypermethrin Permethrin CAS No.490-1..910-5.24) 1.710) . cis-permethrin.410) .155-.202 (.2-dimethylcyclopropane carboxylic acid is a metabolite formed from cis-permethrin.54) . trans-permethrin.740 (.28) 671 680 518 701 591 957 Limit of detection (LOD.28) 468 580 667 831 816 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD . Generally.21) .270 (. Similarly.440 (.2-dimethylcyclopropane carboxylic acid is a metabolite formed from trans-permethrin. trans-cypermethrin.460-1.280-.630) .52645-53-1 General Information Several pyrethroid pesticides are formulated as a mixture of cis.180 (.370-. In the body.200 (.710-1.580) 1.10) 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 .630 (.630) .890 (.08) 947 1193 1004 1346 99-00 01-02 99-00 01-02 99-00 01-02 * * .120-.1.460 (.600 (.370 (.420-.310) .200) .550) .220-.2-dichlorovinyl)- CAS No.80) .690) .210) 90th .380-.960 (. Kuhn et al. < 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.270 (.730 (.740) 1.180) .350) .220-.200-.470 (. which may vary for some chemicals by year and by individual sample. 1999).44 (.270-.610) .230) .610) .170 (.68) .08) .120-.47 (.50) .2-dimethylcyclopropane carboxylic acid in urine not only reflects the metabolic transformation of any of the three pesticides.2-dichlorovinyl)2. 1999). interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.2-dichlorovinyl)-2.07 (.160 (<LOD-.570-.200-.. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.880 (.920) 1.670-2.2-dichlorovinyl)-2.650-1. Kuhn et al. 1985.12 (.35) 1. cis-3-(2.410) .380 (. cis-cypermethrin.790) .262) * * * < LOD < LOD .530 (.260 (.68) .250 (.110-.500 (.110 (<LOD-. The cis-isomer of permethrin has more potent insecticidal activity than transpermethrin.510 (.500 (.2-Dichlorovinyl)-2.510 (.300 (.770) .220) .220-.150 (.300 (.68 (.32) .15) . 52315-07-8 CAS No. The chemical trans-3(2.740-1.2-dichlorovinyl)-2.380-.200) .850 (.160 (.Pyrethroid Pesticides Cyfluthrin the cis-metabolite is found in the urine.200-.680 (.13 (.330 (.2-dimethylcyclopropane carboxylic acid formed in the environment from the degradation of these pesticides (George.600) .77 (.S.510 (.790-1.630-.520) . more of the trans-metabolite than Urinary cis-3-(2.340) .670 (.680) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .340-.400-.730 (.870) 1.200) < LOD < LOD < LOD .11) .120-.160 (.330) .770-1. Survey Geometric mean (95% conf.380) .300-.140 (<LOD-.470-1.600-1.740-2.210) .670-1.430-.490-1. Cyfluthrin.110-. population from the National Health and Nutrition Examination Survey. The presence of cis-3-(2.240) .240) . but can also reflect exposure to trans-3(2.140 (.700) .2dichlorovinyl)-2. ciscypermethrin and cis-cyfluthrin.820 (.890 (.380-.53) .490-.950-2. but it can also reflect exposure to cis-3-(2.120-. 1985.2-dimethylcyclopropane carboxylic acid that is formed in the environment from the degradation of these pesticides (George.270 (.2dichlorovinyl)-2.790-1.2-dimethylcyclopropane carboxylic acid Metabolite of cis-Permethrin.680-3.790 (.210-.570 (.490-.780) . Fourth National Report on Human Exposure to Environmental Chemicals 163 .35) . and cis-Cypermethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.

540) .380 (. 2004). 2006) and 1177 urban adults and children (Heudorf et al.680 (.510-1.420 (.410) .37) . urinary trans-3-(2.390-.31) .220 (.170 (. 2005).440 (.190) . Lu et al.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 .390 (.380) ... 2001.470-1.540 (.2-dimethylcyclopropane carboxylic acid reflect recent exposure to either their parent pyrethroid pesticides or their environmental degradates.67 (.12-2.S.450 (.640-1.59 (1. 164 Fourth National Report on Human Exposure to Environmental Chemicals .2-Dichlorovinyl)-2.260 (. 2003). Survey Geometric mean (95% conf.550-1.2-dichlorovinyl)-2.180 (.430 (.680-1.Pyrethroid Pesticides 2.550 (.580) .2dichlorovinyl)-2..190 (.33) .550-1.400-1.2dimethylcyclopropane carboxylic acids at the 95th percentile that were similar or slightly less than the 95th percentiles in the U.200-.200) .580-1.2-dichlorovinyl)-2.560) . the median and 95th percentile of urinary levels of cis-3-(2.340) .890) .300) .67) .890 (.250) .11) 1.230-.250) 90th .750 (.190) . Urinary levels of the two chemicals in adults were similar to those in children in these studies (Heudorf et al.and trans-3-(2.150-. 2006). Cyfluthrin.700) .and trans-3(2..150-.270-.11) .59) .640 (.540 (.500 (.710-3.450-1.430-1.080-. 2002)..320-. urinary levels of cis-3-(2.550) .590) .810 (.2-dimethylcyclopropane carboxylic acid did not increase.640) 1.370-.104-.11) 947 1193 1004 1345 99-00 01-02 99-00 01-02 99-00 01-02 * * .260-. 2003).710 (.2dichlorovinyl)-2.360-1.380-.138 (.800 (..560) 1. Estimated daily pyrethroid intakes based on urinary levels in the German children were below the acceptable daily tolerances (Heudorf et al.550) .230 (.180-.530 (. 2005). 2004. 2006.230-.2-dichlorovinyl)-2.200-. 2006. though the 95th percentile levels increased several fold after exposure to nearby pest control operations (Leng et al.270 (.350 (.11) . In a study of urban residents in Germany (Berger-Preiss et al. In these volunteers.320) .210-.2-dimethylcyclopropane carboxylic acid levels at the 95th percentile were about one-third of the 95th percentile in the NHANES 20012002 subsample (CDC.900 (.140-. the levels at 24-72 hours were slightly less than the 95th percentile in the NHANES 2001-2002 subsample (CDC.840 (..880) .160 (<LOD-.08) 468 580 667 830 816 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .290) .2-dimethylcyclopropane carboxylic acids in children were related to residential pesticide use and house dust levels (Becker et al.340-. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1. In the same residents.690-1.250-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.182) * * * < LOD < LOD ..840 (.14) 671 680 518 700 591 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.640-.590 (.370-.350) .290 (. median urinary levels of trans-3-(2.570) ..59) . 2005). Studies in Germany of 396 children and adolescents (Becker et al.270) .2-dimethylcyclopropane carboxylic acid did not increase at 24-72 hours after exposure to nearby pest control operations (Leng et al.250-.12 (.150-.300) . 2001) showed urinary levels of cis.400 (.290) .440-.260 (.170) < LOD < LOD < LOD .340) .220) .170 (.280 (.33 (.120 (.250 (<LOD-. In a study of volunteers.2dimethylcyclopropane carboxylic acid at the 95th percentile were about half the 95th percentile in the NHANES 20012002 subsample (CDC.780) 1.700) .920 (.250) . population from the National Health and Nutrition Examination Survey. the levels at 24-72 hours were slightly less than the 95th percentile in the NHANES 2001-2002 subsample (CDC.240 (<LOD-.130-.530 (. 2006).260 (.520) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .300-.430-.. and cis-Cypermethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.680-1.. These studies indicated that intake is mainly from the diet and that dermal absorption contributes little to intake (Heudorf et al. 2005) In a small group of indoor pest-control operators.300 (.390-.780 (.24) .250-.220 (. post- Urinary cis-3-(2.300 (. Schettgen et al.200 (.600 (.830) .80) .260) .640-1.21) .750-1. 2005).230-.290-.440 (.2-dichlorovinyl)-2. Other studies have provided evidence that urinary levels of cis.49) . 2002).S.450-.11 (.2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of cis-Permethrin.440-.03) 1.700-2.280-.29 (.370-. representative NHANES 2001-2002 subsample (CDC.270) .

4.63) 1.500-.19 (3.920-1.39 (1.810-1.59 (1.58) 961 1184 1015 1341 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .01 (1.520) .55-3.4 and 0.11-2.470 (<LOD-. interval) Selected percentiles ( 95% confidence interval) Sample 95th 3.2-dimethylcyclopropane carboxylic acid in urine does not mean that the level causes an adverse health effect.20 (.14-2.55-5.76-3.13) .87 (1.700) .820) .14-6.19 (2.28 (2.03-1.2-dimethylcyclopropane carboxylic acid (Hardt and Angerer.77) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .520-. Biomonitoring studies on urinary levels of cisor trans-3-(2.49-5.41-14.85) 4.910-1.43) 2.49-3.700-1.550 (.97-11.77 (1.39-5.60) 1.710 (.56) 2.01) 4. Finding a measurable amount of cis.60-4.970 (. The maximum post-application urinary levels. population from the National Health and Nutrition Examination Survey.2-dimethylcyclopropane carboxylic acid Metabolite of Cyfluthrin.55-4. and trans-Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.54) 4.62 (1.420 (<LOD-.Pyrethroid Pesticides application median urinary levels of summed cis.840-1.480-.91 (1.760) .500) .11-1.2-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.860) .63) 1. < LOD means less than the limit of detection.2-dichlorovinyl)-2.66) 691 680 518 690 595 954 Limit of detection (LOD.54 (1.750) .490-1.68-2.or trans-3-(2. trans-Cypermethrin.56) 2.40 (1.19) 1.7) 2.41 (1.08-6.77) 1.17 (.56 (1.780 (.60) .940 (.850-1.670) .94 (1.2-dichlorovinyl)-2.20 (.09 (.69 (1.17 (.620) < LOD 2.68) 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 .17-1.490 (<LOD-.and trans-3-(2.670) .610) 1.69) 1.08) 1.410-.560 (. 2005).530) .680-1.470 (.35) 1.580 (.42) 1.410 (<LOD-.48) 4.20 (.50 (1.660) 1.68) 1.800-1.560 (.81) 2.23 (. Survey Geometric mean (95% conf.68) 2.570) 90th 1.68-3.56 (1.410-. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.27 (1.77) 2.07-3.14) 1.400 (<LOD-.830-1.2dichlorovinyl)-2.23) 2. were up to 27 times higher than the 95th percentile for adults in the NHANES 2001-2002 subsample (CDC.22 (1.500 (. Fourth National Report on Human Exposure to Environmental Chemicals 165 .410 (<LOD-.2-Dichlorovinyl)-2.S.440 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.03-1. 2003) were similar to the 95th percentiles for adults in the NHANES 2001-2002 subsample (CDC.66) 478 576 675 826 823 1123 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .12-6.5) 2.560 (.64-4. which may vary for some chemicals by year and by individual sample. 2005).42 (2.84 (1.90) 1. however.26 (.460-.37 (1.08-4.07 (1.460-.10) 2.76-4.16) 1. Urinary trans-3-(2.28 (1.89 (2.49-3.400-.95) 2.66) .95) 3.25-3.730) .25 (1.910-1.

* Not calculated: proportion of results below limit of detection was too high to provide a valid result.780 (<LOD-.19 (1.48 (1.33 (1.610-.87) 1.2-Dichlorovinyl)-2.530 (<LOD-.16 (1.47-2.07-2.740) . Survey Geometric mean (95% conf.56 (1.570-.780) 90th 1.11) 478 576 675 825 823 1123 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .700 (.11) .800-1.700 (.480-.20 (1.580 (.42) 1.730) .27-2.15) 2.91 (1.42 (.750) .S.880 (<LOD-1.60) 2.07-3.08 (.91) 1.15-3.970 (.850) 1.570 (<LOD-.00-5.900 (<LOD-1. 166 Fourth National Report on Human Exposure to Environmental Chemicals .33-1.64 (1.13) 1.07-1.470-.45-2. and trans-Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.3) 2.31 (.720 (<LOD-.580) .86 (2.02-1.22) 1.47 (1.39) 1.44) 2.36 (1.48-2.91-11.60) 2.470 (.34-3. trans-Cypermethrin.22-1.11) 691 680 518 689 595 954 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.74) .770) < LOD 2.440-.540) .410-.00) 5.15 (1.74) 2.65) 1.30-3.87-8.31) 1.47-2.520 (<LOD-.35) 1.20-2.55 (2.40-2.12-1.15-3.55 (2.780) .2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of Cyfluthrin.720-1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.26 (1.00 (1.07) 2.15) 3.57 (1.800-1.560 (.88) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 1.55 (2.530 (.33-2.12 (.Pyrethroid Pesticides Urinary trans-3-(2.30-6.930-1.36) 2.35 (1.29) 1.70 (.660) . population from the National Health and Nutrition Examination Survey.00) 1.19) .640) .56-2.34-4.75 (1.00) 1.39 (1.880-1.08 (.87-3.07) 2.670) .61) 1.13) .22-2.500-.89) 2.27-2.37 (1.60 (1.19) 961 1184 1015 1340 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .98 (1.28) 2.45 (1.700-.81 (2.760 (.87 (1.41) 1.57) 3.10) size 1976 2524 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD 75th .31 (2.880 (.56-5.68) 3.850) .820-2.67 (2.850-3.570 (.720-1.65 (2.15-3.87) 1.80) 1.

Permethrin and its two metabolite residues in seven agricultural crops. Int Arch Occup Environ Health 2003. Pyrethroid exposure of the general population-is this due to diet? Toxicol Lett 2002.62:101-108. Angerer J. Berger-Preiss E. Fourth National Report on Human Exposure to Environmental Chemicals 167 . Schulz C. Berger-Preiss E. Leng G. Heudorf U. Ball M. Biological monitoring of workers after the application of insecticidal pyrethroids.206(2):85-92.Pyrethroid Pesticides References Becker K. Int J Hyg Environ Health 2003. Hardt J. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Environ Health Perspect 2001. Toxicokinetics of pyrethroids in humans: consequences for biological monitoring. Heudorf U. Bartell S. Ranft U.77(1):67-72.209(3):221-233. Barr DB.205(6):459-472. Third National Report on Human Exposure to Environmental Chemicals.209(3):293-299.134(1-3):141-145. Drexler H. Centers for Disease Control and Prevention (CDC). Sugiri D. Idel H. Kolossa-Gehring M. Levsen K. Heudorf U. Angerer J. Hoppe HW. Drexler H. Atlanta (GA). George DA. Environ Health Perspect 2006. Bull Environ Contam Toxicol 1999. Leng G.76(7):492-498. Angerer J.109(3):213-217. Leng G. Sugiri D. Lu C. Idel H. Pearson M. Angerer J.114(9):14191423. Int Arch Occup Environ Health 2004.68(6):1160-1163. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides. Seiwert M. Wieseler B. Hadnagy W. Angerer J. 2005. et al. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine. Heudorf U. Angerer J. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. A longitudinal approach to assessing urban and suburban children’s exposure to pyrethroid pesticides. Int J Hyg Environ Health 2002. Ranft U. J AOAC 1985. Kuhn K. Butte W. Bravo R. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. Int J Hyg Environ Health 2006. Indoor pyrethroid exposure in homes with woollen textile floor coverings. Idel H. Int J Hyg Environ Health 2006. Schettgen T.

Baker et al.2-dimethylcyclopropane carboxylic acid in the urine may reflect exposure to deltamethrin or to cis-3-(2..2-dimethylcyclopropane carboxylic acid at the 95th percentile ranged slightly higher (0.2dimethylcyclopropane carboxylic acid formed in the environment... 2005).S. in detection of cis-3-(2.2-dibromovinyl)-2. (2004) reported a geometric mean concentration of cis-3(2. Urinary levels for adults and children in these studies were similar (Heudorf et al. mean peak urinary levels of cis-3-(2.2-dibromovinyl)-2.2-dimethylcyclopropane carboxylic acid of 0.5 μg/L) than the detection limit (0. 2005). Biomonitoring Information Urinary levels of cis-3-(2.2-dibromovinyl)-2.2-dibromovinyl)-2. urinary levels of cis-3-(2. 168 Fourth National Report on Human Exposure to Environmental Chemicals . 1990). Outside the U. 2001) showed that urinary levels of cis-3-(2. 2006) and 1177 urban adults and children (Heudorf et al. Following residential spraying with deltamethrin for malaria protection in Mexico...3-0. 2004). Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.2-dimethylcyclopropane carboxylic acid were below the limit of detection (CDC.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. In the NHANES 2001-2002 subsample. 2006) and estimated daily intakes based on urinary levels in children were considered to be below acceptable daily intakes (Heudorf et al. Deltamethrin can degrade to cis-3(2.1 μg/L) for the NHANES 2001-2002 subsample (CDC.. 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. In an analysis of 217 urine specimens from a nonrandom sample of United States residents. 2005).39 µg/L. Finding a measurable amount of cis-3-(2.2-dibromovinyl)-2. Studies in Germany of 396 children and adolescents (Becker et al.2-dibromovinyl)2.2-dimethylcyclopropane carboxylic acid is a metabolite of the pyrethroid insecticide deltamethrin.2-dimethylcyclopropane carboxylic acid in urine does not mean that the level will result in an adverse health effect.2dimethylcyclopropane carboxylic acid reflect recent exposure to deltamethrin or its environmental degradate. 52918-63-5 General Information Cis-3-(2. Biomonitoring studies provide physicians and public health officials with reference values so that they can determine whether other people have been exposed to higher levels of deltamethrin than levels found in the general population.2-dibromovinyl)-2. 2001.2-dimethylcyclopropane carboxylic acid in the environment (IPCS. deltamethrin has been used against mosquitoes that carry malaria.Pyrethroid Pesticides Deltamethrin CAS No.2-dibromovinyl)-2.2-dibromovinyl)-2. in some situations replacing the use of DDT. Thus.

* Not calculated: proportion of results below limit of detection was too high to provide a valid result.1. population from the National Health and Nutrition Examination Survey.S. < LOD means less than the limit of detection. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. Survey Geometric mean (95% conf.2-dimethylcyclopropane carboxylic acid Metabolite of Deltamethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.Pyrethroid Pesticides Urinary cis-3-(2.2-Dibromovinyl)-2. Fourth National Report on Human Exposure to Environmental Chemicals 169 .1 and 0. 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. which may vary for some chemicals by year and by individual sample.

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

2005.org/documents/ehc/ehc/ ehc97. Environmental health assessment of deltamethrin in a malarious area of Mexico: environmental persistence. Angerer J. Grimaldo M.inchem. Schulz C. Angerer J. Atlanta (GA). Int Arch Occup Environ Health 2004.109(3):213-217. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides.Pyrethroid Pesticides References Becker K. [online] 1990. Fourth National Report on Human Exposure to Environmental Chemicals 171 . Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine. Butte W. Int J Hyg Environ Health 2006. Available at URL: http://www.209(3):293-299. Batres LE. Heudorf U. Environ Health Perspect 2005. et al.209(3):221-233. Lopez-Guzman OD. and genotoxicity in exposed children.77(1):67-72. Angerer J. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides. Ball M. Seiwert M. Centers for Disease Control and Prevention (CDC). Kolossa-Gehring M. Carranza C. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany.113(6):782-786. Drexler H. Int J Hyg Environ Health 2006. Heudorf U. International Programme On Chemical Safety (IPCS). Deltamethrin. 5/26/09 Ortiz-Perez MD. Third National Report on Human Exposure to Environmental Chemicals. toxicokinetics. Heudorf U. Hoppe HW. Environmental Health Criteria 97. Angerer J. Torres-Dosal A.htm. Environ Health Perspect 2001. et al.

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

238-.280 (.226-.1) 3.820) .05) .300) .05) 1.26-2.300 (.46) .560-1.35 (2.46) 2.780) 4.200-.560-.434) .595) .510-.65 (1.406) .700 (.25-1.490-.440) .288 (.32 (1.240 (.41-2.76 (1.830-2.384) .530-.320 (.260 (.292 (.370) .35) 1.1 and 0.62-6.34) 8.360) .49 (1.50 (2.710 (.190-.52-5.71 (1.16) 1.41-3.52-4.23 (2.311 (.740 (.78) 1.295) .25 (2.73) 1.49-2.266-.570-1.320) .55 (1.78 (1.353 (.417 (.30 (1.340) .210-.27-2.314 (.277-.93 (1.35 (1.18 (2.800 (.273 (.48-2.230-.13) .288-.33 (2.54) 1.260-.260 (.220-.364) .48-2.320) . and Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.650 (.13 (.32 (2.373) .630) .230-. interval) .267 (.250 (.79) 3.25-7.590-.670 (.90) 1.450 (.355) .328 (.16) 974 1193 1024 1346 99-00 01-02 99-00 01-02 99-00 01-02 .330) .190-.470-.49 (1.292-.64) 697 680 524 701 603 957 Limit of detection (LOD.730 (.160-.44) 5.25 (2.300 (.81 (1.8) 3.38 (2.32-21.276-.60) .320) .62-8.314) . population from the National Health and Nutrition Examination Survey.586) .14-6.300 (.570-.04) .16-1.427) .960 (.233-.230 (.27-2.02-6. Fourth National Report on Human Exposure to Environmental Chemicals 173 .65-2.56-5.430-.250 (.240 (.590 (.390) .35) 2.321 (.51-6.940) 1.190-.315 (.750-1. Survey Geometric mean (95% conf.374) 99-00 01-02 99-00 01-02 99-00 01-02 .16) 483 580 682 831 833 1128 99-00 01-02 99-00 01-02 .63-3.454 (.250-.336 (.350-.92-3.42-2.39) 2.340) 1.270) .03 (3.640 (.Pyrethroid Pesticides Urinary 3-Phenoxybenzoic acid Metabolite of Cypermethrin.420) .28) 1.610) .04-5.12) 4.30 (.260 (.750) .26) 2.180-.18 (1.490) .800) 1.510-.72 (1.750) .840-1.12 (.760 (.820) .345) Selected percentiles ( 95% confidence interval) Sample 95th 4.51-3.83-11.78) 6.29-1.362) .850) .25-4.265-.1) 3.89-71.330) .27-11.297 (.41 (1.34 (2.620-1.30) 3. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.850) .325 (.43) 3.63 (3.870 (.246-.298 (.253-.53-3. Deltamethrin.227-.190-.810) 1.387) .230-.69) 3.69 (1.520 (.12) .369) .600 (.53) 1.680 (.S.560-.41) 3.601) .247-.26) 2.21 (2.1.33 (1.830) 90th 1.200-.33) .36) 1.507 (.210-.700-1.250 (.550-.352-.38 (2.290 (.1) 3.78) 1.271-.75 (1.340) 75th .270 (.45 (2.160-.428-.35) 2.430-.45-5.49-2.01 (1.320) .62) 5.230 (.530-.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 .990) .710 (.740 (.34-6.86 (1.200-.

640 (.272) .03-1.270 (.51-7.570) .250 (. Deltamethrin.300-.44 (1.91) .05-3.09-2.437) .280 (.810) 1.330) .11 (.49) 1.370-.311 (. population from the National Health and Nutrition Examination Survey.90) 3.25-5.309 (.173-.740) .860-1.220-.264 (.299-.270 (.61-2.410) .278) .67) 1.590-1.650) .270-.230-.240 (.677) .253) .309) .60) 1.240 (.280 (.400-.202-.490-. and Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.401) .304) Selected percentiles ( 95% confidence interval) Sample 95th 3.74) 3.238-.480 (.530-.378 (.72 (1.330) .316 (.280) .274 (.510 (.00) 1.27) 1.13 (.580 (.160-.510 (.02 (2.440-.40 (1.640 (.11 (.670) .54 (1.09 (.200-.229-.190-.55) 3. interval) .53 (1.240-.246 (.312 (.860-1.48 (1.210 (.490 (.330) 75th .590) .390-.362 (.290) .530-.43 (2.10 (2.290-.62) 1.310) .13-1.270) .19) 2.300-.67 (1.Pyrethroid Pesticides Urinary 3-Phenoxybenzoic acid (creatinine corrected) Metabolite of Cypermethrin.200-.670) 3.450 (.84 (1.730-1.04 (.21-4.290) .446) .15-2.86 (1.88) 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 .387) .420-.35 (1.280-.06-3.19) 974 1193 1024 1345 99-00 01-02 99-00 01-02 99-00 01-02 .83 (1.534) .210 (.07-5.75-8.00) 1.91) 9.230) .550 (.94 (1.320) .490 (.22 (1.225-.460-.49 (1.67 (1.02-1.91 (2.590) .261-.39) 1.250) .62) .580) .36-6.224-.25-2.930) .730) .83) 1.200-.480-.49-2.55 (1.48) 697 680 524 700 603 957 174 Fourth National Report on Human Exposure to Environmental Chemicals .43) 1.730) .329) .35) .700-1.64-5.590) .321-.365) 99-00 01-02 99-00 01-02 99-00 01-02 .550 (.440-.216-.610 (.0) 3.25) 2.410-.190-.271-.178-.37 (1.630) .357) .17-1.91-4.92) 483 580 682 830 833 1128 99-00 01-02 99-00 01-02 .335-.37) 1.95) 1.35) 1.07) 2.63-3.52) 2.21 (1.275 (.272 (.400) .80) 4.49) 3.240-.00) 5.240-.200-.860 (.550 (.19-6.720) 90th 1.274-.400-.840-1.760) .63) 1.13-1.350 (.510 (.44) 2.04 (3.73) 1.230-. Survey Geometric mean (95% conf.60-4.43-64.280) .19 (2.500) .720 (.323 (.16-4.227 (.32 (2.372) .73-4.03 (.329) .41) 1.440-.270) .560 (.330) 1.36 (1.88-5.423 (.960-1.40) 2.750-1.09-2.330 (.09) 3.35-3.240 (.210-.190 (.350) .328) .81 (1.380 (.261 (.380-.41-4.370 (.43 (1.17 (.234 (.930) 1.226-.220 (.96 (1.52 (1.280 (.540 (.240-.240 (.250 (.150-.S.460-.

Sugiri D. Sugiri D. Berger-Preiss E. Environ Health Perspect 2003. et al. A longitudinal approach to assessing urban and suburban children’s exposure to pyrethroid pesticides. Environ Health Perspect 2006. Lopez-Guzman OD.46(3):281-288. Deych E. Int Arch Occup Environ Health 2003. Liu Z.206(2):85-92. Exposure to indoor pesticides during pregnancy in a multiethnic. Int J Hyg Environ Health 2002.76(7):492-498. Ortiz-Perez MD. et al. Angerer J. Isotope dilution highperformance liquid chromatography-tandem mass spectrometry method for quantifying urinary metabolites of synthetic pyrethroid insecticides. Idel H. Barr DB. Godbold J. Hadnagy W.114(9):14191423. Centers for Disease Control and Prevention (CDC). GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Olsson AO. et al. Levsen K. Lapinski R. urban cohort. Barr DB. Arch Environ Contam Toxicol 2004. Becker K.205(6):459-472. Batres LE. and genotoxicity in exposed children. Kolossa-Gehring M. Indoor pyrethroid exposure in homes with woollen textile floor coverings. Hoppe HW. Biological monitoring of workers after the application of insecticidal pyrethroids. Berkowitz GS. Leng G. Fourth National Report on Human Exposure to Environmental Chemicals 175 . Bartell S.209(3):221-233. Environ Health Perspect 2005. Obel J. Seiwert M. Int J Hyg Environ Health 2006. Bravo R. Hardt J. Leng G. Idel H. Ball M. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. Environmental health assessment of deltamethrin in a malarious area of Mexico: environmental persistence.Pyrethroid Pesticides References Baker SE. Lu C. Berger-Preiss E. Carranza C. Grimaldo M. Atlanta (GA). Angerer J. Torres-Dosal A. Pearson M. Ranft U.113(6):782-786. toxicokinetics. Int J Hyg Environ Health 2003. 2005. Ranft U.111(1):79-84. Third National Report on Human Exposure to Environmental Chemicals.

< LOD means less than the limit of detection.103) . Dermal contact with soil.142 (.164-.090 (.250-.04.210-.130) .230-.S.120 (. solder.180-.200) .280) .500) .310 (.210-.430 (.300) . fireworks.090-.280 (.170 (.180 (.112-.390-.300 (.400) .320-.470) .230-.200-.110-.160) .093 (.410) .290-.320) Total .460 (.133) * .190-.178) .340) .160-.146 (.170-.260 (. to a lesser extent.440 (.105 (.390) .300-.140) .230) .130 (.560) .120-.280-.230-.160) .130 (.180 (.170-.141-. 0. It is used in metal alloys.130-.175 (. 7440-36-0 General Information Antimony is found in ores or other minerals.250 (.180-.140 (.140) . and glass.350) .110-.130) .131-.240 (.220-.119-.109-.190 (.500) .095-.070 (<LOD-.100-.160 (.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 .230-.130-.130-.160-.330-.290 (. water.154) .080-.100-.210) .230) .180-.470 (.290-.320-.210 (.410) .390-.350 (.300-.100) .100 (.190 (. and +5.190-.240-.330 (. and excretion of antimony vary depending on its oxidation state.120-.099 (.180 (. The absorption.190-.240 (.120-.390) . population from the National Health and Nutrition Examination Survey. see Data Analysis section) for Survey years 99-00.220 (.350 (. and pewter.190 (.390-.207) . and as a fire-retardant in textiles and plastics.250 (.130-.240) .130 (.100 (.190) .070-.710) .340 (.210 (.220-.460) .088-.360) .140) .180-.270 (.169 (.490) .270) .250-.280-.360 (.310) .350) .117-.180) .190) .140) .095 (.360) .140) .310) .170 (.320) 787 683 618 554 667 723 768 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.200) .320-.190) .330) .260 (.145) Selected percentiles ( 95% confidence interval) 50th .157) .170-.200 (.230 (.260-.180 (.240 (.180-.330) .220) .360-.230) .250-.154) .190) .200-.070 (<LOD-.130 (.115-.390) .300) .310-.210) . which may vary for some chemicals by year and by individual sample. 0. enamels.160-.350-.110 (.280 (.330 (.140 (.080) .120 (.150 (.320-.130-.220) 95th . often combined with oxygen to form antimony trioxide or with sulfur to form stibnite.114) .280) .250 (.117-.440) .150) .130 (.150-.330) .108-.160-.135) * . sheet and pipe metal. distribution.320) .098-.120-.330 (.132 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.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 .430 (.176 (.260) .160) . 176 Fourth National Report on Human Exposure to Environmental Chemicals .184) .510) .158 (.490 (.280-.250) .143 (.132 (.180 (.400 (. metal bearings.190-.220) .108 (.350-.200 (.142) * Sample size 2276 2690 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .125 (.134 (.370) .120-.200-.320 (.240 (.140) .230-.340 (.115) . or other substances containing antimony is another means of exposure. coal-fired plants. Stibine is a metal hydride form of antimony used in the semiconductor industry.120 (.210) .04.260) .220-.350 (.400) .120 (.140 (.145 (.270 (.310 (.210) .470) .220) .150) .400 (.150) .350) . Two antimony compounds (sodium stibogluconate and antimony potassium tartrate) have been used as antiparasitic medications. ammunition.220-.150-. People are exposed to antimony primarily through food and.570) . +3.190 (.150 (.Metals Antimony CAS No.430 (.140-.126 (.270 (.197) .260 (.120) .150-. and 03-04 are 0.410-.440) .390) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.160) .130 (.120) .160 (.090 (<LOD-.200 (.130-.320 (. interval) .310-.460 (.130-.130 (.260) .370-. Antimony can exist in one of four valences in its various chemical and physical forms: -3.350 (.200 (.154-.120-.148-. and refuse incinerators that process or release antimony.134-.144) .160) .230 (.150-.230 (.110-.080) .136) * .160 (.310 (.110-.190 (.200-.110) .250-.156-. 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.220 (.170-.137) .120 (.180 (.136-.190-.200) .360 (.128 (. ceramics.460 (.130) < LOD .130) . and 0.090-.530) .120-.240 (. from air and drinking water. castings.280) .200 (.126-.120-. It is also used in paints.120) .600) .160) .150) 90th .170) . 01-02. Antimony enters the environment from natural sources and from its use in industry. storage batteries.140 (.220-.200) .150 (.161) .270 (.270-.390 (.130 (.400 (.087-.300-.420) .079-.190) . respectively.123 (.300 (.260-.170-.080 (<LOD-.119) .200 (.280-.120) .220-.400-.280) .350) .150-.350-.128 (.122 (.120-.350 (.330) .300) .07.330-.280-.090) 75th .180) .400) .210) .270) .240-.310 (. Workplace exposures can occur at smelters.137) .

121) .102-.230-.181) .143) 90th .147) .195-.125-.115 (.414) .188) .245) . population from the National Health and Nutrition Examination Survey.087) . skin.211) ..189 (.078 (.185 (.104-.333 (. diarrhea.076-.118 (.338 (.315) .200-.068 (.250-.127) .198) .430) .164) .187) .126-.261) . 1986).149) .295 (.115) .176 (.095-.124-.069-. 1995).156-.238 (.143) .129 (.148-.250-.107-.281-.276 (.195-.113-.145) .321) . and route of exposure (Elinder and Friberg.167-.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.130) .228 (.191 (.081) .130) .152) .074 (.170 (.123 (.421) .205-.135 (.131-.079 (<LOD-.116 (.447 (.148) * .098) .131 (.209-.320-.111 (.310 (. 1986).138-.253-.071-.263 (.129 (.320-.250-.112 (.131) .120 (.294) Total . An elimination half-life of approximately 95 hours has been estimated after occupational exposures (Kentner et al.192) .084) .178-.102-.176 (.300) .333) .119-.173 (.152) .163 (.233-.127) .181) .115 (.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 .107-.310) .089) .138 (.241-.183) .120 (.129) .112 (.061-.30) .343 (.209 (.225 (.156 (.203) .167 (.352) .082 (<LOD-.146-.238) .242-.317) . Dysrhythmias and T-wave changes on electrocardiogram have also been noted after both therapeutic (Berman.500) .127) .228 (.298 (.112-.086) 75th .236 (. species.417) .161) . 1944).109-.143) Selected percentiles ( 95% confidence interval) 50th .255) .193 (.137 (.265-.338 (.256 (.300 (.140) .308) .233) .096-.173 (.167 (.106-.400 (.150-. abdominal pain.113) .208 (.286 (.136) .128-.280-.132 (.391) .172-.144-.108-.429) .138) * .134) .171) ... Acute inhalation of antimony has been associated with irritation of the respiratory tract and impaired pulmonary function (Renes.103-.105-.204-. interval) .127 (.114 (.271-.135) .121 (.150-.265 (.160 (.130) .267-.364 (.241-.146-.092) .333-. Acute antimony poisoning may cause a metallic taste.178 (.227-.186) .308-.122 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.162-.278 (.108-.097-.333-1.153-.222 (.471) .444) .095-.320) .. and ulcers (Werrin.115-.380 (.247) .207) .269 (. Human health effects from antimony at low environmental doses or at biomonitored levels from low environmental exposures are unknown.143) .116-.080 (.727) .214) .253 (..268) .148-.357) . 1953).233 (.138-.S.126 (.352 (.257) .250-.391) .082) .099-.209) .333 (. The toxicity of stibine after acute inhalational exposure is similar to that of arsine.235-.080 (<LOD-.250) .288 (.357-.209) .075 (.364 (.263-.203) .192-. and kidney have been demonstrated in high dose animal studies depending on the dose.120 (.100 (.213 (.266 (. and eyes.425) .200-.300) .154-.250 (.117-.206-.126) .135) .119-.181) .238) .135 (.175 (. Ming-Hsin et al.117-.163 (. Inorganic antimony salts irritate the mucous membranes.107-.208-.333 (.248-.098-.320 (.114 (.444) .146-.139 (. 1954).109 (.373) . 1973).113-.068-.167 (.086 (. myocardium.108 (.151) .099-.471 (.Metals than for trivalent compounds (Elinder and Friberg.225) .130 (.115-.122 (.125 (.200-.106-.159-.250 (.081 (<LOD-.224 (.199-.111-.085) .115 (.272) .103-.124 (.118 (.480) .147-.098-.092-.069-.120 (.185 (.108-.267) .318-.333-.082) .077) .417) .320 (.173-.741 (.149-.159-.259 (.278) .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 .230) 95th .182 (.333-.194-.196 (.217 (.229-.385 (.161) .310) .121 (.188-.195 (.076-. liver.132) .318-.193) .127) .109 (.438) .485) .133) . resulting in hemolysis with abdominal and back pain (Dernehl et al.140) < LOD .226 (.143 (.371 (.313-. 1988.741) .139 (.317) .228-.153 (.248) .104-.280 (.179-.135) .075 (. 1962).164 (. Pulmonary edema may occur in severe cases of inhalation exposure (Cordasco et al.185-.267 (.277 (.338) .114 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.244-.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 . Histopathologic inflammatory and degenerative changes in the lung.164-.255-.124-.173) . 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.124) .192 (. 1958) and occupational exposures (Briegner et al.123) .129) * .119 (.429 (.117-. and gastrointestinal symptoms such as vomiting.317) .176-.239-.220) .146) .200) . Fourth National Report on Human Exposure to Environmental Chemicals 177 .159-.405) .

Information about external exposure (i.158:165-190. 2004.html. 2002. Costeloe K. Finding a measurable amount of antimony in urine does not mean that the level of antimony causes an adverse health effect. et al. Handbook on the toxicology of metals. Third National Report on Human Exposure to Environmental Chemicals. Kuo-Juie Y.)1954.S. Carelli G. Ludersdorf et al. indium. Leinemann M. et al. Kiberd B. Cullen A. Roland H. Levels of urinary antimony in infants appeared to be similar to those reported by CDC (2005) for young children (Cullen et al. gallium. et al. Apostoli P. Earlier measurements in general populations (Minoia et al. Iavicoli I. which may be due to methodologic. Ming-Hsin H. Fuchs A. New York: Elsevier. Antimony in blood and urine of infants. Nordberg GF. Trace element reference values in tissues from inhabitants of the European community I.. and hydrogen sulfide. eds. 1987). Human biomonitoring of arsenic and antimony in case of an elevated geogenic exposure. Biological assessment of exposure to antimony and lead in the glass-producing industry. Sabbioni E. Suchenwirth R. Gallorini M. Urinary antimony in infancy. HH.64(2):182-185.16: 33-39. Rev Infect Dis 1988.76(2):103-115. and future strategies. Bolten C. Stone FD. Chin Med J 1958. Environ Health Perspect 1998. A study of 46 elements 178 Fourth National Report on Human Exposure to Environmental Chemicals .13:361-362. Pietra R. Mechanism and treatment of cardiac arrhythmias in tartar emetic intoxication.atsdr. gov/toxpro2. Lauwerys R. Mahieu P. 1998.. Petrucci F. Stead FM. Briegner H.Metals to antimony have been established by OSHA and ACGIH. Several investigations of airborne antimony exposures in workers have found urinary levels that are many times higher than those seen in NHANES 1999-2000. Int Arch Occup Environ Health 1987. Biomonitoring of a worker population exposed to low antimony trioxide levels. stibine. Kentner et al.59:469-474. Stasney J. Arsine.48:93-97. Bailly R. J Occup Environ Med 2004. 1997).106:33-39. 1986. 1998). respectively.. Industrial Medicine 1944. Iavicoli et al. J Trace Elem Med Biol 2002. Kentner M. 2nd ed. Antimony trioxide is rated by IARC as a possible human carcinogen. and a drinking water standard has been established by the U. Dezateux C.67:119-123. 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. Centers for Disease Control and Prevention (CDC). Vouk VB.. 1990. Delves HT. Dernehl CU. Pilgrim L.. Minoia C. 2005. Br J Ind Med 1991. Semisch CW.76:432436. Ho C-K. Pozzoli L. clinical efficacy.cdc. 1995. 1994) have reported values slightly higher than those in this Report. J Clin Pathol 1998.46:931-936. Lenert G. Wu M-T. Dezateux et al. Matthews T. population. Caroli S. Industrial antimony poisoning. Van der Venne MT. Liao Y-H et al. Atlanta (GA). Stocks J. Hamilton EI. Industrial Medicine and Surgery (Dec. Experimental and human studies on antimony metabolism: their relevance for the biological monitoring of workers exposed to inorganic antimony.521-523. Chia-Yu H. environmental levels) and health effects is available from ATSDR at: http://www. Nau CA. Friberg L. Piatnek DA. even when exposure levels were below workplace air standards (Bailly et al. Skulsukai G. Yu H-S. Wade A. plasma and urine and a critical evaluation of reference values for the United Kingdom population. Mayne P. Dunkelberg. Schaller KH. Review of elements in blood. Urinary antimony was not associated with locally elevated soil levels in a study of more than 200 German residents (Gebel et al. 1998) or compiled reference ranges (Hamilton et al. External and internal antimony exposure in starter battery production. Biological monitoring of exposures to aluminum. Antimony. pp. Chemotherapy for leishmaniasis: Biochemical mechanisms.51:238-240. Sci Total Environ 1994. Konings J..e. Chest 1973. Biomonitoring Information Levels of urinary antimony reflect recent exposure.. or exposure differences. Int Arch Occup Environ Health 1995. O’Regan M. Gebel TW. Schacke G. Luedersdorf R.. Cheng-Wei L. Sabbioni E. Weltle D. Ju-Sun P. Arch Dis Child 1997. and antimony in optoelectronic industry workers. Liao Y-H. Alimonti A. 26-42. References Berman JD. Yang C-Y. Chen J-R. Cordasco EM.. In: Friberg L. Buchet JP. and 2003-2004. EPA. Element reference values in tissues from inhabitants of the European community..10(3):560-586. Elinder CG. Delves HT. VI. 20012002. Shao-Chi C. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. arsenic.. Paschal et al. 1991. Pulmonary edema of environmental origin. Mayer P..

95:89-105.76(1):53-59. Werrin M. blood.99-108. Paschal DC. Jackson RJ. Morrow JC. Industrial Hygiene and Occupational Medicine 1953. Ting BG. Chemical food poisoning. Pirkle JL. Trace metals in urine of United States residents: reference range concentrations. and serum of Italian subjects. Fourth National Report on Human Exposure to Environmental Chemicals 179 .Metals in urine. Sci Total Environ 1990. et al. Antimony poisoning in industry. Renes LE. 27:38-45. Sampson EJ. Quarterly Bulletin of the Association of Food and Drug Officials 1962. Environ Res 1998.

5 (23. such as arsenopyrite (FeAsS) and realgar (As4S4).2-61. General population exposure to inorganic arsenic can occur through consumption of drinking water and.90-8.7 (11.8) 29. though in some locations arsenite may be prevalent (WHO. and gray forms).6 (13. meats.34-9. and. 2001). a trivalent compound known as white arsenic) is a common natural and commercial form that can be released into the air during volcanic action. arsenic compounds.84) 8.12 (6.1) 7.5) 95th 65. lead.1) 290 725 1542 03-04 03-04 9.70 (6. from coal burning.1-18.25-9.7) 65.4 (48.1) 1281 1276 03-04 03-04 03-04 9.19-9.6-35. population from the National Health and Nutrition Examination Survey.9 (17. alloys. ocean and fresh waters. and arsenates (oxidation states of -3. referred to as inorganic arsenic compounds.000 metric tons annually.7-95. lead hydrogen arsenate.0 (22. Water sources contain mostly inorganic arsenate. and other metals.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 7.5 (14.8-61. chromated copper arsenate (CCA) has been used to treat outdoor timbers and pressure-treated woods to prevent wood rot. were used as treatments for syphilis. as alloy in metal bearings.6 (9. retaining walls. and arsenosugars.77) 6. Arsenic trioxide (As2O3.4-65.00 (6. cacodylic acid.4) 13. see Data Analysis section) for Survey year 03-04 is 0. and as homicidal poisons.40) 7.8) 34. Groundwater Urinary Total Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.5-52.80) 6. arsenocholine.66-8.70) 8.84) 8. Survey years 03-04 Geometric mean (95% conf.10) 10.8) 7.8) 17.90 (7.08 (5.5-41.2 (12.9) 68.30) 17.70-9.1) 15.27) 9.6-43. copper arsenates.5-178) 46. Arsenic trioxide is approved to treat acute promyelocytic leukemia.50-14.7-83.2 (13.9-34. Arsenic and its compounds have had many uses in the past and present as medicines. and foods. black.80 (5.90-14. Roxarsone and other organic arsenicals are anticoccidial agents added to poultry feed. arsenites.80-9.S. and monosodium methyl arsenate were used as pesticides but contemporary uses are restricted.8) 30.2) 46. gaseous hydride manufactured in small quantities for use in the semiconductor industry.Metals Arsenic CAS No. mental disorders. cancers.5-19. psoriasis. Arsenic can also combine with organic substances in nature to form such organic arsenic compounds as arsenobetaine.4 (24. and in lead-acid storage battery grids. +3 and +5).3-15.8 (48. 7440-38-2 General Information Arsenic is an element that is widely distributed in the earth’s surface in small amounts.5) 43.2 (51. to a lesser extent.6 (32. In nature.9-46. Before the 20th century.57) Selected percentiles ( 95% confidence interval) 50th 7.4 (7.90 (5.4 (31.0-60.8) 7. the smelting of copper. Since the 1940s. and indium arsenides are used in the semiconductor industry.4 (26.9-62.90-7.5 (34.10 (6. and produce.2 (41.9) 21.3) 10.90-8.90) 16. grain.10-10.90-11. aluminum.6-141) 53.30 (6.30 (7. it is found in over 200 crystalline or mineral forms.3-19.1-40.1 (32.4) 60. trimethylarsine oxide.9 (8.8) 33. 180 Fourth National Report on Human Exposure to Environmental Chemicals . and as a cosmetic to lighten complexion.0 (43.0 (15.00-9. Although it is still widely used in the United States. 2005). semiconductors. Various arsenic compounds were used in paint pigments and for tanning animal hides.6 (15. mostly for use in wood preservation (ATSDR.4) 40.0 (14. Also.20 (8.0 (11. Arsenic can combine with such non-carbon chemicals as sulfur and oxygen to form arsenides. CCA-treated wood has been restricted since 2003 and no longer can be used in residential applications such as decks. arsenic as elemental metalloids may be used in some ammunition. Arsenic is measurable in most soils. sodium arsenite.8-77. and play sets.12-10.2-93.5 (40.90) 75th 16.50 (8.5 (36.55 (7.7) 24.6) 618 722 1074 Limit of detection (LOD.10-7. pesticides.1 (38.2-20.02-8.7) 90th 37.6) 11. In the last century.2-17. or rarely as elemental metalloids (yellow.34-10.41 (7.2) 15. Arsine (AsH3) is a reactive.5) 66.3-111) 78. The United States no longer produces arsenic from mining but imports about 22.90 (7. Gallium.97) 8. Various forms of inorganic arsenic can occur in groundwater from natural sources or as a result of soil application or industrial waste. to a lesser extent.0-19.29 (8.5) 41.13-8. interval) 8. particularly arsenic trioxide.74. solders.

58-10.7 (9. dose level.06 (4.64 (7.5-17.1) 8. Arsenate is reduced in the body to arsenite (oxidation state +3).8-32.28-7. Steinmaus et al. population from the National Health and Nutrition Examination Survey.50 (6..0-38.7-35.10-8.1) 58. interval) 8.3) 6. Arsenite is then oxidatively methylated to the monomethylarsonic acid (MMA) and dimethylarsinic acid (DMA) with subsequent excretion primarily in the urine (NRC. but is poorly absorbed dermally (WHO.8 (27.33 (6.4-64. EPA’s maximum contaminant level (Hughes. Smoking tobacco is also a source of inorganic arsenic.12-10.7 (11. Inorganic forms of arsenic demonstrate high acute toxicity.2) 15.30-9.2-15.5) 290 725 1542 03-04 03-04 8.40) 8.6 (10.8 (20.7-17.6 (17.2) 90th 30.S.96) 12.18 (5. Inorganic arsenic is well absorbed from the gastrointestinal tract and absorbed to a lesser degree through inhalation. kelp.00 (6. Though modest bioconcentration occurs in some aquatic life. arsenocholine. 2001). Inorganic arsenic and its metabolites have elimination half-lives of approximately 2–4 days (Lauwerys and Hoet.81-9.5) 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 8.0 (31.1 (11. WHO. In aquatic sediments.. and some other seafood can contain organic forms of arsenic including arsenobetaine.4) 32.38-10.45) 5. 2001). 2006. though some reduction may occur in the gut prior to absorption. trimethylarsine oxide (TMAO).2-46.66-8.0) 1281 1276 03-04 03-04 03-04 8. 2001).3-53. organic arsenic can be converted back to methylated and inorganic arsenic. 2001). Chowdhury et al. 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. EPA. cacodylic acid and monosodium methyl arsenate.20-9.59) Selected percentiles ( 95% confidence interval) 50th 7. 2001..4 (24. 2001.. selenium. 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.7) 28. 2007.32 (5.9) 53. and contact with CCA-preserved wood structures.24 (7.8) 27.0) 14.Metals sources of drinking water often have measurable arsenic and several regions of the United States have naturally higher arsenic levels than the U. arsenocholine is converted to arsenobetaine and also to small amounts of TMAO (Christakopoulos et al.41) 6.8 (12.13) 8.S.3-64.3-62. with trivalent inorganic arsenic (arsenite) being more toxic than pentavalent inorganic arsenic (arsenate) (NRC.61 (7.47-6. 2006.9) 13. shellfish. 2001).3 (24.4 (40.8) 22..35) 7. Children may have additional exposures from ingestion of contaminated soils (e. and arsenosugars.44-11.2) 40.8-62.5-120) 40. Ingestion of arsenosugars in kelp and algae can also lead to the excretion of DMA.25-9.7) 95th 50. NRC.6 (35. dust.04) 7.8-75.9) 618 722 1074 Fourth National Report on Human Exposure to Environmental Chemicals 181 .8 (11.99-9.75) 13.0) 33. 2007.4 (26. 2001).0) 26.76 (6.0) 12.0-18.1-36. Gamble et al.93-8. TMAO is also formed in the environment from microbiological action and is a metabolite of arsenic in certain mammals.93-9.1) 7.11 (5.75 (5.7-34.33-10. 2003. After absorption. are used in enclosed ultraclean operations within the semiconductor industry. 2007.4 (12. Smelter workers can have significant inhalational exposures to airborne arsenic trioxide for which air standards have been established.01) 11. 2001). Fish.66-8.7 (25.1) 6. Extremely high groundwater arsenic levels.1) 24. The semiconductor dopants.4) 54.6-17. U.6) 45.0-69.7-188) 27. Survey years 03-04 Geometric mean (95% conf..7-18.25 (6. These organic forms of arsenic from seafood are absorbed and quickly excreted in the urine (WHO. age.3-41.0) 42.4 (42.8 (21.9-56.86-17.9 (45.3) 9.47 (7. mine tailings). WHO.S.01) 7.44) 6. Tseng.g.5 (9. gallium arsenide and indium arsenide. inorganic arsenic is widely distributed within the body.4 (11.23-7.31 (6. have caused clinical arsenic poisoning.1 (14. In aquatic organisms.47 (6.51) 75th 14.5) 17.88 (5.88) 7. as observed in Bangladesh where millions of people have been exposed.04 (5. arsenic does not show biomagnification in the food chain (WHO.0-26. Direct exposure to DMA and MMA may result from use of the two pesticides.10-16. 2001).07-9.2 (12. and folate status (Chen et al.66 (7. 1988).0 (17.3 (27. so exposure to the general population is extremely limited.

20 (<LOD-1. can cause peripheral sensorimotor neuropathies. 2006) and newly discovered thioarsenic metabolites may also be as toxic (Naranmandura et al.Metals +3) shows greater toxicity than arsenite itself (Aposhian et al. WHO.30) 1. which may vary for some chemicals by year and by individual sample. With chronic exposure. Survey years 03-04 Geometric mean (95% conf. 2001). 2007. Bredfeldt et al.g.20 (<LOD-1.80) 1. respectively. Studies of arsenic at levels typical of U.20 (<LOD-1. see Data Analysis section) for Survey year 03-04 is 1. and environmental standards for arsenic and arsenic Urinary Arsenic (V) Acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.. and bladder cancer (IARC.. OSHA and ACGIH have established workplace standards and guidelines for arsenic exposure and monitoring.. 2001). Such actions may lead to decreased energy production. and hyperpigmentation of the skin (NRC. 2004). including drinking water sources with elevated arsenic levels (e. Chronic elevated arsenic intakes have been associated with diabetes. and DNA repair inhibition (Cohen et al. drinking water have not been associated with increased cancer rates (Schoen et al. leading to a decrease in adenosine triphosphate energy production. including inhibition of numerous enzymes. 2006. 2001). cell transformations. hypertension. Arsenic has many actions demonstrated in cellular studies.50) 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD 1..10 (<LOD-1. Acute toxicity resulting from the ingestion of large amounts of trivalent arsenic (e. arsenic trioxide) includes hemorrhagic gastritis with nausea. Although arsenate is reduced in the body to arsenite. WHO. 2006) or when exposure occurs in smokers (Chen et al.. gluconeogenesis. fatty acid oxidation. and endothelial injury (Kumagai and Sumi. apoptosis.60) 1.50) 2568 95th 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. and production of glutathione may be affected as well.10 (<LOD-1.30) 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1. Chronic human intake of arsenic at less than acutely toxic doses. and altered gene expression.S. substitution in phosphate metabolism. arsenite will inhibit cellular pyruvate dehydrogenase by binding to the sulfhydryl groups of dihydrolipoamide. food residue. increased oxidative stress. but additional or confirmatory research is needed (Kapaj et al.EPA has established drinking water. 2006. The risk of lung cancer appears more pronounced when large environmental exposures start in childhood (Smith et al.60) 1. peripheral vascular disease. Laboratory studies using inorganic arsenic have shown chromosomal aberrations. Raml et al. hematocytopenias. 2007. noncirrhotic portal hypertension. Cardiac arrhythmias..g. 2001). 2001. and it also will inhibit succinate dehydrogenase.S. Taiwan.20 (<LOD-1.. cytotoxicity..S. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th < LOD 90th < LOD Sample size 1. hyperkeratosis. Bangladesh. population from the National Health and Nutrition Examination Survey. 2006. lung. Acute unintentional inhalation of arsine gas can produce hemolysis of red blood cells. 2001).10 (<LOD-1.0. 2007). Chile). Cellular glucose uptake. 2001. interference in signal transduction pathways.10 (<LOD-1. hepatotoxicity. and by uncoupling oxidative phosphorylation (NRC.50) 621 725 1078 Limit of detection (LOD. Chronic arsenic exposure in humans is considered to be a cause of skin..EPA. and peripheral neuropathy may also occur with large doses or after surviving an acute overdose. it may have its own separate toxic action by substituting for phosphate in glycolysis and other pathways. < LOD means less than the limit of detection. 2000.. Cohen et al. 2004..10 (<LOD-1. NRC. The organic forms of arsenic occurring in seafood have little known toxicity. some of these effects may take years to develop. vomiting. U. renal failure. WHO. Acutely. 2004). which can lead to dehydration and shock. 182 Fourth National Report on Human Exposure to Environmental Chemicals .50) 1.. WHO. and diarrhea. NRC. 1998. 2001). and childhood neurodevelopmental effects in observational human studies.S. The U.

IARC and NTP recognize inorganic arsenic and arsenic compounds as human carcinogens. gov/toxpro2... Meza et al.18 (<LOD-3. 2006. Additional information about external exposure (i. 2000). Shalat et al. Consequently. urinary arsenic levels have been accepted as a good biomarker of dose (WHO. DMA produced bladder cancer in some chronic rat studies (Cohen et al. and were about two-fold lower than those for the U. Caldwell et al. 1998.33 (<LOD-3. and the FDA has established a bottled drinking water standard. 2003. Survey years 03-04 Geometric mean (95% conf. higher mean or median total urinary arsenic levels have been reported among people living in specific western areas of North America (Calderon et al.Metals compounds... 1999. environmental levels) and health effects is available from ATSDR at: http://www. population from the National Health and Nutrition Examination Survey. Pellizzari and Clayton. Pellizzari and Clayton. 2001).50) 2568 95th 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2. 2006.61 (<LOD-3. 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. Vahter et al. Though CCA-treated wood contains several thousand times more arsenic than untreated wood.e. In a Nevada town where groundwater levels were naturally elevated.33 (<LOD-3. Pellizzari and Clayton 2006). Josyula et al.S..75 (<LOD-2. although urinary arsenic levels were not associated with CCA contact (Shalat et al. 2000. Caldwell et al. population in the National Health and Nutrition Examination Survey (NHANES) 2003–2004 were similar to levels reported in the National Human Exposure Assessment Survey (NHEXAS) 1995–1996 for about 80 children residing in the Great Lakes region (Caldwell et al..html..41) 3.04 (<LOD-3. 1986).S. 2001).. In animal studies. though air levels of arsenic fume and dust are correlated with urinary arsenic levels at higher occupational inhalational exposures (Jakubowski et al.. Levels of total urinary arsenic in the U.S. 2008).atsdr. Fourth National Report on Human Exposure to Environmental Chemicals 183 . 2006).75 (<LOD-2. Compared with this Report.19) 3..50) 1. 2007.95) 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. the median total urinary arsenic in about 200 people was approximately four times higher than that of the U..70) 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD 2. Offergelt et al. 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. 2001).89) 1284 1284 03-04 03-04 03-04 * * * < 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. Calderon et al. Shalat et al. Daily variation in creatinine-corrected urinary arsenic is relatively small when intake is constant (Calderon et al. population in NHANES 2003–2004 (Schulz et al. 1992. 2004... 1999. Valenzuela et al. 2006).. median urinary total arsenic levels in 4052 adults varied with seafood intake. WHO. population (Rubin et al. 1999).18) 3. had decreased since the prior 1990– 1992 survey.... 2006).. 2006). 2006. Biomonitoring Information Urinary arsenic levels reflect recent exposures and are moderately to highly correlated with arsenic intakes from drinking water and dietary sources (Ahsan et al.69 (<LOD-3.00) 1.80 (<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 Sample size 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. 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. but generally only at maternally toxic doses (WHO. 2008)... 2007. 2008.. In the German Environmental Survey III of 1998.. arsenic has been fetotoxic and teratogenic.cdc.S.

Tseng et al.900-1. 2008. 1990.9) 13.. 2008).8 (17. 2008).20) 3.700-1. with DMA. For residents of Inner Mongolia.68) . methylation capacity. 2006).. and duration of exposure are also considered important.00-4.30 (1.6 (11. Aposhian et al.6.28) 1.1-94.5 (14.93) 1. The higher percentiles of total urinary arsenic levels in the U.30) 10. Also.9 (6.83) Selected percentiles ( 95% confidence interval) 50th 1. 2001.2-38.17-1.1) 45. arsenobetaine and arsenocholine will greatly increase the level of total urinary arsenic and comprise the highest percentage of the total urinary arsenic level.5 (26.. when seafood organic arsenic is subtracted).4) 31. 2007) with higher levels of arsenic in the drinking water.40-6. Valenzuela et al. Median and mean total urinary arsenic levels for residents in some districts in Bangladesh were reported to be about 50-fold higher than respective levels in the U. arsenite. 2008. geometric mean levels were about 70-fold higher than for the U.00-6..20-3. Chowdhury et al.20 (2. 2007). Survey years 03-04 Geometric mean (95% conf.4. China. When seafood intake is avoided. see Data Analysis section) for Survey year 03-04 is 0.40) 5.50) . In most human studies. In the residents of a Chilean town who consumed water with high levels of arsenic.10) 4.7-22.800-1. a control population of 696 Tacoma residents had median urinary DMA levels similar to those for NHANES 2003–2004 (Kalman et al.6. Urinary Arsenobetaine Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U..3 (21.g.70 (3.11-1. Arsenate. arsenite.80 (3.8.6-44.60) 1. 2005.40) 75th 5..60-3.5) 32..600 (..70 (5.20 (1. arsenocholine. population from the National Health and Nutrition Examination Survey.871-1. population in the NHANES 2003–2004 subsample. respectively. Individually measurable species resulting from inorganic arsenic exposure are arsenate. Pellizzari and Clayton. DMA has been the predominant metabolite composing the majority of measurable inorganic-related arsenic in the urine (i.3 (9. population showed a higher contribution of arsenobetaine (Caldwell et al.3-39.70-21.40-7.0) 4. median levels of urinary DMA were about 40-fold higher than the adult median reported in NHANES 2003– 2004.3) 1284 1284 03-04 03-04 03-04 1.9 (7.400-. 1996.. Total arsenic measured in the urine includes all species of inorganic and organic arsenic. dermal keratosis.1) 18. 2000.20 (.20) 7.00) 3.00 (1. 2000. DMA and MMA. < LOD means less than the limit of detection.50-6.19 (.20 (4.00 (.43-1.. 2001)..6 (13.8-50. Great Lakes region residents had median urinary DMA levels that were slightly less than median levels in NHANES 2003-2004 (Caldwell et al. After recent seafood ingestion.5) 621 725 1078 Limit of detection (LOD.20) 18. Sun et al. WHO.30 (2. Measurable organic arsenic species in this Report are three biologically generated environmental forms.0-23.1-51.S. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Caldwell et al.S. and arsenobetaine being the main contributors to the total urinary arsenic levels (Caldwell et al.37 (1. and urinary DMA represented about 67% of the total urinary arsenic (Hopenhayn-Rich et al.1-25.3% of a representative sample of the U.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. and TMAO.10 (4...29 (1.00-12.66 (1.. MMA.5) 29. Caldwell et al. which may vary for some chemicals by year and by individual sample.70) 6.8) 35.Metals other areas of the world (Ahsan et al. 4.7) 15.800 (. arsenocholine. population (Ahsan et al.31-1..50) .80) 1. Blom et al.S.4 (16.9-23. DMA and MMA compose most (about 75%) of the total arsenic species measured in urine.90-7.45 (1.90-29.. as evidenced by trace or nondetectable levels of arsenobetaine and arsenocholine in the urine.80-5. 2005.800-4.62) 2. and two methylated metabolic products.e.20-190) 31. 184 Fourth National Report on Human Exposure to Environmental Chemicals . in NHEXAS 1995–1996.80 (4.4-35.48-2.20-25.0 (26.8-40.900 (. Some noncancer effects of arsenic (e. vasospasm.05) < LOD .800 (.80 (. 2003).7) 13.10) 8.. In the late 1980s.70-21.2 (6.800) 1.0 (27.3) 35..00-1.8 (12.S. and other factors such as nutrition.7 (13.30) 2. and peripheral neuropathy) have been associated with urinary levels as low as 50–100 μg/L in chronically exposed populations (ACGIH.50) 90th 16. interval) 1.5) 292 728 1548 03-04 03-04 1. Caceres et al..7 (21. 2008). 1985. and 0. arsenobetaine. population (Sun et al.S.74 (1.500-1.700-1. and TMAO were detected in only 7.2-35. 2008).4) 23.. These associations are stronger at higher urinary levels.0) 29. 2005. 1. 2000.3) 95th 35.6 (25.55 (1. Levels of DMA and MMA increase in approximate proportion to the intake of inorganic arsenic. Caldwell et al. Detectable levels of MMA reported in NHANES 2003–2004 were found only at the upper percentiles and.

3) 95th 29. interval) 1.50-7.7) 30.938-1. WHO.11 (.30) 1. Sun et al.4-28.19-2.6 (9.54 (1.61-6. 1992.1 (26.0-36.36) 2.70) 5. 2001).400-.80-153) 17. 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.2 (13.67) 1. 1998.40) 1.78 (3.58 (3.83) 8.4) 292 728 1548 03-04 03-04 1.14 (1.638) 1.93 (1.82) 4.612-1.13-39.6-29.4) 13.901-2. population from the National Health and Nutrition Examination Survey.88 (5.29-14.43) 14. 1986..15-4.39-3.81 (4.40 (1.29 (4.88) 2.6) 19.3-24.5-20.55) 1.78-5. 2008).68 (1.51) 5.0) 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.91) 90th 16.5 (18.6-32.531 (.50-15.4-21. Information about the biological exposure indices is provided here for comparison.25 (.2 (12.5 (18.877 (.47 (1.73-6.21) 5.S.83) 2.18-1.909-1.00 (3. Caldwell et al. Survey years 03-04 Geometric mean (95% conf.10 (.9 (13.4-82. 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. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.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. The 95th percentile of the U.2 (4.45) 1.9 μg/L. not to imply a safety level for general population exposure.62-6. Urinary Arsenobetaine (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.1) 26.5) 17.43) 75th 5. Fourth National Report on Human Exposure to Environmental Chemicals 185 .9) 32.12) < LOD ..6 (6.44 (1. occupational monitoring and research studies have focused on the sum of inorganic-related species (arsenate + arsenite + DMA + MMA) as a measure of inorganic arsenic intake.0 (9.00 (1.786-1.3 (10.28) 1.4) 32.51-2. 2007).1-36. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects..76-27.82) Selected percentiles ( 95% confidence interval) 50th 1.1-18.64-29.47 (2.9-18.15-1.32-7.3) 1284 1284 03-04 03-04 03-04 1.833-1..9 (25.72) 12.. which is below the ACGIH BEI (Caldwell et al. Finding a measurable amount of arsenic in urine does not mean that the level of arsenic causes an adverse health effect.5) 26..53 (..05 (.959-1.9) 14.37-2.16 (.91 (4. In recent years.80) . population for the sum of inorganic related species was 18. Vahter et al. 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.25-7.15-1. Offergelt et al.7) 17. 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. 2006.S..Metals as with DMA.4 (11.3 (10.7) 9. 2003. 2008).30-1.4 (24.67) 4.8) 29. 2001).79 (1. these levels were much lower than those found in other studies where environmental exposures were highly elevated (Chowdhury et al.65 (1.2 (12.6-46.05) 1.

Urinary Arsenocholine (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th < LOD 90th < LOD 95th < LOD Sample size 2568 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 621 725 1078 Limit of detection (LOD. * 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.Metals Urinary Arsenocholine Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.S.S. 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. see Data Analysis section) for Survey year 03-04 is 0.6. 186 Fourth National Report on Human Exposure to Environmental Chemicals . Survey years 03-04 Geometric mean (95% conf. which may vary for some chemicals by year and by individual sample. 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. < LOD means less than the limit of detection.

08 (<LOD-4.29) < LOD 621 725 1078 < 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. Urinary Arsenous (III) Acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.00) 1.20 (<LOD-1. Survey years 03-04 Geometric mean (95% conf.80) < LOD 621 725 1078 Limit of detection (LOD.Metals Urinary Arsenous (III) Acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.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. * 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. < LOD means less than the limit of detection.00 (<LOD-3. Fourth National Report on Human Exposure to Environmental Chemicals 187 . see Data Analysis section) for Survey year 03-04 is 1.40 (<LOD-1. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th < LOD 90th < LOD 95th < LOD Sample size 2568 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1.S.44) 2.2. which may vary for some chemicals by year and by individual sample. 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-2.70) < 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. Survey years 03-04 Geometric mean (95% conf.00 (<LOD-2.

22) 4.00-11.31) 4.24) 3.00) 6.59 (6.0) 11.32-10.45 (8.0) 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 4.80) 7.94) 3.00-5.10) 3.00-12.00-12.0) 10.0 (8.16 (2.67) 9.42) 3.00-15.0-25.00) 6. Survey years 03-04 Geometric mean (95% conf.S.90) 2.50 (4.61-16.31-4.34) 3.08 (2.00-15.00-4.7) 12.3 (7.0 (13.00) 4.00-4.00-4.0 (14.4 (7.0 (8.0) 16.0) 9.32 (8.0) 13.0 (10.11 (3.0 (10.90) 5.0 (10.00 (6.17-6.48 (3.62) 4.S.9 (11.80-6.0-12.70-4.86-21.61-11.9) 11.00 (5.00-7.00) 12.14) Selected percentiles ( 95% confidence interval) 50th 3.17 (2.0) 95th 16.0-19.0-18.88 (4.00) 90th 11.71 (3.78 (4.60-6. see Data Analysis section) for Survey year 03-04 is 1.0 (9.1 (8.0-16.00-10.50-15.7) 1284 1284 03-04 03-04 03-04 4.32 (4.06) 5.91) 75th 5.24-4.00-4.00 (7.0-17.69-3.48 (2.00-3.82-9.0) 292 728 1548 03-04 03-04 4.49) 10.19) Selected percentiles ( 95% confidence interval) 50th 3.00) 4.29-4.84-8.00 (4.00 (6.44) 5.44 (2.03 (3.2) 10.46 (4.57-5.00 (5.13-4.11) 4.80) 2.57 (3. Urinary Dimethylarsinic Acid (creatinine corrected) Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.27-2.7) 13.05) 3.27 (2.80-3.00) 75th 6.60-4.00-4.00) 3.90 (3.33-4.30 (7.5) 12.34 (3.97-3.27 (3.80-5.00-11. population from the National Health and Nutrition Examination Survey. interval) 3.0 (9.00 (3.00) 3.98) 4.69 (3.20) 11.8) 7.16-11.30) 3.00-13.16 (4.05) 5.7 (10.4) 621 725 1078 188 Fourth National Report on Human Exposure to Environmental Chemicals .1-15.9) 12.49-4.3 (8. Survey years 03-04 Geometric mean (95% conf.0) 16.28) 2.70-12.1-18.00-7.60-3.9) 13.15) 4.0 (13.12-4.0) 14.00 (3.6) 292 728 1548 03-04 03-04 3.95-4.20-4.0 (12.95 (4.5 (11.65-6.92) 3. interval) 3.12 (3.00 (3.8) 7.00 (3.3 (8.00 (3.50-5.34-4.25 (4.69-6.95-3.82-5.0 (10.78) 4.17-4.00-11.94-3.00-8.14) 3.8) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites Sample size 2568 03-04 03-04 03-04 3.1-22.38 (3.37 (3.33) 3.00) 7.18 (6.09 (7.00 (7.86 (2.82) 3.Metals Urinary Dimethylarsinic Acid Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.0 (12.05) 10.72 (4.45) 8.85 (3.71 (4.00) 6.00-15.77 (3.27-5.34 (3.6-18.6 (9.69 (3.00-4.0) 17.0) 11.7.60-7.00-9.0) 13.74) 90th 9.0-16.92-12.74 (2.52) 3.0) 621 725 1078 Limit of detection (LOD.0) 12.71-4.80 (4.45) 3.00-3.00 (5.89 (3.70 (3.7-16.67) 8.9 (7.84-18.0) 17.39-3.79 (3.00) 5.00 (3.00) 6.20-12.00-22.5) 95th 13.9) 5. population from the National Health and Nutrition Examination Survey.0 (11.70-3.00-7.0-17.00 (6.86-7.70) 5.0 (9.34-4.00 (5.0) 9.95-6.71) 3.00 (5.10) 6.0) 9.00) 9.65-8.81 (5.73) 6.37 (2.03-6.00-7.73 (3.6) 1284 1284 03-04 03-04 03-04 4.55 (2.

31-3.36) 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.61) 2.20 (1.10-1.93) .10) 2.52 (2.40) 1.30 (1.985) 1.00) 1.30) 2.30-1.80-2.10 (<LOD-1.50-2.00) 1.00) 2.70-2. population from the National Health and Nutrition Examination Survey.50) 621 725 1077 Limit of detection (LOD.00) 2.07 (1.S.80) Sample size 2567 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.53) Sample size 2567 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.816 (<LOD-.853-1.30-1.60) 2.45) 3.28 (1. Survey years 03-04 Geometric mean (95% conf.20-3.90 (1.61-3.53-2.96-2.88 (1.80 (1.80 (2.46-2.80 (1. see Data Analysis section) for Survey year 03-04 is 0.30 (1.00) 1.60) 1283 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.18-1.40) 2.70-2.30-2.31 (1.70-2.60) 292 728 1547 03-04 03-04 * * < LOD < LOD 1.80 (1.86) 3.30) 1.07) 2.80 (1. < LOD means less than the limit of detection.40-3.20-1.30) 1.20 (1.28 (1.46 (1. Survey years 03-04 Geometric mean (95% conf.86 (2.15-1.20 (1.07-3.50 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.30) 90th 1. Urinary Monomethylarsonic Acid (creatinine corrected) Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.40 (2.82-2.00 (1.Metals Urinary Monomethylarsonic Acid Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.10 (1.9.50 (2.14-1.90 (2.50 (1.85) 2.73-2.81) 1.90) 2.36 (1.23) 1.90) 1.88 (1.00 (2.00-2.00-4. which may vary for some chemicals by year and by individual sample.82-2.50) 1.00-2.57) 95th 2.S.35-3.40-2. population from the National Health and Nutrition Examination Survey.63 (<LOD-1.33 (1.00 (2.30 (2.10) 95th 2.10 (.40) 1.80) 1.18-1. 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 1.50 (<LOD-1.60 (2.70) 2.20 (1.20 (1.00-1.17) 2.20) 2.60 (1.34) 2.20 (1.10-3.53) 292 728 1547 03-04 03-04 * * < LOD < LOD 1.77) 1.86) 2.53 (1.70-2.60) 2.37 (1.11-1.80) 1.90) 2.85) 1.80-2.75) 621 725 1077 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.16 (2.86 (2.22 (1.79) 2.88-2.33 (1.05-1.10-1.60) 1. Fourth National Report on Human Exposure to Environmental Chemicals 189 .40-3.84-3.53) 1283 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.00 (<LOD-1.00 (<LOD-1.40-2.10 (.58) 2.40 (1.10 (1.00-1.54) 90th 2.62) 2.900-1.70-3.60-2.43-3.22) 3. 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 1.30 (1.71-2.

Urinary Trimethylarsine oxide (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. which may vary for some chemicals by year and by individual sample.S. Survey years 03-04 Geometric mean (95% conf. 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. 190 Fourth National Report on Human Exposure to Environmental Chemicals . * Not calculated: proportion of results below limit of detection was too high to provide a valid result. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th < LOD 90th < LOD 95th < LOD Sample size 2568 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 621 725 1078 Limit of detection (LOD. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.Metals Urinary Trimethylarsine oxide Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. Survey years 03-04 Geometric mean (95% conf. population from the National Health and Nutrition Examination Survey. < LOD means less than the limit of detection. population from the National Health and Nutrition Examination Survey.S. see Data Analysis section) for Survey year 03-04 is 1.0.

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87 (6.45 (1.39 (1.59-11. respectively.71-9.02 (7.50 (4. barium sulfate and barium carbonate).27 (1.37) 1.50 (4.53-5. fireworks. Barium compounds are used by the oil and gas industries to make drilling muds.50 (3.Metals Barium CAS No.15) 5.28-1. it combines with other chemicals such as sulfur or carbon and oxygen.87-9.56 (1.12) 6.10 (4.82) 2. and ceramics.90 (4. In nature.01 (4.21 (1.07 (2.60) 1.60-6.39 (1.80 (2.71 (2.40) 7.32-1.78) 1.S. 01-02.70) 1.60 (1.67) 6.72) 1.74-3.20-6.05% of the earth’s crust.85) 1.92) 2.57) 3.30-2.73 (6.51) 7.74) 3.35 (3.50-1.80) 6.43) 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 1.35 (1.15 (6.40-13.20-8.84) 5.30 (1.85) 1.40 (1.30) 5. Urinary Barium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.60) 1.32) 8.4) 9.18-1.94-6.43 (1.30) 2.80 (5.14 (6.36) 5. and 0.62) 1.14-1.30) 4.43) 2.61 (3.50 (1.10 (2.17-1.65-8.21-8.11 (3.49-9.85 (2.76-7.30) 5.46) 1.68 (1.30-3.48) 1.50 (6. water.40 (1.10 (3.46-1.36 (1.63) Total 1.22-1.19) 2.76-3.48) 1. 0.45) 7.10-4.90-2.38 (1.90 (6.86 (4.88 (5.80-7.08-8.39-1.36 (4.20-5.88) 7.95-6.63) 1.80-5.50 (1.56 (6.73 (5.35-1.56) 1. barium sulfate is used as a contrast medium for taking radiographs of the gastrointestinal tract.57-7.50 (2.63) 1.20-1.54-1.73) 3.30) 5.00) 6.15-11.70-6.54) 2.15-1.54) 1.90) 2.31 (2.10) 5.28) 90th 5.82-6. such as brazil nuts.54) 1.70 (5.41-1.50-6.51) 2.20-8.70-3.80 (1.76 (3.97 (1.88) 1.50 (1.18 (6.61 (1.99-5.00) 1.66) Selected percentiles ( 95% confidence interval) 50th 1.00 (2..78-2.86-4. Barium salts have also been available as rodenticides.62 (1.30 (2.60-2.39) 4. see Data Analysis section) for Survey years 99-00.53) 2. glass.70) 3.70-2.49) 11.22) 6.70-5.70) 1.63 (8.87) 7.00-8.56) 4.15 (2.36-1.8 (6.30-5.47) 4.16) 5.38) 8.50) 1.62) 1. In single dose animal studies. Some barium salts are freely soluble in water.50) 2.30) 8.77) 1.60) 3.41) 1.00-3.11 (2.87-14.47-1.80 (1.24 (4.26-7.36-1.81-2.00-76.26) 5.09 (2.20-1.90) 1.50-1. and food.21-2.60) 4.03 (1.50 (1.20 (4.61 (5.25 (1.49) 2.90) 4.70-8.04-2.76) 1.49) 8.50 (4. Ingested soluble barium General Information Elemental barium is a silver-white metal which comprises approximately 0.80-3.70) 5. interval) 1.04-6.54-8.21 (1.10-5.73-5.95 (4.51 (1.86-5.55-3.1) 9.76-2.19-1.49 (1.29-1.78-3.32-7.30-2.60 (2.91 (2.40 (5.27) 2.8) 5.31.75-3.93-8.43 (1.91) 2.62 (1.20 (1.9) 5.80 (2.80-2.40) 7.69 (1.65) 3. 2001).59) 3.49) 4.64) 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 2.15-1.54-1.87 (5.25-11.72) 75th 3.70 (1.27 (1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. The general population can be exposed to low amounts of barium in air.37) 5.90 (1.46) 1.50 (5.10) 3.81-3.60-3.64 (1.93-2.77-3.54 (2.12 (2.g.37-1.80) 1.14-6.35 (2.37 (4. depilatories.26-1.12.88) 4. bricks.48-4.44 (1. 7440-39-3 Medically.31-2.34 (1.26) 2.70) 4.50 (1.30 (5.12 (2.71) 2.05-2. were relatively well absorbed following inhalation (60-80% of a dose) or ingestion (11-32 % of a dose). whereas others are practically insoluble (e.90-13.12-1.86 (4.09 (1.57 (5.01-7.87-7.42 (1. are high in barium (Genter.08 (6.61 (2.4) 7.35-4.78) 1.30) 3. population from the National Health and Nutrition Examination Survey.40 (1.61 (1.30-1.60-6. such as barium chloride.18) 3.40 (5.48 (6.75) 2.00) 1.12.38 (1.39) 1.56 (2.96-2.30 (5.33 (1.52 (4.40 (4.53) 1. rubber.65 (5.06-1.25-1.44-5.37-8.12) 7.56 (1.40 (5.63 (5.64-3.43) 6.35-1.11-1.50-6.20) 2.65) 1.35) 5.70) 7.20-1. Small amounts of barium can be released into the air during mining and other industrial processes.34 (1.71) 95th 6.90) 2.63 (2.29) 5.41-3.63 (1.06-2.52 (1.20 (3.74-2.50) 4.99 (4.44-2.87-3. Fourth National Report on Human Exposure to Environmental Chemicals 193 .48-4.00) 4.61-8.54 (6.16 (1.30 (3.80 (1.8) 9.24-1.4) 6. Barium compounds are also used commercially in paint.30-1.11 (3.29-5.65-5.43 (5.20-1.66 (4.53) 692 683 618 540 667 723 765 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.65-1.98) 1. soluble forms of barium. Workers employed by industries that make or use barium compounds can be exposed to barium dust. Certain foods.81-2.90-9.73) 1.51) 1.55-7.77 (3.47-1.72) 4.15 (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 1.20-8.38) 2.00 (1.40) 3.24-1.22-1.91) 6.50) 2.71) 1.65) 1. tiles.82) 1.2) 6.86) 6.34) 2.93 (4.49-1.34 (2. and 03-04 are 0.60-10.70-2.80) 7.

96) 7.47) 1.62 (2.27 (2. 1989).68-3.48-3.921 (. The health effects of exposure to barium compounds depend on the dose. Toxicity from soluble barium salts is rare.79-5.21 (1.70) 1.56 (1.78 (2.00) 6.4 (5.92) 2. Insoluble barium salts.38) 1.26-1. 1986).41) 4.29 (3.24) 3.30) 2.37-2.46) 2.35-3.38) 1.42 (4.68) 3. population from the National Health and Nutrition Examination Survey.72) 4.00 (2.68 (3.26-4.30 (1.42) 1.04) 1.39 (2.32 (1.37-1.69 (5.28-6.00-1.22-4. are not absorbed when administered.880-1.40-1.82) 1. Barium is not rated for human carcinogenicity. Symptoms following acute high dose include perioral paresthesias.91-2.86 (2.28-11.34-3.38-5.53) .52 (3.49-1.76 (2.64 (1.22-1.27-1.57-10. a benign condition that may occur among barite ore miners.46) 1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.34 (1.54 (1.56) 4.12) 2.39-1.42) 1. Barium blocks cellular efflux of potassium resulting in profound hypokalemia.26-1.20-1. 1984.58) 75th 2.84) 2. and cardiac dysrhythmias.47) 4..19-1.18 (1.39 (3.63) 1.92 (4.29-4.55) .56-3.74) 1.39 (2.46) 3.49-1.24-1.37 (1.24 (5.65 (5.47) 1.39) 4.01 (5.58-6.91 (3.04 (2.53 (2.74) 1.26-1.75) 2.62 (1.70) 4.70) 10.72) 6.00-7.19-1.34-1.64 (1.72 (2.59 (1.02-5.00) 4.11) .75) 1.45-8.45) 1.45-1.87) 1.45-1. Following intravenous injection in animals.64 (1.55 (4.36 (1.32) 2.48 (1.25 (1.54) 1.23-1.33) 1. vomiting.51-3.33 (1.51 (1.19-1.24-11.5) 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 1.48-5.36-1.S.4) 5.76) 2.60 (2. interval) 1.00) 4.99 (2.34-5.20 (1.61 (4..29-1.62 (4.36-2. 1985.77) 1.00 (3.11) .45 (3.60 (2.76) 2.63-4.41) 5.27) 692 682 618 540 667 723 765 1132 1074 Non-Hispanic blacks Non-Hispanic whites 194 Fourth National Report on Human Exposure to Environmental Chemicals .46 (2.77) Total 1.55 (1.52) 2.777-1.905 (.46-22. in urine. 1994.60 (1.73-4.39-5.86-7.98 (2.25-11.49 (1.32 (2.28-7.85-5. about 75 % of a dose of soluble barium was eliminated within 3 days (Reeves.75-3.31 (1.51) 4.38 (1.58) 1.44-2.Metals was eliminated primarily in feces and to a lesser extent.03) 2.29-4.16-1.00) 1.48-1. Perry et al.10-1.38-7.81-6.08-2.25) 4.16 (1.24-1.27-3.59-7.891 (.91) 2.81-6.26-1.04) 5.881 (.36 (5.45-6.23-5.69-9.53-21.39-10.710-1.61) 2.31-1.31) 5.00 (3.86) 5..57 (6.10-2. chemical form.38) 4.51 (1.10) 3.29-7.31-1.96) 4.03-1.30 (1.77) 5.32 (1.40 (1.99 (4.96 (4.37) 2.48) 2.40 (1.96) 4.96-6.03) 1. Chronic accumulation of inhaled barium dust in the lung tissue may cause baritosis. water solubility.24 (3.57-7.41 (1.60 (5.54) 2.35-1.84-5.00 (5.64) 7.915 (.88 (2. paralysis.18 (1.76 (4.41 (2.97 (5.76) 1.22-1.28 (1. diarrhea.31-1.77) 1.76-3.33 (5.73-2. such as those used in medical radiographic procedures.50 (4.84 (3.52-4.89) 90th 4.64 (1.67-6. but can occur after intentional or accidental ingestion of barium carbonate in rodenticides (Genter.34) 1.47 (5.01 (4.75) 1.0) 7.26) 4.83) 2.80) 3.37 (1.54 (2.51) 4.29 (1.32) 2.08-1.44-2.754-1.80-6.36 (1.55-6.91 (3.60) 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 2.68 (3.43) 1.68) 1.83) 3. 1990).28) 5.96 (4.97-4.38 (1.16) 11.51) 6.39-1.88 (6.56 (1.52-10.58 (2.703-1.96) 4.02) 4.23-2.09) 6.13-2. Chronic high doses in animals resulted in kidney damage (McCauley et al.45) 95th 6.14-2.52) 7.2) 5.48 (1. Chronic exposures to natural low levels of barium in drinking water have not produced general health effects or evidence of cardiovascular risk (Brenniman and Levy.89 (2.40 (1.10) 6.24-6.50) 297 368 290 621 762 725 1262 1559 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 1.97) 1.03-1.01) 1. Urinary Barium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. hypertension.20-2.76 (3.59) 1.28-1.38 (4.99) 1.11-2.75) 2.97-3.0) 5.8) 4.22-2.13-3.29-3.47 (2.55 (5.52) 1.963 (.0) 6.55-5.57-5.58) 4.62) 2.50) 1.27) 7.02 (3.64) 7. weakness.20) 4.58 (4.33 (1.15-4. NTP. and route of exposure.35-1.84-2.60 (1.59) 1.24-3.80) 4.33-4.90-2. Wones et al.65 (2.43-6.2) 6.73) 2.02) .36 (3.45 (1.77) 1.97 (4.05-1. Human health effects from barium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.33-1.68-3.36-1.55 (1.56) Selected percentiles ( 95% confidence interval) 50th 1.38-1.49 (1.10 (6.59) 2.82) 1.832-1.06) .3 (6.41 (1.20-8.48 (1. 2001).38 (4.31 (4.47-8.44 (1.36 (3.19-2.51 (3.3) 6.49-1.03) 3.29) 1.39 (2.06) 2.79) 1.71 (5.24-6.77-5.57) 2.33) 6.81-7.68 (2.47) 10.74 (5.75-22.50) 2.59 (1.66 (1.50) 1.2 (3.

e. Zschiesche W. Studies reporting urinary levels of barium in general populations have found values generally similar to those reported in NHANES 1999-2000.197210. eds. Investigations into the effect of drinking water barium on rats. and serum of Italian subjects. Pietra R. 1998).95:89-105. Gallorini M. Environ Res 1998. 1984. NTP. 1990.gov/toxpro2.. pp. Environ Health Perspect 1990. Stadler BL.html. et al. Princeton NJ: Princeton Scientific Publications. EPA. Calabrese EJ.. blood. ed.28(3):373-388. Barium levels determined in clinically submitted specimens were broadly comparable (Komaromy-Hiller et al. Paschal et al. A study of 46 elements in urine. and a drinking water standard has been established by U. Minoia et al. Perry EF. Ash KO.nih. Sci Total Environ 1990. calcium. Urinary concentrations in acute poisonings are often hundreds to thousands of times higher than in this Report. Atlanta (GA). p. Morrow JC.85:355-359.64(1):13-23. Handbook on the Toxicology of Metals. strontium. Sampson EJ.. McCauley PT. New York: John Wiley & Sons. and radium In: Bingham A. Patty’s toxicology. et al.76(1):53-59. 2005. p.nih. Laurie RD.gov/ntp/htdocs/LT_rpts/tr432. environmental levels) and health effects is available from ATSDR at: http://www.296(1-2):71-90. Hypertension and associated cardiovascular abnormalities induced by chronic barium feeding. Kopp SJ. Advances in modern toxicology..gov:8080/cs. New York: Elsevier.. Available at URL: http://ntp. Princeton (NJ): Princeton Scientific Publications. Vouk VB. Ting BG. LA. 1992). patient population and literature reference intervals for urinary trace elements. Trace element reference values in tissues from inhabitants of the European community I. Vol 2: Specific Metals. 1989. the welders had no obvious adverse clinical effects (Zschiesche et al. In Friberg L. Third National Report on Human Exposure to Environmental Chemicals. In: Inorganics in drinking water and cardiovascular disease. 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. Frohman.cdc.S. Apostoli P. National Toxicology Program (NTP).atsdr. J Toxicol Environ Health.Metals Workplace standards for external air exposure to various barium salts have been established by OSHA. p.niehs. 2000) to levels in NHANES 1999-2000 and 2001-2002. Weltle D. Epidemiological study of barium in Illinois drinking water supplies. PS. Welders of barium-containing electrodes had median urinary levels of barium that were 60 times higher than the median levels in this Report. 2nd Ed. 2001-2002.. Reeves AL. technical report on the toxicology and carcinogenesis studies of barium chloride dehydrate (CAS no. Int Arch Occup Environ Health 1992. barium. Cohressen B.niehs. 1994. Finding a measurable amount of barium in urine does not mean that the level of barium causes an adverse health effect. 221-252 Komaromy-Hiller G. Clin Chim Acta 2000. Trace metals in urine of United States residents: reference range concentrations. [online]. 2001. Pirkle JL. Wones RG. References Brenniman GR.. Jackson RJ. In: Calabrese EJ. 5th ed.pd f&qt=barium+chloride+dehydrate+1994&col=020rpt&n=3&la= en. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Information about external exposure (i. 1986.. 2005. Sabbioni E. Exposure to soluble barium compounds: an interventional study in arc welders. ed. 4/8/09 Paschal DC. et al. 231-249. Centers for Disease Control and Prevention (CDC). Perry HM. Levy. Schaller KH. 84-94. Nordberg GF. 10326-27-9) in F344/N rats and B6C3F1 mice (drinking water studies). Comparison of representative ranges based on U. Minoia C. Inc.html?charset=iso-88591&url=http%3A//ntp. Lack of effect of drinking water barium on cardiovascular risk factor. Genter MB.. Barium. Biomonitoring Information Levels of urinary barium reflect recent exposure. Jr. Powell C. eds. and 2003-2004 (CDC. Pozzoli L. et al. Howerton K.S. Douglas BH. Magnesium. Costa R. 1985. Fourth National Report on Human Exposure to Environmental Chemicals 195 .

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 . Beryllium is also used in the production of sports equipment such as golf clubs and bike frames. aircraft. 7440-41-7 General Information Pure beryllium is a hard gray metal.140 (<LOD-. Two types of minerals.13. and refined beryllium is used in mirrors and special metal alloys for the automobile. Low-level beryllium exposure in the general population can occur through breathing air.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 . 196 Fourth National Report on Human Exposure to Environmental Chemicals . and dental bridges. or drinking water containing the metal. and can be found in mineral rocks.S. which may vary for some chemicals by year and by individual sample. and 0. electrical. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. computer.130 (<LOD-.Metals Beryllium CAS No.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 . inhaled insoluble beryllium sulfate was retained in the lungs and nearby lymph nodes. Burning coal and oil can produce small amounts of beryllium dust that can be released into the air. less than one percent of the inhaled dose was slowly absorbed into the blood and eventually incorporated into the skeleton. Exposure to beryllium occurs mostly in the workplace. 01-02. and machine-parts industries. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. coal. 0. are mined for commercial recovery of beryllium. x-ray machines. see Data Analysis section) for Survey years 99-00. eating food. In studies of laboratory animals. near some hazardous waste sites. beryllium is used in instruments. population from the National Health and Nutrition Examination Survey. and 03-04 are 0. and volcanic dust. < LOD means less than the limit of detection. nuclear.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. and from breathing tobacco smoke. the lightest of all metals. respectively. In medicine.13.13. soil.130 (<LOD-. bertrandite and beryl. A half-life of 450 Urinary Beryllium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. Beryllium compounds are commercially mined.

based upon excess lung and central nervous system cancers in studies of workers. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. S. Genetic factors modify individual sensitivity to beryllium and susceptibility to developing chronic beryllium disease (McCanlies et al. which produces pneumonitis. is a granulomatous interstitial lung disease that is caused by chronic beryllium inhalation and the resultant immunologic response. 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.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 . and drinking water and environmental standards have been established by U. 1990). NTP considers beryllium to be a known human carcinogen. EPA. Maier. or berylliosis. population from the National Health and Nutrition Examination Survey. Chronic beryllium disease. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. 2003. 2002).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.231 (<LOD-. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th < LOD < LOD < LOD 90th < LOD < LOD < LOD 95th < LOD < LOD < LOD Sample size 2465 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 . including contact dermatitis and subcutaneous nodules.346 (<LOD-.Metals days has been calculated for beryllium elimination from the human skeleton (IPCS. IARC has classified beryllium as a human carcinogen.. Fourth National Report on Human Exposure to Environmental Chemicals 197 .273) < LOD < LOD < LOD < LOD 340 368 290 719 762 725 1406 1559 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . Human health effects from beryllium at low environmental doses or at biomonitored levels from low environmental exposures are unknown. Workplace air standards and guidelines for external exposure have been established by OSHA and ACGIH.281 (<LOD-. 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. The effects of occupational exposure to beryllium depend on the concentration of beryllium in the inhaled air and the duration of air exposure.S. respectively.

Minoia et al. Pirkle JL.htm. less than 0. Int Arch Occup Environ Health 2001.html. it is likely that urinary beryllium levels in the U. References Apostoli P.S. Paschal DC. 0. Gallorini M.Metals (i.. Given these results. blood. McCanlies EC. Ting BG. Urinary beryllium--a suitable tool for assessing occupational and environmental beryllium exposure.15 μg/L in workers exposed at the recommended threshold limit value (Apostoli and Schaller. and 2003-2004. Sci Total Environ 1994. Kriess K. Sampson EJ. In other studies.. Apostoli P.95:89-105. patient population and literature reference intervals for urinary trace elements. Minoia C.e. Van der Venne MT.296(1-2):71-90. Review of elements in blood. 106. Costa R. urinary levels for general populations have been either undetectable or had different detection limits than in this Report (KomaromyHiller et al. Hamilton et al.13 μg/L..158:165-190. 1990. They reported urinary beryllium levels ranging from 0. Paschal et al. Environmental Health Criteria. Howerton K. Finding a measurable amount of beryllium in urine does not mean that the level of beryllium causes an adverse health effect.23:827-839. 2000. 198 Fourth National Report on Human Exposure to Environmental Chemicals . Levels of beryllium in urine for the U.12 to 0. Andrew M. Beryllium [online].. Element reference values in tissues from inhabitants of the European community. 20012002. Environ Res 1998.inchem.1 μg/L). Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. and the 95th percentile for males in NHANES 2001-2002. Centers for Disease Control and Prevention (CDC). Sabbioni E.76(1):53-59. Jackson RJ.atsdr.cdc. Hamilton EI. Sci Total Environ 1990. 1998).org/documents/ehc/ehc/ ehc106. and the fact that most NHANES participant levels were undetectable. HLA-DPB1 and chronic beryllium disease: a HuGE review.S. and serum of Italian subjects. Atlanta (GA) 2005. (1994) noted that analytical methods used in several general population studies appeared to have limits of detection that were insufficiently low (i. Genetic and exposure risks for chronic beryllium disease. et al. International Programme on Chemical Safety (IPCS). Morrow JC. Sabbioni E. Weston A. 1990. Third National Report on Human Exposure to Environmental Chemicals. population were generally undetectable in NHANES 1999-2000. Ash KO. Clin Chest Med 2002. Available at URL: http://www. Trace element reference values in tissues from inhabitants of the European community I. Apostoli and Schaller (2001) stated that detection limits in earlier studies were inadequate to estimate nonoccupational exposures. A study of 46 elements in urine. Pozzoli L. which approximate this Report’s limit of detection.157:388-398. Pietra R. Am J Epidemiol 2003. plasma and urine and a critical evaluation of reference values for the United Kingdom population. et al. Comparison of representative ranges based on U.. VI. environmental levels) and health effects is available from ATSDR at: http://www.e. 3/27/08 Komaromy-Hiller G.gov/toxpro2. 2001). Biomonitoring Information Urinary beryllium levels represent recent and accumulated exposure. Maier L.S. population are lower than levels in workers. Clin Chim Acta 2000.74:162-166. Trace metals in urine of United States residents: reference range concentrations. Schaller KH. 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.

400-.200-.400-.300) . 01-02.800) 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 .400 (.3.00-1.00) . cadmium use has declined in response to environmental concerns (http:// minerals.400) .00 (1.376-.200) .400) < LOD .300 (.700) .300) .300 (.300) .500) .300 (.60 (1.400 (.200 (<LOD-.400) .359-.300-.30-1.10) 1. malleable.20) 1.600) 1.50 (1. Since 2001.400 (.460) .20-1.800 (.500-.600 (.800-1.700-1.300-.30-1.500-. Fourth National Report on Human Exposure to Environmental Chemicals 199 .378-.400 (.395 (.600 (.200 (.10) 1.900-1.80) 1.300) .70) 1.400 (.20) 1. and 0.400) .00-1.400) .00-1. population from the National Health and Nutrition Examination Survey.400-.50-1.300 (.300-.300-.700) .600 (. and 03-04 are 0. Blood Cadmium Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.10 (.500-.368-.00-1.300-.700 (.500) .300 (.400 (.20) 1.600) 90th 1.600) .300-.S.500 (.30) 1. respectively.300 (.300-.70) 2742 2268 2085 1842 2219 2292 2716 3806 3478 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.00 (.60 (1.60) 1.300) .600 (. < LOD means less than the limit of detection.600) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.400 (.470) * . The predominant commercial use of cadmium is in battery manufacturing.216-.400) .30 (1.800) .500-.300 (<LOD-.700) . which may vary for some chemicals by year and by individual sample. Cadmium also may be emitted into the air from zinc.255) .80) 1.235 (.500-. 7440-43-9 General Information Cadmium is a soft.10) 1.300) .30) 1.304 (.700-1.400-.40-1.304-.300-.50 (1.90) 1.200-.427) * .300-.20-1.500-. and nonferrous alloys.900-1.266-.500 (. as zinc sulfide) and to a lesser extent.421 (.70) 1.600) .700-1.400) < LOD .400 (.300 (.600) .60) 1.400-.300) .300-.900-1.500-.60) Total * .400 (.403 (.700) .10) 1.320) Sample size 7970 8945 8372 Age group 1-5 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * .400 (.900 (.200-.200) .40) 1. 0.20) 95th 1.60 (1.500-.00-1.400) .60) 1.300-.313 (.50 (1.600 (.10 (1.400) .20-1.900-1.40 (1.70) 1.600-. and incineration of municipal waste materials.gov/minerals/pubs/commodity/cadmium). during refining of lead and copper from sulfide ore.70) 1.500) .80 (1.700) .60-1.500) .500-.300 (.600) .386-.40 (1.412 (.300-.10) 1.20) 1.S.600) .500 (.600 (.300-.20 (1.366) * * .10 (1.70) 3913 4339 4131 4057 4606 4241 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .400) .300-.600) .500-.800) .00 (.300 (<LOD-.40 (1.300 (.500-.14.300) .700) .500 (.600 (.40 (1.800 (.40-1.400 (.400) .600) .20-1.400-.283 (.300-.20-1.10 (1.500 (.426-.20) 1.50-1.452) . lead.300-.200-.400-.400-.900-1.3.300) .50-1.441) * .600 (.337) .300 (.600-.60 (1.500 (. bluish-white metal that is obtained chiefly as a by-product of processing zinccontaining ores (principally sphalerite.275-.500-.10 (1.00 (.600 (.500-.900-1.420 (.500) .300 (<LOD-.400 (.362-.300) 75th .400-.10) 1.600 (.400) .900-1.20) .500-.900-1.30-1.60 (1.10) 1.200 (.20) .468 (.400 (.400) < LOD .00 (.700) 1.200 (<LOD-.600 (.500-.326 (.20) 1.400-.40) 1.500 (.400) .296-.449) Selected percentiles ( 95% confidence interval) 50th .00 (.10 (1.500-.50-1.600 (.500) .30-1.300-.700) .425 (. plastic stabilizers. Other uses include pigment production.300-.20-1.300) .500-.00 (.400) .500) .378 (.400 (.Metals Cadmium CAS No.00 (.300 (. interval) .40 (1.300-.300 (.900-1.usgs.382 (.361-.20) 1.333 (.00 (.10 (1.393 (.403) .600 (.00-1.200 (.300-.50 (1.300 (.00-1.289-.600 (.30-1. or copper smelters (U.900 (.600-.367-.20-1.331) .600) .00-1.40 (1.300) . EPA.20) 1.00 (1.513) .800-1.400 (.30) .309-.00 (.400 (.10 (1.30) 1.400 (.300) 1.10) 1.50) 1.300-.20 (. U.398) < LOD < LOD < LOD < LOD < LOD < LOD .300) .304 (.50) 1.500 (.300) .40 (1.400) .200-.50) 1.00 (.00) .400) < LOD < LOD < LOD .424) * .300-. see Data Analysis section) for Survey years 99-00.344) . Important sources of airborne cadmium in the environment are burning fossil fuels such as coal or oil.300 (<LOD-.300 (.900-1.500-.00-1.400-.600-1.500 (.700) .400) .S. coatings and plating.

741-1.843-1.170-.257) .238-.295) .327 (.28-1.226) Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 * .175 (.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..249) .255) .219 (.38) .17 (.077 (.231) .940-1.436-.980-1.210 (.148) .201 (.12-1.330-.490) 1.120 (. individual values vary and are affected by factors such as dietary intake of essential nutrients (iron.423-.839 (.520-.686-.280 (.700-.400-.170-.180 (.322 (.04 (.48 (1.818 (.302 (.184-.191-.313) . With chronic exposure.191 (.466 (.700-. zinc.519) .190-.551) . 200 Fourth National Report on Human Exposure to Environmental Chemicals .507) .210 (.17 (. 2004a.300 (.300) .227 (.03) .500) 90th .210 (.713) .284) .175 (.193 (.221) .203) .065-.329 (.239 (.476-.339) .06.74) 1. The estimated half-life of cadmium in the kidney is from one to four decades (ATSDR.200 (.20 (1.490) .875) .246) .243-.963-1.290-.251) .067-. 2003.130 (.433-.219 (.500) .281 (.221 (.206 (.354) .210) .350 (.262) .189-.820) 1.247) .25) 1.633-1.241) .20-1.700-.220-.394-.109 (.206) .230) 75th .207-.187 (.202-.253-.237-.173) .192-.153-.178-.813 (.633 (.493-.539) . including many food crops such as cereal grains. For nonsmokers who are not exposed to cadmium in the workplace.551 (.135-.875 (. Diamond et al.714-1.216 (.249-.15) 1.820-1.160) .316 (.235) .183-. rice.200 (.114-.260-.234 (.148-.171-.733) .980-1.38) . About one-third to one half of the total body burden accumulates in the kidney tissues (Nordberg and Nordberg.211-.220) Selected percentiles ( 95% confidence interval) Sample 95th 1.400-. 2003).189-.705-..01) .199 (.13) .492 (.15) .09-1.06-1.530 (.061-. The kidney is a critical target and shows the earliest sign of cadmium toxicity.38) 1.890 (.445 (.263) ..43) 1.179-.04 (.210) . To a lesser extent.233) .265 (.326) .919) .160 (.189) .121 (.170 (.452 (.498-..72) 1. 2003).169-.229) .960 (.240-.892-1.462 (.810-1.238) .202 (.299) .858 (. 2001).360) .13-1.192-.167-.972 (.475 (.279 (.24) 1.381-.220-.980 (.230) .100-.26) size 2257 2690 2543 Total years 99-00 01-02 03-04 50th .204 (.285-.596) .766 (.886) .150) .820 (.753-.07-1.200-.219 (.559 (.092) . 0.860) 1.83) 1.20) 1.730-. Urinary Cadmium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.607) .S.763-.128 (.510) . Renal tubular and glomerular damage.366-.351-.261-.306 (. a factor that may contribute to the higher absorption of cadmium by women (Diamond et al. Cadmium in soil is absorbed by plants.289-.366) .06) .255) .283 (. respectively. calcium. and 03-04 are 0.800 (.157) .440-.372) .270 (. wheat.362) .482) .260 (.229-.870) .19) 1. ingestion through food is the largest source of exposure..17 (.836-1.790 (.817 (.17) .440 (.198) .892 (.090) .22 (1.136) .214-.470-.479) .990) .06-1.233) .232 (.210 (.109-.748-1.38) 1. and various seeds. drinking water is a source for cadmium intake.450 (.20 (1.150-.310 (.226) .41 (.190-.177-.** Survey Geometric mean (95% conf.223 (.115-.078 (.440 (.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 .255) .196-.52 (1.126) . 1999.087-.640) .387) .430-.680 (.151-.265) .733-.01-1.36) 1.388-.02-1.57) 1.20 (1.977) .261-.13 (.481) .270 (. whose body burdens of cadmium can be approximately twice that of nonsmokers.28 (1. **All results are corrected for molybdenum oxide interference in the ICP-MS method.610) . and 0.890-1.458 (.277 (.980) . however.82) 1. copper) and protein. cadmium accumulates in the liver and kidneys where it is bound to metallothionein.34) 1.140 (.200-.112-.426 (.193-.550 (.390 (.240) .209 (. population from the National Health and Nutrition Examination Survey.880) .989-1. potatoes. 1994).519) .390-.06.450 (.800-.960) 1.848 (.211 (.456-.220) .067-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.220 (.717-.208-.32 (1.272-.817 (. Cadmium is absorbed via inhalation and ingestion.430) . Horiguchi et al.061 (<LOD-.806) .194-.190-.080 (.530) ..232) .366-.320) . interval) .28) 1.393-.25 (1.101) .510-.589 (.412) .203 (. an inducible metal binding protein.230 (.092 (.229) .980) . The gastrointestinal absorption of dietary cadmium is about 5% in adult men and 10% or higher in women (Diamond et al.918-1.210 (.191-.165-.110-.580) .886-1. see Data Analysis section) for Survey years 99-00.308) .160) .15 (.10 (1.222) .540) .282 (.47) 1.081) .310) .01 (.077 (.157-.445 (.141 (.257-. Cadmium absorption may be increased with iron deficiency (Berglund et al.545 (.336) .181 (.790 (.06.195-.160-.273 (.134) .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 .855-1.30-1.455 (. 01-02.090) .060-. 2003).390-.260-.51 (1.135 (.12 (.623) .480) .Metals 2000).107-. Inhalation of cigarette smoke is a predominant source of exposure in smokers. Kikuchi et al.22 (.447 (.

716) .216-.123-.667) .13) .292) .560-.318 (.267 (.227-.404 (.421 (.440) .316) .212 (.184-.175 (.235) .228-. Noonan et al.884) .Metals manifested by irreversible proteinuria and progressive reduction in glomerular filtration rate.209) Selected percentiles ( 95% confidence interval) Sample 95th .826-1.700) .631) .245 (.148 (.137 (.818) .688-.261 (.209) .085-.255-.156 (.293-.289) . 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.617 (.415) . **All results are corrected for molybdenum oxide interference in the ICP-MS method.622 (.909-1.05) 1.10) 1.176 (.364) .282 (..690-. can result from high dose chronic exposure.533) .382) .470) .126 (.779 (.767 (..074-.182) .998) .545) .802 (.100 (.247-.266) .38) .175-.157-.818) .097) .16) .336-.207) .077-.07 (.472) .985 (.663 (.086 (.917) .691-.331 (.813-..278) .00 (.316 (.308) .166 (..096) .754) .470) .325 (.927-1.433-.197-.051-.789 (.098) .122 (.449) .210 (.093 (. Olsson et al.668-.156) .268 (. interval) .827) .296 (.067-.090 (.202 (.757 (.263 (. 2004b).329 (.204-.238) .075 (<LOD-.247-.690 (.686 (.176 (..184) .154-.101) .173 (.678-.398-.181 (.218) .387-.440) .140-.830) .962) .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 .431) .304-.232) .795) 1.792 (.240) . 2002.352) .441-. 2002.551) .219 (.094) .423-.224 (.** Survey Geometric mean (95% conf.273 (.828) .806-1.874-1.210) .507-.716-.219) Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 * .432 (.813-1.207-.281) .250) .232) .143-.650-.487 (.253) . population from the National Health and Nutrition Examination Survey.289) .226) 75th .491-.382-.757) .150-.239-. 1999).123-.091 (.205 (.696-.219 (.221 (.607) .481 (.270 (.191 (.490 (.00 (.187) .215 (.211 (.729 (.163 (. Fourth National Report on Human Exposure to Environmental Chemicals 201 .02 (.225) .340) .767) . However.181-.208 (.940 (.288) .170 (.850) .614) .700 (.147-.091 (.104) .08) .143) .979 (.168 (.708-1.839) . 2002.178-.078-. At lower environmental exposures.071 (.078 (.156-.234-.177) .919 (.075-. 2004).191) .225) .690-.343-.476) .236-.484 (.242) ..950) .104) .171-.112) .388-. 2000.906) .162 (.350) .178) .541) .769 (.562-.674-1.722-. 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.208-.185) .653) .183 (.856 (.175 (.083-.136-.538) .687-.182) .740 (.261) .189-.266-. 1999).434 (.725-1.240) .263-.288 (.678 (.157-.146-.173-.07) .16) 1..174-.438-.137-. During the 1950’s and 1960’s.536 (.303) .234 (.917 (.063-.234) .144-.381-.693 (. most often a result of occupational exposure (Roels et al.666-.136-.559-.850) .444-.414 (.233 (.084-.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.300-..185 (. 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.308 (.190 (.826-1..931 (.865 (.830-1.09 (.473 (.256-.274) 1.261-.131-.712 (.501 (. Staessen et al.154 (.085 (..241) .391-.281) .170-.161-. Jarup et al.518) .283 (.199 (.158-.229) .338 (.321) .687 (.531 (.418) .404) .253 (.438) 90th .184-.267 (.387 (.04) size 2257 2689 2543 Total years 99-00 01-02 03-04 50th .783) .163) .17) .377-.873 (.140-.304) .06 (.182) .940-1.159 (.784) .201-.147-.833-1.516-.297) . 2003. two studies in Japan did not find an association between cadmium in urine and renal biomarkers (Ezaki et al.220 (.143-.423 (.446) .12) 1.500-.113-.192) .194-. 1996.941 (.479 (.198) . 1999).130-.414-.147 (.537-.084 (.199-.876-1.191-.783 (. a condition known as “itaiitai” (“ouch-ouch”) affected postmenopausal women living in a cadmium-polluted region of Japan.111-.223) .091) .929) .168-.311) .196 (.247-.645-.221-.206-. Horiguchi et al.647-.135) .222-.418-.183) .168-.210 (.718 (.S.238-.426-.630-.591 (.288-. 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.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 .106) .252 (.159 (.856) .181) .719 (.412 (.187-.181 (.335 (.107) . 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.190 (.727-.200 (.280 (.

Cadmium can produce lung. Ezaki et al. 1999)..1 mg/L (Alfven et al.S. 2004b). 2002. In the typical environmental exposure. blood cadmium was also slightly higher in Mexican Americans and participants 20 years and older (CDC..46 mg/gram of creatinine) (Ezaki 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.. 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.. In adults aged 60 years and older.. Biomonitoring Information Blood cadmium reflects both recent and cumulative exposures. maternal blood or maternal urine and birth weight (Nishijo et al. Horiguchi et al. Jarup et al. Friedman et al.. Blood and urine cadmium levels are typically higher 202 in cigarette smokers.. Olsson et al. the risk of low bone mineral density increased by nearly three-fold when the blood cadmium exceeded 1. environmental levels) and health effects is available from ATSDR at: http://www. EPA. intermediate in former smokers and lower in never-smokers (Becker et al.e..Metals greater urine cadmium levels may have an increased risk for bone fracture and diminished bone mineral density (Alfven et al. respectively. 2002). Wennberg et al. However. Biomonitoring studies on levels of cadmium provide physicians and public health officials Fourth National Report on Human Exposure to Environmental Chemicals . urinary cadmium reflects both cumulative exposure and the concentration of cadmium in the kidney. 2002. Becker et al. Jarup et al. respectively. 2003. and drinking water and environmental standards have been established by U. Olsson et al. 2004. Jin et al.. Acute and heavy exposure to airborne dusts and fumes. Olsson et al. approached these values associated with subclinical changes in renal function and bone mineral density.. 2002) and length at birth (Nishijo et al. 2005... Blood cadmium levels are about twice as high in smokers compared to nonsmokers (Becker et al. Chronic inhalation exposure to cadmium particulates was associated with changes in pulmonary function and chest radiographs that were consistent with emphysema (Davidson et al. CDC. Small epidemiologic studies have noted an inverse relationship between cadmium in cord blood. 1999. 2000). Staessen et al. 2002... Animal studies have demonstrated reproductive and teratogenic effects. Staessen et al.. Both IARC and NTP consider cadmium a human carcinogen. study subjects living near a former zinc smelter were similar to those from an unexposed community and to those in this Report (Noonan et al. Zhang et al. People who are occupationally exposed may have blood and urine cadmium levels that are higher than those of the general population.... In this Report the urinary and blood cadmium levels at the 95th and 90th percentiles.cdc. 2005. Wilhelm et al. 2002).. 2006. 2003... 2000. 2005.. Surveys of populations not known to have increased cadmium exposure have reported similar urine and blood levels (Becker et al. Occupational standards are provided here for comparison only. 2006).html. Moriguchi et al. 2002). 1996. Horiguchi et al. data (CDC. 2004. 2005). 2002. 1996)... Information about external exposure (i.. 2003). Salpietro et al..S. Further research is needed to address the public health consequences of such exposure in the United States. Waalkes (2003) provides an overview and summarizes potential mechanisms for carcinogenicity. 2003. 2000. 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. Mannino et al.. Wennberg et al. 2003. 2002. Komaromy-Hiller et al... pituitary gland and kidney tumors in animals and has been associated with lung cancer in humans in occupational epidemiologic studies..26 and 3. Ezaki et al.. Workplace standards and guidelines for air exposure to cadmium have been established by OSHA and ACGIH. with peak values observed in the fifth to sixth decades (CDC. 2006. 2004. Becker et al. 2002. Finding a measurable amount of cadmium in blood or urine does not mean that the levels of cadmium cause an adverse health effect. 1999).. 2002). 2002).. Creatinine-corrected urine cadmium values in U. Staessen et al.. not to imply a safety level for general population exposure.. 2005. Workplace exposure to airborne cadmium particulates was associated with decreases in olfactory function (Mascagni et al.. For NHANES 19992000.gov/ toxpro2. 2003. Women had higher blood and urine cadmium levels compared to men of similar ages. 1988). In postmenopausal women.S. has resulted in severe.. 2004.. decreased bone density was correlated with mean urinary cadmium levels of approximately 1 mg/gram of creatinine (Staessen et al. 2004b. The 95th percentiles for cadmium levels in this Report were less than the OSHA standards for both blood cadmium (5 mg/L) and urine cadmium (3 mg/gram of creatinine).. as may occur from welding cadmium-alloyed metals. Noonan et al. 2006). Becker et al. potentially fatal pneumonitis (Fernandez et al. 2003.. Suwazono et al. 2004). 2000..atsdr..

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Nakagawa H. Lybarger JA. Bruiglia S. EPA). Bergdahl IA. et al. 2001. Staessen J. Nordberg GF. Stegmayr B. age. Noonan CW.epa.84 (Section A):4455. Olsson IM. Tawara K. Cadmium concentration in maternal and cord blood and infant birth weight: a study on healthy non-smoking women. Usefulness of biomarkers of exposure to inorganic mercury. Schultz C. Tanebe K. Nogawa K. Merlino MV. Zhang YL. Kido T. Hazard Summary. Zhao YC. Stelitano A. Mutat Res 2003. 2004.3:26-41. Vangronsveld J. Revised 2000 [online]. In: Clarkson TW. 4/8/09 Waalkes MP.353:1140-1144. et al. et al. Buchet JP. Cadmium carcinogenesis. Bensryd I. Staessen JA.209:301305. Lijnen P. Wang JX. Environ Res 2006. 2000. United States Environmental Protection Agency (U. J Perinat Med 2002. et al. Lauwerys R. Cadmium compounds. 204 Fourth National Report on Human Exposure to Environmental Chemicals . Roels HA. Sarasua SM. Kathman SJ.59:394-397. cadmium. Arch Environ Health. Lundh T. Emelianov D. et al. Nordberg M. Effects of maternal exposure to cadmium on pregnancy outcome and breast milk. Campagna D. Oskarsson A. or cadmium in controlling occupational and environmental risks of nephrotoxicity. Sager PR. and mercury in blood or urine of children: Basis for validation of human biomonitoring data in environmental medicine. Cadmium in blood and urine – impact of sex. lead.Metals Nishijo M. and risk of fractures: prospective population study. J Environ Sci Health B 2004.21(3-4):251-262. Skerfving S. Tanebe K. Environ Health Perspect 2002. Effect of environmental exposure to cadmium on pregnancy outcome and fetal growth: a study on healthy pregnant women in China. forearm bone density. J Cardiovasc Risk 1996. Salpietro CD. Environ Res 2000. 151-168. pp. eds. Nordberg GF. Honda R. Revised and new reference values for arsenic.110:151-155. Nakagawa H. et al. Minciullo PL. Kobayashi E. Nishijo M. Biological monitoring of cadmium. Zhu HD.39:2507-2515. Environ Health Perspect 2002. Toyama. Fan YG. Ginucchio G.30(5):395-399. created 1992. Liu QF. Biological monitoring of toxic metals. Lison D. Jansson J-H. Saito S.S. Available at URL: www. and mercury in the population of northern Sweden. Friberg L. lead. Okubo Y. iron status. Int J Hyg Environ Health 2006. Time trends in burdens of cadmium. Relationship between newborn size and mother’s blood cadmium levels. Roels H. Lundh T. Suwazono Y. Nakagawa H. Ottosson H.59(1):22-25. Schwenk M. Environmental exposure to cadmium. Public health implications of environmental exposure to cadmium and lead: an overview of epidemiological studies in Belgium. New York: Plenum Press. Gallmans G.gov/ttn/atw/ hlthef/cadmium. Wilhelm M. Occup Environ Med 2002. Effects of exposure to low levels of environmental cadmium on renal biomarkers. Ren Fail 1999. Wennberg M. Japan. Gangemi S. and former smoking – association of renal effects. Renal effects of cadmium exposure in cadmium nonpolluted areas in Japan. Kuznetsova T. Honda R. Mueller PW. Hoet P. Thijs L. lead.110:1185-1190.100:330-338.html. Lancet 1999. Roels HA.533(12):107-120. dietary intake.

20) 8.26 (3.00-8.64-10.68) 9.0) 9.27 (7.01) 7. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.10 (8.99-11.2 (9.03 (4.40-11.30-5. For absorbed cesium salts.40-5.77 (4.3 (8.89) 5.08-5.00-4. and high-power gas-ion devices.83-4.35 (4.95-4.12-11.40) 7. respectively.70 (4.20 (6. although cesium was generally of low toxicity when given to animals.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 4.8) 12.43-8.2-13.25-5.8-13.70 (6.09-5.0 (10.49) 75th 7.82) 5.76-6.5-14.2-14.26) 4.80-6.40) 5.30-10.27) 4.56 (4.10-8.1 (10.8) 9.01-6.91 (7.97-7.84-9.7-14.50) 9.25 (3.70 (8.56 (4.6 (11.30) 7.36 (3.40-5. However.32 (3.1) 11.05-5.64) 5.23-4.8 (10. and 03-04 are 0.49 (4.6) 11.02 (4.50-7.90-8.94-4. diarrhea.4) 10.45-5.87 (4.77 (9. Human health effects from cesium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.70 (5.1) 9.3) 10.5) 9.42-7.90-10.5) 12.97) 4.60) 7.3) 9.84 (4.69-6.3) 10.60) 7.2) 12.77 (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 4.08 (6.12 (4.39-4.1) 11.60) 5.04) 7.26) 7.71-8. 01-02.59) 7.08-5.46) 7.90 (6. the body half-life is estimated to be 70-109 days based on 137Cs exposures.56) 5.05) 5.99-6.00-10.2-13.Metals Cesium CAS No.00) 7.55 (7.4) 95th 11.40-11.68 (7.80-10.94 (4.59-5.2-12. photographic emulsions.60-12. Case investigations of ingestions of large doses of cesium chloride have reported decreased appetite.74 (4. Workplace guidelines for cesium hydroxide are available from ACGIH and NIOSH.70) 5.87-7.53 (6.70) 7. Urinary Cesium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.13 (5.13-8.74-5.37) 7.20-5.70-8.8 (11.8) 12.09) 5.5-13.40-5.10 (6.99) 7.7 (9. Little is known about the health effects of this metal.88 (8.6 (11.66 (7.7 (10. scintillation counters.90) 5.6) 10.71-5.99-11.90) 9.86-12.72) 4.80-10.47-4.3-13.27-5.80) 7.94) 4.79 (4.64) 4.50 (4.1 (11.4) 10.0-13.57-5.9) Total 4.17) 4.80 (8.00-9.13 (7.81) 9. 0.35 (4.90-12. Most human exposure to cesium occurs through the diet.74) Selected percentiles ( 95% confidence interval) 50th 4.71 (8.3) 10.12) 5.13 (8.8) 11.10-7.1-12.71-9.05) 5.4-13.8) 9.1-12.7 (9.04 (4. see Data Analysis section) for Survey years 99-00.34 (4.9 (11.7 (11.80-11.80 (4.73-11.40-5.00-8.98 (7.4 (9.89) 4.7) 884 683 618 568 667 723 821 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.2) 11.00) 6.38) 5.39) 7.87 (4.12-5.4 (10.01-8.45-8.7) 10.50) 5. and as polymerization catalysts.81 (4.5) 10.33 (5.17-6.49 (5.60-6.3 (8.43 (5.56-11.4) 9.5-14. Inorganic cesium compounds are used in photomultiplier and vacuum tubes.9 (11.25) 4.10-9.9) 8.0) 11.1-13.15-8.29 (4.32-5.30) 5.87 (4.72-7.17 (6. and 0.63) 6.6 (9.9 (10.36 (6.91-8.90) 4.83) 6.10 (6. nausea.1) 9.60-7.21 (4.61-6.3-13.3) 12.20-8.26-11.9) 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 4.9) 11.40-7.9 (11.96 (6.0-15.5-16.47-8.40 (4. Fourth National Report on Human Exposure to Environmental Chemicals 205 . and cardiac arrhythmia (ATSDR.22 (4.92-13.80 (4.95 (3.03 (4.29) 4.6 (9.1) 10.7) 11.22-4.55 (4.86 (7.33 (6.70 (8.59-5.87) 5.1 (9.60-5.71) 4. population from the National Health and Nutrition Examination Survey.7) 11.23) 9.77-8.20-7.30 (6.7 (9.63 (4.7 (8.63-4.42) 6.80 (8.54-11.14.0 (9.60 (7.3-15.64-5.59-5.05-5.59 (5.60 (8.07-11.4) 11.54) 4.4) 12.70 (9.20-4.10 (8.0) 12.95) 5. interval) 4.30 (6.4) 12.20) 5.70 (6.2-13.5 (10. soil.81) 4.8 (10.62) 4.9) 12.73-5.40) 5.6 (9.70-5.89-5.81) 4.81-14.90-12.21) 90th 9.90-10. cesium hydroxide is corrosive and irritating at high concentrations. Whether cesium compounds are carcinogenic is unknown.00) 4. semiconductors.67 (4.0) 12.31-8.07) 4.64) 5.03-4.97 (7. Radioactive 137Cs has been used medically to treat cancer.9 (10.86-11.14.2 (9.20) 7.32) 4.4 (9. and clay.84) 8.35-5.80-13.60-6.9 (11.5 (8.49) 4.16-6.80 (8.50 (4.53-11.60-7.36) 3.50 (6.S.71 (4. 2004).0) 11.98 (7.8) 11.08 (7.0) 12.80-10.08) 7.00 (7.14 (4.50 (7.80 (4.7 (10.50 (4.84-5.90-10.90) 7.42) 7.20) 4.7 (10.93 (4.37) 5.52) 7.16-6.84) 5.52-9.90) 5.44 (8.70) 5.62 (5.2.20 (4.33-5.0) 10.10-5.64 (4.55-11.3) 10.34) 9.99) 9.82-4.94 (4. infrared lamps.24) 4. 7440-46-2 General Information Cesium is a silver-white metal that is found naturally in rock.61) 7.7) 10.8) 12.62 (5.90 (4.6 (9.

23 (7.57) 3.91) 5.96 (4.45 (4.58) 8.25) Selected percentiles ( 95% confidence interval) 50th 4.25) 4.14 (6.07) 8.55-5.97) 8.67) 5.05) 6.00-5.56) 4.05-3.58) 3.74) 3.50) 4.90-8.41-4.06 (3.16-8.83) 8.43) 8.72-5.84-9.95) 4.87) Sample size 2464 2689 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 5.64-6.56) 3.20) 5.03) 5.91) 4.47) 4.96) 4.95-12. population.5) 9.5) 7.82) 7.66 (5.96-4.18-6.38) 10..99-9.3 (8.12-6.79) 9.6) 6.06) 5.17 (6.28) 8.40) 7.18-7.74 (5.77 (4.75 (6.18 (7.61-3.79-5.46) 6.91 (5.8 (9.14) 4.27-6.06) 4.73 (3.15 (7.84-11.63-6.95) 8..93-9.10-4.97-4.95 (5. Urinary Cesium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.58-5.82-4.50) 4.00-9.96) 4.51 (4.30-4.45-6.62-8.8) 10.3 (9.91-6.91) 5.08) 4.53) 6.24-4.44-9.7) 10.85) 5.49) 3.98 (7.81 (4.70) 6.28 (4.9 (9. interval) 4.50 (7.95 (3.50) 4.68-11.87-4.12 (3.68) 6.31-6.46-8.59) 4.05-4. population from the National Health and Nutrition Examination Survey.50) 8.44) 3.17) 9.7-12.8) 5.52-5.09) 8.79 (5. and were also roughly similar to those in this Report.64) 4.26-6.42-4.22 (3.43 (3.92 (5. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.02-4.41) 9.34 (5.37-3.60-10.70 (7.51) 4.83-7.78 (3.27 (6.66 (5.83-6.41-7.6 (9.35 (3.65-3.87 (5.98) 5.97-5.64 (8.77-5.31 (4.5) 9.51 (4.07 (5.99-4.88-10.42 (4.08 (5.30-4.28 (5.19-3.41 (5.26 (4.04) 6. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.78 (3.2 (8.64) 9.10 (3.08-3.13-9. Using clinically submitted specimens.46-4.14) 4.13) 7.2) 11.43-11.9 (10.68) 4.68 (4.55 (3..05-3.79) 4.77 (6.20-4.06 (5.54 (4.63-6.53) 3.6 (9.42-6.47) 6.56) 4.56 (4.95) 10.7) 10.04-11.05 (4.72 (4.68) 3.04) 5.07-4.29) 4.48) 7.91-9.62) 5. (2000) found urinary cesium levels that were slightly lower than those reported for the U.71 (7.59-8.19-6.10 (3.51 (7.21 (2.44-5.63 (7.90-3.35-11.93-7.27 (8.90-8. Finding a measurable amount of cesium in the urine does not mean that the levels of cesium cause an adverse health effect.1) 11.44 (4.14-6.96-4.63 (4.48) 90th 7.38-12.54 (5. Komaromy-Hiller et al.40) 6.36-6. Urinary cesium levels were similar in a group of forest fire fighters and residents living near the fire area (Wolfe et al.30) 10.43 (8.70) 7. Two small studies of European populations reported urinary cesium levels similar to U.64) 5.30 (3.5 (9.09 (4.8) 6.27 (6.22) 6.16-5.58 (4.0) Total 4.02 (5.51 (3.74 (4.54 (3.41 (8.99) 4.09) 4.16-8.08 (6.65 (6.03-6.50 (6.S.20-8.00-10.74) 75th 5.98 (6.43 (4.9) 10.36-3.88-4.47 (7.58 (6.72) 4.21-5.66-6.18) 8.2 (8.28) 7.05) 3.81 (4.80) 6.64 (4.3 (10.Metals Biomonitoring Information Urinary cesium levels reflect recent exposure.24-10.24 (3.76-9. 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.79) 6.41) 4.40-5.61 (7.0 (7. 1990).0) 7.00-5.00) 6.31 (4.53 (6.S.51 (3.60-20.77) 4.35 (4.33-8.S.60 (3. population results shown in this Report (Alimonti et al.35-7. 2005.42-4.78) 4.10) 7.43-6.2) 340 368 290 718 762 725 1406 1559 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 3.3) 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 3.44 (8.33 (5.13 (3.76-6.94) 7.85) 4.29-3.11 (5.46 (8.00 (8.12) 3.73-4.71) 6.39) 8. 2004).38-7.00-4.3) 11.92) 3.15-4.21-4.08) 4.56-10.11 (5.84-7.78) 4.3-15.85-4.29) 5.41 (4.27) 4.95-6.42 (5.39 (5.15) 95th 8.03-5.99 (3.14-7. Minoia et al.03) 6.00-8.67 (5.10 (5.38 (3.55) 4.47) 7.17-4.07) 8.30 (7.98) 5.20-4.31-4.84-9.75-11.14-4.30 (4.99-9.20-4.0) 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 .04-5.38 (3.17) 4.91-7.87) 5.50-5.08) 3.4) 10.60 (5.86 (4.91 (5.53 (4.63) 6.08-7.29-3.29) 4.01-8.08 (3.3) 9.21-3.30) 10.35) 3.33-3.65-4.75 (7.66 (6.60) 3.54 (4.27-4.43 (4.94 (5.46 (7.22-11.33 (5.67 (6.36-10.89-4.77 (7.15-11.37) 4.48-6.90 (7.26 (3.47 (4.39) 5.50 (5.84-7.16) 5.63 (6.47) 6.74-11.13-9.

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

480-.470) .950 (.05) 1.26) Total .502) .32) 1.46 (1.419) Selected percentiles ( 95% confidence interval) 50th .450-.620-.550) 90th .410 (.850) 1.800-.294 (.340) .910-1. Cobalt is used as a drying agent in paints.398 (.404) .390-.01 (.427-.373-.16) 1.327-.26) 1.500 (.24 (1.470 (. population from the National Health and Nutrition Examination Survey. It is emitted into the environment from burning coal and oil and car and truck exhaust.600) .360-.740 (.26-1.09) .04-1.540) 1.26-2.310-.469-.496) .530-.520 (.386) .32) 1.940-1.900-1.600 (.630 (.390 (.410 (.48) 1.12) 1. 7440-48-4 General Information Cobalt is a magnetic element that occurs in nature either as a steel-gray.370-.520 (.540-.380 (.590-.940 (.410-. 208 Fourth National Report on Human Exposure to Environmental Chemicals .374 (.16 (.73) 1. hard metal (alloys of cobalt and tungsten carbide).418 (.510) 1.710) 1.550 (.610-.930-1.750 (. and 03-04 are 0.68 (1.540-. and in synthesizing polyester and other materials.580 (.343 (.610) .790-.430) .32-2.570 (. Cobalt compounds are also used in manufacturing battery electrodes.880 (.820 (.950-1.380 (.750 (.640) .460 (. varnishes.519 (.410 (.09 (.670-.430 (.280-.03 (.32 (1.32 (1.860 (.81) 1.04-1.417) .Metals Cobalt CAS No.450) .530) .920-1. hard metal or in combination with other elements.750 (.05 (.270-.454 (.420) .460 (. and magnetic recording media.350-.350-.410 (.22) 1.06-1.73) 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 .99) 1. respectively.310 (.870 (.22-1.364-.520-.890) 95th 1.580 (.37-1.47 (1.320 (.360-.540-.360-.367 (.410) .S.17-1.28 (1.07-1.950-1.33-1.398) .26) 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.44) 1.690-.07. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.53) 1.01-1.428-.24 (.04 (.09 (.740-.650 (.463-.16) 1.350 (.570) .940-1. steel-belted radial tires. 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.379 (.S.410 (.45 (1.390) .690 (. It is also a component of porcelain enamel applied to steel bathroom fixtures.434 (.394) .890-1.950 (.316 (.330) .350) 75th . Medical uses include joint and dental prostheses and radioactive cobalt in cancer chemotherapy. and 0.630 (.520 (. and kitchenware.431) .319) .900-1.980) .980-1.259-.372) .36) 1.333-.350-.870 (.770) .890-1.580 (.480 (.03 (.564) .02-1.300-. automobile airbags.19) .00) .420 (.410-.21) 1.930) .520-.359 (.670-.431) .39) 1.17 (1.450-.14-1. interval) .800-.313) .15-1.590) .730) 1.338-. Among its many uses are manufacturing superalloys used in gas turbines in aircraft engines.75 (1.300 (.377-.660) .14) .370-.760) .487) .560 (.900) .333-.435 (.920) 1.06 (.465) .12) 1.340-.17 (.640) .03) .760 (.42) 1. Usual human exposure is from food sources.670 (.570) .430 (.336-.460-.550-.28 (1.07-1.13) 1.620-.67) 1.620-.820 (. The cobalt used in U.790 (.50 (1.291-. see Data Analysis section) for Survey years 99-00.390 (.379 (.352 (.850-1.640) .308-.600-.29 (1.331-.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 .400-.650 (.08) .420) .960-1.660) .05 (.81) 1. industry is imported or obtained by recycling scrap metal that contains cobalt.28 (1.28-2.59 (1. blue-colored pigments.750-.52 (1.490-.285 (.430 (.450) . seawater.520) .25-1.16 (1.370) .850-1.355-.316-.64) 1.800) . and soil.410) .340-.950) .850) .424) .47) 1.330-.870-1.710 (.583) .388-.520-.810) .301 (.523) . shiny.23-2.830-1.33 (1.343) Sample size 2465 2690 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .670 (.16 (1.530 (.680) .880-1.452 (.540-.07.410-.900) .499 (.380-.650-.520-.680 (.670 (.930 (.380 (.50) 1.414) .22 (1.460) .47 (1.348-.06 (.330 (.440-.405-.07 (.890) .810-.340 (. Cobalt compounds are used as catalysts in producing oil and gas.08-1.08.680) .810) .480 (.430) .47) 1.490-.348-.03-1.460) .900) .380-.03) 1.65) 1.339 (.390 (.590-.23) .820 (.543) .48) 1.620) .16-1.570-.305-.520 (. and fertilizers.399) .461 (.373) .04-1.60 (1.690-.16-1.01-2.660-.700) .450) .840) .700) .450) .520) .92) 1.04) 1.01 (.270-.15 (1.290-. and inks.430-.630-.610 (.375 (. large appliances.393-.515 (.03) 1. 0.610) .56) 1. 01-02.740-.570-.890-1.710) .270-. Cobalt occurs naturally in airborne dust.371 (.369 (.581) .590 (. diamond-polishing wheels.500) .17 (1.370-.460) .370 (.340) .416) .334) .790) .680 (.20 (1.

368) .11-1.707) .50) 1.543) .911-1.09) 1.16 (.426 (.976 (.400 (.632-.00 (.615) .57) 1.301) .850 (.955) .785) .12 (.402 (.638-1.296) . respectively.19) ..346 (.634-.457) .844 (.275-.363) .407) .963) .409) .515 (.563-.804) 1.848 (.824 (.215-.352) .391) Selected percentiles ( 95% confidence interval) 50th .533 (.326-.33) 1.462) .449) .00 (.60) 1.15 (.16 (.522) .331-.73) 1.750) .376 (.895-1.00) .Metals fabricated from cobalt alloys (Lhotka et al.279) .850-1.03 (.392 (.396) .727 (.879-1.313-. Cobalt constitutes 4% by weight of vitamin B-12 (cobalamin).382-.324) .360) .554 (.296-.256-.983) .488) .316 (.550-. Once absorbed and distributed in the body.333-.29) 1.983-1.329 (.471-.27) 1.36) 1.561) .290 (. cobalt is excreted predominantly in the urine.960 (.328 (.83) 1.740-1.457 (.753-. Cobalt is absorbed by oral and pulmonary routes.700 (..500-.33) .248-.361 (.277-.963) . 1994).251-.600-.898 (.593) . Lung retention of relatively insoluble cobalt compounds such as cobalt oxide may be prolonged. A portion of cobalt retained for long periods is concentrated in the liver.317 (.487-.792 (. Urinary Cobalt (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.324-.290 (.744) 1.487-.388 (.16 (1.353 (.500 (.369 (.268 (.753) 1.917) .60) 1.361 (.463-.975 (.378-.728) .457-.313-.349) .327 (.361-.44 (.23 (1. 1979).428-.10-1.386 (..452-.306 (.234 (.425-.938) .781-1. using hard metal cutting tools.272-.343-.598 (.342-.774 (.29 (1.368) .362 (. and to a lesser extent.50 (1.29) .434-.297-.335 (.861 (.421) .334) .640) .14 (.11-1.03-1.548 (.313 (.393 (.06 (.352 (.290 (.833-1.728 (.523 (.257 (.333-.04 (. with pulmonary clearance half-lives of from one to two years (Hedge et al.328 (.630-.343 (.660-.36) 1.821 (.708) .35) 1.937 (.302-.387) .319-.547 (.736-.294-.391 (. refining or processing alloys.286) .29 (1.337) .792-1.404-.. 1994.594) .25 (.304-.30 (1.826-1.738 (.847) . Workplace standards and guidelines for external air exposure to cobalt and several of its compounds have been established by OSHA and ACGIH.513) .781) 95th 1.964 (.704-.738 (.24) . in the feces.683-.461) .362-.17) .435-.289) .691 (.02 (.542 (.362) .703-.10) .777-.279 (.830 (.S.50) 1.12-1.503-.361-.393-.259-.339-.310) .949) .328) .271 (.247 (.309) .378 (.323) .673-.344-.378-.365-.756 (. but with a minor fraction (10-15 %) exhibiting a half-life of several years (Mosconi et al.313-.10) Total .851 (.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 .273 (.562) .49) 1.534 (.963-1.700 (.00 (.857-1.257-.449-.669) .523 (. or using diamond-polishing wheels that contain cobalt metal.00 (.955) .384) .303-.476-.611) .513 (.329-.04-1.932-1.355) .990-1.475 (. A nutritional requirement for cobalt other than that contained within dietary cobalamin has not been established.237-.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 .278 (.442-.630-.417) . an essential human nutrient.821-3.325) 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 . 1972).297) .433) .952 (.28) 1.259 (.408 (.282 (.00) .606 (.481) 90th .280-.471-. 2003).560-. Elimination reflects a multi-compartmental model dominated by compartments with half-lives on the order of several hours to a week.25 (. Human studies with 60Co administered as soluble cobalt chloride have reported oral absorption ranging from approximately 1 to 25 % (Smith et al.372) .574-.419) ..348) .733-1.938-1.471 (.259) .585) .616-.667-1.298 (.293 (.861-1.608 (.365) .407 (.275-.611) .380-.278-.304) .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 .300) .479) .394) .378-.929) .10 (.737 (.508-.425) .479-.895-1. interval) .439) .872 (.396) .829-1.417 (.381) .609) .327-.54) 1.723 (.250) .274-.554 (.239-.829) .552 (..591 (.282-. Smith et al.635 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.626-.505) .582-.429) 1.537 (.529 (.500-.757-1.455 (.281) .513-.562) . population from the National Health and Nutrition Examination Survey.368 (.905) .694) .353-.689 (.760-1.29 (1. Exposure in the workplace may come from electroplating.306) 75th .647) .599) .301-.644 (.842) .313-.333 (.750-.990) .534-.786-.963-1.438) .444 (.291 (.595) .388 (.15) 1.314 (.679-.333-.35) .352 (.838 (.469-.358 (.900-1.581) .55) . 1972).667-1.243-.662) .337 (.467-.435 (. Recent inhalation exposure to soluble cobalt compounds can be monitored by measuring cobalt in urine or blood (Lison et al.00-1.27) 1.16) .495 (.468) .313-.248-.

. “Hard metal” disease. Pharmaceutical preparations of cobalt used in the past as hematinics were associated with the development of overt hypothyroidism (Kriss et al. 1994. Cobalt was once added as a foaming agent to beer. Roycroft JR. a distinction is made between soluble and insoluble (oxides and metallic) cobalt (Christensen and Poulsen. Finding a measurable amount of cobalt in the urine does not mean that the levels of cobalt cause an adverse health effect. usually in combination with tungsten carbide (Cugell et al. The extent to which cobalt exposure alone causes interstitial lung disease is unknown (Linna et al. Smaller population surveys of European adults reported urinary cobalt levels that were roughly similar U. Shirakawa et al. Swennen et al. 2001...cdc. Correlations between air exposure levels and urinary cobalt levels in hard metal fabricators are well documented (Ichikawa et al. 1993)... Atlanta (GA). et al. 1988). Toxicol Sci 1999. Persons with occupational exposure to cobalt often have urinary cobalt levels that are many times higher than those of the general population. population (CDC. Lauwerys and Hoet. A subclinical decrease in thyroid production was observed in a study of cobalt production workers (Swennen et al. Morgan WKC.S. Lisi.. A clinical and pathological study of twenty-eight cases. although substantial occupational exposures have produced elevated urinary levels for many weeks. 1994). 1994. 2001)..e. MacDonald et al.html. 2001.50(13):95-104. Thomassen et al. with mean levels that were about 15-20 times higher than in the general U. biological levels and health effects following exposure to soluble or insoluble cobalt compounds in cobalt blue dyes. Information about the BEI is provided here for comparison..43(4):299-303. Perkins DG. Third National Report on Human Exposure to Environmental Chemicals. Grumbein SL. 1955). White and Sabbioni. For workers exposed to cobalt in the air. 1985. An industry-wide study of hard metal workers in France observed an increased mortality from lung cancer (Moulin et al. 1998). Inhalation toxicity and carcinogenicity studies of cobalt sulfate. Small studies of patients with hip replacements using metal alloy prostheses reported increased urinary cobalt concentrations.. 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. 2005. Bucher JR. Poulsen OM.gov/ exposurereport/. 2001. Occupational exposure to cobaltcontaining dusts has caused occupational asthma (Pisati and Zedda. Haseman JK. The ACGIH biological exposure index (BEI) for inorganic forms of cobalt (except insoluble cobalt oxides) is 15 mg/L.atsdr. Rubin A.49:56-67. Case reports have also suggested a link between occupational cobalt exposure and cardiomyopathy (Jarvis et al. 1989). Alexandersson R.. 2003) and produced lung cancer in rats and mice after chronic inhalation (Bucher et al. Blood and urinary concentrations as estimators of cobalt exposure. 1997. Dunstan et al. 4/3/08 Christensen JM. not to imply that the BEI is a safe level for general population exposure.. Centers for Disease Control and Prevention (CDC).. 2003. 2005. Daniel et al. Information about external exposure (i. Cugell DW. Arch Environ Health 1988. Krause et al. Lison et al. 2006. Cobalt compounds elicited numerous genotoxic effects in both in vitro and in vivo assays (De Boeck et al. Available at URL: http://www... 1972).cdc..S.gov/toxpro2. A 1982-1992 surveillance programme on Danish pottery painters. 1998). has been associated with exposure to dusts that contain cobalt. Cobalt compounds appear to stimulate erythropoietin production and were formerly used in the treatment of anemia (Goldberg et al. Urinary measurements mainly reflect recent exposure. References Alexander CS. 1992). and this caused outbreaks of cardiomyopathy among heavy drinkers in the mid-1960’s (Alexander et al. 210 2006.Metals Toxic effects of cobalt have been encountered in workplace settings.. 1988). 2003). 1997). 2003. IARC has classified cobalt metal with tungsten carbide and other soluble cobalt salts as possibly carcinogenic to humans. Sills RC.. Biomonitoring Information Urinary levels of cobalt decline rapidly within 24 hours after exposure ceases (Alexandersson et al. Hailey JR. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects...53:395417. Exposure to soluble cobalt salts will produce proportionately higher urinary levels because they are absorbed better. 2005 [online]. Iavicoli et al.. Linnainmaa and Kiilunen. 1993). Am J Med 1972.. 1999). The respiratory Fourth National Report on Human Exposure to Environmental Chemicals .. Sci Total Environ 1994. Cobalt compounds are a recognized cause of allergic contact dermatitis (Dickel et al... population results in this Report (Kristiansen et al. Cobalt-beer cardiomyopathy.. 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.

White MA.242:1412-1415.” Contact Dermatitis 2001.51(7):447450. Sci Total Environ 1997. Ziaee H. Occupational asthma from cobalt sensitivity in workers exposed to hard metal dust. et al. Metal-on-metal versus polyethylene in hip arthroplasty: a randomized clinical trial. A report of two cases from mineral assay laboratories and a review of the literature. Zhuber K. McCalden RW. Ichikawa Y. The effect of the diameter of metal-on-metal bearings on systemic exposure to cobalt and chromium. J Trace Elem Med Biol 2006. Boca Raton (FL): Lewis Publishers. Chest 1989. Buchet JP. Hammon E. Pisati G. Bacis M. Molders J. Zweymuller K.150:177-183. Thakker DM. Cresti R. Sabbioni E.34:620-626. Oksa P. Iversen BS. et al. Regulation of the erythropoietin gene: evidence that the oxygen sensor is a heme protein. Absorption and retention of cobalt in man by whole-body counting. Smith T. Hedge AG.20(1):25-31. salt. Leghissa P. The release of metals from metal-onmetal surface arthroplasty of the hip. Vitali MT.148:241-248. Health Phys 1972. Angerer J. Robinson C. Zobelein P. Am J Ind Med 2003. Lauwerys RB. Schank M. Kiilunen M. Exposure assessment in the hard metal manufacturing industry with special regard to tungsten and its compounds. Lauwerys R. Romazini S. Clin Orthop Relat Res 2003. Iavicoli I. Salama A. Kirsch-Volders M. Dunstan E. Metal ion levels after metal-on-metal proximal femoral replacements: a 30-year follow-up. Ghat IS. Dunning SP. Sci Total Environ 1994. Meyer zum Buschenfelde K-H. Bunn HF.55(4):269-276. De Boeck M. et al. Rorabeck CH. Bozec C. Peltier A. Szekeres T. Toxic trace element reference levels in blood and urine: influence of gender and lifestyle factors. Int Arch Occup Environ Health 1997. Lasfargues G.150.Metals effects of cobalt.216:253-270. Fujimura N. HoffmannB. Pradhan C. Uitti J. Lison D. J Bone Joint Surg Br 2005. Steffan I. Kriss JP. Br J Ind Med 1993. Salvatori S. Mosconi G. Moulin JJ.406:282-296. X. Science 1988.22:359367. Health Phys 1979. Thabe H.21(2):189-195. Palmroos P. Epidemiological survey of workers exposed to cobalt oxides. et al. Diepgen TL. 3rd ed. Outcome of occupational asthma due to cobalt hypersensitivity. Occupationallyinduced “isolated cobalt sensitization. Gross RT.204:147-160.95:29-37. Cannon SR. Lison D. et al.88(4):443448.87(5):628-631. Dickel H. et al. Sci Total Environ 1994. Mutat Res 2003. Linna A. J Bone Joint Surg Br 2006. 1985. MacDonald SJ. Swennen B. Sanghrajka AP.150(1-3):167-171. Goto S.533:135-152. a study of 13 elements in blood and urine of a United Kingdom population. and cobalt metals. Tilley S. Blunn G. Weyher I. Four-year study of cobalt and chromium blood levels in patients managed with two different metal-on-metal total hip replacements. Hypothyroidism and thyroid hyperplasia in patients treated with cobalt JAMA 1955.28(5):1121-1128. Carnes WH.157:117121. Cleland D. Linnainmaa M. Occup Environ Med 1994. Laippala P. Am J Epidemiol 1998. cobalt salts. Bourne RB. Goto S. Alessandrelli M. Contact Dermatitis 2003. Falcone G. oxides. and hard metal dust. Lisi P. Cobalt excretion in urine: results of a study on workers producing diamond grinding tools and on a control group. Int Arch Occup Environ Health. Occup Environ Med 2001. Unwin P. Heki S. Trace element reference values in tissues from inhabitants of the European Union. Meier R. Zedda S. Respiratory health of cobalt production workers. Weber A. Hoet P. Kusaka Y. Goldberg MA. Chess DG.36:732-734. Edmonds CJ. Urinary cobalt as a measure of exposure in the wet sharpening of hard metal and satellite blades. Biological monitoring of cobalt exposure based on cobalt concentrations in blood and urine.(1-3):133-139. Lung cancer risk in hard-metal workers. 2001.45:246-247. Lhotka C. Daniel J. Sabbioni E. Kristiansen J.48:172-173.58(10):631-634. McMinn DJ. Kraus T. Long-term clearance of inhaled 60Co. Cobalt cardiomyopathy. Hoher T. Radulescu M. Wild P.50(9):835-842. Barnaby CF.69(3):193-200. DeSantis V. Kuska Y. Thomassen H. Roto P. J Orthop Res 2003. Lauwerys R. J Occup Med 1992. Schramel P. Sabbioni E. Fourth National Report on Human Exposure to Environmental Chemicals 211 . Stanescu D. J Rheumatol 2001. Kato M. Biological monitoring of workers exposed to cobalt metal. Sci Total Environ 1998. Schaller KH. Cobalt and antimony: genotoxicity and carcinogenicity. Cobalt-specific T lymphocytes in synovial tissue after an allergic reaction to cobalt alloy joint prosthesis. Arch Intern Med 1990. Shirakawa T. Industrial Chemical Exposure: Guidelines for Biological Monitoring. Jarvis JQ. Buchet JP.44:124-132. Co-sensitivity between cobalt and other transition metals. Swennen B. Lison D. Christensen JM.

80 (1.50-4.60) 1.70) 1.69 (1.10-8.20) 3.50 (2.37 (1.40) 1.00) 3.40-2.90-2.30 (4.00-4.10) 1.90-3.00) 1.878-1.90 (2.90) 1.60) 5.20 (3.50) 1.00-4.90-6.36) 1.95) 1.10-1.80 (1.60-1.20 (3.87 (1.60 (2.70 (2.70) 4.50-2.00) 4.50) 1.75-2.70 (1.90) 1.80-3.20 (4.10-3.50-6.90 (3.50-2.70) 2.00) 1.S.40-5.40) 5.30 (1.70-2.20) 90th 3.942 (.20 (3.70) 3.90-4.40) 1.72) Selected percentiles ( 95% confidence interval) 50th 1.20-2.40-3.30 (2.60-2.40-6.30-1.60) 1. metal alloys (e.00 (6.20-3.10) 5.00) 2. 0.00) 1.20 (1.25) 1.65 (1.30-2.22 (1.60) 1.51) 1.70-1.68-1.17) .51 (1.20 (2.50-1.10 (1.50 (1.10-1.43) 1.62-1.45-1.70) 1.60) 1.50) 75th 2. Lead was used in plumbing for centuries and may still be present.60) 2.30-1.00) 6.10) 3.10 (2.60 (1.50 (1.80 (4.20-6.36-1.g. Elemental lead can be combined with other elements to form inorganic and organic compounds.90) 3.70-4.10-3.90-2.30 (1.00) 2.40 (1.946 (.60) 3.80 (3. Aerosolized lead is either inhaled or ingested after it is deposited on surfaces and food crops.50) 5.50-5.32-1.00) .10-2.80-4.75-1.60 (2.10 (2.40) 3.70) 3.80 (1.20 (1.00 (4.34-1.50-5.50 (4.40-1.56 (1.40-2.20 (3.80) 1.02) 1. dense. 7439-92-1 General Information Elemental lead is a soft.53) 1.46 (1.50) 4.77 (1.00 (4.90 (4.10-2.40 (3. and 0.40 (1.49-1.90) 5.50 (2.50-3.00) 1.60-1.43) 1.00 (2.60-4.60 (1.20 (3.60) 4.60-2.30 (2.14-1.60) 3.23 (1. interval) 1.50-1.78 (1. Lead is most often mined from ores or recycled from scrap metal or batteries.60 (3.90-2.899-.40 (4.90 (3.20 (1.50-1.40 (1.20-3.900 (.20) 3.40 (2.55-1.60 (2. Before the 1980’s.10) 3.20-1.37-1.28.70-2.50) 2.60 (1.20 (2.80-4.43 (1.10-2.3. the main source of lead exposure for the general U.50-4.70 (1.30) 2.71-1.14-1.20 (1.10-4.70-6.55-1.10 (2.75 (1.30-2.70-3.87) 1.40) 1.00-1.09) 1.30-1.00) 5.30-4.40-6.60 (3.986) .93-2.60 (2.30) 1.20 (3.45 (1. malleable.80) 1.20) 3.30 (1.70) 1.90 (3.40) Total 1.39) 1.40-1.80) 1.00-5.40-1.10-1.20) 2.60) 3.70) 4.00-6.900 (.60 (4.00) 2.10 (3.86) 1.66 (1.90-4.50-1.60 (1.30 (2.90 (1.90) 2.40-1.70 (1.04-1.50-2.40) 2.S.60) 2.20) 4.90) 3.60) 2.48) 1.70 (5.90) 2.12-1.50 (2.75) 1.30 (4. brass.80 (1.20) 5. respectively.52 (1.60 (2.91) 1.39-1.00 (1.00 (1.10-2.36-1.10) 3.00) 4. antique-molded or cast ornaments.20) .40-2. population was aerosolized lead emitted from combustion engines that used leaded gasoline.40-3.30-1.20) 1.40 (2. 01-02.81) 1.70 (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. Since lead has been eliminated from gasoline. blue-gray metal that occurs naturally in soils and rocks.70 (1.43-1.10) 1. and for radiation shielding.60 (1.00 (5. ceramic glazes.52-1.80) 3.30 (2.60) 2.50-1.14-1.50) Sample size 7970 8945 8373 Age group 1-5 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 2.30 (4.70-1. In the past.60) 4.30-5.70) 4.40-1.89) 1.60) 3.80 (2.90 (3.10-3.10) 4.10 (4.50) 5.69 (1.20 (1.96-2.80 (5.50) 3.60 (3.50 (2.10) 2. such as lead phosphate and tetraethyl lead.90-4. leaded glass.25 (1.10 (1.30) 2742 2268 2085 1842 2219 2293 2716 3806 3478 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.60) 4.32-1.60-6.70 (3.90) 1.60-4.30 (1.10-6.90 (2.90 (3.40 (1.80 (4.70) 1.50) 1.50 (2.30 (2.80-3.90-4.800-1.80) 2. population from the National Health and Nutrition Examination Survey.20-2.40) 2.43 (1.30 (3. 212 Fourth National Report on Human Exposure to Environmental Chemicals .40) 2.10-2.60) 1.40-3.80-3. solders.69) 1.19 (1.60-1.25 (1.30) 95th 5.10 (1.10-3.10-6.70) 3.70-1.00-2.70) 4.30-6.60) 2.90-2.50 (3.70 (2.60) 723 898 911 905 1044 856 2135 2231 2081 4207 4772 4525 6-11 years 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 2.62 (1.900-1.20) 3.80) 2. see Data Analysis section) for Survey years 99-00.30-1.40-1.60 (3.30) 5.50) 1.80 (2.30-2.10) 1.10) 2.40) 4.90) 2.00-1.20-3. Lead has a variety of uses in manufacturing: storage batteries.55 (1.80) 1.00 (3.31) 1. and 03-04 are 0.Metals Lead CAS No.50) 7.30) 2.40 (5.60-3.70) 1.20) 4.80-2.50-3.70-5. plastics.50 (1.00-4.70-2.30-1.40-4.66) 1.50) 4.30-2.60) 4. bronze).60-1.30 (2.50 (4.10-2.20-3. adult lead exposures tend to be limited to Blood Lead Geometric mean and selected percentiles of blood concentrations (in µg/dL) for the U.50-2.30 (2.20-4.00) 3. ammunition.40) 2.90) 2.00) 2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.80-3.80 (1.80) 2.80-5.80) 1.52-1.83 (1.60 (1.20 (3.62) 1.00) 1.3.20-1.80) 2.90 (1.37 (1.30) 2.90) 2.10-4.01 (1.60 (2.80 (2. lead was added to gasoline and residential paints and used in soldering the seams of food cans.50) 2.70 (3.69) 1.80 (1.60 (1.80 (5.50 (3.50 (1.80-4.60) 5.

810-1.50-2.06) .800) .80) 1.900 (.40 (2.60 (2. battery and radiator manufacturing) and recreational sources.20) .30) 1. stained glass framing.70) 1.00 (2. imported children’s trinkets and toys.10-1.10-1.00) .90 (2.10) 2.800 (.610 (.910-.20 (1.730 (.33.820-1.50-3.480-.20 (2.90-2. Fourth National Report on Human Exposure to Environmental Chemicals 213 .579-. 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.690) 75th 1.70) 1.920 (.40-5.833 (.20 (1.500-.572-.700-.60 (1.40) 3.749) .50-1.700 (.50 (2.80) 2.90-2.960-1.90) 2.49 (1.800) .600 (.700-.04 (.90-3.20) 1.822-1.600 (. absorbed lead is bound to erythrocytes and then is distributed initially to multiple soft tissues and eventually into bone.800-.30 (3.59-2.80) 2.90 (2. see Data Analysis section) for Survey years 99-00.50) 3.40-1.30) 1. Approximately half of the absorbed lead may be incorporated into bone.800-1.600-.90 (2.10-3.30 (2.90-2.40) 1.14-1.915-1.800) .900-1.10) .695 (.620) 1.815 (.07 (.80 (1.40) 2.70) 3.674) 1.20 (1.30) .613) .990) 1.862) .60 (1. lead-containing folk remedies and cosmetics.680-.13) .757-.22) 1.86-2.00) .955-1.935) 1.808 (.80) 1.04 (.50) 2.50) 1.828) Selected percentiles ( 95% confidence interval) 50th .738) .23) .90 (1.990) 2.700 (.677 (.848 (.30-1.40) 1. pewter utensils and drinking vessels.11) 2.13-3.00 (1.1. interval) . respectively.540 (.700 (. However.00-1.900-1.70-3.688 (.941) .651) .78-2.40 (2.20-2.70 (2.900 (.10 (1.556-. or water contaminated by mining or smelting operations.970-1.900) .641-.642 (.731 (. and 0.710-.800) .640 (.30 (1.766 (.10-1.32 (1.03 (1.00) .30) 1.50 (2.700 (.640-.573 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.10 (.02 (.60-3.80 (1.23-4.790 (.10-5. 2000).03-2.700-.29) 2.10 (1.800-.80-2.33 (2.00 (1.923 (.10 (.553-.70) 1.11 (1.00) 2.75) 4.40-1.78-2.70 (2.40 (1.680) Sample size 2465 2690 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.900) .82 (1.50 (2.960-1.30) 2. population from the National Health and Nutrition Examination Survey.80) 2.628) 1.09) 1.591 (.900) .10 (1.41) 2.40-2.600-.857) .10) .10-3.900 (.570-.20) 1.773) .700-.02) 1.20 (1.82 (2.35 (.30) 2. 1991).00-2.700) .70 (2.900-1.86 (1.86) 95th 2.10 (1.600-.600) .90-3.89) 2.29 (2.986) . which is the site of approximately Urinary Lead Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.700-.80-2.00) .661-.40 (1.616) . lead-contaminated dust in indoor firing ranges.600-.18-1. Children may also be exposed to lead brought into the home on the work clothes of adults whose work involves lead.605) . Less common sources of incidental or unique lead exposure are numerous: lead-glazed ceramic pottery.20 (3.589-.00 (1.78-2.40) 2.00-1.04) 2.708-.80) 3.700) 1.66 (2.70 (1.564 (.60-2.60-2. 2007.59) 1.90) 2.21 (2.590 (.818) .800 (.90-2.701) .20 (1.630 (.44-2.40 (1.00 (.50-2.600-.960 (.560-.30-5.60-1.671-.745-. bullet fragments retained in human tissue.62-4. and 03-04 are 0.40 (2.00) 2.900-1.14 (1.00-2.90-4.70) 2..752 (.20-1.49) 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 .17 (1.40 (2.20) . In the blood. 0.900) .S.52-1.636 (.80) 3.30) 1.20) .20) 1.80) 2.40-1.840 (.660) .50 (1.60) 2.80 (2.700 (.70 (2.50 (1.800-1.24-1.00 (1.10 (.72) 1.30) 2.718) .625 (.70) 3.680-.80-3..50-2.20-1. or after soluble lead compounds are ingested.00-2.40) 1.12) 90th 2.1.700 (. CDC.80) 2.700-1.90 (1.19 (1.04-2.506-.50) 2.97) 4.75) 3.833-1.27 (1.07-1.20 (1.600) .800 (.33-2.31-3.20-1.625-.10-1.691-.659 (.850 (. Lead is absorbed into the body after fine lead particulates or fumes are inhaled.10-3.80) 1.90) 2.558 (.52 (1.40 (1. dust.10) 2.40-3.20-2.729-.62) Total .86) 1.30-1.40) 1.650) 1.27) 1.04) .637-.31 (1.580-.70-2.60 (1.51) 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.20) . lead-based painted surfaces undergoing renovation or demolition.785) .40) 1.900) .680) .73 (1.30) 1.540-.30-3.64) 2.931) .579-.90 (1. 01-02. Small amounts of environmental lead also may result from burning fossil fuels (ATSDR.50) 1.30-2.30-1.91) 2.800 (.40) 2.10-1.50) 1.710-1.90) 1.900) .753 (.920 (. the primary source of exposure in children is from deteriorated lead-based paint and the resulting dust and soil contamination (Manton et al.40) 2.66 (2.30) 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 (2.Metals occupational (e.595-.620 (.60 (1.795 (.604 (.40-1.52-1.00-1.940 (.535-.g.14 (1. older plumbing systems with leaded pipes or lead soldered connections.20 (2.40 (1. and contact with soil.60-3.10) 1.526-.00) 1.30-1.800) .

88) 1.00) .Metals 90% of the body lead burden in most adults.52) 1.27 (1.28) 2.00 (1.20) .551-.50-1.70 (1.917-1. abdominal pain.742) .01 (.781-1. Approximately 70% of lead excretion occurs via the urine.55 (1.31) 1.71-2.43) 1.655) 75th 1.22-1.559-.753) .588-.00 (.709 (.28-1. 2004.988-1.10) 884 682 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites 214 Fourth National Report on Human Exposure to Environmental Chemicals . 1991.625 (.06) .712 (.10) 1.645-.14) 1.606-.541-.579-.721 (.603-.75-2.18) 1.67-4.569 (.746) .938-1.496 (.35) 2.68 (1. through the inhibition of certain enzymes. O’Flaherty.22-2.05 (.31 (2.508) .617-.43 (2.03) 2.460-.02-1.603-.404-.644 (.432 (.31 (1.03 (.718) 1.05 (1.47 (1.670) 1.66 (1. 2003.698) .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 .25-1.98) 2.790) .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 .914 (. For instance.02) 1.19-5.681-.469 (.920-1.61) 1. and paralysis.50 (1.41 (1.06 (1.18) 1.11 (1.43 (1.61) 1.607-.26) Total .03) 1.957-1.997-1.50-2.92) 2.56 (1.98 (1. 1993).28) .33-1.655-.15-2.667) .623 (. Schwartz.586-.48 (1.65 (1.18) .00 (1. In 1991.725) .04-3.62-2.11 (.38 (2.608-.86 (1.74 (1.56-3.535) .375 (. based on prospective population studies.667-.946-1.62-3.662) 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.S.63) 1.24 (1. Lead can cross the placenta and enter the developing fetal brain.696 (. and iron.19) 1.33) 1. BLLs and associated toxic effects differ in children and adults.09-1.926 (.380-..50) 1.03) .22) .33 (1.63) 4.914-1.731-. 1996).22) 1.975-1.679-.33) 2.436) .608 (. 1995.838) .648 (..79 (1.43) 2.79) 1.707 (.49 (1.58) 1.83 (2.01) .75 (2.612-.72-2.918-1.677) . with lesser amounts eliminated via the feces.11) 1. kidney injury.622 (.720 (.571-.79) 2.893) . 1993.583-.639 (.51) 1.10 (1.64-2.710) . and approximately 40 to 70% of lead in blood comes from the skeleton in environmentally exposed adults (Smith et al.988 (.594-.47 (2.05-1.673) .73-2.618 (.97-18.96 (1.07) .604-.718) . 1995).15) 1.870 (.981-1. The skeleton acts as a storage depot.701 (.22) 1.633 (.03) 1.03 (1.97) 1.61) 1.851) .25-1.688) .708 (.693 (.77) 2.722 (.78 (2.62) 2.638 (.40-1. Equilibrated blood lead levels (BLLs) after chronic intake are associated with certain toxic effects.683-.887 (.61) 3. Lead is cleared from the blood and soft tissues with a half-life of 1 to 2 months and more slowly from the skeleton.69 (1.588-.18 (1.14 (1.37-1.408-.46 (2.82) 1.654) .09) 1.09-1.658 (.47) 1.722 (.862-.06 (. interval) .03-2.20-3.88) 2.88) 2.652 (.41-1.655) .800-.940 (.933-1.383-.649 (.44 (1.0) 3.615 (.977) 1. and nails (Leggett.97 (1.09-1.793-1.44 (1.635 (.39-1.428) .603 (. 2007).701) . population from the National Health and Nutrition Examination Survey.742) Selected percentiles ( 95% confidence interval) 50th .615 (. Large amounts of lead in the body can cause anemia.56) 3.50-2.11 (.03) 90th 1.64) 2. Nash et al.85 (1.592-.72-2.639) .853-1.03) .641 (.07-1.734) . CDC.763) .12-1.26) 2.11-1.587-.605-.609 (.03 (.44) 1.765) .725) .66) 2.94-2.971 (.571-.37-1.05-1.828) .23 (1.71 (1.623 (.50-2.404 (.400) .38 (2.18) 2. with a half-life of years to decades.78-4.510-.810 (.659-.702) .644) .29 (1.08) .933) .51 (1.938 (.17-1.03 (.65-2.492-.668-.85) 1.31 (1.758) . Staessen et al.671 (.962 (.703) .900 (.739) .681-.992-1.07 (. scant amounts are lost through sweat.882-1.682) .31) 1.64) 95th 2.667-.404 (.72) .87) 1.56-2.55 (1.08) .11 (1.679) 1. BLLs near 10 µg/dL can affect blood pressure in adults and neurodevelopment in children (Bellinger.812-1.645-. hair.34-1.632 (.963-1.59-3.38 (2.53) 1.529-.677 (.83) 1.700-.914 (. seizures.45 (1.990 (.676) .774 (.03) 2.702-.841-1.17 (.561-.85-2.41) .992-1.601-.97) 1. and through binding to ion channels and regulatory proteins.85-2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.88 (1.876-1.593 (.720 (. Additional mechanisms include generating reactive oxygen species and altering gene expression (ATSDR.979 (.08-2.15-2.10 (.00 (1.52 (1.61) 1.98-2.898) .15) 1.36-2.342-. zinc.62-1.702) .20) .828-1.639 (.755 (.04) 2.64 (1.53-1.657) 1.11) .461) .43-1.89-2.918 (.66 (1.730) 1. encephalopathy.639 (. 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.686) .15-3. The toxic effects of lead result from its interference with the physiologic actions of calcium.621 (.698) .89-5.594-..677-.94 (1.46 (1.88-2.796-1.73) 2.06) 1.

6%) were lower than those from NHANES 1991-1994. Workplace standards and guidelines for lead exposure and monitoring have been established by OSHA and ACGIH. Data submitted through state public health programs from 2006 showed that 1.. Schwartz. both the geometric mean (1.xls).. IARC considers inorganic lead compounds probable human carcinogens.. 2003. higher than 100-200 µg/dL). BLLs greater than 10 µg/dL continue to be more prevalent among children with known risk factors. Schwartz et al.07 µg/dL (Becker et al. 1995. Bellinger 2005. 1995) and associations between increased bone lead concentrations and blood pressure (Hu et al. CDC.4% in NHANES 1999-2004. urban residence. when the geometric mean BLL was 2.. adults in the 19992000 NHANES sample (Apostoli et al.. 1996. NTP considers lead and its compounds reasonably anticipated to be human carcinogens. 1996. adult residents. Both drinking water and ambient air standards for lead have been established by the U.. 2006).S. and organic lead compounds not classifiable with respect to human carcinogenicity. 2005a). with overt encephalopathy.2 µg/dL in males and 3.000 higher-risk children and adolescents who were tested from 2001 to 2002 at an urban medical center had higher BLLs than the NHANES sample. may alter sperm morphology. 1987. 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. Muntner et al.5 per 100. particularly in the skeleton..4% of children had BLLs of 10µg/dL or higher (CDC. Low level environmental lead exposure may be associated with small decrements in renal function (Kim et al. Pirkle et al. almost double the geometric mean of 1.atsdr. Recent studies have suggested that neurodevelopmental effects may occur at BLLs lower than 10 µg/dL (Canfield et al. In NHANES 1999-2002 in children 1-5 years old. 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. 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.21% of approximately 3. though there is greater individual variation in urine lead than in blood and greater potential for contamination. Jones et al (2009) showed that the prevalence of BLLs of 10 µg/dL or greater decreased from 8.html. 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. 2009). Biomonitoring Information Blood lead measurement is the preferred method of evaluating lead exposure and its human health effects. and low family income (CDC. environmental levels) and health effects is available from ATSDR at: http://www. including minority race or ethnicity. adult population has similar or slightly lower BLLs than adults in other developed nations (CDC. A decrease in BLLs is evident also in adult NHANES results reported over past decades (CDC.S. premature delivery.75 µg/dL in U. Urine levels may reflect recently absorbed lead. seizures. 2006).9 µg/dL) and percentage of children with BLLs greater than 10 µg/dL (1. 2005b). Jones et al.000 adults. usually with BLLs greater than 40 mg/dL. Lanphear et al. Overall. approximately 11. 2000). 2003.. and peripheral neuropathy generally occurring at much higher levels (e. Fourth National Report on Human Exposure to Environmental Chemicals 215 . and decrease fertility (Alexander et al. 1996. 1998). 2002..3 million children tested had BLLs of 10 mg/dL or higher (http://www.. 2002a).cdc. A general population survey of adults Germany in 1998 reported a geometric mean blood lead concentration of 3. subtle or nonspecific neurocognitive effects have been reported at BLLs as low as 20-30 µg/dL (Mantere et al. 1999). Korrick et al.0 µg/dL in females (Soldin et al. In occupationally exposed adults. Payton et al. For example. A general population survey of adults in Italy tested in 2000 found BLLs slightly more than double those reported for U. Temporal declines in children’s BLLs have been found in other developed countries (Wilhelm et al.cdc... reduce sperm count..gov/toxpro2.g. Surveillance data reported by U.. 1999)... adults in the 1999-2000 NHANES sample. the geometric mean BLL was 3.S. 1991. Information about external exposure (i. 2007).7 µg/dL and 4.Metals µg/dL or higher as the level of concern in children. which is an 84% decline. 2003). respectively. The U.gov/nceh/lead/surv/database/State_ Confirmed_byYear_1997_to_2006.S. lead in women may be associated with hypertension during pregnancy.S. 2003. BLLs reflect both recent intake and equilibration with stored lead in other tissues. EPA. 1994). the prevalence rate has declined annually since 1994 (CDC. More recently. residing in housing built before the 1950’s. However.6% in NHANES 1988-1991 to 1. At low environmental exposures.e... High dose occupational lead exposure. 2000). 2001). 2005b.. the national prevalence rate for adults with BLLs 25 mg/dL or higher was 7... 2002). and spontaneous abortion (Baghurst et al. Borja-Aburto et al. 1984. Staessen et al. Telisman et al.. Many animal studies have established the multiple neurotoxic effects of lead (ATSDR.S..

Caldwell KL. Blood lead reference values: the results of an Italian polycentric study. A prospective follow-up study on psychological effects in workers exposed to low levels of lead.gov/toxprofiles/tp13. Rojas LM. Vimpani FB. Hu H.89:330-335.htm. Jacobson JL. Jones RL. MMWR Morb Mortal Wkly Rep 2006. Hernberg S. Neurotoxicol Teratol 2004. Korrick SA. Neurotoxicol 1987.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. Aug 2007 [online]. 1991 [online]. Angle CR. Blanco J. Semen quality of men employed at a lead smelter. Hunter DJ.atsdr. Hänninen H. Speizer FE. Batuman V.gov/nceh/lead/ CaseManagement/caseManage_main. Bavazzano P. Available at URL: http://www. Pediatrics 2009. References Agency for Toxic Substances and Disease Registry (ATSDR). Chiodo LM. Rotnitzky A. Atlanta (GA). JAMA 1996. Lanphear BP. 4/14/09 Centers for Disease Control and Prevention (CDC). Hu H. 4/14/09 Centers for Disease Control and Prevention (CDC). Acquisition and retention of lead by young children. Mantere P. N Engl J Med 2003. Available at URL: http://www.cdc. Aro A. CDC. Blood lead levels measured prospectively and risk of spontaneous abortion. doi:10. Toxicological profile for lead. Teratogen update: lead and pregnancy. et al. 2005. IARC Monogr Eval Carcinog Risks Hum 2006.87:1-471. Blood lead and chronic kidney disease in the general United States population: 216 Fourth National Report on Human Exposure to Environmental Chemicals . Lead. Am J Epidemiol 1999. Homa DM.150(6):590-597. Pirkle JL. Recommendations from the Advisory Committee on Childhood Lead Poisoning Prevention. Checkoway H. Managing Elevated Blood Lead Levels Among Young Children. Henderson CR. Stanek KL. Rios C. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Canfield RL. Neurodevelopmental effects of postnatal lead exposure at very low levels. et al. gov/mmwr/preview/mmwrhtml/mm5420a5. Atlanta (GA). Bellinger D.gov/nceh/lead/publications/ books/plpyc/contents. The Port Pirie cohort study: lead effects on pregnancy outcome and early childhood development. Brody DJ. Am J Public Health 1999. McMichael AJ. Kim R.82:60-80. Krause C. Ga.cdc. Robertson EF. 2005b.cdc. Age-specific kinetic model of lead metal in humans. Birth Defects Research (Part A). Wigg NR. 2003-2004. Borja-Aburto VH. Payton M. Muller CH. Inorganic and Organic Lead Compounds.8(3):395-401. The relationship of bone and blood lead to hypertension. Trends in blood lead levels and blood lead testing among US children aged 1 to 5 yeas.123:e376-e385. Weiss ST. Ewers TG. Available from URL: http://www. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.1542/peds:2007-3608. Muntner P. Farias P. 1999-2002. Seiwert M. Cory-Slechta DA. Cox C. Manton WI.53:411-416. Sparrow D. Rotnitzky A. Hu H. Int J Hyg Environ Health 2002. Schulz C. Kaus S. Adult blood lead epidemiology and surveillance—United States. Auinger P.275:1177-1181. Weiss ST.73:409-420. et al. van Netten C.html. Occup Environ Med 1996.htm. 4/14/09 Centers for Disease Control and Prevention (CDC). Meyer PA.113(4):1016-1022. Environ Health Perspect 1993. MMWR Morb Mortal Wkly Rep 2005a. Becker K.htm. Baghurst PA.275(15):1171-1176.gov/mmwr/preview/mmwrhtml/ mm5532a2. Scand J Work Environ Health 1984. Ronchi L. et al. Cognitive deficits with blood lead concentrations < 10 µg/dL in US children and adolescents.26:359-371.205:297-308. Jacobson SW.101(7):598-616. Public Health Rep 2000. Wager C. Dietrich K. Baj A. Korrick S. et al. Luukkonen R. Blood lead levels—United States.htm. Pediatrics 2004. Neri A. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Available at URL: http://www. Kuehnemann TJ. Kaufman JD. 4/14/09 Alexander BH. Ganzi A. Preventing Lead Poisoning in Young Children. Lead and hypertension in a sample of middle-aged women. Intellectual impairment in children with blood lead concentrations below 10 µg/dL. Leggett RW.55(32):876-879. JAMA 1996. 1988-2004. Available at URL: http://www.cdc.cdc. Third National Report on Human Exposure to Environmental Chemicals. Reese YR. Bellinger D.287:1-11. Vupputyuri S. Coresh J. Cox C. Environ Res 2000.10:43-50. Roberts RR. Hertz-Picciotto I. Lepom P. 4/14/09 Centers for Disease Control and Prevention (CDC). Jusko TA.115:521-529. Apostoli P. Sparrow D. Centers for Disease Control and Prevention (CDC). Atlanta. Sci Total Environ 2002.348:15171526. A longitudinal study of low-level lead exposure and impairment of renal function: the Normative Aging Study. 2002 [online]. Lanphear BP.54(20):513-516.

blood pressure and cardiovascular disease in men.S. Kaufmann R. zinc. Osterloh JD. Schwenk M. Hanak B. Blood lead concentrations in children: new ranges. and hypertension in perimenopausal and postmenopausal women. blood pressure. Revised and new reference values for arsenic. stable lead isotopes to determine release of lead from the skeleton. Physiologically based models for bone-seeking elements. Wilhelm M. Environ Health Perspect 2000. Pizent A. Lauwerys RR. and mercury in blood or urine of children: basis for validation of human biomonitoring data in environmental medicine. Soldin SJ. Sherwin R. Cvitkovic P. Use of endogenous. Rocic B. and tibia lead with neurobehavioral test scores in South Korean lead workers. 50:31-37. cadmium. et al. Am J Epidemiol 1994. Brody DJ. Soldin OP. Smith DR. Hwang KY. Hickman T.327:109-113. population to lead: 1991-1994. IV. Fourth National Report on Human Exposure to Environmental Chemicals 217 . Toxicol Appl Pharmacol 1993. dimercaptosuccinic acidchelatable lead. Semen quality and reproductive endocrine function in relation to biomarkers of lead. Kinetics of lead disposition in humans. Lead.108(1):45-53. Rubin R. Gunter EW. Am J Epidemiol 2001. Association of blood lead. O’Flaherty EJ. Staessen JA. Lee GS. Lee BK. Pirkle JL. Jurasovic J. Magder L. Stewar WF. Environ Health Perspect 1998. Nash D. Blood lead. Exposure of the U. Clin Chim Acta 2003. Arch Environ Health 1995. et al. Lustberg M. Roels H.209:301305.Metals results from NHANES III. Int J Hyg Environ Health 2006. Gavella M. cadmium. Payton M.289(12):1523-1531.106:745-750. Amery A. Kidney Int 2003.140:821-829. Low-level lead exposure and renal function in the Normative Aging Study. Paschal DC. JAMA 2003. lead. Flegal AR. Kaufmann RB. Hu H. Low-level lead exposure and blood pressure.9:303-327. Weiss ST.118:16-29. and copper in men. Schwartz J. J Hum Hypertens 1995.153(5):453464. Sparrow D.104(1):60-66. Telisman S. Environ Health Perspect 1996. Schwartz BS. Schulz D. Lee SS.63:1044-1050.

800-1.30) 3.40 (3.40-2.70 (3.80 (1. 7439-97-6 General Information Mercury is a naturally occurring metal that has elemental (metallic).20-4.900) 1.00 (. synthetic organomercury compounds were once used in pharmaceutical applications.2.50-3.40-1. electrical lamps. 1980.30-2.800 (.00) 1. Hursh et al.00-5. water can be contaminated by the direct release of elemental and inorganic mercury from industrial discharges.886) .703-.814 (.90 (1. 1998.30-4. IARC..00-1.90 (1.00) .700 (.60-5. silver-white liquid (quicksilver) obtained predominantly from the refining of mercuric sulfide in cinnabar ore.50) 2. Some cosmetic skin creams from countries other than the U. with the highest concentrations occurring in the kidneys (Barregard et al. and mercury compounds are still used as preservatives (e. mercuric chloride).60 (2.00 (.372) .10-3.00 (2.g.903) Selected percentiles ( 95% confidence interval) 50th . which create an episodic potential for volatization and inhalation of mercury vapor.90) 3. Imported folk and alternative medicines occasionally are contaminated with inorganic mercury.60-2.90) 95th 4.g. sphygmomanometers and barometers. an organic form of mercury. Inorganic mercury compounds such as mercuric oxide are used in producing batteries and pigments and in synthesizing many organic chemicals. 218 Fourth National Report on Human Exposure to Environmental Chemicals .80) 3.800-1.40 (3.80 (1. and dental amalgam.60) 2085 2293 3478 Limit of detection (LOD..40-3. Metabolism of mercury by microorganisms in aquatic sediments creates methyl mercury.30) 1.80) 1.80 (1.g.800-1.20-3.50-1.70 (1. such as chlorine (e.40) 3. population from the National Health and Nutrition Examination Survey.40 (4.900) 75th 1.70-2.70 (4. predominantly from fish and other seafood.40) 1.285-. Elemental mercury is used to produce chlorine gas and caustic soda for industrial applications. thermometers. and mining and smelting.781 (. have often required public health intervention (Zeitz et al.40-1.700-.500 (.400-. Woods et al.40 (4. 1994. Kingman et al.90-3. The ingestion of methyl mercury.02) .40-2.12) . sulfur.689-.860-1. and is distributed to most tissues. Also. Inhalation of elemental mercury volatilized from dental amalgam is a major source of mercury exposure in the general population (Halbach.655-.563 (. interval) . Accidental spills of elemental mercury.700) .753-1. which can bioaccumulate in aquatic and terrestrial food chains.20 (2.472-.80) 4.00) 3. it is oxidized in Total Blood Mercury—2003-2004 Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U.Metals Mercury CAS No. may contain inorganic mercury.900) .00) 1.S.30 (2.919) . 2007).10) .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 .60-6. merbromin). Atmospheric elemental mercury can be deposited on land and water.70) 911 856 2081 4525 03-04 03-04 . inorganic.90 (4.30-6. phenylmercuric acetate) or topical antiseptics (e. Inorganic mercury exists in two oxidative states (mercurous and mercuric) that combine with other elements.30) 3.900 (.800 (. Elemental mercury is released into the air from the combustion of fossil fuels (primarily coal).326 (.600) 1.877 (. After elemental mercury is absorbed.00) 4.800 (.00 (2.300-.418-.419 (. The kinetics of the different forms of mercury vary considerably.80 (3.30) 5.00 (.500-.490 (.400-.700-.700-.00 (2.50) 4. see Data Analysis section) for Survey year 03-04 is 0.714-.00 (1.00 (.70 (1.g. Survey years 03-04 Geometric mean (95% conf. to form inorganic mercury compounds or salts. elemental mercury is absorbed mainly by inhaling volatilized vapor.574) .672) .20-4.30-5..700) .700-. or oxygen. constitutes the main source of dietary mercury exposure in the general population.300 (.60) 1.363-.797 (.400 (.20) 2.60-3.30 (1.800 (. 2002). and organic forms..60) 1. elemental mercury is used in rituals practiced in some Latin American and Caribbean communities.. 1993). Apart from methyl mercury.30) 1.50) 5.500 (. solid-waste incineration. thimerosal.50) 1. Poorly absorbed from the gastrointestinal tract.500-.. Elemental mercury is a shiny. thermostats and switches).484) . In addition.800-1.300) .979 (. 1999 .600 (.60 (1.60-6..900) 1.S.50-2..500) . Other major uses include electrical equipment (e.700-.60 (1.927) .30) 4132 4241 03-04 03-04 03-04 .776 (.800-1.900) 1..90) 90th 3.

833 (.70 (1.30) 3.80-3. Jonsson et al.70 (1.40-2.300 (.50) 2. Excretion occurs by renal and fecal routes.20 (2.30-2.20 (.00-2.10 (5.300 (..600) . 1998).00-3. 1990). Suzuki et al.00-2.318 (. Inorganic mercury and methyl mercury are distributed into human breast milk in relatively low concentrations. and peak urine levels can lag behind peak blood levels by days to a few weeks (Barregard et al.300 (.475) .20) .300) .7) 4.30 (1.300) .900 (.00) 4.824) 1. a measure of accumulated dose (Cernichiari et al.800 (.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 .60 (3.40) 2.00) 6. 1995. Transplacental transport of methyl mercury and elemental mercury has been demonstrated in animals (Kajiwara et al.800) 1. 1999-2002.726-1.00) .541-. 2004.90 (4. 1971)..10) .30 (1.10 (.30) 1.3) 4.40 (1.20-3.00) 1.50 (2.40 (1.90) 90th 1. 1998). 1999).30-4.40) 1. McDowell et al..700 (. 2003).30) 1.200-.800-1.700 (. The fraction of methyl mercury absorbed from the gastrointestinal tract is about 95% (Aberg et al. Vahter et al.30 (1.00) 2.500-. Smith et al.377) .700-1.90) 2.256-.268-.60 (3. 1991.. Methyl mercury is incorporated into growing hair. Miettinen et al. Fourth National Report on Human Exposure to Environmental Chemicals 219 . After exposure to elemental mercury.800-1..90 (1.738-.00-1.20-2.14 and 0.. 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.00-6.900-1.50) 3.200-..600) . Smith and Farris.30-6..300) .200-.200-.664-1.01) .00) 1. The slow-phase half-life may be several weeks longer in persons with chronic occupational exposure (Sallsten et al.800) .Metals the tissues to mercurous and mercuric inorganic forms..50) 1.70-5.500 (.60 (1.900 (. Geometric mean Survey years (95% conf.299-..800) 75th .70) 4. 1975.40) 5.697-.919) .500-.27) .50-3.200-.50-2.29) . Sandborgh-Englund et al..940) Race/ethnicity (females.500-.35 (1. 1994).30 (.10-3.10 (1. 1996.820 (. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.60 (1..80) 1.50 (1.600 (.80) 579 527 370 436 588 806 Limit of detection (LOD. Less than 15% of inorganic mercury is absorbed from the human gastrointestinal tract (Rahola et al. 1992.90 (4.50) 1.395) .20-3.70 (1.70-3. population. 1992).825-1.200 (. Methyl mercury enters the brain and other tissues (Vahter et al. 1993)..10 (3.200 (..800) 1.23) .50-12. 1994.300) .369) 1... 1996). and the newborn’s levels decline gradually over several weeks (Bjornberg et al.317 (.343 (.944 (.10 (1.14..700 (.10) 1.06 (. Myers et al. 1993).S.20-11.00 (2.00 (3..60 (2.500-.73) 1.70) 4.30-5. 1992 and 1999.60) 1. Vimy et al. urinary mercury levels decline with a half-life of approximately 1-3 months (Roels et al. excretion of mercury occurs predominantly through the kidney (Sandborgh-Englund et al.30-4.00) 7.297-.10) . 2005).70-6. and a useful marker of exposure in epidemiologic studies (Grandjean et al.10-1.60) 3.60) 2.800-1.. 1994) and then undergoes slow dealkylation to inorganic mercury.800) .02 (.20) .700) 2.500 (.300) ..40-2.20-3.90) 3.700 (.80 (1. Lesser penetration of inorganic mercury occurs through the bloodbrain barrier than occurs with either elemental or methyl mercury (Hattula and Rahola.30-6.90 (3.700-1.700-.30-3. 1973). thereafter.329 (.300) .50) 95th 2.00 (2.10 (1.0) 4..400-.06-1. 2003). for both acute and chronic exposures. The half-life of inorganic mercury in blood is similar to the slow-phase half-life of mercury after inhalation of elemental mercury.. 1969.20) 1.70) 1.40-1.871-1.374) .60 (1.265-.500-.307 (.10 (.200-.269-. 16-49 years) Mexican Americans Non-hispanic blacks Non-hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 . Mercury levels in the cord blood are higher than in the mother’s blood (Stern and Smith.00 (1.70-3.90) 2. Human pharmacokinetic studies indicate that methyl mercury declines in blood and the whole body with a half-life of approximately 50 days.900-1.30-11.80 (3.667 (.700-.90 (1.377 (. 1984.800 (. interval) Selected percentiles (95% confidence interval) 50th .800 (. with most elimination occurring through in the feces (Sherlock et al.407) .00 (2.500-1. Blood concentrations decline initially with a rapid halflife of approximately 1-3 days followed by a slower half-life of approximately 1-3 weeks (Barregard et al.70-5.300 (.30-6.60) 1. National Health and Nutrition Examination Survey.90) 5.00-2.900 (.

Survey Geometric mean (95% conf. 2004). Vupputuri et al. Acute.600-. Inorganic mercury exposure usually occurs by ingestion.600-. overt signs and symptoms of chronic inhalation may include tremor.500-. 2005). maculopapular rash. Smith et al. 2002. 1998.. and neurocognitive and behavioral disturbances. 2000). ataxia.500 (. 220 Fourth National Report on Human Exposure to Environmental Chemicals . depression. which may vary for some chemicals by year and by individual sample.700) 2007 2240 3406 Limit of detection (LOD. and cerebral palsy (NRC.500-.500) .500-.500-.600) . and pinkish discoloration of the hands and feet (Tunnessen et al. Factor-Litvak et al. and a drinking water Inorganic Blood Mercury Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U. Overt poisoning from methyl mercury primarily affects the central nervous system. Smith et al. 2000.700) 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 . short-term memory loss. 1987). typically after a latent period of weeks to months. particularly irritability. Salonen et al.500-.42. 2000. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 2003).500-..600 (.700) . 2004).700-. 2006.600-.. Rice.800) . < LOD means less than the limit of detection.500 (<LOD-. Rissanen et al.600 (. 2006. DeRouen et al. high-dose exposure to elemental mercury vapor may cause severe pneumonitis. Workplace standards for inorganic mercury exposure have been established by OSHA and ACGIH.800) .600) . High-level prenatal exposure may result in a constellation of developmental deficits that includes mental retardation. causing parasthesias. 1951.700 (. fatigue.600) .700-.600) . Oskarsson et al. Large amounts may cause irritant or corrosive effects on the gastrointestinal tract (Sanchez-Sicilia et al. In recent epidemiologic studies. altered physical growth.500-. 1963).600) . The constellation of findings may include anorexia. 1993)..600 (.700 (. and sleep disturbance (Bidstrup et al. anorexia.500-.700 (. Although recent investigations have suggested a possible link between chronic ingestion of methyl mercury and an increased risk for cardiovascular disease..800) 792 842 2060 4453 03-04 03-04 * * < LOD < LOD < LOD < LOD . 1970. Sakamoto et al. limb deformities.700 (. At levels below those that cause acute lung injury.. insomnia.600-. Drexler and Schaller.700 (...600 (... hearing impairment. 2004. dysarthria. Once absorbed..600 (.. Mercury levels in breast milk also decline in the weeks after birth (Bjornberg et al.500-. sensory impairments.Metals may be more efficient for inorganic mercury (Grandjean et al. interval) Selected percentiles ( 95% confidence interval) Sample 95th .800) 4015 4132 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD .600 (.600) * 03-04 03-04 03-04 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .600) . Acrodynia is a sporadic and predominantly pediatric syndrome historically associated with calomel (mercuric oxide) in teething powders and occasionally other inorganic forms of mercury. population from the National Health and Nutrition Examination Survey... 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.500 (. gingivitis.700-. Occupational exposure to elemental mercury vapor has been associated with subclinical effects on biomarkers of renal dysfunction (Cardenas et al. Sakamoto et al. and progressive constriction of the visual fields. hypertension. 1983). 2004.S. the existence of a causal relation is unresolved (Chan and Egeland. pain in the extremities. dysarthria. 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. irritability..600) . 1995.500 (<LOD-. see Data Analysis section) for Survey year 03-04 is 0.600) . Stern 2005. the most prominent effect is on the kidneys where mercury accumulates and may lead to renal tubular necrosis. cerebellar ataxia.. 1996). Bellinger et al. 1995. 2005.600 (..700 (. Low-level exposure from dental amalgams has not been associated with neurologic effects in children or adults (Bates et al.600 (..600) .

89) 3..97) 2.358 (..330-. range 40 years to 78 years) had an average total blood mercury concentration of 2. 1998).93 (1. IARC considers methylmercury to be a possible human carcinogen and elemental and inorganic mercury to be unclassifiable with regard to human carcinogenicity.700 (. However.cdc. Fourth National Report on Human Exposure to Environmental Chemicals 221 . Grandjean et al.24 (2. Total blood mercury levels increase with greater fish consumption (Dewailly et al.23) 2.463) .01 (.870-1.420 (.42) 95th 3.580) . Mahaffey et al.530) .67-3.88-3.250) .00) 1.14) 90th 2. total blood mercury geometric mean levels in females aged 16-49 years did not change. 2009).66) 3. 1995. and increased slightly in non-Hispanic white children (Caldwell.430) .07 (.360 (. 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. Urinary mercury consists mostly of inorganic mercury (Cianciola et al.9 years).68 (2.254 (. Urine mercury levels increase as more occlusal surfaces of teeth are filled with mercury-containing amalgams (Becker et al.39-3.570) .63-2. adult women in several ethnic subgroups (Hightower et al.492) Selected percentiles ( 95% confidence interval) 50th .60) 619 713 1066 Limit of detection (LOD.410-.340-. the total blood mercury concentration is due mostly to the dietary intake of organic forms.433 (.65) 1.870-1.60 (1.440 (.330 (.610-1. From 1996 through 1998.330-.03-4. interval) .370) .29) 1.549) . who participated in a 1998 representative population survey (Becker et al. Survey years 03-04 Geometric mean (95% conf. 2004.200 (.290-. average age 9. the developing fetus may be the most susceptible to the effects of ongoing methyl mercury exposure (NRC.46) 3.413-.99-6.31) 1266 1272 03-04 03-04 03-04 . see Data Analysis section) for Survey year 03-04 is 0.23) .55) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites Sample size 2538 03-04 03-04 03-04 .24) 1. 1998).76-4.88) 287 722 1529 03-04 03-04 .700-1.77-2. These men had no occupational exposure to mercury but previously had received dental amalgams at military facilities (Kingman et al.08 (1.16 (.20 (1.18) 2. These distinctions can help interpret mercury blood levels in people.396-. particularly methyl mercury..280-. Urinary Mercury—2003-2004 Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. total blood mercury increased with age. Information about external exposure (i. the median concentration of blood mercury was 0.76-3. slightly higher total blood mercury levels were found in U. (2000) studied 1216 blood donors in the Czech Republic (896 men and 320 women.52) 2.gov/toxprofiles. EPA.S.534) . In NHANES 19992002. Schober et al. aged 18 to 69 years.360-. Sanzo et al..430 (.05) 3.495 (. Clinically observable signs of ataxia and paresthesias may occur when blood mercury levels increase to approximately 100 µg/L after methyl mercury poisoning.epa. 758 children.96 (1.67-2.213-.28) 1..940 (.16 (1.304) .460) .350-.840-1. Over the NHANES 1999-2006 survey periods. 2006).. environmental levels) and health effects is available from the U.e. EPA at: http://www. average age 33 years. military veterans (mean age 52.58 µg/L for 4645 adults.85-2.420 (.atsdr..840) 1.96 (1.90) 2.476 (.14.360-. 2003).330-.54 (2..441 (. Among the three racial/ethnic groups.61) 1.46 µg/L for children. During the same survey periods.442-.160-.31) 2.78 µg/L for adults and 0.770-1. Biomonitoring Information In the general population.S.509) .430 (.55 µg/L..gov/mercury and from ATSDR at: http:// www..12 (. 2000).509) .480) 75th 1.890 (.30) 3. 2001. 2003).34-3.530) .382-.14-2. Benes et al. and the age-related changes differed across the groups (Caldwell et al.19 (2. 2002). 2009).78-2. Kingman et al. et al.840-1.480 (.. A cohort of 1127 U.405-.406-.520) .S. In Germany the geometric mean for blood mercury was 0.08 (1.930-1..05) 1.S.555) .33 (2.S.88 (1.400 (.76-3.13-2.960 (.09 (2.60-2.530-.Metals standard for inorganic mercury has been established by U.313-. 2001.408) . although non-Hispanic black females had higher levels than non-Hispanic white or Mexican American females..8 years. 1997.460 (.00 (.416 (. population from the National Health and Nutrition Examination Survey..447 (.26 (1. total blood mercury levels declined slightly in non-Hispanic black and Mexican American children.19 (1.

64-2.276 (..307-.472-. The ACGIH (2007) currently recommends that urinary inorganic mercury in workers not exceed 35 µg/g of creatinine. 1992).00 (.16) 1.S.. ACGIH recommends that the blood levels due to inorganic mercury exposure in workers not exceed 15 µg/L.362 (.464 (.365 (. women of childbearing age have generally been much lower than these levels (CDC. DeRouen et al.00) 286 722 1529 03-04 03-04 .40-1.687) .09) 1.619-. Urinary mercury levels in recent German (Becker et al.25 (.246-. not to imply a safety level for general population exposure. and on average.31 (1.392-.07) 1.265-.480) .385-.18-1.87) 2.498) 75th .76 (1.01) 2.537) .616) .486) Selected percentiles ( 95% confidence interval) 50th .S.65 (1.61) 1. 1988.347) .343 (. 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.463 (.391) ..714-1.208-. Biomonitoring data will also help scientists plan and conduct research on exposure and health effects.400-.90) 618 713 1066 222 Fourth National Report on Human Exposure to Environmental Chemicals .909 (.306 (.485 (.588) .358) .990) .784) 1. et al.13 (1.46-2.S.964-1.54 (2.S. Survey years 03-04 Geometric mean (95% conf. reversible increase in urinary N-acetyl-glucosaminidase. Urinary Mercury (creatinine corrected)—2003-2004 Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U..11-2.875-1.289) .23-2.35 (1. 2003).87 (1.30) 2.13-2.476 (.32 (1.Metals 2000). and Italian (Apostoli et al.297 (. a biomarker of perturbation in renal tubular function. 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.1 µg/L.06 (.12-3.62 (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 .391-. 1998)..384 (.88-2.443 (.40 (1. 2009). among workers with urinary mercury concentrations of 25-35 µg/L or greater (Barregard et al..275) .630) .447 (.79 (1.525 (.. Langworth et al.376-.67 (1. interval) . 2002).32-2.969-1.545 (.404-.535) 1.365 (. Levels in U. Czech (Benes et al.652) .301-.28 (.400) . mean urinary mercury was 3.280-.63) 1.41-2.88 (1.785-1.44) 1.88-2.21) 1.56) 1266 1271 03-04 03-04 03-04 . In the study of U.30) 1.04-3.78-4.86) 95th 2.39) 1. the urine mercury increased by approximately 0. Finding a measurable amount of mercury in blood or urine does not mean that the level of mercury causes an adverse health effect.309-. Department of Health and Human Services noted that several studies have observed a modest. Information about the biological exposure indices is provided here for comparison.508 (. Blood mercury levels of women and children in NHANES 19992006 were also below levels established as occupational exposure guidelines (Caldwell.225-.77 (2.768 (.S.417) . 2006). military veterans with dental amalgams.368) . 2006.532 (. 2002) adult population surveys were similar to those in a U.667-1.587 (.1 µg/L for each surface with a dental amalgam (Kingman et al. 2005).196-.. population from the National Health and Nutrition Examination Survey. et al.566) .599) .970 (.455-.455) . 2009).51-2.06 (.522-. An expert-panel report recently prepared for the U.00) 90th 1. Urine mercury and the number of dental amalgams were correlated.455-.696 (.217 (.800-1.67 (1.79) 1.255 (..620-.11) 1.333-.447-.03) 2.11) 2. representative sample of women aged 1649 years reported in NHANES 1999-2006 (Caldwell..

502-.79) 3.91-7.833) .68 (3.46-4.72) 1. Geometric mean (95% conf.92) 3.742-1.Metals Urinary Mercury−Females Aged 16-49 Years Old.85-3.50 (2.68) 3.824) .616-.846) .569-. 1999-2002.41-6.25) 2. population.620 (.580-.51 (3.910) .31-1.56) 4.760 (.27 (1.43-1.46) 3.832-1.420-.724 (.18) 3.850-1.76) 2.81-6.37 (1.605-.831) .30 (2.98 (5.32-3. National Health and Nutrition Examination Survey.670) 75th 1.07-2.723 (.99-2.606 (.00 (2.51) .10-4. population.97 (1. Urinary Mercury (creatinine corrected)−Females Aged 16-49 Years Old.665) .14-1.00) 2.32) 2.39) Sample size 1748 1960 Age group (females) 16-49 years Race/ethnicity (females.27-1.37) 1.565 (.94) 1.17) 95th 5.658 (.610-.83-3. National Health and Nutrition Examination Survey.516 (.596 (.53) 595 531 381 442 594 826 Fourth National Report on Human Exposure to Environmental Chemicals 223 .790) . 1999-2002.21 (1.665) Mexican Americans Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .05 (2.42) 2.3) 5.501-.15-1.806) .31 (1.28 (1.00 (3. interval) Selected percentiles (95% confidence interval) 50th .99) 1.44) 3.578-.615 (.709) .21-3.710 (.966) .32 (1.45-2.744) 1.07) 1.560-.740 (.84 (2.23-1.520-.97) 2.637) .387-.500-.639 (.656-.69-3.632 (.45-3.55-3.39-3.930) .92) 4.650 (.57-4.48 (2.04-10.809) .522 (.426-.54) 595 531 381 442 594 826 Limit of detection (LOD.61) 1.50-4.03 (.664) Mexican Americans Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 . 16-49 years) 99-00 01-02 .580 (.41 (2.09-1.85) 4.70 (2.56) 3.65) 1.99 (3.13-4.624-.62 (1.30-2.47) 1.89 (2.87-4.52) 3.69 (1.45) 2.631-.636-.45) 95th 3.909-1.553-.41 (1.540 (.14-2.79) 1.650 (.691) .03 (.97) 2.06 (.410-.710) 1.799) .62 (3.77) 1. 1999-2002 Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for females aged 16 to 49 years in the U.35 (1.450-.686) .14) 3.35) .24) 6.22 (.84 (2.45 (1.557-.655 (.76-5.657 (.91 (2.03) 1.S.09-1.540-.650) 1.774) .50 (1.68-3.59-5.07-5.772 (.710 (.61-6.709) 75th 1.47) 1.97) 2. 16-49 years) 99-00 01-02 .892) .65-4.99 (2.30 (2.45) 2.62 (4.24-1.810) .05 (3.04-1.15 (2.38) 4.55) 90th 3.27 (2.622-.46 (1.600 (.21 (2.92) 2. 1999-2002 Geometric mean and selected percentiles of urine concentrations (in µg/L) for females aged 16 to 49 years in the U.14.S. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.76 (1.831) .56 (1.22-3.03-2.699) 1.664) .475-.508-.95 (2.30 (1.81 (3.592 (.10-2.23-1.579-.53-3.41 (1.719 (.42) 90th 2.63) Sample size 1748 1960 Age group (females) 16-49 years Race/ethnicity (females.18 (3.13 (2.42-3.721 (.14 and 0. Geometric mean Survey years (95% conf.16) 5.582-.526-.706 (.560 (.685 (. interval) Selected percentiles (95% confidence interval) Survey years 50th .16-5.520-.870) .77) 2.

Sci Total Environ 2002. Total blood mercury concentrations in the U. Martin MD. Jarvholm B. Hultberg B.7(3):176-184. Geier J. Lauwerys RR. Mercury derived from dental amalgams and neuropsychologic function. Brewer R.212:588-598. Sandborgh-englund B. Neurotoxicology 1995. Drexler H. Marsh DO. Neuropsychological and renal effects of dental amalgam in children: a randomized clinical trial. Cardenas A. Cincinnati (OH): Signature Publications. Exposure of the Inuit population of Nunavik (Arctic Quebec) to lead and mercury. Bates MN. Pb.33:1-9. Kinetics of mercury in blood and urine after brief occupational exposure. Int J Hyg Environ Health 2009. Bidstrup PL. Br J Ind Med 1993. Levallois P. Am J Epidemiol 1999.56(4):350-357. Markers of early renal changes induced by industrial pollutants. Assessment of reference values for mercury in urine: the results of an Italian polycentric study. Subrt P. Luis H. Garrett N.50:17-27. Barregard L. Cianciola ME. Aposian HV. Locket S. Barregard L.149:301-305. Int Arch Occup Environ Health 1999.295(15):1775-1783. Fawcett J.61:65-69. Videro T. Smid J. Krause C.111:719-723. Grandjean P. Buchet JP. et al.72:169-173. Harvey DG. Falk R. mercury exposure. JAMA 2006. 2007 TLVs and BEIs. JAMA 2006. Bonnell JA. Bernardo M. Schulz C. Osterloh JD.8(2):117-119. McKinlay S. Schutz A. Spevackova V. Martin MD. Monitoring methylmercury during pregnancy: maternal hari predicts fetal brain exposure. Attewell R. et al. Bellinger DC. Mangili A. population: 19992006. Becker K.16(4):705-710. Cox C. Arch Environ Health 1969. The mercury concentration in breast milk resulting from amalgam fillings and dietary habits. ACGIH.295(15):17841792.47(3):185-195. Berglund B. 206:15-24.19:478-484. Int JHyg Environ Health 2002. et al. Cernichiari E. and Se in blood of the population in the Czech Republic. Trachtenberg F.289:1324. Leroux BG. 2005. Seiwert M. Kjellstrom T. Castro-Caldas A. White RF. Environ Res 1998. Lapham LW. Egeland FM. Kaus S. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Kaus S. Weber JP. Environ Health Perspect 2005. et al. Seiwert M. Sallsten G. Cent Eur J Public Health 2000. Budtz-Jorgensen E. Martins IP. 52:19-33. Echeverria D. Arch Environ Health 2001. Health effects of dental amalgam exposure: a retrospective cohort study. Jones RL. Jacobs D. Third National Report on Human Exposure to Environmental Chemicals. Nutr Rev 2004. Barbon R.113(10):1381-1385. Jorgensen PJ.Metals References Aberg B. Debes F. Weihe P.S. selenium. et al. Cernichiari E. Barregard L. Cernichiari E. Drago I. Gagliardi T. Tavares M. J Toxicol Environ Health 1997. and heart diseases. Application to workers exposed to mercury vapour. Weihe P. Transport of methylmercury and inorganic mercury to the fetus and breast-fed infant. Benes B. Bruneau S. Cejchanova M. Arch Environ Health 1992. Caldwell KL. Environ Health Perspect 2003. Rosenbaum G. Tissue levels of mercury determined in a deceased worker after occupational exposure. Hasselgren G. Schulz C. Lancet 1951. Jorgensen PJ. Niklasson B. Neurobehavioral effects of dental amalgam in children: a randomized clinical trial.77(2):124-129. Grandjean P. Roels H.205:297-308. Impact of maternal seafood diet on fetal exposure to mercury. Hg. Atlanta (GA). Barregard L. Apostoli P. Greitz U. Int J Hyg Environ Health 2003. Elia G. Bjornberg KA. Caudill SP.. Arch Environ Health 1992. et al. Fish consumption. Chronic mercury poisoning in men repairing direct-current meters. Woods JS. Biennow M. Ekman L. Townes BD.62(2):68-72. Schaller KH. Cu. DeRouen TA. Factor-Litvak P. Centers for Disease Control and Prevention (CDC). Based on the Documentation of the Threshold Limit Values for Chemical Substances and Physical Agents and Biological Exposure Indices. Enzymuria in workers exposed to inorganic mercury. Chan JM. Int J Epidemiol 2004. Cutress T. Epidemiologic assessment of measures used to indicate lowlevel exposure to mercury vapor (Hgo). German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Int Arch Occup Environ Health 1988. Bernard AM. Lepom P. Myers GJ. Cortesi I. The concentration levels of Cd. Conradi N. Sallsten G. Dewailly E. Methylmercury exposure biomarkers as indicators of neurotoxicity in children aged 7 years. Persson G. Vahter M. Kline J. Clarkson T. Sallsten G. Woods JS. Metabolism of methyl mercury (203Hg) compounds in man. Begg M. I. Schuzt A. Skerfving S. Lebel G. Zn. and lead. Cerna M. Ayotte P. Becker K. Mortensen ME.2:856-861. Daniel D. Leitão J. Snihs JO. Seifert B. 224 Fourth National Report on Human Exposure to Environmental Chemicals . et al.

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Amurrio A. Vahter M. Azpiri MA. Environ Health Perspect 2003. Bernardo MF. McDowell M. Kaye WE. Hongo T.37:245-252. Turner MD. Topping G. The hair-organ relationship in mercury concentration in contemporary Japanese. Stern AH. Methyl mercury pharmacokinetics in man: a reevaluation. Sherlock J. Burbacher T. Smith JC. Patil LS. Vorwald AJ. Aguinagalde FX. Estimation and validation of mercury intake associated with fish consumption in an EPIC cohort of Spain. Smith RG. Maternal-fetal distribution of mercury (203Hg) released from dental amalgam fillings. Martin MD. Schober SE. DeRouen TA. Environ Health Perspect 2002. Jones RL.97(2):195-200.128(2):25125-25126. Smith JC. Suzuki T. Woods JS. Leroux BG. Most B. Toxicol Appl Pharmacol 1996. Elevation of mercury in human blood from controlled ingestion of methyl mercury in fish.124:221-229.258(4 Pt 2):R939-945. et al.79:786789. The contribution of dental amalgam to urinary mercury excretion in children. McMahon KJ.4(5):981-988. Goldberg J. Am J Physiol 1990. Zeitz P. 226 Fourth National Report on Human Exposure to Environmental Chemicals . Public health consequences of mercury spills: hazardous substances emergency events surveillance system. Environ Res 2005. Mottet NK. Farris FF. Longnecker MP. Tunnessen WW.31:687-700.110:129-132. Acrodynia: exposure to mercury from fluorescent light bulbs. Allen PV. Nakazawa M. Public Health Nutr 2001. Stern AH. Arch Environ Health 1993. Speciation of mercury in the primate blood and brain following long-term exposure to methyl mercury. Whittle K.111(12):1465-1470. Sinks TH. Imai H. Osterloh J. 1999-2000. Takahashi Y. 1993-1998. Yoshinaga J. Fisher HL. Mooney TF. Orr MF.40:413-419.289(13):1667-1674. Blood mercury level and blood pressure among US women: results from the National Health and Nutrition Examination Survey 1999-2000. Effects of occupational exposure to elemental mercury on short term memory. Effects of exposure to mercury in the manufacture of chlorine. Lorscheider FL. Blood mercury levels in US children and women of childbearing age.2:117-131. Leitao JG. Hum Toxicol 1984. Smith PJ.115(10):1527-1531. The kinetics of intravenously administered methyl mercury in man. Br J Ind Med 1983. Hislop D. Vupputuri S. An assessment of the cord blood: maternal blood methyl mercury ratio: implications for risk assessment. Amiano P. Daniels JL.48(4):221229. Toxicol Appl Pharmacol 1994. et al. Smith AE. Friberg L. Baser M. Guo S. Shen DD. Matsuo N. JAMA 2003. A review of the studies of the cardiovascular health effects of methylmercury with consideration of their suitability for risk assessment. et al. Pediatrics 1987. Sandler DP. Vimy MJ. Langolf GD. Lind B. Toxicol Appl Pharmacol 1994. Environ Res 2005. Dorronsoro M. Hall LL. Bolger PM.Metals Sanzo JM. Newton G. Environ Health Perspect 2007.98(1):133-142. Am Ind Hyg Assoc J 1970.

01-02.4) 41.7-84.8) 46.9 (34.4-75.9) 62.6) 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 (99.0-110) 90.7) 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 78.8 (85.0-71.1 (91.Metals Molybdenum or ore deposits.8-108) 87.4) 56.8.3-47.2) 40.4 (79. Fourth National Report on Human Exposure to Environmental Chemicals 227 . 2001).5-124) 108 (92.2) 48.7-91.0-62.5 (41.7 (36.9 (73.3-75. lubricants.4) 49. The recommended dietary allowance for adult men and women is 45 µg/day (IOM.9-55.7) 51.2 (55.7-60.5-65.3 (37.9 (40. 0.8) 40.0 (43.0-65.1 (38.3-91.2) 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 (98.3-115) 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 (49.2) 37.6 (55.9 (37. hydrogenation catalysts.0-85.0) 84.1) 59.1) 57.5.3 (55.7-51. chemical reagents in hospital laboratories.5 (48. More recently.9 (44.8 (67.7 (45.0) 55.3 (47.2) 52. and in pigments for ceramics.5 (49.6-111) 267 (159-840) 197 (161-291) 181 (138-235) 188 (146-216) 179 (155-227) 143 (130-156) 168 (143-206) 150 (130-166) 133 (119-144) 310 368 290 648 762 725 1299 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 52.2 (69.4-52.2) 53.8-94.0) 97.9-85.0-53.6 (55.5 (43..8) 44.3 (53.2 (38.1-51.2) 41.1-63.9-56.8-106) 88.3) 37.6-82.7 (50.1-52.2 (63.9) 67.4) 42.3) 90th 135 (125-146) 124 (117-130) 111 (105-118) 95th 180 (154-216) 165 (145-176) 138 (133-146) Total 45.4 (48.1-88.6) 71. which exert homeostatic regulation over molybdenum balance.5) 47.3 (38.0) 39. 7439-98-7 General Information Elemental molybdenum is a silver-white.0 (46. and paints.3 (73.5 (41.7) 75th 84.4) 45. At a daily oral molybdenum dose of 24 µg. and the average dietary daily intake of molybdenum is approximately 100 µg/day (IOM.6 (52.2-79.9-83.8-46.6 (73.6-62.0-56.7-73.0-100) 63.7-105) 69.7-41.2 (40.7 (58.1-48.7) 45.7) 86.3 (46.3 (55.8-90.1) 126 (106-147) 109 (94.3) 54.3 (79.4 (72.0-101) 82.6 (40.4 (80.2-59.2 (49.1 (71. urinary excretion over six days CAS No. and xanthine oxidase (Kisker et al. interval) 45.1-55.6-96. Excretion occurs predominantly via the kidneys.6-42. 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.5-46. hard metal widely used to add strength and hardness and retard corrosion in metal alloys.5 (74.5) 80.4 (48.7-92.7 (73.6 (43.9 (52.6-72.8.5) 85.1-44. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.8 (82.7) 78.7) 57.3 (71.6-55.3 (64.6) 71.0 (48.5-91.5-52.6) 51.6) Selected percentiles ( 95% confidence interval) 50th 50.3) 83.0 (41. 1997).4 (34.5-41. In humans.7-68.5) 60.8) 39.3) 65.3 (84. Gastrointestinal absorption of molybdenum averages 8893% for dietary intakes of 22-1490 µg/day.0 (76. semiconductor and battery industries have begun to use molybdenum. Molybdenum is a nutritionally essential trace element that enters the body primarily from dietary sources.1-59.8-49.5) 80.7-39.0) 62.7) 46.3) 47.8) 75.9 (33.5 (67. 1996).7 (37.5-68.7 (71.9 (32.1) 46.9-55.6-58.9) 34.0) 54.4) 52.2-70.3) 85.5-66.4-61.5 (37.2-37.7-122) 93.4-82.3-108) 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. molybdenum is a cofactor for three enzyme classes— sulfite oxidase.1-52. inks.1) 60.7 (51.0) 60.7-96.2 (61.3) 41.7-47. and 1.6-46.2 (56.9-82.2-42. aldehyde dehydrogenase.1) 35.3-44.2-53. population from the National Health and Nutrition Examination survey.S.5-52.5) 44.0) 45.6) 93.8 (42.2) 150 (128-187) 130 (120-141) 119 (112-130) 119 (105-138) 115 (104-128) 101 (97.0-38. and 03-04 are 0.5 (81.0 (42.4) 76.6 (40. Compounds of molybdenum are also used as corrosion inhibitors. see Data Analysis section) for survey years 99-00.8) 48.7) 77.0-77. 2001.2) 79.7 (44.9 (78.6) 53. WHO.0 (42.2 (83.7) 78. respectively.0 (81.1 (34.1) 82.2-59.2-91.9-109) 97.7-50.

dust and other fine particles produced during refining or shaping of molybdenum or molybdenumcontaining alloys are inhalational pathways of exposure.2-121) 107 (92.5) 71. 1993). Biomonitoring Information Molybdenum is an essential element for health.5-119) 90.0) 39.5) 72.2-46.3-102) 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 40.3) 37.6) Selected percentiles ( 95% confidence interval) 50th 41.4) 44.1 (49.6-45.3 (58.8-84.8) 79.2 (43.2-40. Human health effects from molybdenum at low environmental doses or at biomonitored levels from low environmental exposures are unknown.5 (40.8 (90. Molybdenum is generally considered to be of low human toxicity.9) 40.9-40.3 (37.4-42.2) 43.3) 56.9 mg/kg/day and established a tolerable upper intake level of 0.4 (59.7-43.3) 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 85.2 (40.5-62.5-44.5 (38.4-118) 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 .1-39.2 (52.9 (73.9 (64.5-50.4) 47.1-67.4 (56.2-80.03 mg/kg/day in humans (IOM.5 (36.0-120) 85.1 (44. Based on studies finding adverse reproductive effects in rats and mice.8-47.7-62.4) 122 (107-133) 109 (99.3) 57.4) 116 (101-126) 104 (88.5 (50.7-44.0) 39.5 (35.9-68.4) 89.0) 72.3-59.1-40.2-96. and urinary levels reflect intake from all sources.0-38.2-65.1-81.7-52.5) 214 (154-1040) 185 (165-219) 160 (129-257) 112 (78.5 (80.6-88.8 (36.5 (65.5 (39.2-49.3) 43.0) 88.4-41. interval) 43.4-120) 101 (84.6-41.3-68.2) 37.6 (71.S.7-120) 87.8 (75.0) 44.9) 41.6-63.9 (35.8-47.3 (71.8-66.2 (69.6-76.3 (36.1) 101 (83.2-47.7) 57.8) 61.8) 62.8-46.3-52.1-109) 89.4) 40.8) 37.3 (36.1-100) 86. U.1) 37.9 (40.1-112) 78.1-43. Levels of molybdenum Urinary Molybdenum (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.8-52.6-78.6) 39. 1999).7-100) 77.0-103) 103 (90.5-69.3-43.8) 38.7) 112 (95.1 (39.1 (54.5) 60.4 (55.1 (82.9-117) 57.0) 36.3-46.6-61.7) 42.2) 55.7) 53.5 (37.9 (39.5 (41.2 (57. and molybdenum has not been systematically evaluated for carcinogenicity by IARC.2 (40.4-39.7) 75th 63.2 (40..7-93.5 (39.7) 62. EPA.6 (38. of the ingested dose (Turnlund et al.4) 77.9 (64.4 (44.9-118) 91.0) 62.0 (74.2 (73. and clinical or epidemiologic evidence of adverse effects is limited.7) 115 (93.3) 64.8-65.5-70.0 (58.9-61.6) 39.9 (39.7-40.1 (42.5 (59.1 (40.1) 40.2 (33.5 (40.6) 36.7) 41.9-45.3 (51.4-106) 85.5 (35.7 (77.0-41.0-46.1-45.5-48.9 (49.2 (50.6) 48.9-96.5 (34.4 (37.2) 37.1-34.3 (55.4-66. at daily oral doses of 95 µg and 428 µg.9) 173 (130-243) 159 (129-170) 132 (107-158) 85.8-67.8 (37.7 (30.5-45.5 (41.9-71.3 (53. One case-control study suggested a possible link between occupational exposure to molybdenum and lung cancer (Droste et al.5 (54.3) 40.4-185) 106 (94.2) 42.8 (56.4) 60.1 (30. population from the National Health and Nutrition Examination survey.8) 45.5-60.9-42.3 (71. 1995).1) 43.3-56.5-35.8) 38.5 (78. In industry. 1997).2-96. respectively.1-41.1-127) 90.8) 71.5 (37.3-141) 109 (81.0-56.0-46.4) 48.9 (36.8) 39.3) 41.1 (38.1) 56.0-133) 119 (88.2) 58.2 (37.9-45. urinary excretion over six days rose to 50% and 67%.0) 38.0) 33.1-79.5 (83.2) 39.5-92.2) 42.0) 95th 144 (125-171) 130 (120-149) 120 (107-135) Total 42.Metals was 18% of the ingested dose.1) 65.6 (36.S.2-41.1 (37. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.5-46.2) 38.4 (40.7-137) 129 (109-155) 112 (97.1) 37.4 (53.3 (83.1-39.5-99.8 (57.0) 53.3) 61.2-103) 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 42.0 (35.5 (79.9 (79.4-107) 85.3-44.2 (36.3-115) 98. the Panel on Micronutrients of the Institute of Medicine identified a no observed adverse effect level (NOAEL) of 0. but available epidemiologic data are scant.4) 61.6-63. 1961.0 (80.5 (65.4 (67.7-38.7 (66.9) 31. 2001).7) 45.9-41.2) 39.6) 43.3) 44.7 (75.9-87..1 (33.3-45.3 (37.1-38.. A long term inhalation bioassay of molybdenum trioxide in mice yielded “some evidence” of carcinogenicity (NTP.9) 44.8-118) 81.4 (78.9) 92.5) 90th 108 (97.6 (59.4-76.8-42.5) 73.5-97. Chronic exposure to very high levels may result in higher serum uric acid levels and a gout-like illness (Koval’skiy et al.4) 58.6 (42.6 (36.6 (57.6-61.5) 63.9) 79.1-43.1 (38.

In: Trace elements in human nutrition and health. (DC): National Academy Press. X. White and Sabbioni. Rapid Comm Mass Spectrom 2002. iodine.22(3):179-191. Molybdenum in infancy: methodical investigation of urinary excretion. 420-441.htm.niehs. Inductively coupled plasma mass spectrometric determination of molybdenum in urine. copper. 2005). and zinc: a report of the Panel on Micronutrients. vanadium. molybdenum. Van Meerbeeck JP. pp. Sabbioni E.. Inductively coupled plasma mass spectrometric determination of molybdenum in urine from a Danish population.epa. Zhurnal Obshchey Biologii 1961. 1998. Turnlund JR. 56:322-327. Molybdenum-cofactorcontaining enzymes: structure and mechanism.Metals in urine for the U. boron.nih. Molybdenum. TR-462. Turci R. Rees DC.. 4/14/09 White MA. 1998). Gatti A. Kristiansen J. Urinary molybdenum concentrations in infants may be slightly lower than those in other age groups (Sievers et al. Christensen JM. iron. Molybdenum absorption. edu/openbook. Food and Nutrition Board.66:233-267.15(2-3):149-154. Schleyerbach U. Geneva: WHO. 2005.nap. Minoia C. Schindelin H. Droste JHJ. World Health Organization (WHO). Minoia et al. Washington. Am J Clin Nutr 1995. Aprea C.gov/iris/ subst/0425. Occupational risk factors of lung cancer: a hospital based case-control study. Environmental Protection Agency (U. EPA). Trace element reference values in tissues from inhabitants of the European Union.S. manganese. Changes of purine metabolism in man and animals under conditions of molybdenum biogeochemical provinces. vitamin K. Toxicology and carcinogenesis studies of molybdenum trioxide (CAS No. U. Dietary reference intakes for vitamin A. Third National Report on Human Exposure to Environmental Chemicals. arsenic. Sabbioni E.gov/index. Molybdenum 1993 [online]. silicon. References Centers for Disease Control and Prevention (CDC). Institute of Medicine (IOM). 1313-27-5) in F344 Rats and B6C3F1 Mice (inhalation studies) 1997 [online]. Schaub J. Kisker C. Atlanta (GA). Ronchi A. 1996. Ann Rev Biochem 1997. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Fourth National Report on Human Exposure to Environmental Chemicals 229 .62(4):790-796. pp. Menne C. Occup Environ Med 1999..S. Sci Total Environ 1998. Shmavonyan DM. and retention studied with stable isotopes in young men at five intakes of dietary molybdenum. et al. Finding a measurable amount of molybdenum in the urine does not mean that the level of molybdenum causes an adverse health effect.S. Weyler JJ.216:253-270. population were well characterized in NHANES 1999-2000 and 2001-2002 (CDC. National Toxicology Program (NTP). Available at URL: http://ntp. 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.php?record_id=10026&page=420. Sciarra G. Standing Committee on the Scientific Evaluation of Dietary Reference Intakes. chromium. 2001. Vermeire PA. 4/14/09 Iversen BS.123(1):81-85. cfm?objectid=070A72C6-E9C1-AE67-4BFAB97AD0F427E8. 2002. Analyst 1998. van Sprundel MP. White MA. Available at URL: http://books. 4/14/09 Sievers E. Peiffer GL. Koval’skiy GA. nickel. 144-154. these levels were comparable to those reported for adults in smaller European population surveys (Iversen et al. 16:1313-1319. A study of 13 elements in blood and urine of a United Kingdom population. Available at URL: http://www. Yarovaya GA. excretion. J Trace Elem Med Biol 2001. 2001). Keyes WR.

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

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

Moore W Jr. Schulz C. Nickel. Seiwert M. Schierl R. pp. Kelly J. New York: John Wiley & Sons. Schierl. Several studies have shown that background concentrations in general populations were usually less than 0. Hebert R. Saindelle A. Environ Res 1975a. Herr et al. 3/31/08 Moore W Jr. Influences on human internal exposure to environmental platinum. Hysell D. Stara J: Preliminary studies on the toxicity and metabolism of palladium and platinum. Stara J: Biological fate of a single administration of 191Pt in rats following different routes of exposure.55(2):138-140.9:152-158. and in blood and urine in the United Kingdom. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Kulka U. 5th ed. Int Arch Occup Environ Health 1997. Ensslin AS.org/documents/ehc/ehc/ ehc125.htm.. Hysell D.4(1):27-36. 2003. Blanks R. Available at URL: http://www. Kaus S. Gieler U. 232 Fourth National Report on Human Exposure to Environmental Chemicals . Environ Health Perspect 1975b. 1999. Farago ME. Patty’s Toxicology.. 289-380. Turfeld M. References Becker K. Int J Hyg Environ Health 2004. Neuendorf J. Nowak D.. Pethran et al. Campbell K. Fries HG. Urinary excretion of platinum from platinum-industry workers. Schierl et al. 2003).10:63-71. Finding a measurable amount of platinum in the urine does not mean that the level of platinum causes an adverse health effect.70(3):205-208. 2003. Powell CH. Biomonitoring of traffic police officers exposed to airborne platinum.inchem. Duneman L:Long-term urinary platinum. J Expo Anal Environ Epidemiol 2003. et al. Int Arch Occup Environ Health 2003. Part 1: monitoring of urinary concentrations. Jankofsky M. Iavicoli I.005 µg/L (Iavicoli et al.35:313-321. Begerow J. Petrucci F. 2004) or less than 0.. One study found that traffic-control officers had no greater urinary platinum concentrations than office-based control subjects (Iavicoli et al. Cohrssen B.S..inchem. Ewers U.13(1):24-30. Arch Environ Health:1969. Gromiec JP. Alimonti A. Hall L. Parrot JL.19:685-691. palladium. 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. 2000. Arch Environ Health 2001. Environmental Health Criteria 125.. Biomonitoring Information Urinary platinum levels reflect recent exposure. which elevate urinary platinum by five to twelve-fold (Begerow et al. 206:15-24. population were below the limit of detection (0. Platinum concentrations in urban road dust and soil. Crocker W. Angerer J. 1997. Ruff F: Histamine release by sodium cholorplatinate. Revised and new reference values for some trace elements in blood and urine for human biomonitoring in environmental medicine..61(7):636-9. Pethran A. Huber R. ruthenium. palladium. Biomarkers 1999. Analyst 1998. 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..org/documents/ehc/ehc/ehc125.56(3):283-286. Saindelle A. Kazantzis G. 2004. van de Weyer C.htm. Platinum-industry and precious-metal workers had urinary concentrations about one-thousand times higher than general populations (Schierl et al. Herr CE. Uptake of antineoplastic agents in pharmacy and hospital personnel. In: Bingham E. Biological monitoring of hospital pharmacy personnel occupationally exposed to cytostatic drugs: urinary excretion and cytogenetic studies. Czerczak S. Levels of platinum in urine for the U. Allergy and histamine release due to some platinum salts. Kavanagh P. Wilhelm et al. Stilianakis NI. Hauff K. Rommelt H. Schierl R.76(1):5-10. Bocca B.. Occup Environ Med 2004. Ruff F: Platinum and platinosis.. rhodium. 2003. Boos KS. and gold excretion of patients after insertion of noble-metal dental alloys. Schierl R. et al. Gold-platinum dental restorations were correlated with increased urinary platinum concentrations. 2004). Carelli G. Grimm CH. 1991 [online].207(1):69-73. 1998).01 µg/L (Becker et al. Wilhelm M. Seifert B. Kuster W.04 µg/L) in this Report. Herr et al.. International Programme on Chemical Safety (IPCS). 1998).123(3):451-454. et al.Metals the International Programme on Chemical Safety at http:// www. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Schierl R. Pethran A. et al. Fruhmann G. Br J Pharmacol 1969. and platinum. Thornton I. Senofonte O. International Journal of Hygiene and Environmental Health 2003. 2001). osmium. eds. Raab W. Platinum. Urinary platinum levels associated with dental gold alloys. Occup Environ Med 1998. Schulz C.

200 (.239) . the latter being the current major industrial consumer of thallium in this country.165 (.200 (.250-. Human health effects from thallium at low environmental CAS No.390 (.210 (.260 (.300 (.290 (.225) . Elimination from the body tissues occurs slowly through urine and feces (Blanchardon et al.170-.171 (.340) .340-.150-.200) .410 (.160-.220 (.440 (.240) .410-.250-.154-.400-.200-.450 (.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 .290) .280) .230) .640) .240-.490) .150-.191 (.156) .149 (.144 (.184 (.210 (.179-.160-.370) .400 (. and 0.300) .450 (.158) .420-.390) .260) .420-.260-.330) .370 (.430-.470 (.185 (.170-.218) . Thallium exposure occurs primarily from industrial processes such as coal-burning and smelting.400-.420) .243) .300) .360-.240-.370 (.201 (.330-.380 (.420-.210-.410 (.250-.330-.360 (.190 (.360-.400) .420) .280 (.147-.163) .390) .370) .450 (.170-.190 (.250-.280-.250-.230) .180 (.160 (.430 (.230-.260 (.480) .190 (.300) .135-.400) 95th .202 (.420 (. representing distribution into other tissues.430-.290) .440) .360 (.330) .159 (.370-.490 (.177) .230 (.240) .190 (.197-.480) .196) .500) .270 (.200) .200) .380 (.230-.360-.159 (.200) .160 (.350 (.220 (.280) .155 (.172 (.133-.430) .290 (.500) .160-.350) .470) .400) .170 (.201 (.400 (. thallium was obtained as a by-product of smelting other metals.188) .173) .183) .290-.202) .430 (.410-.147-.440-.390) .430 (.160 (.370 (.175) .200 (. see Data Analysis section) for Survey years 99-00.220) .200 (.180 (.200-.230) .170-.157-.290) 90th . 0.134-.350-.190-.400 (. thallium readily crosses the placenta and also distributes into breast milk.210) .420-.390-.400 (.400-.330-.250 (.340-.390-. however.270) .160-.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 .173-.270) .260-.182-.390-.510 (.167-.180-.146 (.250) .340-.460) .350-.340) .520 (.180-. In the past.350-.300 (.350-.202 (.370 (.330-.440) .300) .360 (.470) .190 (.420) .330-. It is still used in relatively small amounts in pharmaceutical and electronics manufacturing.480) .290 (. interval) . respectively.181-.460) 861 675 618 561 657 723 801 1114 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.220) .153-.430) .220 (.370-.380) .520) .185-.167-.510) .480) . In the United States.330) .330-.450 (.490) Total .310) .470) .180-.180 (..410 (.220 (.170 (.400) .162-.140-.370 (.370-.270 (.180) 75th .183) .270 (.170) .220 (.290 (.200-.690) .280 (.137-.230-.167 (. From these and other sources.390) .360) .190 (.450 (.156-.178) .320-.320) .180-.450 (.159 (.380-.173) .310 (.150-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.S.Metals Thallium depilatory cosmetics. 01-02.490) .520) .150-. In addition.200) . Thallium disappears from the blood with a half-life of several days.02.02.590) .217) .440 (.440 (.200 (.170-.520) .410 (.350) .470 (.410-.220) .290) .270-.420) .170) .370 (.320) .218) .340 (. it has not been specifically mined or refined in the United States since 1984.410 (.145-.440) .215) .270-.250-.148-.300-.250-.02.280-. Fourth National Report on Human Exposure to Environmental Chemicals 233 .187-.260-.450 (.390-.145-.172 (.420) .400) .320 (.217 (.196) .330) .290) .300 (.490) .260 (.160 (.320) .192) Selected percentiles ( 95% confidence interval) 50th . 7440-28-0 General Information Elemental thallium is a blue-white metal found in small amounts in soil and in sulfide-based minerals.630) .172) .145 (.590) .270 (.330-.220) .280) .240) .420) .410-.410-.450 (.260-. population from the National Health and Nutrition Examination Survey.180) .197 (.410-.350-.290 (.170) .430-.200 (.350-.290 (.160 (.270 (. 2005).360 (.220) .370 (.460) 336 362 290 697 746 725 1380 1545 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .290-.410) .480) .170-.400 (.147-.170-.430 (.440 (.280 (.460-.150-.156) .360-. and 03-04 are 0.420) .500 (.500) .150-.240-.450) .270-.350 (.310 (.550 (.200) .370-.170 (.260-.250-.310 (.450 (.230) .560) .310-.410 (.400-.340-.380-.250 (.390 (.220-.160-.200-.400-. thallium is produced in a fine particulate form that can be absorbed through inhalation or ingestion.176 (.206) .220) .360-. 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.460 (.

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

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.. Minoia C. White and Sabbioni.. Ting BG..html.47(3):223-231.48(4):375-389. et al. Valentin H. Manke G. Cassot G. Finding a measurable amount of thallium in urine does not mean that the level of thallium causes an adverse health effect.216:253-270. 2005. 1980. 2005.cdc. 1985). Trace element reference values in tissues from inhabitants of the European Union. Minoia et al. Schmidt M. Paschal DC. Dolger R.5 μg/L. White MA. Jackson RJ. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Fourth National Report on Human Exposure to Environmental Chemicals 235 . population) are thought to correspond to workplace exposures at the threshold limit value of 0.265 people living near a thallium-emitting cement plant in Germany.1 mg/m3 (Marcus. Wiegand H. Martin J-C. Seventy-eight percent of the urine specimens in that study contained greater than 1 μg/L. J Soc Occup Med 1985. Sampson EJ. Atlanta (GA). Soddemann H. Int Arch Occup Environ Health 1980. 1992 [online]. Brockhaus A. Morrow JC. Long term retention and excretion of 201Tl in a patient after myocardial perfusion imaging. blood. Biomonitoring studies on levels of thallium provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of thallium than are found in the general population. These urine levels are generally comparable to levels observed in earlier studies of general populations (Brockhaus et al. Third National Report on Human Exposure to Environmental Chemicals. 1998). 1990. References Agency for Toxic Substances and Disease Registry (ATSDR). and serum of Italian subjects. Schaller KH. Sci Total Environ 1998. Available at URL: http://www.gov/toxprofiles/tp54. Centers for Disease Control and Prevention. Toxicological profile for thallium. Schaller et al. Raithel HJ. et al. A study of 13 elements in blood and urine of a United Kingdom population. Sabbioni E. Challeton-de Vathaire C. Urinary concentrations of 100 μg/L in asymptomatic workers (500 times higher than median levels in the U. Trace element reference values in tissues from inhabitants of the European community I. Brockhaus et al. with concentrations ranging up to 76. et al. Trace metals in urine of United States residents: reference range concentrations.35(1):4-9. (1981) studied 1.95:89-105. Buhlmeyer G. Pirkle JL. Investigation of a working population exposed to thallium. Apostoli P. Gallorini M.76(1):53-59. Pietra R. Int Arch Occup Environ Health 1981. Marcus RL. Paschal et al.atsdr. 7/15/09 Blanchardon E. Radiat Prot Dosim. 2005) and are shown with results from NHANES 2003-2004 in this Report. Environ Res 1998. Sci Total Environ 1990. 1981. Investigations of thallium-exposed workers in cement factories. Kramer U.S.113(1):47-53. Nearby residents were exposed by eating garden plants that had been contaminated by the thallium. Intake and health effects of thallium among a population living in the vicinity of a cement plant emitting thallium-containing dust. A study of 46 elements in urine. Celier D. Ewers U. 1998. Pozzoli L. Boisson P.Metals (CDC.. Sabbioni E.

105 (. which are used in rock drills and metal-cutting tools.400 (. Tungsten compounds are used as lubricating agents.073 (.090-. population from the National Health and Nutrition Examination Survey.460 (.096-.101-.093-. Occupational exposure is from dusts released during grinding or drilling of hard metals.050-.065 (.082) .113 (.320-.101 (.210-.620) .180-.800) .100) .140 (.160 (.070-.400) .150 (.070-.160) .160-.135) .078-.250) .410 (.116) .810) .110 (.770 (.210 (.073-.290-.420-.140-.S.530 (.120) .220) .270-.310-.190-.280 (.120-.170) .530 (.080 (.350) .062 (.430 (.330 (.310-.00) .062 (.066-.350-1.190-.120 (.320) .090-.270 (.100) .060 (.440) .560 (.320 (.04.132) .490 (.110) .080) . and for producing ferrotungsten.140) 90th .060-.280-.100) .120) .260-.520) .450-.071-.130-.110 (.630) .065-.590) .070) .082 (.100-.380-.137 (.170-. bronzes in pigments.060-.100) . 0.170 (.800) . their illness may stem from exposure to cobalt mixed with tungsten carbide rather than to tungsten alone.280 (. see Data Analysis section) for Survey years 99-00.380) . Although workers occupationally exposed to tungsten carbide may develop serious lung disease (“hard metal disease”).290) .230 (.100 (.290) .110-.060 (.250) .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 .300 (.470 (.160-.160-.060 (.130 (.230-.500 (. Most background environmental exposures to tungsten are from the soluble forms such as tungstate salts that may occur in drinking water.090-.073-.095-. interval) .095-.090-.050-.430 (.090 (.180-.113 (.190 (.091) .310-. filaments for incandescent lamps.510-1.240-. respectively. Little information is available on the toxicity of tungsten.081 (.310) .090) .050-.088) .550) .260-.310-.330) .160 (.080-.204) .080-.200-.580) .550 (.158 (.110 (.104) .120) .060-.076 (.430) . Human health effects from tungsten at low environmental doses or at biomonitored levels from low environmental exposures are unknown.220 (.340) .109) .140-.090) .300-.210 (.087) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf. and 03-04 are 0.105) .080 (.560) .113 (.250) .420-.100 (.110-.130) .180) .490) .380 (.270 (.084) .310 (. mainly as scheelite (CaWO4).470) .300 (.073) .240 (.260 (.093 (.082 (.084 (.120-.310-.450 (.290 (.640 (.460 (.140 (.070-.480) Total .370 (.150) .170) .170) .560) .520) .140 (.080-.090) .570 (.150 (.120-.290-.330-.090-.340-.360 (.060 (.056-.350 (.110 (.140 (.320-.360 (.133) .270-.390) .560) .460 (.550) .470 (.110-.380-.070-.092) .330-.086 (.110 (.100 (. and as catalysts in the petroleum industry.060-.080) .130-.130) .090) .500 (.400 (.122) .080 (.150 (.090-.260-.180 (.510 (.080) 75th .150-.113 (.100 (.230-.790) .410) 790 680 618 562 649 723 802 1117 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.230) .230) .210 (.120-.380-.260) .200) .190) .320 (.520) .090-.082-.410-.060 (.110) .210 (.360-.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 .220-.070) .220) .340-.120-.260 (.090 (.Metals Tungsten CAS No.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 .071 (.100-. 236 Fourth National Report on Human Exposure to Environmental Chemicals .060 (.04.460) .096 (.04.370 (.510-.340-.160 (.120-.300) .180) .250-.400 (.370-.400-.550) .400 (.050-.058-.690) .200 (.560) .190-.570 (.470) .160 (.090-.126) .380 (.056-.270-.120) .120) .460) .300) 95th .170 (.093) .290-.084-.180) .180) .080 (. and 0.070) .370 (.350) .250) . Evidence is lacking for the carcinogenicity of tungsten.360) .350) .190-.950) .210 (.180-.130-.670) .530 (.100) .250-.180-.360 (.370-.270-.330) .060-.077-.830) . which is used in the steel industry.430-.300 (.210) .160-.068) .100-.070) .107 (.123-.070 (.060-.130 (.360-.130) .190 (.092 (.180 (.380-.620 (. and it has not been classified with respect to its carcinogenicity by either IARC or NTP.160 (. 7440-33-7 General Information Tungsten is a steel-gray to tin-white metal that occurs naturally in the earth’s crust.070 (.088 (.270 (. Urinary Tungsten Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.430 (.430-. 01-02.111-.076 (.151) .620) .070 (.250) .220) . Tungsten is used mainly for producing hard metals.250) .53) .087-.069) .070-.069-.230-.130-.100) Selected percentiles ( 95% confidence interval) 50th .470-.170) .120) .370) .160) .092 (.650) .130) .090 (.230-.390 (.130) .500) .074-.064-.080) .080 (.097-.

333-.079) .165) .120) .215) .255-.484) .453) .122-.083 (.143-.067 (.072-.055-.439) 1160 1306 1281 1178 1345 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .084) .240-.124 (.069 (.333 (.582) .739) .28) .103-.081-.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 .279 (.S.098-.120) .258-.081 (.090-.062 (.100) .188-.078-.364 (.354) .381) .092) .301) .065-.823) .500) .079) .216-.253 (.158) .184 (.146 (.(Kraus et al.150 (.360 (.077-.203-.138) .. Patients with medically-inserted tungsten found at increased levels in drinking water.231 (.150-.158) .482 (.065-.341 (.074) 75th .275 (.139) .237) .117 (.258 (.079 (.300 (.087 (.083-.414) .284) .152-. A study of 14 unexposed adults yielded values that were similar to the 95th percentiles in this Report.187) .383 (.060 (.136-.098) .082) .218 (.116) .139-.151 (.054-.497 (.098-.111 (. interval) .333) .074-.317 (.063 (.071 (.150-.286-.267-.333 (.214) .317) .181 (.077-.091) .075 (.465) .053-.375) .080 (.143 (. In whereas the tungsten-worker group had mean urine levels a Nevada community where tungsten was measured and 35 times higher.217-.272-.174) .075-. 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.063-.131-.237-.209-.155-.079) .091 (.084) .452-.086) .063-.439 (.484 (. or exposure that a control group of non-metal workers had mean levels differences.253-.199 (.301) .439) Total .073 (.190) .294 (.133) .339 (.200-.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 .161) .216-.250-.125) . 1998). 2001).354-.667 (.333) .301) .063-.167) .124-.208-.136-.158) .086) .245-.197) .554) .084 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.100 (.117) .308) .059-.075-.431) . Nicolaou et al.090-.197-.061-.126-.121-. 2005).061-.082 (.201 (.462) .261-.078) .066 (.359 (.333 (.075) .084 (.089) .119-. 2003.072 (..059-.426) . measure urinary tungsten.250 (.157) .176-.426) .063 (.109-.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 .315-.108-. population in the NHANES 1999-2000 slightly higher values than those found in NHANES 1999.353 (.164 (.179-.306) .056-.300) .074-.880) .075 (.392) .136 (.073 (.133) 90th .386) .064-.436) .096) .339 (.095) Selected percentiles ( 95% confidence interval) 50th .105 (.065 (. Workers involved in grinding operations that released tungsten metal into the air had elevated urinary levels that Levels of urinary tungsten reflect recent exposure.329-.067-.085-.215 (.130-. 2001-2002.465) .116 (.130 (. similar to those in this Report (Schramel et al. population (CDC.060-.Metals Workplace air standards for external exposure have been established by ACGIH and recommended by NIOSH.216 (. Biomonitoring Information median urinary levels were as much as 15-fold higher than median levels in the U.086-.079 (.153-.231-.206-.279 (.133) .105 (.056-.439 (.071 (.071) .300-.073 (.250 (.385 (.068-.186 (.198-.107-.167-.065) .167) .058-.093) .121 (.074) .069-.233-.083 (.081) .065-.154) .201) .098-.063-.069 (.216-.379 (.344-.148) .070 (.170-.S.667) .138 (.085) .081 (.139 (.255 (. Using neutron activation analysis to 2000.146 (.410-.091 (.158 (.317-.214-.412 (.078 (.270 (.059 (.071-.122-.459) .144-.091) .065 (.088) .049-.091) .082) .197) .222-.083) .136-.255 (.S.211 (.308) .358) .148 (.073 (.125 (.145 (.078 (.179-.237) .054-.116-.100) .089 (.094) .154) .085 (.333-.057-.727) .169) . and 2003-2004 (Paschal et al. population from the National Health and Nutrition Examination Survey.071 (.285) .153) .436-1.174 (. A were more than 900 times higher than the overall geometric nonrandom subsample from NHANES III demonstrated mean of the U.329 (.091) .098 (.283) .198) .326) .068 (.080-.555 (.064-.431) .061-.168 (.075) .797) .287) .059-.087) .265 (.431) . 1997).176-.057-.060-..302-.167-.340 (.088) .200-.199 (.136-.302-. population.331-.109 (.078) .104-.094-.222) .144 (.138 (.108) .070 (.278-.093-.634 (.071) .119 (.071) .146) .080-.216 (.079) .197 (.122 (.279 (.077) .605) .169 (.072-. (1987) found possibly due to methodologic.180-.086) .267) .095-.347 (.300-.080 (.066 (.224) .067 (.217-.106 (.083) .205-.538) .353 (.077) .253) 95th .094) .099-.359 (.074 (.333 (.293 (.299 (.

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

014 (.054) .028 (.042) .009) .011 (.050) .037) .007) .050) .009) . 0. and 0.055 (.010 (.009-.037) Total .009) .007-.023-.026 (.028-. Natural uranium is a mixture of three isotopes: 238 U (greater than 99%).009-.018 (.023 (.022-.033) .011) . including nuclear weapons.006-.013 (.020-.008-.008 (.065) .012) .044 (.011) .026) .021 (.016-. interval) .040) .007-.010-.007 (.021-.046 (.021-.047 (.027 (.005-.017-.012 (.007-.009) .022-.022 (. and as an aid in electron microscopy and photography.032 (.007 (.026 (.031 (.010-.012) .013-. 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.008 (.007 (.114 (. Uranium has many commercial uses.026) 95th .013 (.045) .062) .008 (.065) . Thus.008 (.021 (.009) * .010) .009) .008-.027) .030 (.007-.008 (.009 (.007-.016) .020-.031 (.008) .010-.012 (.008-.009) Selected percentiles ( 95% confidence interval) 50th . in some ceramics.069) .008) .037-.053) .009-.021) .011 (.007 (.011) .073) .007 (.007 (. and 234U. DU has been used by the military in armor-piercing ammunition and as a component of protective armor for tanks.015 (.035-.012-.022-.021 (.016 (.006-.036 (.024-.008 (.034) .009 (.056) .046 (.011-.018 (.023 (.010 (.016) .013 (.006 (.008) .006-.028 (.011) .009) .013 (.031-.009) .054) .012) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.031 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.008) .008) .034-.009 (. and 03-04 are 0.014 (.008 (.005-.011) .013) 90th .039) .015) .009) .009) .018) .014 (.038) .022) .008 (.088) .010-.007-.005.017) .027-.008 (.017-.039-.010) .010 (.030) . human exposure occurs primarily by inhaling dust and other small particles.021) .045) .008-.007-.040 (.041 (.027 (.009) .027) .020) .029-.017) .007-.009-.008 (.031 (.046) .009-.039) .017 (.024 (.006-.013-.006 (.008 (.033 (.007 (.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 .009 (.019-.010 (.006-. 235U (about 0. population from the National Health and Nutrition Examination Survey.008-.007) .052 (.014 (.023-.015-.029 (.033-.008-. Exposure to DU may occur in military personnel from retention internal shrapnel that contains DU or exposure to dust generated from ammunition Urinary Uranium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.010 (.017-.006 (.008-.009 (.009-.006 (.063) .009 (.007) .158) .025-.012 (.006-.011-.026) . nuclear fuel.020-.009 (.040) .049) .046-.040-.279) .035) .011-.007-.066) .017) .S.007) .011) .007-.027 (.009-.037) .010-. the primary exposure sources for nonoccupationally exposed persons are dietary (especially root vegetables) and drinking water.010-.038 (.020 (.012 (.007 (.010) . or processing.009 (.006-.008-.019-.016) .049) .026-.007-.012-.006-.015 (.017-.043) .018) .024-.008 (.023-.020-.054-.004.011-.006-.007-.009) .007-.009 (.009-.007-.030 (. Variable concentrations of uranium occur naturally in drinking water sources.013 (.009) .006-.007-.020) .036) .029-.016-.013 (.008 (.Metals Uranium CAS No.012) .048) .024-.023-.034-.053 (.035) .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 .028 (.027) .037 (.007-.009 (.005-.010) .007-. 01-02.006-.037) .008 (.031 (.019-.016) .017) .046 (.027 (.011-.004.016) .016) .007) 75th . respectively.019 (. Since the 1990’s.067) .010) * .006-.008 (. Fourth National Report on Human Exposure to Environmental Chemicals 239 .043 (.036-.028-.010) .014 (.064 (.006-.040 (.012-.023 (.007-.014 (.017) .010) * . It usually occurs as an oxide and is extracted from ores containing less than 1% natural uranium.036) 883 683 618 568 667 722 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.026-.005-. milling.005-.016-.008 (.72%).027-.072) .056) .018) .017 (.009-.030 (.010) .042 (.048 (.011-.027) .015 (.008 (.030-.020-.010) .127) .023) .046 (.012-.033 (.023) .051) .026 (.010) .015) .013 (. In workplaces that involve uranium mining.013-. see Data Analysis section) for Survey years 99-00.012 (.021) .019-.015 (.018-.041 (.013) .007) .017-.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 .009-.036) .007 (.036 (.007 (.027-.012-.067) .023) .009) .012 (. 7440-61-1 General Information Uranium is a silver-white metal that is extremely dense and weakly radioactive.040-.060 (.007 (.018) .036-.012-.011) .011-.017-.

006 (.006) .041) .048) .026 (.008 (. In cases of retained DU shrapnel.007 (.014) .037 (.009) .006-.006-.006-. After long term or repeated exposure.067) .028) .038) 340 368 289 719 762 725 1405 1559 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .007 (.012-.017) .012 (.008 (. the initial half-life of uranium is about 15 days (Bhattacharyya et al.005 (.009) .014) .024) .015 (.039) .028) .007 (.005 (.019-.019 (.015) .017-.029 (.006-.013 (.007 (.021) .009) .030 (.014 (. about 50% of the absorbed dose is eliminated in the urine within the first 24 hours.012 (. which can occur occasionally from high occupational exposure.028 (.044) .011 (.019 (.048) .006-.034) . Inhaled uranium-containing particles are retained in the lungs.017) .007 (. population from the National Health and Nutrition Examination Survey.015-.017-.006-.040 (. and bones can accumulate uranium with the largest amounts being stored in bones (Li et al.008-.015) .027-.007 (.013 (.S. the half-life of insoluble uranium in the lungs is several years (Durakovic et al.028-. 240 Fourth National Report on Human Exposure to Environmental Chemicals .015) . After exposure to soluble uranium salts.032) .014) 90th .016) .012 (.015 (.010-.004-.018-. 1992).007) .009-.013 (.050) .010 (.024) .007-.027) .008 (.007 (.019 (.010-.013 (.025-.019-.019) .016-. liver.004-.028) .007-. the shrapnel acts as a source of chronic.020) .005-.007 (.008) 75th .033 (.034-.007 (.063) .024 (.015-.006-.021 (.014 (.013-.021 (.008) .006) .009) .026-.007 (.011-.009) .009) .026) .030 (.012-.011) * .011-.006-. 0.024 (.007-.015) . After inhalation.010) .020-. low level exposure.010) .033) .008) .010-.039) .012 (.029 (.016) .008-.012) .009) Selected percentiles ( 95% confidence interval) 50th .008 (.011-.034 (. Human health effects from uranium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.014-.016-.017-.051) .009 (.100 (.006-.008) .009-.010 (.030 (.016) .016) .007-.005-.050 (.008) .061) .007) .053) .006-.006 (.013 (.006) .008 (.009) ..007-.013) . 2005).016-.020-.025 (.025-. Soluble forms of uranium salts are poorly absorbed in the gastrointestinal tract.009) * .027-.1%-6% of an ingested dose may be absorbed.025-.270) .024) .007 (.025) 95th .029 (.059 (.006) .029) . Health effects from uranium exposure result from chemical toxicity to the kidney.006-.019-.018) .009) .007) .006) .074) . Uranium is eliminated in feces and urine.011-.007 (.009) .018-.006 (.011) .033 (. with much slower elimination from bone.011 (.027 (.006 (.015 (.027-.024-.034 (.047) .020 (.054) .035 (.020-.009 (.006-.024) .039) . which represents distribution and excretion.016) .034 (.008-.027 (.017) .013 (.019) .026 (.013) .006-.010 (.008) Sample size 2464 2689 2557 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .022 (.012) .007 (.039) Total .009) .014) .030) .010-.010 (.005 (.008-.013 (.030-.006-.008) .010-.006 (.008 (.006-.016 (.030) .008) .013 (.007 (.007 (.051) .013) .010 (.014-.017-.013 (.006-.033 (.006-.042) .007 (.016) .015 (. 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.009-.042) . Radiation risks from exposure to natural uranium are very low.009-.006-.011) .007 (.031 (.030-.029) .011-.009 (.021 (.010-.007 (. where limited absorption occurs (less than 5%). 2003). interval) .023-.009 (.011-.146) .019-.029) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.015-.016) .026 (.016) .006 (.018-.025 (.027 (.005-.007-.035 (.034 (.Metals impact.012 (.058) .005-.010-. Depending upon the specific compound and solubility.025-.024-.010) . kidneys.007-.008) .013 (.045 (.024 (.008) .018-.008) .005-.008-.080) .006-.043 (.007 (.056) .007-.034-.022-.006-.005-.034 (.042-.005-.007-.011-.051) .017 (.010) .027-.021 (.010) .021-.011-.019-.007-.008 (.022 (.008) .007 (.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.010-.018 (.009) .007 (..032) .050) .017 (.006-.022) .016-.015-.010) * .009 (..005 (.058) .014-.020-.077) .020 (.012) .053) .024-.011) .033 (.015-.010-.051 (.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 .006-.006-.010) .010-.009-.022-.009-.008) .008 (.008-.027) .008 (.022-.010-.008 (.028 (.029) .012 (.012 (.024) .031-.022 (.011-.028) .020 (.018-.006-.

. Uranium content of blood.078 μg/L (ranging up to 5. 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. 2000). and 2003-2004 (Dang et al.. population. 2002. Stradling GN. soldiers evaluated before. McDiarmid et al. (Kurttio et al. 1992. In: Gerber GB. Karpas et al. Biomonitoring Information Levels of urinary uranium reflect recent and accumulated exposure. Guidebook for the treatment of accidental internal radionuclide contamination of workers. Sci Total Environ 1991. urinary levels of uranium were as high as 9. 1999) and other small populations have shown urinary concentrations that are similar to those in NHANES 1999-2000. respectively. Boyd P. the geometric mean urinary uranium concentration was 0. urine and hair of exposed and non-exposed persons determined by radiochemical neutron activation analysis.. Breitenstein BD. Information about external exposure (i. soldiers who had been injured and had embedded DU shrapnel for as long as eight years. 2006).62:562-566. In a study of 105 persons exposed to natural uranium in well water. 2006). 2001-2002.168(8):600-605. McDiarmid M.1996. Carmichael AJ.65 μg/L). Kent (England): Nuclear Technology Publishing..Metals injury associated with elevated urinary uranium levels (Kurttio et al. The U. NRC. In the same study. 2006). Dang HS.61 μg/g creatinine. Finding a measurable amount of uranium in urine does not mean that the level of uranium causes an adverse health effect. the median urinary uranium concentration was 2.html. 2000).. Metivier H. IARC and NTP have no ratings for uranium human carcinogenicity. and no consistent effects on multiple endpoints of kidney function were found. Follow up of 32 veterans with embedded shrapnel showed that increased urinary uranium levels persisted more than 12 years after the first exposure (McDiarmid et al. Zimmerman I. Benedik L. Byrne AR. or wound contamination. 2004). 2005...gov/ toxpro2. 1978).. Eighty-five percent of those levels were above the 95th percentile of the NHANES 1999-2000 population. Tolmachev et al. Dietz LA. Six workers in a depleted uranium program showed concentrations of 0..066 μg/g creatinine (Gwiazda et al. A cohort of 46 U. Pullat VR. Volf V.e.1992. 2004).78:143-146. In 17 U. Drinking water and other environmental standards have been established by U. Hamilton MM. Komaromy-Hiller et al.atsdr. but in whom no shrapnel was embedded. Horan P. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Ejnik JW. Health Phys 2000. 2006).. the median urinary concentration was 0. 41 (1).S.107:143-157... Third National Report on Human Exposure to Environmental Chemicals. 1994.162 μg/L) (Orloff et al. Fourth National Report on Human Exposure to Environmental Chemicals 241 . 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. 1991.011 μg/L (McDiarmid et al.S. Squibb K. in that the levels were below their respective detection limits (Byrne et al. Vol. ingestion. 1-49. References Bhattacharyya MH. eds. 2006. Older studies have demonstrated urinary uranium concentrations that are consistent with levels in the U. A previous nonrandom subsample from NHANES III (n = 499) (Ting et al.S. Pillai KC.. 2004). environmental levels) and health effects is available from ATSDR at: http://www.cdc. Mil Med 2003.S. EPA. Centers for Disease Control and Prevention (CDC). In two studies of a Finnish population with high natural uranium concentrations in their drinking water. Atlanta (GA). Nuclear Regulatory Commission (NRC) has set an action level of 15 μg/L urinary uranium to protect people who are occupationally exposed (U. Determination of the isotopic composition of uranium in urine by inductively coupled plasma mass spectrometry.. with emphasis on quality control.110 to 45 μg/L (Ejnik et al. Workplace air standards and guidelines for external exposure to soluble and insoluble uranium compounds have been established by OSHA and ACGIH. Muggenburg BA. during. (May et al. 2003.55 μg/L (median 0.S.. 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. Durakovic A. Urinary uranium measurements in 103 Canadian military personnel showed mean urinary levels slightly less than geometric mean in this Report (Ough et al.. et al. pp.. had a mean urinary uranium concentration of 0. 2004). Radiation protection dosimetry. Hamilton et al. although slightly increased during and after deployment. 28 soldiers who may have been exposed to DU by inhalation. Recent studies of veterans have been conducted to examine concerns about DU exposure during military conflicts. 2002). In a much larger study of 446 Gulf War veterans who were concerned about past exposure to DU.S. Health Phys 1992. Galletti. Thomas RG. Determining the normal concentration of uranium in urine and application of the data to its biokinetics..

Ash KO. VI.44:29-40. Environ Health Perspect 2002. Element reference values in tissues from inhabitants of the European community. Bennett LG. Hollriegl V. Howerton K.47(6):972-982. J Toxicol Environ Health A 2004. Halicz L. Lewis BM. Kalinsky V.67(8-10):697-714. Radiat Environ Biophys 2005. Paretzke HG.S. Sampson EJ.158:165-190. Smith D. Kurttio P. Health Phys 2004. Gucer P. Metcalf S. Jarrett JM. Li WB.91(2):144-153. Health Phys 2004. Paschal DC.S. Auvinen A. Gwiazda RH. Englehardt SA. et al.79(1):11-21. Kuwabara J. U. Katorza E. Pekkanen J. Inductively coupled plasma mass spectrometry as a simple. McDiarmid M. Biologic monitoring for urinary uranium in Gulf War I veterans. Renal effects of uranium in drinking water.94:319-326. Health Phys 2002. Marino R. Heller J. Ejnik J. Health Phys 1996. Harmionen A. Environ Res 1999. An examination of uranium levels in Canadian forces personnel who served in the Gulf War and Kosovo.S. Oliver M. Detection of depleted uranium in urine of veterans from the 1991 Gulf War. Pinto V. Pirkle JL. Squibb K. July 1978. Health Phys 2006. Saha H. Scott K. Health Phys 2003. Auvinen A. Salonen L. Komulainen H. Wilson PD. Orloff KG. Oberbroekling KJ. Review of elements in blood.Metals Galletti M. Salonen L. and inexpensive method for determination of uranium in urine and fresh water: comparison with LIF. Hancock RG.22–Bioassay at uranium mills. Biokinetic modeling of uranium in man after injection and ingestion. Sabbioni E. Andrews WS. Mistry K. U. Roth P. Am J Kidney Dis 2006. Kurttio P. Kane R. Jackson RJ. Van der Venne MT. Komaromy-Hiller G. D’Annibale L. Engelhardt SM. Ough EA. et al. Roiz J.85:228-235. et al. Sci Total Environ 1994. Shelly T. Clin Chim Acta 2000. Nuclear Regulatory Commission (U. Squibb K. plasma and urine and a critical evaluation of reference values for the United Kingdom population.81:45-51. et al. Wahl W. Uranium and thorium in urine of United States residents: reference range concentrations. Cordero S. patient population and literature reference intervals for urinary trace elements.87:51-56. Karpas Z. Washington (DC): NRC. Lorber A. Karpas Z. Marko R. Military deployment human exposure assessment: urine total and isotopic uranium sampling results. Makelainen I. et al. Kidney toxicity of ingested uranium from drinking water. Tolmachev S. Human exposure to uranium in groundwater. McDiarmid MA. Hamilton EI. Biological monitoring and surveillance results of Gulf War I veterans exposed to depleted uranium. Comparison of representative ranges based on U.296(1-2):71-90. Oeh U. 242 Fourth National Report on Human Exposure to Environmental Chemicals .110(4):337-342. Environ Res 2004. concentration and daily excretion of uranium in urine of Japanese. May LM. Noguchi H. Charp P.S. rapid.86:12-18. Ting BG. NRC). McDiarmid MA. Uranium daily intake and urinary excretion: a preliminary study in Italy.82(4): 527-532. Cremisini C. et al. Int Arch Occup Environ Health 2006.71(6):879-85. Nuclear Regulatory Commission (NRC) Guide 8. Costa R. Saha H.

0 (11.40) 3. certain catalytic metals.60) 5.20 (6.50) 5.10-11.0 (12.00-6.0) 9.50 (5.0 (12.39-4.0) 9.40-6.80 (3.90 (4.0-29. matches.30-17.0 (11.40) 3.50) 5.51 (3.80-8.22 (2.10-12.07-4. fabric dyeing.0 (11.90-3.0) 10.40 (5. lettuce) can be the main sources of intake for humans (FDA.51 (3.70) 3. Perchlorate has been characterized as a mobile and persistent ground and surface water contaminant.0) 13.40-4.80) 12.84) 14. 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.20-12.0-15. 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.56) 3.68) 4.00-5. Survey years 01-02 03-04 Geometric mean (95% conf.65) 3.76 (3..0 (9.0) 11.0 (8.S.30 (5.80 (3.40 (4.0) 9.80 (7.0 (9.31) 2.66) 3.0) 374 314 828 721 1618 1487 01-02 03-04 01-02 03-04 4.90 (5.19 (3.0-19.50) 11.0-18.60-7.20 (4.67-5.22-5.20) 4. In addition. and limited applications in pharmaceutics.12) 3.19-4.0) 14.10-4.40-13.40 (5.29-3.90-11.60 (4.80-12.40-5.10) 3.40) 3.0) 13.0) 8.0) 14.0-23.0) 9. 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.70-12. 2005).0) 13.0-17.0 (8.80-15.0) 8.03) 3.09) 3.80-4.75-3.0) 13.30-6.0 (9.20 (8.40) 4. Other manufactured uses include fireworks.55) Sample size 2820 2522 01-02 03-04 01-02 03-04 01-02 03-04 4. Perchlorate is excreted unchanged from the human body with an estimated elimination half-life of about 7.0-17.05.70 (3.10-11.49-3.0) 15.0 (9.50) 3.50) 6.0) 12. population from the National Health and Nutrition Examination Survey.47-4.11) 3.26 (2.g. but has strong oxidant properties in the presence of concentrated acids. see Data Analysis section) for Survey years 01-02 and 03-04 are 0.93 (4.0 (8.00) 3.0) 13. and reducing agents. 7601-90-3 General Information Perchlorate is an inorganic chemical containing one chlorine and four oxygen atoms.0 (11.90) 6.70-6.0 (9.05 and 0.40 (4.50-3.90-10.00) 5.40) 2.81) Selected percentiles ( 95% confidence interval) 50th 3.0) 11. Perchlorate is stable under most environmental and physiological conditions.38) 5.70-7.90) 5.60) 8.75 (3.0 (9.45-4.80 (6.02 (3.10 (5.44-4.01 (2.20-3.0) 13.80-6.30 (5.0 (12. 2007).10) 3.50-7.0 (11.20 (7.0) 19.93-4.90-3. 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.76) 4.0) 15.0) 14.0 (11.62 (3. small amounts of perchlorate can form naturally in the atmosphere (Dasgupta et al.0-14. 1998).0 (12. Perchlorate was added to the U.20) 7.0 (13.60 (4.80) 7.20 (5.40 (8.96 (3.0 (10.54 (3.20) 3.0) 11.21 (2.50 (8.20-4.00) 7.20 (2.50-11.0 (11.18-3.0) 10.10 (6. Animal and human studies have shown that perchlorate can inhibit thyroid hormone production (NAS.0-15.40) 6. Large doses of perchlorate have been used as a medicine to treat hyperthyroidism and to diagnose disorders related to thyroid or iodine metabolism.0-17.10 (2.70-5.08-3.35 (3.S. leather tanning.30-19.60-6.90-11..30-7.00) 3.40 (5.79 (2.90-12.10-7. 2001-2002 performed on surplus samples (variable unavailable of NHANES website) Fourth National Report on Human Exposure to Environmental Chemicals 243 .90 (5.0-18.5 hours and has a small estimated volume of distribution (Crump and Gibbs.60 (7.10) 5.30) 6. It is normally found and produced as the anion of a sodium.88) 3.40-7.20-11.0 (8.0-17.0 (8.0-18. 2005).70 (3.0) 9.40 (3.0-17.0 (11.87-3.50-4.70-9.81-16.20 (4. and electroplating. interval) 3.90-9.0-17.40 (3.0) 1335 1229 1485 1293 01-02 03-04 01-02 03-04 01-02 03-04 4. and certain plants with high water content (e.20-4.30-7.00) 4.80) 3.10 (7.10 (6.80-4.EPA.11) 4.70-3.30 (2.00-6.0) 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 3.90 (5.0) 95th 14.30) 6.90 (3.40-4.70-11.10) 12.40-11.0) 708 617 681 652 1228 1092 Limit of detection (LOD.80) 75th 6. Drinking water.60) 3.90-6.0) 13.46) 3.74-3.20 (2.S.16) 3.0-20.0 (11.0) 16.70-3.50-4.05 (2.0) 9.93-3.0) 10.Perchlorate Perchlorate (Urbansky.90 (2.0 (11.70 (3.30 (2. potassium. laboratory analysis.90-9.89-3.0 (9.32 (3.40) 90th 10. or ammonium salt.10) 5. 2002). milk.50 (3.0) 13.

.33-12.87) 2. it is known that maternal and congenital hypothyroidism adversely effects neurological development and decreases learning capability.34-3.3-14.45) 3.0-14.3) 12.2) 8. levels.6) 20. 2000).58) 2.00 (2.90 (4.0-19.0 (11.60-5.33 (7.50 (6.90 (2.22-4.54 (2.90-3.36 (8.g.02) 3.70) 2. nitrate. In the U.1 (8.52 (8. but without effects on serum levels of thyroid stimulating hormone or thyroxine (Braverman et al.00-3.4) 8.90-2.30) 5.50) 6.30) 90th 9. dietary iodine intake.00-2. 2005). 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 (8.70 (2.22-6.40 (3.90-15.0 (11. women with urinary levels of iodine less than 100 micrograms per day. 2005).87-3. Also. age. although iodine intake was higher than U.41) Sample size 2818 2504 01-02 03-04 01-02 03-04 01-02 03-04 5.81-3.93-5.00) 3.50) 2. Steinmaus et al.44) 3. 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.87 (5.80 (7. in a representative sample of U.90 (7. 2003.20) 8.35 (4.S.0 (10.4 (8.5) 8.0-14.93-7.60-6.10 (1.10) 6.1) 8.80 (4.20-9.61-10.0) 708 616 680 648 1227 1080 2001-2002 performed on surplus samples (variable unavailable of NHANES website) 244 Fourth National Report on Human Exposure to Environmental Chemicals .90-11.60-15.. 1999.0) 14.70) 10.61-5.90) 5. Lamm and Doemland. 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.0) 1335 1220 1483 1284 01-02 03-04 01-02 03-04 01-02 03-04 3.03 (2.20-3.00) 4.35) 3.30 (3.08) 3.4 (10.1-14. menopausal status.76 (3.0) 374 313 827 715 1617 1476 01-02 03-04 01-02 03-04 3.08 (3.29) 2.S.6-17.33-6.93-5.10 (4. 2005).20-4.25 (3. 2001.05 (4.10 (4.S.59) 3. 2006. Li et al.3) 8.4-16.60-3.26) 4.60) 3.40) 3.51-4.09) 3.1-13.0) 4. levels and sufficient in most participants (Tellez et al.20 (4.43) 6.S. Survey years 01-02 03-04 Geometric mean (95% conf. 2005.51 (3. However.89 (2. congenital hypothyroidism is a condition for which nearly all newborn blood is screened.00-11.0-17.70-3.18-3.0) 12.70 (2.20 (7.0) 7.8 (11. gender.25) 5.07 (2. Though it produces follicular cell thyroid tumors in animal studies at goitrogenic doses.20-10.7 (11.60 (3.82 (5.EPA.26 (3.1 (11.91) 4.50-3.99 (5. During gestation and infancy.50) 95th 12. Lawrence et al.39 (3.60) 8. suggesting its tumorgenic effect is a result of a chronic increase in thyroid stimulating hormone indirectly resulting from iodine uptake inhibition.60) 10.74) 7..14 (2.12-2.09 (7.80) Selected percentiles ( 95% confidence interval) 50th 3.72 (3.96) 2.40 (4.19-6.24-2.84) 2.20-3.52-9.0) 12.20 (6.37-13.40-10.04-3. up to 68% RUI has been demonstrated.67) 5.87) 7.40 (7.30-10.50) 9.0 (9.44-6.0) 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 3.1-16.2) 8.32) 5..25) 5.73) 3.22-4. altered thyroid function was not found in Chilean pregnant women or their newborns with mean urinary perchlorate levels about 40-fold higher than average U.60-8.80 (7.24 (4.46-4.30 (6. population from the National Health and Nutrition Examination Survey.42 (3.50 (3.50) 5. 2002.60-8.3) 11. 2005.90 (2.40) 17.12 (6.00) 9.77 (3. chronicity of exposure.40 (3.50-9.0) 10.15-12.60-11.22 (2.0) 6.S..35 (2.29-6.30) 75th 5.66) 3.61 (5. interval) 3.53 (2.0) 9.10) 13.97-5.10) 3.1-22.20 (2.70-5.93) 3. thiocyanate.0) 9.20) 3.64-3..75) 3.99-3.76-3.0) 11.25) 5.6) 12.21 (2.56-3.0) 13.30-5.0) 13.83 (5.64) 5.0 (8.95 (2.87 (7.56 (3. 2007).47) 2..86) 4..40) 5..19-10.0) 12.30) 3.10-7.37 (4. NAS.70 (4.39-4.S.39) 2.EPA.71 (5.3 (10.0 (9.10 (2. Greer et al.46-13.5 (13. perchlorate is negative in most genotoxic assays (U.30 (5.80-3.54 (3.10) 4.50-5.50) 2.60-5. 2002. Short term human studies of the effect of perchlorate on RUI have been used for risk estimation (Greer et al.0) 12.70-15.20 (3.4 (11.00 (6.0 (11. Ecologic studies from screening programs with elevated perchlorate in the regional drinking water have indicated no increased prevalence of abnormal neonatal screening tests for this disorder in these regions (Kelsh et al.10 (6.41-9..45-2.0 (9.04-3.0-44.70-4.10-3.98) 3.S. Many factors may be important in consideration of perchlorate action on the thyroid: dose.46 (3.Perchlorate inhibition (RUI).93-8.30-5.4) 13. 2002).00 (4.90-20.89-3.16-3. medications).90-9.02-4. U. and the presence of other substances known to affect thyroid function (e.4 (11.60-11.80-3.

113(11):A732. and environmental perchlorate exposure among residents of a Southern California community. Benchmark calculations for perchlorate from three human cohorts.40(21):6608-6614.html and from ATSDR at: http://www. Blount BC. Landingham CB. Urinary perchlorate and thyroid hormone levels in adolescent and adult men and women living in the United States. Valentin-Blasini L. National Academy of Sciences (NAS). Pirkle JL. Erratum in: J Occup Environ Med 2004. Pleus RC. Skeels MR.S. 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. Byrd D.fda. He X. Lamm SH. Blount et al.17(4):400-407. most of the population is considered to be below the U. Mauldin JP. Thyroid 2001.S.115(9):1333-1338. Doemland M. Greer SE. Erratum in: Environ Health Perspect 2005. et al. Gibbs JP.htm. 2005. 2007). Howd R.atsdr. 2001-2002. et al. Preliminary Estimation of Perchlorate Dietary Exposure Based on FDA 2004/2005 Exploratory Data. Lamm SH. thiocyanate. Environ Health Perspect 2005. et al. Sesser DE. and nitrate on thyroid function in workers exposed to perchlorate long-term. J Occup Environ Med 2000. Caldwell KL. Lau EC. Health effects assessment for environmental perchlorate contamination: the dose response for inhibition of thyroidal radioiodine uptake in humans. Primary congenital hypothyroidism. Dyke JV. Perchlorate in the United States. Richman K. Crump KS. Lawrence J. Also. Goodman G. 2005). Health Implications of Perchlorate Ingestion. Steinmaus C. 2005).45(10):1116-1127. References Blount BC. Jackson WA. Environ Sci Technol 2006. Valentin-Blasini L.. Kirk AB. Analysis of relative source contributions to the food chain. Pino S. Neonatal thyroxine level and perchlorate in drinking water. Compared to a previous study of pregnant women in three Chilean communities with varying perchlorate levels in the drinking water.113(8):10011008. 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. 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. Finding a measurable amount of perchlorate in urine does not mean that the level of perchlorate causes an adverse health effect. Kelsh MA. J Occup Environ Med 2003. Braverman LE. Has perchlorate in drinking water increased the rate of congenital hypothyroidism? J Occup Environ Med 1999. Pino S. et al. Abarca CR. Deyhle GM. Li FX. Tellez RT. Cross M. Blount BC.EPA at: http://www. Long-term environmental exposure to perchlorate through drinking water and thyroid function during Fourth National Report on Human Exposure to Environmental Chemicals 245 .. population. The effect of perchlorate.gov/toxpro2. Lawrence JE. May 2007. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Osterloh JD. The effect of short-term low-dose perchlorate on various aspects of thyroid function.11(3):295.41(5):409-411.S.gov/Food/FoodSafety/ FoodContaminantsAdulteration/ChemicalContaminants/ Perchlorate/ucm077653. Page Last Updated: 05/28/2009.html..Perchlorate be unlikely to occur without overt perturbation of thyroid homeostasis. Lamm SH. newborn thyroid function.46(5):509. Barnard JC.114(12):1865-1871. J Clin Endocrinol Metab 2005. 6/2/09 Greer MA. Perchlorate Exposure of the US Population.110(9):927-937. The levels seen in NHANES 20032004 show a similar pattern to NHANES 2001-2002. Low dose perchlorate (3 mg daily) and thyroid function. Washington (DC): National Academy Press. J Expo Sci Environ Epidemiol 2007. Thyroid 2000. CFSAN/Office of Plant & Dairy Foods. EPA reference dose (Blount et al. Lamm S.gov/safewater/ccl/perchlorate/perchlorate. Braverman LE. Buffler PA. Crump KS. Environ Health Perspect 2002. Environ Health Perspect 2006. Miller MD. Pirkle JL. National Research Council of the National Academies. Li Z. Daaboul JJ. Rutherford GW.10(8):659-663.42(2):200-205. Available at URL: http://www. Additional information about exposure and health effects is available from the U. Dasgupta PK. Braverman LE. When these NHANES 2001-2002 urinary levels of perchlorate are used to calculate daily oral intakes for the U. Osterloh JD. epa. Magnani B. Food and Drug Administration (FDA).cdc. Environ Health Perspect 2007. (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. Biomonitoring Information Urinary perchlorate levels reflect recent exposure. Impact of smoking and thiocyanate on perchlorate and thyroid hormone associations in the 2001-2002 national health and nutrition examination survey.90(2):700-706. Chacon PM.

Drinking Water Contaminant Candidate List.epa. Integrated Risk Information System (IRIS).1/15/06 U.S.15(9):963-975. EPA). cfm?substance_nmbr=1007.S. EPA/600/F-98/002 Washington (DC).gov/iris/quickview. Thyroid 2005. Available from URL: http://cfpub. 246 Fourth National Report on Human Exposure to Environmental Chemicals . Revised 2/11/05.9(3):187-192. Perchlorate. Perchlorate as an environmental contaminant. Doc.Perchlorate pregnancy and the neonatal period. 1988. U. Urbansky TF. EPA). Environmental Protection Agency (U. Environmental Protection Agency (U. Environ Sci Pollut Res Int 2002.S.S. No.

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

1993). and in human blood and semen (Calafat et al. Both PFOA and perfluorodecanoic acid have been shown to reduce androgen levels in laboratory animal studies (Biegel et al. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. but still can have long residence times in the body. Survey Geometric mean (95% conf. For instance..5 years and for PFOS..S.. In some cases. but the relevance of peroxisomal pathways in humans is unclear (Kennedy et al. < LOD means less than the limit of detection.. Unlike many organohalogen contaminant chemicals.. 2005). It is unclear if environmentally degraded telomer products are a major source of other PFCs..Perfluorochemicals PFOS greater than 2000-fold over aquatic levels). Vanden Heuvel et al. Excepting PFOS and PFOA. EPA. the 8-2 telomer. and in offspring. PFOS and PFOA levels in archived bird eggs from Sweden have increased thirtyfold from 1968 to 2003 (Holmstrom et al. Human health effects from PFCs at low environmental doses or at biomonitored levels from low environmental exposures are unknown. the perfluoroalkyl acids (PFOA and PFOS) do not tend to accumulate in fat tissue. The elimination half-life of PFOA in humans is roughly estimated to be 3. The liver toxicity of several PFCs is evident by vacuolization and lipid accumulation in both rodent and monkey livers (Seacat et al. population from the National Health and Nutrition Examination Survey.. in a wide variety of marine and land animals (Kannan et al. 2004). 2000. 2003.4. environmental fate. 2006. 2004) and may be attributable to the ability of PFCs to affect intracellular lipid binding proteins.. 2005. by high protein binding in plasma and other proteins. 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. The ammonium salt of PFOA has been tested at high doses in mammalian animal studies and produced altered weights of the liver. 2007).. PFOA (and probably other perfluoroalkyl acids) exist in the anionic state at physiologic and environmental pHs and their distribution in the body is determined... endocrine and immune effects.. Bookstaff et al. 2006a. 248 Fourth National Report on Human Exposure to Environmental Chemicals . PFCs have been identified in surface coastal and ocean waters (Yamashita et al. C6. 2005). 2005. human toxicokinetics.. PFOA preparations used in many studies may also contain a small percentage of other chain length perfluoroalkyl acids (i. Lau et al.. Kannan et al. 2003). and β-oxidation of lipids (Kudo et al.. 2004. 1995. PFOA has been reported to cause liver.. in part. but limited observations in humans suggest that only one-fifth of the total body clearance is renal (Harada et al. 2003a and 2004a).. hepatotoxicity. C5... approximately 4. PFOA is mostly excreted in the urine in animal studies.. Some of the effects in animals may be mediated through peroxisomal proliferation. 1990). All sources of human exposure are uncertain. 2004. growth retardation and delayed sexual maturation (Kennedy et al. Serum Perfluorobutane sulfonic acid (PFBuS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U. including immunologic effects and tumor induction. 2004. but probably include dietary sources (Kannan et al. Guruge et al. C7). 2004. Lau et al. may metabolize or degrade to PFOA (Dinglasan et al.. 2005). Keller et al.. pancreas. 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. 2005.. thymus and spleen. 2003). or effects of other PFCs.8 years (Olsen et al.S. kidney. 2004). 2007a).e. U. Taniyasu et al. which may vary for some chemicals by year and by individual sample. 2002. heptadecafluoro-1-decanol. peroxisomal proliferation. Olsen et al. there is limited information on the sources.. see Data Analysis section) for Survey year 03-04 is 0.. Tittlemier et al. Prevedouros et al. The PFCs often measured in human serum are listed in the table.

500 (..108 times higher than background serum levels in humans (Butenoff et al.500 (<LOD-1.. Harada et al. 2005). see Data Analysis section) for Survey year 03-04 is 0. Olsen et al.50) . Kennedy et al.500-1. monkeys.600 (.800) 1. PFOA. 2003a).. PFOS.800 (. 2007a..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 .00 (. hepatotoxicity. Twelve different PFCs were measured in the sera of NHANES 2003-2004 participants..00) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 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. Fei et al..800 (. At high but non-toxic maternal doses of PFOS. 2003. and there was no clear evidence of excess all-cause or diseasespecific mortality.500-3. the potential to estimate risks to humans from animal doses is uncertain. population from the National Health and Nutrition Examination Survey. developmental and teratogenic effects were demonstrated in offspring..500-1.400-1.300-1. Roughly similar levels of PFCs in serum have also been measured previously in other samples of the U. U.400 (<LOD-. the median PFCs values tend to be roughly similar in these age categories (Olsen et al..300 (<LOD-.S. population. In such studies. 2007b. 2004).500-1. Olsen et al. Late gestational exposure to PFOS in animal studies has also demonstrated early neonatal lethality.. 2007). At doses causing maternal toxicity.400 (<LOD-.400-1. Olsen et al.10 (.. reproductive.800 (. thyroidal). development in offspring was stunted and hypothyroxinemia was observed.. EPA. 1992.. 2003a.20) . 2003. which may vary for some chemicals by year and by individual sample.Perfluorochemicals and testicular tumors in high dose animal testing (Biegel et al. Serum Perfluorodecanoic acid (PFDeA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.700 (. In comparing three separate reports on adults. 2001. possibly related to lung immaturity (Lau et al. PFOA. 2003).10) .400-. EPA. 2003a.700) . Fourth National Report on Human Exposure to Environmental Chemicals 249 . 2007a.. and other PFCs have not been classified as to human carcinogenicity by IARC or NTP. 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..400-1. animal and human serum PFOA levels have been compared: serum levels associated with toxic effects in animals are 66-11. Biomonitoring Information Serum levels of PFCs (particularly PFOA and PFOS) tend to reflect cumulative exposure over several years. Two recent cross-sectional human studies observed a negative correlation of birth weight with serum levels of PFOA (Apelberg et al. 1999..300 (<LOD-. Animal studies of PFOS have demonstrated weight loss..00) .S. and no substantial age trends were seen within adults ages 20-69 (Olsen et al.500) . Due to marked intergender differences in the elimination of PFOA in rats and substantial differences in the half-life of PFOA in rats.300 (<LOD-. Cook et al. U.10) * 03-04 03-04 * * < LOD < LOD < LOD .400) . 2004a. < LOD means less than the limit of detection.20) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD .600 (. 2005). 2004. However..500-1.600 (. Effects on serum liver enzymes in limited observational studies of human occupational exposures are unclear.500 (.500) . 2007b). A study of workers chronically exposed to primarily PFOA showed no biochemical evidence of hepatotoxicity or hormonal changes (adrenal.600-2. 2003a. Lau et al.500) 90th .40) . and changes in thyroid hormone concentrations (Grasty et al.400-1..500-.3.500) .400-1. 2003a). 2004. 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.500) . Thibodeaux et al. 2003. 2003).800 (.S.S. PFOS..00) . 2004b).400 (<LOD-.400-. Slightly higher levels of PFOS and PFOA in males than females have been noted in several other studies (Calafat et al. interval) Selected percentiles ( 95% confidence interval) Sample 95th . 2004). Survey Geometric mean (95% conf. and humans.80) 640 1454 03-04 03-04 * * < LOD < LOD . elderly and children. perfluorohexanesulfonate (PFHxS).900 (. 2007..800) 1. 2003).80) 485 538 962 Limit of detection (LOD.900 (. or increased cancer rates (Alexander et al.10) ..900 (.

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

300-. see Data Analysis section) for Survey year 03-04 is 0. < LOD means less than the limit of detection.300 (<LOD-. which may vary for some chemicals by year and by individual sample. population from the National Health and Nutrition Examination Survey.300 (<LOD-.400 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.500) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th < LOD 90th * 03-04 03-04 * * < LOD < LOD < LOD < LOD . see Data Analysis section) for Survey year 03-04 is 1. Survey Geometric mean (95% conf.S.900) < LOD 640 1454 03-04 03-04 * * < LOD < LOD < 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 < LOD < LOD 485 538 962 Limit of detection (LOD.400) .500-. Serum Perfluoroheptanoic acid (PFHpA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.500) 485 538 962 Limit of detection (LOD.400 (<LOD-. interval) Selected percentiles ( 95% confidence interval) Sample 95th .900) < LOD .600 (.0.600) < LOD . population from the National Health and Nutrition Examination Survey. which may vary for some chemicals by year and by individual sample.400 (<LOD-.3. < LOD means less than the limit of detection. Survey Geometric mean (95% conf. Fourth National Report on Human Exposure to Environmental Chemicals 251 . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.500 (<LOD-.S.Perfluorochemicals Serum Perfluorododecanoic acid (PFDoA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.600) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .

30 (1.30) .60) 1.90-19.10) 1.70) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 1.30 (3.60 (1.852 (.70-5.90) 1.80-4.900-1.S.900-1.800-1.90 (2.30) 3.44 (2.72 (1.40-1.14) Selected percentiles ( 95% confidence interval) Sample 95th 3.50 (1.30-2.60 (1.800 (.00-1.12) .70) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 1.40-3.90) 8.809) 1.70) 13.80-8.20-1.20-3.60-3.60-2.900-1.70) 1.70) 3.51) 1.10) 5.05-2.80) 1.54) .10 (1. see Data Analysis section) for Survey year 03-04 is 0.40) .10) 6.40-1.90 (1.30-6.00 (5.697-1.70) 1.40 (1.10) 1053 1041 03-04 03-04 03-04 .30-12.30) 03-04 03-04 .721-1.60-8. Serum Perfluorononanoic acid (PFNA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.20-1.17-1.00 (2.80-4.70-7.10 (4.10-9.10 (.20 (1.10-5.50 (1.27) 1.80 (1.Perfluorochemicals Serum Perfluorohexane sulfonic acid (PFHxS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.50 (1.40 (1.00) 1.10) 4.10 (.689 (.30 (1.16) Selected percentiles ( 95% confidence interval) Sample 95th 8.93 (1.6) 7.70-2.826-1.50 (4.50) 2.20 (1.50-6.80) 4.834-1.00) 1.50-3.00 (1.80) 90th 2.80-2.20 (1.50 (4. Survey Geometric mean (95% conf.50 (2.60-4.10 (4.912-1.40 (1.90 (1.30 (1.20 (6.1.90) 1.80) 5.30) 3.60-3.10) 6.00 (1.20-1.900-1.60-7. see Data Analysis section) for Survey year 03-04 is 0. interval) 1.90 (4.40) 4.20) 1.90) 90th 5.80-3.50) 2.87-2.00 (.40) 2.984 (.42 (1.30 (7.67-2.90 (1.60 (1.90-2.00) 2.900) 1.80-8.80-7.00-6. population from the National Health and Nutrition Examination Survey.5) 8.16) .00 (1.20 (1.91) 2.90) 1.70 (2.20) 1.77-2.62-2.60-2. population from the National Health and Nutrition Examination Survey.80) 3.60 (6.20) 2.30 (6.3 (9.00) 3.40) 1.56-1.60-4.80-12.00 (.80 (4.08) 2. interval) .60) 2.20-2.90 (4.30 (2.40 (1.09 (.20) 485 538 962 Limit of detection (LOD.40) 1.70-10.80 (1.10-9.700-1.80-6.03) 1. 252 Fourth National Report on Human Exposure to Environmental Chemicals .60-2.92 (1.0) 8.26) 2.70) 2.10) 8.50 (6.60) 9.20-1.80-3.0) 1053 1041 03-04 03-04 03-04 1.20) 03-04 03-04 2.20) .90-10.10) 75th 1.00-7.861 (.900-1.900 (.S.600-.835-1. Survey Geometric mean (95% conf.700 (.963 (.70-6.30-9.10) 75th 3.40 (2.70 (1.50 (1.50-10.3.816-1.70) 2.900-1.00-1.90) 3.50) 6.72) 1.1) 485 538 962 Limit of detection (LOD.5) 5.30) 3.70-2.01 (1.17 (1.60) 3.20 (6.40) 640 1454 03-04 03-04 2.04) .80-4.86 (1.900 (.50-6.10 (.73-2.00 (1.90 (1.10) 4.50 (6.00-8.40) 640 1454 03-04 03-04 1.30 (1.10) 1.586-.30 (2.14 (.966 (.80-7.

10) 5.20) 10.5-33.9 (19.60-14.6-24.70-5.1 (19.20 (4.1.7 (35.90 (7.90-4.4) 75th 30.4) 640 1454 03-04 03-04 23.21-3.89 (3.60 (5.9-19.85-4.1-52.40) 3.9) 22. population from the National Health and Nutrition Examination Survey.35) 3.5) 8.50-6.8 (45.2 (18.6 (44.4 (19.53) 3.0) 21.27) 4.60 (4.4-25. Serum Perfluorooctane sulfonic acid (PFOS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.79) 4.70 (5.20 (4.7-23.4) 21.30-8.60 (6.0-66.S.8) 32.3 (44.00 (3.60-9.8-22.30) 7.8-35.6 (19.7 (35.60-6.6 (42.10 (3.9 (13.1) 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 4.1-33.1) 15.90 (5.70-9.4-17.9-38.6) 35. see Data Analysis section) for Survey year 03-04 is 0. Fourth National Report on Human Exposure to Environmental Chemicals 253 .90 (7.2-57.3) 41.8-81.5) 32.9 (22.90) 6.4 (23.5) 9.5) 19.47 (4.60-13. population from the National Health and Nutrition Examination Survey.8) 27.65-4.8) 46.0) 485 538 962 Limit of detection (LOD.4 (28.0-16.40-14.95 (3.9-23.6-45.90-4.50 (4.3 (35.1-25.37 (2.6) 9.50 (3.40-17.5 (28.60) 03-04 03-04 3.8 (34.0-20.Perfluorochemicals Serum Perfluorooctanoic acid (PFOA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.00 (5.0) 03-04 03-04 19.4) 20.40) 90th 7.0) 21.60 (3.70) 3.0) 36.6) 42.60 (7.5) 1053 1041 03-04 03-04 03-04 14.10-3.0 (27.00) 3.6) 21.20-4.30) 6.4) 56.3-61.11 (2.1 (23.80-9.8-78. Survey Geometric mean (95% conf.5) 7.20-9.20) 5.70 (3.82) 4.0) 23.18 (3.2) 30.30 (3.80 (6.9) 9.0) 43.6-50.S.20-5.30 (5.1) 57.10 (3.50) 7.20) 7.8-22.70-7. interval) 20.3 (28.2) 30.4-42.80) 8.70) 6.0) 90th 41.07-4.6) 62.9 (17.90-12.7 (43.30-3.96 (3.10 (6.8 (37.99-3.80-12.7-33.9) 27.3 (17.3) 42.30-11.60 (6.1 (24.3 (35.70) 4.40) 5.4 (17.70 (5.5) 18.2) 640 1454 03-04 03-04 4.7) 39.2 (19.30-5.4 (19.9) 22. interval) 3.6) 1053 1041 03-04 03-04 03-04 3.40 (6.7 (13.5-23.1-35.80 (7.2-22.3) 28.90 (7.2) 45.80-4.1-36.3-22.20) 4.50) 4.30 (3.5) 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. Survey Geometric mean (95% conf.7 (43.5-21.4.3) Selected percentiles ( 95% confidence interval) Sample 95th 54.7-30.70-7.60) 8.40-10.8-30.7-49.7-53.40 (4.40-6.0-70.80 (6.00 (5.50-4.6) 7.91) 3.2 (28.7 (7.84-3.2 (16.5) 57.40-6.0 (20.50-13.6 (35.7-69.3) 485 538 962 Limit of detection (LOD.5-62.1-24.70-10.30-6.7 (19.40) 75th 5.27) Selected percentiles ( 95% confidence interval) Sample 95th 9.20) 7.67-4.2 (27.8-22.47-4.5 (28.2 (21.20) 5. see Data Analysis section) for Survey year 03-04 is 0.80 (5.6) 18.

300) * 03-04 03-04 * * < LOD < LOD < LOD < LOD .500) 485 538 962 Limit of detection (LOD.300 (.300-.300 (.200-.300-.400 (<LOD-.2.300 (.200-.300 (.200-.400) 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD .300 (. population from the National Health and Nutrition Examination Survey.S. < LOD means less than the limit of detection.300) . Survey Geometric mean (95% conf.500) . population from the National Health and Nutrition Examination Survey.300 (.300) . 254 Fourth National Report on Human Exposure to Environmental Chemicals .300) .200-.300 (. which may vary for some chemicals by year and by individual sample.200-.300) . < LOD means less than the limit of detection.300 (.500) .200-.S.300-.300 (.300) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Survey Geometric mean (95% conf.200-.200 (<LOD-.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. see Data Analysis section) for Survey year 03-04 is 0.300 (.500) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .Perfluorochemicals Serum Perfluorooctane sulfonamide (PFOSA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.200-.300) .300-.200-.500) < LOD 485 538 962 Limit of detection (LOD.300) . interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th < LOD 90th * 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result. see Data Analysis section) for Survey year 03-04 is 0.200-.300 (.300 (. which may vary for some chemicals by year and by individual sample.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 . interval) Selected percentiles ( 95% confidence interval) Sample 95th .500) .4.300 (.

500 (<LOD-.30) .10 (1.700 (<LOD-.600 (<LOD-1.800 (<LOD-.700 (<LOD-2.S.40) 1.10) * 03-04 03-04 * * < LOD < LOD .700 (<LOD-.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 .900-1. < LOD means less than the limit of detection.30 (1.900) . interval) Selected percentiles ( 95% confidence interval) Sample 95th .300-2.10) .30 (1.700 (<LOD-.70) 1.900) 485 538 962 Limit of detection (LOD. see Data Analysis section) for Survey year 03-04 is 0.900 (.80) 1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.50 (1.10) 1.00 (.30 (1. < LOD means less than the limit of detection. Survey Geometric mean (95% conf.30) 1.900-1.10-1.700 (<LOD-. population from the National Health and Nutrition Examination Survey.80) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD .700) 1. which may vary for some chemicals by year and by individual sample.20 (1.700) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .50 (1.Perfluorochemicals Serum 2-(N-Methyl-perfluorooctane sulfonamido) acetic acid (Me-PFOSA-AcOH) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.20) 1. population from the National Health and Nutrition Examination Survey.600) .900-1.20-1.400 (<LOD-.10 (.900-1.60) 485 538 962 Limit of detection (LOD.10) 1.60) 640 1454 03-04 03-04 * * < LOD < LOD .30) 1.80) 1. which may vary for some chemicals by year and by individual sample.10-1.900-1.800) . Survey Geometric mean (95% conf.00 (.300 (<LOD-1. Fourth National Report on Human Exposure to Environmental Chemicals 255 .300 (<LOD-. Serum Perfluoroundecanoic acid (PFUA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.10 (.6.S.10-1.900-1.00 (.40) < LOD < LOD .00 (.800) .400 (<LOD-1. see Data Analysis section) for Survey year 03-04 is 0.10 (.700) 1.900-1.600 (<LOD-1.00) < LOD .600 (<LOD-1.40) 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD .700 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.3.900 (<LOD-1.10-1.900) 1.50) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD 75th .10-1.700) 90th 1.600 (<LOD-.700 (<LOD-.700) .90) .00-1.10) .

Calafat AM. Halden RU. and perfluorinated contaminants in livers of polar bears from Alaska. Environ Sci Technol 2006a. Witter FR. Arendt MD. Toxicol Sci 2001. Characterization of risk for general population exposure to perfluorooctanoate.34(4):351-384. McLaughlin JK. Toxicol Appl Pharmacol 1992. Induction of Leydig cell adenomas by ammonium perfluorooctanoate: a possible endocrine-related mechanism. Mandel JS. Kuklenyik Z. Environ Health Perspect 2007. Environ Sci Technol 2004. O’Connor JC. Guruge KS. Kannan K. and ex vivo studies. et al.68(6):465-471.7(4):371-377.39(1):80-84. Birth Defects Res B Dev Reprod Toxicol 2003. Kuklenyik Z. Frame SR. Inoue K. Laane RW. Serum concentrations of 11 polyfluoroalkyl compounds in the U.115(11):1677-1682. Moore RW. Day RD. Chemosphere 2006b. Cook JC. Toxicol Appl Pharmacol 1990. Perfluorinated organic compounds in human blood serum and seminal plasma: a study of urban and rural tea worker populations in Sri Lanka. de Voogt P. Perfluorooctanesulfonate and related fluorochemicals in human blood from several countries. Chlorinated. Temporal trends of PFOS and PFOA in guillemot eggs from the Baltic Sea. Environ Res 2005. et al.115(11):1596-1602.99(2):253-261. Taniyasu S. Needham LL. brominated. Mortality of employees of a perfluorooctanesulphonyl fluoride manufacturing facility. Edwards EA.60(1):44-55. Yun SH. Watanabe T. Environ Sci Technol 2005. Evans TJ.63:490496.38(17):4489-4495. et al. Biegel LB. The influence of time. Kamiyama S. Mandel JH. Inoue K. Herbstman JB. Needham LL. Environ Health Perspect 2007. et al. Murray SM. Chem Biol Interact 2000. Cord serum concentrations of perfluorooctane sulfonate and perfluorooctanoate in relation to weight and size at birth. Ye Y. Burris JM. Morikawa A. Perkins RG. Cook JC. Prenatal window of susceptibility to perfluorooctane sulfonate-induced neonatal mortality in the Sprague-Dawley rat. Katakura M. Hurtt ME. Liu RC. Aguilar-Villalobos M. Dinglasan MJ. Seneviratne HR. Olsen J. Kudo N. Tully JS.39(3):363-380. Environ Sci Technol 2005. Caudill SP. Environ Sci Technol 2007a. Needham LL. population: Data from the National Health and Nutrition Examination Survey (NHANES) 1999–2000. Sasaki S. Holmstrom KE. Mechanisms of extrahepatic tumor induction by peroxisome proliferators in male CD rats. Wong LY. Environmental and toxicity effects of perfluoroalkylated substances. Kawashima Y.S.124(2):119-132. et al. Saito N.179:99-121.40:21282134.115(11):1670-1676. Suzuki E. Perfluorinated chemicals and fetal growth: A study within the Danish National Birth cohort. Reidy JA. Jarnberg U.41:2237-2242.1968--2003. Yamashita N. Rodricks J. Butenhoff JL. Perfluorinated chemicals in selected residents of the American continent.Perfluorochemicals References Alexander BH. sex and geographic factors on levels of perfluorooctanesulfonate and perfluorooctanoate in human serum over the last 25 years. Effects of ammonium perfluorooctanoate on Leydig cell function: in vitro. 256 Fourth National Report on Human Exposure to Environmental Chemicals . Hekster FM. Kennedy GL Jr. Perfluorinated compounds in the plasma of loggerhead and Kemp’s ridley sea turtles from the southeastern coast of the United States. Tarone RE. Environ Health Perspect. Koizumi A. Mohotti KM. Kuklenyik Z. J Occup Health 2004. Renal clearance of perfluorooctane sulfonate and perfluorooctanoate in humans and their species-specific excretion. Corsolini S. Kannan K. Harada K. Reidy JA. Environ Sci Technol 2005. Yamashita N.104(2):322-333. Wijeratna S. Olsen GW. Loganathan BG. Harada K. Cook JC. Rogers JM. Androgenic deficiency in male rats treated with perfluorodecanoic acid. Bandai N. Kumar KS. Biegel LB. Calafat AM. 2007b. Induction by perfluorinated fatty acids with different carbon chain length of peroxisomal beta-oxidation in the liver of rats.Koizumi A. Gaylor DW. Needham LL. Fei C. Calafat AM. Olsen GW. Butenhoff JL.134(1):18-25. Crit Rev Toxicol 2004. Regul Toxicol Pharmacol 2004. Bookstaff RC. Hurtt ME. Apelberg BJ. Kuklenyik Z. Fillmann G. Environ Sci Technol 2004. O’Connor JC. Taniyasu S.39(23):9057-9063. Bignert A. Grasty RC. Ingall GB.and perfluorinated acids. Saito N. Lau CS. Fluorotelomer alcohol biodegradation yields poly. Hurtt ME.38(10):2857-2864. Reidy JA. Mabury SA. Yoshinaga T. Olsen GW. Grey BE.60(10):722729. Calafat AM. Caudill SP.S. Mandel JH. in vivo. Seacat AM. Moore JA. Occup Environ Med 2003.46(2):141-147. Keller JM. Perfluorochemicals in pooled serum samples from United States residents in 2001 and 2002. Kannan K. Falandysz J. Calafat AM. Frame SR.39(23):9101-9108. J Environ Monit 2005. Polyfluoroalkyl chemicals in the U. Peterson RE. population: data from the National Health and Nutrition Examination Survey (NHANES) 2003-2004 and comparisons with NHANES 1999-2000. Rev Environ Contam Toxicol 2003. The toxicology of perfluorooctanoate. et al. Yoshinaga T. et al. Reidy JA.113(2):209-217. Tully JS. Toxicol Appl Pharmacol 1995.

Hanson RG. Toxicol Appl Pharmacol 2004. Sources.68(1):249-264. Half-life of serum elimination of perfluoroo ctanesulfonate. Environ Health Perspect. Rogers JM. Cao XL et al.198(2):231-241.perfluorohexanesulfonate. J Ag Food Chem 2007. Biol Pharm Bull 2003.2(1):53-76. Burris JM. Hansen KJ. (Erratum in: Environ Health Perspect. Church TR. 2003. Coordinate induction of acyl-CoA binding protein. Exposure to perfluorooctane sulfonate during pregnancy in rat and mouse.82(1):359. Sterchele PF. Butenhoff JL. Horii Y. Burlew MM.26(1):47-51. Ehresman DJ. Olsen GW. Olsen GW. Hanson RG. Mandel JH. Prevedouros K. Grey BE.54(11):1599-1611. birds. Korzeniowski SH. Huang HY. Environmental Protection Agency (U.41(9):799-806. J Children’s Health 2004b. perfluorooctanoate andother fluorochemicals in human blood. Butenhoff JL.epa. Reagen WK. Rogers JM. Petrick G. and perfluorooctanoate in retired fluorochemical production workers. Seymour C. Burris JM. J Occup Environ Med 1999. Preliminary evidence of a decline in perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) concentrations in American Red Cross blood donors. Chemosphere 2007b.111(16):1892-1901. et al. Hansen KJ. et al. Case MT. Toxicol Sci 2003. and food items prepared in their packaging. Kannan K. EPA).S. Moisey J. Cousins IT. Seacat AM. Bronson R.1177(2):183-190. Froehlich JW. Environ Health Perspect 2003a. J Occup Environ Med 2003b. Kannan K. Perfluorooctanesulfonate and other fluorochemicals in the serum of American Red Cross adult blood donors. Zobel LR.113(5):539-545. htm. and humans from Japan. Butenhoff JL. Quantitative evaluation of perfluorooctanesulfonate (PFOS) and other fluorochemicals in the serum of children. A survey of perfluorooctane sulfonate and related perfluorinated organic compounds in water.115(9):1298-1305. Kawashima Y. Exposure to perfluorooctane sulfonate during pregnancy in rat and mouse. Horii Y.51(8-12):658-668. Thibodeaux JR.68:105–111.Perfluorochemicals Kudo N. Lau C. fatty acid binding protein and peroxisomal beta-oxidation by peroxisome proliferators. Peterson RE. Burris JM.gov/opptintr/pfoa/pfoara. Fourth National Report on Human Exposure to Environmental Chemicals 257 . Thibodeaux JR. I: maternal and prenatal evaluations. Rogers JM. Chemosphere 2004a. (Erratum in: Toxicol Sci 2004. Miller JP. Stanton ME. Mar Pollut Bull 2005. A global survey of perfluorinated acids in oceans. Grey BE. Biochim Biophys Acta 1993. Lau C. Mandel JH. Dietary exposure of Canadians to perfluorinated carboxylates and perfluorooctane sulfonate via consumption of meat. Washington. Preliminary Risk Assessment of the Developmental Toxicity Associated with Exposure to Perfluorooctanoic Acid and its Salts. Larson EB. Available from URL: http://www. Yamashita N. Toxicol Sci 2003.74(2):382-392. Epidemiologic assessment of worker serum perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) concentrations and medical surveillance examinations.55:3203-3210. Ehresman DJ. Thomford PJ. Mair DC.40(1):32-44. Buck RC. et al. Yamashita N. Induction of triglyceride accumulation in the liver of rats by perfluorinated fatty acids with different carbon chain lengths: comparison with induction of peroxisomal betaoxidation. Seacat AM. et al. Hansen KJ. Environ Sci Technol 2003. Lundberg JK. fish. fish. Pepper K. Mandel JH. Olsen GW. Ellefson ME. et al. Olsen GW.) Tittlemier SA. Subchronic toxicity studies on perfluorooctanesulfonate potassium salt in cynomolgus monkeys.45(3):260-270. Serum perfluorooctane sulfonate and hepatic and lipid clinical chemistry tests in fluorochemical production employees. Mandel JH. Helzlsouer KJ. Nesbit DJ. 2003a. Olsen GW. Environ Health Perspect 2005. Historical comparison of perfluorooctanesulfonate. Gamo T.37(12):2634-2639. Butenhoff JL. Olsen GW. fast foods. Serum concentrations of perfluorooctanesulfonate and other fluorochemicals in an elderly population from Seattle. Lundberg JK. The developmental toxicity of perfluoroalkyl acids and their derivatives. Hansen KJ. Butenhoff JL. Hansen KJ. Burris JM. 2007a. II: postnatal evaluation. et al. van Belle G. 1/15/06 Vanden Heuvel JP.111(16):1900) Olsen GW. Toxicol Sci 2002. Church TR. Church TR. Hanari N. Richards JH. Olsen GW. Olsen GW. Barbee BD. Taniyasu S. Butenhoff JL.S.74(2):369-381. Environ Sci Technol 2006. fate and transport of perfluorocarboxylates.. Taniyasu S. U. Burris JM.

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

4/20/09 Agency for Toxic Substances and Disease Registry (ATSDR). Part Q: Phthalate Esters. 2003. Population estimates of concentrations of specific phthalate metabolites may differ by age. effects that may be mediated by inhibiting testicular and ovarian steroidogenesis. ovarian abnormalities in the female animals (Jarfelt et al. phthalates have been shown to induce peroxisomal proliferation in rodents. Sauer MJ.. Springer... High doses of di2-ethylhexyl phthalate (DEHP). McKee et al..3. testicular atrophy.cdc.niehs. Albro PW and Lavenhar SR.gov/toxprofiles/ tp135. Assessment of critical exposure pathways.805:49-56.cdc. Dave M. 2004.. Cousins IT. Evaluation of a recombinant yeast cell estrogen screening assay.. 2005). Calafat AM. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. at very high levels. but similar findings were not present in young Swedish men with comparable or higher median levels of urinary metabolites (Jonsson et al.nih. 4/20/09 Albro PW. Mackay D. Toxicological profile for di(2-ethylhexyl)phthalate update [online]. 2007. 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. 1982. Silva MJ. 2001.html.atsdr. Vol.e. 2006). Castle L. 2003. 1982). Environ Health Perspect 1982. interactions with macromolecules and species differences in metabolism of DEHP. atsdr. 2001. McDonnell DP. 2000b.gov/toxpro2. 2004). Information about external exposure (i. Drug Metab Rev 1989. Variation occurs from person to person in the proportions or amounts of a metabolite excreted after similar doses (Anderson et al. Hauser et al. Dirven HA.html. and race/ethnicity (Silva et al. van der Broek PH.. Schroeder JL.cdc. Peck and Albro. Lovekamp-Swan and Davis. References Agency for Toxic Substances and Disease Registry (ATSDR). Matthews HB. efficiency of intestinal absorption. Biomonitoring Information Urinary levels of phthalate metabolites reflect recent exposure to the parent phthalate diester. Hoppin et al. and benzylbutyl phthalate (BzBP) during the fetal period produced lowered testosterone levels. at higher doses.gov/ reports/index. variation also occurs in the same person during repetitive monitoring (Fromme et al. 2000a.New York.. and extent of metabolite conjugation to glucuronide (Albro et al. Jordan S. 2001).. 1985. However. 2002). 2006). Also. 2007).18(12):10681074. peroxisomal proliferation may not be a relevant pathway in humans (Rusyn et al.html. Available at URL: http://www. Food Addit Contam 2001.html). The Handbook of Environmental Chemistry. and Sertoli cell abnormalities in the male animals and. 2004.21:13-34. Toxicological profile for di-n-butyl phthalate update [online]. 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. The proportions of each metabolite for a given phthalate may vary by differing routes of exposure (Liss et al. In Staples CA (ed). Determination of four metabolites of the plasticizer di (2-ethylhexyl) phthalate Fourth National Report on Human Exposure to Environmental Chemicals 259 .. but there are known species-related differences in the hydrolysis of diester phthalates.atsdr. which may be a pathway to the development of liver toxicity and cancers in these animals. Slakman AR. Herbert AR. Metabolism of di(2-ethylhexyl) phthalate. In animals. A biomarker approach to measuring human dietary exposure to certain phthalate diesters... reducing estrogen production. 2004. Environ Health Perspect 1997. Corbett JT. pp. environmental levels) and health effects is also available for some phthalates from ATSDR at: http://www.. 105:734-742. Kessler et al. Needham LL. 1986). Silvapathasundaram S. 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.. Automated solid phase extraction and quantitative analysis of human milk for 13 phthalate metabolites. Scotter MJ. Clark K. Jongeneelen FJ. 2005. Massey RC. dibutyl phthalate (DBP). Hauser et al. NTP-CERHR.gov/ toxprofiles/tp9. Connor C. Coldham NG. gender. 227-262. Phthalate urinary metabolite levels in men evaluated at an infertility clinic were associated with several measures of sperm function and morphology (Duty et al. Rhodes et al. The monoester metabolites are thought to mediate toxic effects for some of the phthalates.. 2000c. J Chromatogr B 2004. Pharmacokinetics. Anderson WA.45:19-25. Available at URL: http://www. 2004. Springall C. 2002. These differences may contribute to species-specific differences in toxicity (ATSDR. 2002)..Phthalates and metabolites have been tested. phthalates produced anti-androgenic effects by reducing testosterone production and.

Mechanisms of phthalate ester toxicity in the female reproductive system. McKee RH. Fromme H. White R. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Meeker JD.nih.niehs. 2006 [online]. Kano K. Calafat AM. Yoshimura M.46(11):643-647. NTP-CERHR. Ladefoged O. Estimation of estrogenic and anti-estrogenic activities of some phthalate diesters and monoesters by MCF-7 cell proliferation assay in vitro.195:142-153. Blood burden of di(2-ethylhexylphthalate (DEHP) and its primary metabolite mono(2-ethylhexyl) phthalate (MEHP) in pregnant and non-pregnant rats and marmosets.nih. Int J Hyg Environ Health 2007. A variety of environmentally persistent chemicals including some phthalate plasticizers are weakly estrogenic. Hauser R.html. Liss GM. Tsukino H. Milligan SR. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Main KM. Csanády G. Anal Bioanal Chem 2005. 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Monograph on the Potential Human Reproductive and Developmental Effects of Din-Butyl Phthalate (DBP). Filser J. Brock JW. 2000a [online]. Ryan L. 6/2/09 Okubo T. Urine phthalate determinations as an index of occupational exposure to phthalic anhydride and di (2-ethylhexyl) phthalate. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. Urinary phthalate metabolites and biomarkers of reproductive function in young men. et al. Singh NP. Toxicol Appl Pharmacol 2004. Chahoud I. Jarfelt K. 2000c [online]. Akesson B. Brock JW. Park MG.112(17):1740]. Research Triangle Park (NC).18(1):122.19(4):505-515.11(5):381-387.105:802-811. Research Triangle Park (NC).gov/ chemicals/phthalates/bb-phthalate/bbp-eval. Reynolds T. Duty SM. Occurrence and daily variation of phthalate metabolites in the urine of an adult population. 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1-90.S.1 (13.2 (14.1-16. 01-02.8-72.3-18.9-62.5-14.3) 37.4-24.0-85.1) 76.2) 13.3) 63.9-190) 86.7-35.6) 13.2-20.8 (50.3 (29.6 (13.5-35.9 (11.7-16.0 (30.2-31.5 (76.9) 18.4) 35.1) 12.8) 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. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.9 (22.6) 95th 103 (94.1) 14.4 (32.8 (71.3 (44.8-35.5-97.2) 32.4) 108 (96. BzBP can be released into the environment during its production and.4) 14.S.5) 15.8) 24. 262 Fourth National Report on Human Exposure to Environmental Chemicals .7-17.2-17.0 (26.6) 15. including MBzP.3) 94.0) 20.7) 40.0-26.2) 15.8 (71.5 (26.6) 35.1-214) 166 (116-191) 145 (110-213) 88.3.4) 81.2-115) 113 (91.7-13.6 (53.8 (10.1) 32.4) 65.3-43.1 (10.9-87.9-30.6) 35.6 (12.4) 51.5 (57.8-13.5-36. and 2003-2004 were generally similar those reported in U.1 (55.6 (32.9 (16.6 (13.0-106) 58.2-116) 122 (102-143) 101 (84.2 (19.4 (32.4) 38.8-64. NTPCERHR.5 (67.1-116) 122 (93.8-16.1.5-62. 2000).3) 15.3 (12.9-14.1 (20.6) 29.2-16.1-18.8 (12.1-15.4-62.0 (23.2-16.8.6-92.3 (54.9 (12.6) 14.3-34.4-127) 80.7-119) 99.7 (51.9 (70.6-132) 103 (84. Biomonitoring Information The median levels of MBzP in NHANES subsamples from 1999-2000.9) 13.0) 32.7-170) 169 (134-198) 152 (99.6 (66.2) 14. interval) 15. see Data Analysis section) for Survey years 99-00.9 (28. population from the National Health and Nutrition Examination Survey.6-79.5-84. and diet is the major source for general population exposure.8-76. High dose BzBP and its monoester metabolites.8) 14.5-25.1) 68.9) 15.4) 98.7-16.6) 25.1 (32.4 (59.5-18.8 (38.7-15.7) 38. 2001-2002.5-94. People exposed to BzBP will excrete mono-benzyl phthalate (MBzP) and small amounts of mono-n-butyl phthalate in their urine.5) 27.4) 75th 35.7 (11.4 (68.3) 13.6-17.6-116) 122 (102-142) 101 (85.5) 55.4-25.1-39.1-61.1-38.8 (86.2-39..6 (13.3-130) 122 (88.9 (12.9) 14.5) 23.3 (29.4 (27.7-16.4 (10.3 (12.2-40.8-133) 89.8-14.0 (11.2 (10.1-35.1-15.0) 24.2) 22.9) 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 39.9 (39.6) 24.4) 12.6-43. it can be released into the ambient air during use or disposal of the products.4) 33.5 (61.6-38. some personal care products.3 (30.6) 13.3) 13.9) 49.8-121) 79.8) 33. sealants. can produce developmental and reproductive toxicity in rodents.3-125) Total 15.4 (13.2) 12.2 (43.7-82.5 (27. because it is not bound to products in which it is incorporated.3 (12.0 (43.5 (47.0 (30.0) 34.2 (19.5) 65. and 03-04 are 0.1-16.4-16.6) 50.2) 78.2) 17.9) 43.4 (53.9) 14.9-27.2-19.2) 14.6 (13.9 (21.8 (80.3-122) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.0-130) 101 (86.6-29.4) 71.7-14.0 (33.2-183) 101 (78.9 (13.7 (80. 2004.5) 214 (108-399) 235 (183-330) 255 (146-365) 125 (93.4) 49.3-21.2 (25.2) 66.9) 11.3-74.0-55.2-38.0 (55.4 (31.2 (47.6-92.1 (14.0) 33.1) 67.1) 29.0 (20.8 (14.8-16.7-172) 103 (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 13.5-33.3-82.8 (28.3) 54.3-161) 99.5 (55.5-36.8-41.7-25.4) 129 (98.7) 23. particularly male animals (McKee et al.5) 82.7 (82. residents (Blount et al.4 (29.1) Selected percentiles ( 95% confidence interval) 50th 17.8 (21.7 (70.2) 33.2-155) 91.1 (14.1 (19.8-98.9) 12.3-18.9-47.9-49. in a small sample of pregnant women in New Urinary Mono-benzyl phthalate (MBzP) Metabolite of Benzylbutyl phthalate (BzBP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.6) 14.0 (15.6) 67.0 (27.5-40.0 (15.0 (34.8 (53.4-15.6-72.3-75.7-58.6) 16.5-41. 85-68-7 General Information Benzylbutyl phthalate (BzBP) is a solvent and additive used in products such as adhesives.0) 70.7 (53.0) 23.5) 15.8) 28.1-43. 0.8-17..1) 31.5-145) 138 (106-241) 143 (127-179) 120 (99.4-92.5) 16. and to a lesser extent.6) 37. IARC considers BzBP not classifiable with respect to human carcinogenicity.6 (41.4) 80.2) 69.9-16.0) 90th 67.7 (15.0 (12.2 (11.8-14. vinyl tile.3-12.3-27.8-48.7 (13.9-28. Food crops take up BzBP.4 (53. 2000).8-17.2-33.1) 13.6-18.7 (12.6-39.4) 35.3 (22.5) 30.3 (13.6 (21.4 (48.3-91.5 (13.0 (14. and 0.3 (33.6) 63.3-88.4 (10.6-150) 94.1-120) 52.0) 16.1 (13.8-18.4 (63.8 (30. respectively.Phthalates Benzylbutyl Phthalate CAS No. car care products.5 (66.3) 23.8) 63.1 (58.

0 (41.1) 35.4 (12. 2004.8) 71.1) 17.2) 11.7) Sample size 2541 2782 2605 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 40. 2005.8 (13. Finding a measurable amount of MBzP in the urine does not mean that the levels of MBzP or the parent compound cause an adverse health effect.4-18.0-48.1 (18.9-62.3) 13.9-14. 2005).5) 14.5) 78.5 (48.4) 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 12.1 (46.4-142) 134 (116-176) 136 (85.2-21. and females compared to males (Silva et al.5-23.8) 68.3) 13.3) 90.4 (63.6) 25.8) 54.2) 12.7) 56.2) 11.5) 46.0 (12.8-14.8 (50.1-125) 86.6-15.1-58.2) 67. In an annual sample of German university students.7 (54.5) 17.6 (30.5-29.6-47.8-69.9 (24.9) Total 14.8) 56.9 (54.6 (14.4) 13.5-213) 49.1) 80.7 (11.3) 14.4) 14.6) 53.5-13.1 (9.5) 41.9) 100 (80. the adjusted geometric mean levels of urinary MBzP were significantly higher in several subgroups: children compared to adolescents and adults.3 (24.0 (49..69-11.0-51..8 (30.7-56.8) 33.4-14.2-78.8-16.7) 46.9-13.1) 24.2-15.5 (42.3 (13. A small study of African-American women in Washington.4-93.3 (60. Biomonitoring studies on levels of urinary MBzP provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of BzBP than are found in the general population.1-29.9-83.8 (57.6-86.8 (69.3) 89..3) 55.2-15.5-31.3-34.2) 32.6-99.1) 27.8) 15.7-15.8 (10.7) 25.8-64.0 (12.9 (29.2 (69.1 (53.8) 53. 2002.7) 19.1 (21.2-17.4 (33.3 (35.6) 75th 25.4 (10. 2003).5-61.5-76.6) 12.8) 16.5 (10.7) 38.6) 38.3) 14.8) 26.6) 58.9) 12..8-60.7 (12.6 (51.1-12.4 (46.5 (56.4 (34.1 (19.6-26.5) 23.2-26.0) 15.3) 18.9-115) 57.8 (46.5) 10.9) 11.4 (11.6-116) 74.0 (67.4-19.1-14. median urine levels of MBzP were about one-half the median levels in NHANES subsamples from 1999-2002 (Wittassek et al.6 (36.6 (11.0-27.6) 13.5) 95th 77.8-39.8-13.7 (11.9 (22.9 (10.9 (55.6 (24.4-14.3-16.4-99.7 (23.7 (14.6) 30.7 (55.9 (10.2-51..7-19.4) 15.7 (13.6 (11.S.4 (26.7 (59.8-34.8-173) 195 (121-305) 229 (99.2) 11.Phthalates York City (Adibi et al.8) 13. 2007).4 (25. 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.8-85.5-99.9) 12. adolescents compared with adults.4) 17.0 (33. 2007).3 (23.0 (41.3) 12.9 (15.5-79.1 (15.6-12.8) 108 (75. in men attending a Boston infertility clinic (Duty et al.0 (38.3-64.3) 21.3 (38.5-26.7 (21.3) 13.3 (15.9-13.5-58.1-27.4-90.9 (51.1 (21.0-53.7-31.4-116) 73.5-16.9 (39.0 (10.5) 13.1 (21.4 (69.4-79.2) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 12.1 (41.1-79.5-38.6-13.3) 67. Hauser et al.8 (64.6-40. and in a small sample of German residents (Koch et al.9 (15.7-15.9-40.4) 21.8 (11.8 (49.9) 52.0) 24..7-14.0 (62.1 (14.9) 64.1) 23.6 (19.5) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Fourth National Report on Human Exposure to Environmental Chemicals 263 .5-57.6) 12.5 (12.9 (9.8) 53..9 (12. DC reported median urinary MBzP levels that were about twice the levels of adults and females reported in NHANES 1999-2002 (CDC.7-397) 70.4 (11.9-69.1) 24.5 (11.1 (13.7 (13.4-27.2-57.5-42.5) 16.6 (22.3) 29.0) 11.4) 25.5) 20.8) 24.7-20.9) 24.1 (13.8-42.7 (11. 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.4 (13. Hoppin et al.73-12..5 (9.8-27.9-16.8) 46.9) 11.2 (40.2 (27.6-20.0) Selected percentiles ( 95% confidence interval) 50th 13.9-23.7-12.4-42.0) 49.2-117) 95.6-81.3 (39.4) 28.4) 51.1) 142 (99.3) 73.4) 12.4-23.0) 60.4) 60.3) 37.6 (30.5-58.5 (49.5-26.7) 11.2-49.4) 104 (89.9 (24.1) 39.8-48.4 (21.1 (34.1-35. in young Swedish men (Jonsson et al.8-13.3) 16.2 (56.4 (74.7-20. interval) 14.2) 26.2-13.2-13.4 (11.8) 11.7-19.8) 34.4-17..1 (21.7-14.9) 42.8-15.9) 12. 2006).1-120) 77.5 (10.4) 50.2-12.4-15.4-60.0) 24. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.0 (13.6) 73.6 (34.8-15.1 (25..7-69.3-11.4-102) 70.95-14. 2002). 2003). 2004).7 (18.9-104) 62.1) 12.1 (11.0-109) 65.0-26.4 (60.7-123) 77.7-29.8) 80.4) 13. In NHANES 1999-2000.3) 36.0) 12.7 (19.1-12.5 (35.7-61.9 (43.8-14.8 (12. Weuve et al.2 (41.3 (12. population from the National Health and Nutrition Examination Survey.7 (38. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.6 (11.6 (15.3-73.9 (12.3-38.6 (57.7-90.1 (23.9-28.2) 15.8-13.0-90.4) 44.8-80.0) 13.4) 90th 50.8) 33.0-15.1 (43.0 (11.

et al. Epidemiol 2005. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Sanchez GN. Barr D. Brock JW. et al.210(3-4):319-333. 264 Fourth National Report on Human Exposure to Environmental Chemicals .16(4):487-493. Hauser R. Wittassek M. et al. 2005. Hilborn ED. Hoppin JA.112(3):331-338. McKee RH. Phthalate monoesters levels in the urine of young children. Meeker JD. Hodge CC. Hagmar L.108(10):979-982. Needham LL. Ryan L.Phthalates References Adibi JJ. Environ Health Perspect 2003. Environ Health Perspect 2004. Needham LL. Blount BC. Barr DB. Internal phthalate exposure over the last two decades—a retrospective human biomonitoring study. Reprod Toxicol 2004. Centers for Disease Control and Prevention (CDC). Chen Z. Eckard R. Bull Environ Contam Toxicol 2002. Brock JW.nih. Levels of seven urinary phthalate metabolites in a human reference population. J Androl 2004. Prenatal exposures to phthalates among women in New York City and Krakow. Poland. Calafat AM. Environ Health Perspect 2006. Calafat AM.110(5):515-518. et al. NTP-CERHR. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. Hum Reprod 2007. Reproducibility of urinary phthalate metabolites in first morning urine samples. Jacek R. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. Third National Report on Human Exposure to Environmental Chemicals. Caudill SP. Caudill SP. Hu H. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. Environ Health Perspect 2000. Wiesmuller GA. Gans G.gov/ chemicals/phthalates/bb-phthalate/bbp-eval. Jedrychowski W. 2000 [online].111(14):1719-1722.68:309-314. Available at URL: http://cerhr. et al. Jonsson BAG. Duty S. 4/20/09 Silva MJ. Giwercman A. Monograph on the Potential Human Reproductive and Developmental Effects of Butyl Benzyl Phthalate (BBP). Davis BJ. Baird DD. Int J Hyg Environ Health 2007. Sampson EJ. Silva MJ. Duty SM. Koch HM. et al.114(9):1424-1431. Exposure to phthalates in neonatal intensive care unit infants: urinary concentrations of monoesters and oxidative metabolites. Rossbach B. Angerer J. Koch HM.niehs. Urinary phthalate metabolites and biomarkers of reproductive function in young men. Schettler T.18(1):122. Helm D.22(3):688-695. Weuve J. Malek NA.S. 112(5):A270]. Caudill SP. et al. Singh NP. Drexler H. Reidy JA.25(2):293-302. Silva MJ. David RM. Rylander L. Green RA. Atlanta (GA). National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction.93:177-185. Camann DE. Pirkle JL. Dobler L. Urinary levels of seven phthalate metabolites in the U. Environ Health Perspect 2002. Richthoff J. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Silva MJ. Brock JW. Perera FP.html. Silva MJ. Environ Res 2003. Research Triangle Park (NC). Butala JH. Ryan L.

pharmaceutical coatings.9) 15.7) 14. 2007).73 (2.90 (4.1-12.7 (7.5 (17.40 (3. in a small sample of pregnant women in New York City (Adibi et al.82-3.8) 40. referred to as DBP) are industrial solvents or additives used in many personal care products such as nail polish and cosmetics.70) 5.0) 1371 1250 1411 1355 01-02 03-04 01-02 03-04 01-02 03-04 3..50) 8.60 (4.00-11.5) 18.. Compared with the median for 6 to 11 year olds in NHANES 1999-2004 (CDC.22) 3.55 (3.4-12.10) 8.5 (10.3) 33.43) 6.5-16.50 (3. DBP can produce reproductive toxicity in male rodents (McKee et al.0 (13.00) 6.0 (13.71 (2.S.26 (2. interval) 2. Hauser et al.46) 2.7) 15.97) 2. CDC.6 (29.7 (16.80 (5.1) 22.6 (9.40-3.70) 3. about 65% to 80% of a dose is eliminated in urine within 24 hours.6-34.2 (11.56 (3.6 (13. 2003).85-6.3-24.1 (8.8 (9. 2004.20) 4.3-19.2-22.70 (2.20-9.60 (2.6 (14.56 (5.3.30) 10.40-5.30) 5.S.72-3.3-20.1-25. Small amounts of mono-3-carboxypropyl phthalate are also produced from di-n-butyl phthalate.50-2.00) 7. Median MBP levels in two European studies were about two to six times higher than median levels in this Report (Jonsson et al.3 (13.7) 7.37) 6.6) 12.6 (11.20 (7. 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.7 (17. 2000.50) 5.28-5.48 (2..Phthalates Di-n-butyl Phthalate CAS No.94) Selected percentiles ( 95% confidence interval) Sample 95th 17.80-5. 2004.6) 10.80 (2.50-4.6-20.3 (11.66) 2.50) 18.9 (16. Survey Geometric mean (95% conf.0) 9.30 (4.22 (3.40-4.07 (3.0-25.3-48.59) 3. and insecticides.00-9.6 (13.40 (6.0) 24. 2005). exposure to benzylbutyl phthalate (BzBP) will also result in small amounts of mono-n-butyl phthalate appearing in the urine.6) 26.50 (6. Biomonitoring Information Median concentrations reported in the NHANES 19992000.30) 10.97) 4.30-3.8) 677 652 703 699 1216 1088 Limit of detection (LOD. residents (Blount et al.10) 3. People exposed to dibutyl phthalates will excrete mono-n-butyl phthalate (MnBP) and mono-isobutyl phthalate (MiBP) in their urine.9-23.0-18.0) 13.80 (5.46 (2.20-12.20-6.40 (7.30-6.30-6.6) 16.6) 17. population from the National Health and Nutrition Examination Survey.6-18.1-17.0) 20.3 (18.30-7.90-7.5-29.7-18.17 (2.19-3. mostly as MnBP (Anderson et al.80) 75th 5.40-17.56) 3.2-14.10) 11.10) 9.40-9. 2001).20-12. 2005).02) 4.10) 2.70-4. 2005.9 (16.1 (13. Fourth National Report on Human Exposure to Environmental Chemicals 265 .4) 22.60 (8.7 (9.30 (3.30-13.0-38. 2003).50) 7.90-2. and also in some printing inks.00-4.3-18.46 (3.56-4.0 (19.0 and 0.33 (2.9) 10..50) 2.30-2.10-9.68 (2. NTP-CERHR.0) 12.20-2.46-5. 2001-2002 and 2003-2004 subsamples were similar to MBP levels reported in U.97-7.80 (3. they have been referred to as monobutyl phthalate (MBP).. Studies of children found age-related differences in urine MBP levels.60) 3. In addition.20 (6.49-2.8) 21. NIOSH and ACGIH have established guidelines for workplace air exposure to di-n-butyl phthalate.3 (13.5-24.40-4.7-31.90-4.00) 4.11-3.7 (18.90-4.9-14.44-2.3 (19.0 (11.30) 2.00) 4.5) 12.5) 22.3) 3.7) 4.91) 4.20) 7.25) 01-02 03-04 01-02 03-04 01-02 03-04 4.10-2.5 (27.67 (5.5) 19.4 (20.00) 10.3) 18. Neither IARC nor NTP has evaluated dibutyl phthalates with respect to human carcinogenicity.10 (4.80 (2. Koch et al. see Data Analysis section) for Survey years 01-02 and 03-04 are 1.60-6. in men attending a Boston infertility clinic (Duty et al.6 (10.70-4.6 (10.00-6.40-3.7-31.1) 16..63) 3. When total DBP metabolites have been measured.73-5.6-26.40-12.0) 393 342 742 729 1647 1534 01-02 03-04 01-02 03-04 2.6 (14.3-43.84) 4.4) 12.50-10.90 (4.6) 17.96) 3.2-33.30 (1.50) 90th 12. 2000). and in a small sample of Japanese adults (Itoh et al.00-6.70-8.70 (5.1-20.0-14.00 (7.90 (3.1) 25.2 (8.00 (5. OSHA has established a workplace air standard for external exposure to DBP.81 (3.2) 5. Following oral administration of DBP to humans..30-11.5 (11.5) 23.40 (2.5 (20.10-9.20 (3.7 (17. 84-69-5 General Information Dibutyl phthalates (both di-n-butyl and di-isobutyl phthalates.3-30.30) 6.5) 25. 2005).24-8.10 (3.4) 5.17) 4.90 (6.5) 14.10 (4.4 (14.7-20.0) 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 2.55) 2.80-5.60 (5. 84-74-2 Di-isobutyl Phthalate CAS No.7) 18.5) 18.90) 12.3 (16...3 (16.6-14.4-27.5-16.40) 5.50-6.2 (12.6) 16.40 (2.

17-12.52-20.08-2.28-13.95) 10.94) 6.64-10.78) 8.2-13.1) 11. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.82) 4.32 (3. to about two to fourfold higher (Fromme et al. 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. 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.38 (6.03-7.56-4.5 (11.6) 11.61-3.0 (12.51) 2.95-3.7) 19.21 (5.95) 2.1) 677 652 703 699 1216 1088 266 Fourth National Report on Human Exposure to Environmental Chemicals .33) 3.0) 3.83 (2.68) 3.1 (11.9-26.related differences in the adjusted geometric mean levels of urinary MiBP and MnBP (CDC.32) 7. 2005). Studies measuring urinary MnBP have reported variable median values compared to the NHANES 2001-2002 and 2003-2004 subsamples.97-2.5) 13. An analysis of NHANES 2001-2002 showed similar age.. up to four and 13 fold.39-3.43) 3.81) 9.13-6.84 (8.0) 15.78-8.18-10.81) 4.74-3.2) 24.58-3.33 (3.20 (2.81 (6.31) 2.Phthalates for neonates was lower (by about half) and the median for toddlers was higher (by about sixfold) (Brock et al.7 (11.00-3.73 (5.2-15.8 (8.0-18.86-4. 2005)..80-3.7) 10.51) 15.3 (17.8 (9.38-10.1) 4.27-12.6 (10.1-24.17) 90th 8.1-12.68 (2.13 (2.84 (4.35) 3.68) 5.6 (15.85 (2.25) 5.7-28. samples from German university students had consistently higher median urine levels of MnBP and MiBP.04) 7.9 (15.18) 3.18 (4.56) 2.11 (5.76-3.20-2.39) 5.3) 28. 2002.18) 4.7) 1371 1250 1411 1355 01-02 03-04 01-02 03-04 01-02 03-04 3.33-9. ranging from more than one-tenth the NHANES median (Itoh et al. In an analysis of NHANES 1999-2000.30 (6.1) 13.41 (2.8-36.66 (8. Differences in urinary MBP population estimates by gender have also been shown (Silva et al.52-3.76-15.47-12.43) 3.62-12.53-3.79-6.54) 2.18-4. than adults in NHANES subsamples during the same time period.51) 5.4) 7.54 (2.9) 12.82 (4.80) 7.46) 3.5 (9.8-13.53-4.00-7.43) 3.19 (2.89-5.81 (3.75 (4.2 (11.2) 8.89 (3.78) 9.9 (11.69 (2..99-4. Weuve et al.67-5.8) 10. Biomonitoring studies on levels of MnBP and MiBP provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of dibutyl phthalates than are found in the general population.3) 13.58-4.65 (4.47-5.31) 2.52) 3.9-40.7 (9.9 (9.33 (2.66) 2.57 (3. the students’ median values for MiBP levels remained relatively unchanged.46 (2.4 (12..03-11.42) 2.54 (4.44 (3.34 (3.72) 5.30) 2.3) 16.36-2.4-16.24) 3.6-19.94 (5.57 (3.20-4.8-18.69-7.76-3.0) 393 342 742 729 1647 1534 01-02 03-04 01-02 03-04 2.65-4.32 (7.6 (9.01-2. population from the National Health and Nutrition Examination Survey.00) 01-02 03-04 01-02 03-04 01-02 03-04 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 2.29-8.8-18.7 (13. 2004).65-11.20 (2.20 (7.1-25. 2004).86) 6.04) 3.31 (2.47 (3.56) 5..45) 3.02 (7.0 (10. Between 1998 and 2003.2) 9.91-6. Survey Geometric mean (95% conf. 2006).00-3.79 (4.05) 2.S.80 (3.14 (4. the adjusted geometric mean levels of urinary MBP were significantly higher in children aged 6 to 11 years than in either adolescents or adults (Silva et al.07-5.89) 6.2 (10.and gender.76 (3.11) 5.73) Selected percentiles ( 95% confidence interval) Sample 95th 12.99) 7.8 (10.59 (4. Over this time.10-5..1 (10.17 (2. while MnBP declined (Wittassek et al.66) 10.31 (7.6-19.07 (2.20-3.0) 7.6 (8. 2007).69) 6.46-11.08) 75th 4.7) 3.11-2.7 (21.56-15.5) 15.6) 13.03 (5.29-3.53-5. 2007).1) 15.22 (2.64-7.00 (3.94-12.15-4.9-16.72-7.36-7.02-10.92 (7.1) 7.28 (4.3) 18.75 (6.21) 10.64-7.66) 4.69) 4.15) 3.37) 3.6 (8.26-2. respectively.96 (3.55-6.79-8.74 (4.88 (2.4) 15..1-15.93-6.1) 10.57-4.52 (2. interval) 2.98 (2.6 (12.5-19.18 (1.3 (13.3) 13.26 (2.0 (8.62 (6.4) 23.0) 11.04-5.7) 11.09-2.

5) 36.1) 47.9) 46.5 (29.7-26.6-24.1 (62.6-44.0) 30.5) 17.7 (64.8-119) 90.9) 26.2 (78.6 (32.4-20.4 (38.8) 58.9-28.2-33.9) 21.5-43.2) 20.9 (17.5) 24.9-22.5) 26.5) 47.9-22.4 (36.6) 38.4 (19. interval) 24.1-122) 122 (104-137) size 2541 2782 2605 Total years 99-00* 01-02 03-04 50th 26.6) 20.0-24.4 (35.3 (42.9) 75.5-47.0-32.6-69.1) 46.1) 36.2-93.1) 25.3) 40.4) 20. *In the 1999-2000 survey period.6) 166 (127-279) 159 (110-290) 191 (150-243) 165 (121-227) 148 (106-185) 134 (110-158) 143 (117-161) 95.6 (55.3-24.7 (19.6) 39.0 (25.6) 35.6 (16.2-32.3 (37.1-80.8-123) 101 (90.1-82.6-29.7) 52.0 (72.5-47.9 (79.1-27.5-60.1) 23.2) 68.2) 42.0 (36.9) 18.6-31.1) 23. see Data Analysis section) for survey years 99-00.0 (20.0 (31.9-101) 77.6-48.4 (35.4 (25.4) 22.7-121) 97.4 (23.1-29.1.2-23.7-91.4 (35.1 (19.3-21.2 (18.0-19.4-26.3) 23.2) 62.2-49.2) 38.2-63.9 (20.0) 27.3) 19.0 (30.6-29.2 (59. and 03-04 are 0.8) 62.7 (33.8) 75th 51. respectively.5) 37. Fourth National Report on Human Exposure to Environmental Chemicals 267 .9-87.1 (18.1) 20.6 (26.8) 43.9-92.5) 34.4-42.0 (23.3) 21.7-124) 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.8-22.2 (74.5) 85.3 (51.5) Age group 6-11 years 99-00* 01-02 03-04 99-00* 01-02 03-04 41.2-22.5-121) 106 (94.7-117) 118 (108-143) 93.1 (16.3 (23.2-24.7 (28.0-19.9-33.8-111) 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 23.3-79. 1.5) 36.2) 90th 98. and 0.5 (30.2-87.7 (18.9) 71.7 (70.1-51.1-22.8 (57.7) 74.6-37.3-96.6 (65.4 (35.3 (23.5 (28.0-26.5 (74.2 (58.0) 38.2 (21.7) 124 (98.2 (75.7-106) 69.2 (25.7-92.0-73.7) 28.1 (36.8-42.4) 59.6 (48.1 (58.2-21.2 (21.7 (16.9) 29.3) 26.7 (22.7) 92.4 (72.7 (51.4-44.4) Selected percentiles ( 95% confidence interval) Sample 95th 150 (121-169) 108 (94.8) 23.3-60.6) 46.9-53.4-18.5) 31.7-53.1-20.8-165) 167 (143-197) 138 (110-184) 144 (115-168) 142 (111-161) 107 (89. Survey Geometric mean (95% conf.0 (78.3) 18. 01-02.4 (84.7 (18.2) 32.6) 80.4-25.6 (61.3) 36.8-29.4) 52.2-159) 92.5) 78.3 (17.2-56.6) 17.1 (34.4-159) 107 (84.1) 19.5-53.3 (30.1 (26.1 (31.0-21.5-117) 95.1-24.1 (54.6-143) 127 (99.1 (19.7 (24.0) 20.2) 26.3-85.7 (38.1-75.6) 21.1 (51.5) 21.0) 120 (98.5-44.5) 40.1) 31.5) 95.5) 65.1 (19.7) 42.4-31.0 (18.0 (17.0 (15.3 (56.3 (36.5-27.6 (19.6 (90.0) 84.3-67.7-42.1 (19.7 (43.3) 24.1 (28.7-111) 64.6-113) 108 (90.1) 30.6-20.7-34.8) 48.7-24.0) 117 (104-131) 112 (84.1-92.7-20.2 (79.4) 64.9 (79. referred to as monobutyl phthalate (MBP).3 (30.6-40.7-34.S.8) 19.3-76.0 (45.1 (21.0-24.4.9) 36.5-42.0) 31.3-136) 137 (107-162) 119 (90.9.5) 20.6) 71.7-116) 95.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.2-114) 73.1) 17.9-42.3-145) 85.0-51.1 (17.4-60.4 (71.6-49.1 (41.9-114) 116 (97.2 (19.6 (22.7-42.6 (44.4 (21.1) 23.3-40. concentrations of mono-isobutyl phthalate and mono-n-butyl phthalate were measured together and expressed as a combined value. population from the National Health and Nutrition Examination Survey.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 22.8 (19.8-132) 95.8-25.5 (59.0-58.3 (60.6-33.0) 21.9 (17.5 (59.9-79.2 (20.5) 19.2 (17.6-36.

1) 61.4 (16.2) 31.5) 60.8) 19.2) 74.4) 62.4 (19.7-80.9-36.6 (74.3) 18.7-19.6-26.0) 19.5-23.6-155) 91.3-71.9 (64.0-47.5-21.1) 21.6 (27.6 (17.4) 21.9 (21.9 (16.9-26.6 (29.1-32.7 (12.6-42.0-75.1-83.4-47.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.4-103) 117 (83.9-56.3-18.1 (29.6) 31.7) 42.0-90.0 (61.5 (14.3) 17.5-76.1) 42.2-27.0 (16.0 (18.7-39.4) 19.3 (55.3 (71.7 (20.4 (47.3) 35.3 (52.2-106) 64.2) 59.5 (64.3 (17.8) 22.9) 49.9) 91.6) 83.0-38.0) 108 (71.9) 20.0) 35.8) 20.9-68.7-78.7 (60.9 (56.4 (45.3 (69.6-28.8) 34.0) 28.6-24.5 (18.4 (20.2-18.1 (61.2-73.8) 23.6-44.1-128) 97.3-21.0) 75.6-128) 96.2-179) 84.2 (83.4) 15.9 (39.9 (73.3 (28.0 (43.5-22.1 (34.1 (15.3) 52.S.8) 17.8) 35.0) 70.8-235) 137 (108-198) 88.8-43.1 (21.7) 20.4 (18.6-74.7 (60.3) 59.6 (41.1 (56.3-23.4-61.6-23.7-19.5 (18.2) 16.6) 64.3-106) 74.2 (19.1) 17.8) 40.4) 20.9-14.0-92.4 (56.8 (18.6 (61.7-26.4) 16.0) 94.7-42.8-24.6) 37.5-142) 81.9-105) 85.0 (52.8-24.9-84.0 (15.0 (19.8) 17.5-70.9) 28.7 (81.6) 24.1) 20. Survey Geometric mean (95% conf.6 (31.2-86.7) 36.3-38.2 (35.2-61.7) 19. interval) 22.7 (16.5-64.2-108) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites 99-00* 01-02 03-04 *In the 1999-2000 survey period.6-24.0) 59.0-19.9-68.3-49.9 (30.7 (54.3 (17.0) 41.0 (18.4 (31.8) 20.9-34.6-32.6-92.1) 53.3-21.0) 53.3) 19.6-139) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00* 01-02 03-04 99-00* 01-02 03-04 21.4) 53.6) 24.1-18.5) 84.6-27.3 (46.4 (68.6 (72.4) Selected percentiles ( 95% confidence interval) Sample 95th 97.3) 21.8) 63.3) 33.3) 19.0 (50.4-164) 96.4-76.8) 75th 38.3-39.1-115) size 2541 2782 2605 Total years 99-00* 01-02 03-04 50th 21.5) 82.6) 39.6) 23.7-51.9 (35.6-19.0-17.4 (17.8 (22.4-34.8 (50.6) 18.0-60.6) 34.1-23.5 (30.8 (18.4 (31.7 (14.4 (50.3-40.7 (27.3) 20.5) 91.0-113) 104 (83.8-32.2) 21.3-26.7 (28.1) 22.7 (57.9-100) 86.3-32.2-48.1) 44.8 (25.9) 52.6) 65.2-21.2-16.9 (20.0) 81.5) 134 (93.3 (16.3 (60.0 (26.5 (81.5) 17.2) Age group 6-11 years 99-00* 01-02 03-04 99-00* 01-02 03-04 41.2 (16.6-43.5-16.0 (71.6) 38.9) 39.0) 29.9 (30.0 (69.2-22.4 (17.3 (48.8) 28.9 (58.3 (21.2) 65.6-16.3 (52.8 (18.6) 25.8) 34.5-37. concentrations of mono-isobutyl phthalate and mono-n-butyl phthalate were measured together and expressed as a combined value.5-41.7-28.2 (38.0) 55.2) 159 (102-263) 147 (93.6 (25.3-114) 328 393 342 752 742 729 1461 1647 1534 12-19 years 20 years and older 99-00* 01-02 03-04 Gender Males 99-00* 01-02 03-04 99-00* 01-02 03-04 17.5-15.0) 26.1) 35.6-119) 63.4) 15.5-18.6-23.7 (73.8) 13.3 (42.1) 50.2-22.7-23.9 (30.4 (13.6) 14.4-135) 71.7-21.4 (37.4 (16.2-28.7 (43.4 (53.4 (33.1-62.6 (25.1) 20.2-85. 268 Fourth National Report on Human Exposure to Environmental Chemicals .9) 24.7-20.9-49.1 (46.6-44.2-22.0) 25.9 (35.0 (34.5-142) 89.6 (19.8 (17.9 (19.4-65.8 (33.3) 67.4-24.9) 62.9) 14.1 (32.9-38.6-53.9 (37.1-21.0 (70.1-99.4 (50.3) 33.3 (76.8 (16.9) 30.9-70.4-131) 81.1) 37.3 (17.4) 51.5) 39.8) 17.6-22.3-78.4 (23.6-50.2 (19.8 (13.3-81.7-37.1-99. population from the National Health and Nutrition Examination Survey.3-17.6 (57.7 (19.9) 19.3 (19.4 (31.0-41.0 (27.4-72.8 (65.5) 90th 68.3 (24.8) 30.5) 21.8-23.0 (20.5-30.3-20.5 (15.

25(2):293-302. et al. Silva MJ.210(3-4):319-33. Environ Res 2003. Rylander L. 2005.18(12):10681074. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004.16(4):487-493. Itoh H.93:177-185. Epidemiol 2005. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. Koch HM. Calafat AM. Urinary phthalate metabolites and biomarkers of reproductive function in young men.68:309-314.108(10)979-982. et al. Jonsson BAG. Monograph on the Potential Human Reproductive and Developmental Effects of Di-n-Butyl Phthalate (DBP). Anderson WA. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. NTP-CERHR. Brock JW. Third National Report on Human Exposure to Environmental Chemicals. Yoshida K. A biomarker approach to measuring human dietary exposure to certain phthalate diesters. Phthalate monoesters levels in the urine of young children. Springall C. Drexler H. Camann DE. Meeker JD. Eckard R. Duty S. Hilborn ED. Brock JW. Pirkle JL.22(3):688-695.gov/chemicals/ phthalates/dbp/dbp-eval. Sampson EJ. Evaluation of the effect ofa governmental control of human exposure to two phthalates in Japan using a urinary biomarker approach. Ryan L. et al. Needham LL. Centers for Disease Control and Prevention (CDC). Butala JH.18(1):122. Drexler H.114(9):1424-1431. Occurrence and daily variation of phthalate metabolites in the urine of an adult population. Masunaga S. Rossbach B. Chen Z. Angerer J.html. Available at URL: http://cerhr. Schettler T. Environ Health Perspect 2003. Blount BC. Angerer J. Silva MJ. Needham LL. Castle L. Duty SM. Dobler L. Urinary levels of seven phthalate metabolites in the U. et al. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. J Androl 2004. Environ Health Perspect 2004. Green RA. Prenatal exposures to phthalates among women in New York City and Krakow. Barr D. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. Singh NP. Hum Reprod 2007. Scotter MJ. Int J Hyg Environ Health 2005.Phthalates References Adibi JJ. Reidy JA. Gans G. Koch HM. Massey RC.208:237-245. Exposure to phthalates in neonatal intensive care unit infants: urinary concentrations of monoesters and oxidative metabolites. Levels of seven urinary phthalate metabolites in a human reference population. 112(5):A270]. Bolte G. Int J Hyg Environ Health 2007. Environ Health Perspect 2006. et al. Environ Health Perspect 2000. Fromme H. Wittassek M. Wiesmuller GA. Internal phthalate exposure over the last two decades—a retrospective human biomonitoring study. Poland. Caudill SP. Hauser R. Malek NA. Sanchez GN. Richthoff J. Barr DB. Boehmer S. Jacek R. Silva MJ. Weuve J. Perera FP.nih. 2000 [online]. Food Addit Contam 2001.111(14):1719-1722. Reprod Toxicol 2004.210:21-33. David RM. Calafat AM. Hagmar L. Atlanta (GA). Ryan L. Hodge CC.112(3):331-338. 4/20/09 Silva MJ. et al. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Hu H. Research Triangle Park (NC). Caudill SP. et al.niehs. Int J Hyg Environ Health 2007. Bull Environ Contam Toxicol 2002. et al. McKee RH. Silva MJ. Giwercman A. Jedrychowski W.S. Caudill SP. Fourth National Report on Human Exposure to Environmental Chemicals 269 . Koch HM. Helm D.

500) . respectively.300 (.400-.300) < LOD .500) . 0.300-.400 (.400 (<LOD-.400 (<LOD-.500) 1.200-. < LOD means less than the limit of detection.2.500) < LOD 1.500) 1.400 (.500 (. 270 Fourth National Report on Human Exposure to Environmental Chemicals .10 (<LOD-1.70) .300-.90) .500-.500) < LOD < LOD .600) .300-.600 (.50) .200-.300-.9.300 (.00 (<LOD-1.500) .200-. only levels at or above the 90th percentile could be characterized.400 (.00-3. Neither IARC nor NTP has evaluated DCHP with respect to human carcinogenicity.400) < LOD 1.Phthalates Dicyclohexyl Phthalate CAS No.10) .10 (<LOD-2.300 (.300-.400 (<LOD-.500) . and 03-04 are 0. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.400 (.70 (1.300) 328 393 342 752 742 729 1461 1647 1534 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .300-.500 (.400-. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. population from the National Health and Nutrition Examination Survey.300 (.600) .500) 1. 84-61-7 General Information Dicyclohexyl phthalate (DCHP) is used to stabilize some rubbers.500 (.500) < LOD < LOD .500 (.200-.500) < LOD * * * Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1.400) size 2541 2782 2605 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .300 (.200-. In this Report.700) .300 (. People exposed to DCHP will excrete mono-cyclohexyl phthalate (MCHP) in their urine. and polymers. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Urinary Mono-cyclohexyl phthalate (MCHP) Metabolite of Dicyclohexyl phthalate (DCHP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.300-.700) . 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.700) .400) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.600) .300 (<LOD-. polyvinyl acetate. Survey Geometric mean (95% conf.400-.70 (1.50) . 01-02.500 (.500) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .500 (. Biomonitoring studies on levels of urinary MCHP provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of DHCP than are found in the general population.80) .400 (. see Data Analysis section) for Survey years 99-00.600) .200-.400 (<LOD-.900-1.400-. resins.300) < LOD .00) . and 0.400 (. including nitrocellulose.400) 1.300-.400) < LOD < LOD .S.500 (.20) . Finding a measurable amount of MCHP in urine does not mean that the levels of MCHP or the parent compound cause an adverse health effect.400) 1.10 (.200 (<LOD-.300-.400 (.600) < LOD . which may vary for some chemicals by year and by individual sample.00 (<LOD-1.400-.00-2. and polyvinyl chloride.400-.500 (.500 (.400-.300-.300 (.10 (<LOD-1.00 (<LOD-1.3.70) .600) .

420-.910 (.710) .450 (.330 (.22 (<LOD-1.470 (.17) .12-1.480 (.54-6.530) 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.S.36-1.310) < LOD .16) .500) 3.530-.510 (.260-.420-.360-.54) .67 (1.800-1.590 (.18) .10) .510-.420-.53) .500 (.770) < LOD 2. Survey Geometric mean (95% conf.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.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 .33 (<LOD-3.470) 3.05) .270) < LOD .33) .770 (.490) .770-1.74) .770-1.530 (.400-.82) .450 (.410 (.250 (. population from the National Health and Nutrition Examination Survey.16 (<LOD-3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.790-1.00) .14 (<LOD-3.660) .610 (.910 (.330 (.630 (<LOD-.380 (.740) .240-.06) .530-1.44) .310-.43 (1.00 (<LOD-3.220 (<LOD-.560) 1.170-.670 (<LOD-.950 (.770-1.500) size 2541 2782 2605 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th . Fourth National Report on Human Exposure to Environmental Chemicals 271 .830) 1.910 (.690) < LOD < LOD .620) < LOD .660) < LOD < LOD .54 (<LOD-2.350-.690) < LOD 2.530) 1.390 (.630 (<LOD-.690 (.500-.740) < LOD < LOD .500) 328 393 342 752 742 729 1461 1647 1534 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .690-1.370 (<LOD-.910 (.53) .590 (<LOD-.880 (.400-.34) .11) .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 1.290-.06) .940 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th 3.380-.670-1.82 (1.

01-02. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. a sample of young Swedish males entering the military had median urinary MEP levels that were somewhat higher than males in the NHANES subsamples. population from the National Health and Nutrition Examination Survey. 0.2.9 (61.3-110) 211 (160-278) 197 (159-243) 225 (187-270) 190 (164-219) 191 (171-214) 205 (176-238) 75. People exposed to DEP eliminate mono-ethyl phthalate (MEP) in their urine.7) 71. and also in men attending a Boston infertility clinic (Hauser et al. 2007). and 0.1-93. and hand lotions. 272 Fourth National Report on Human Exposure to Environmental Chemicals . deodorants..1 (71. respectively. particularly those containing fragrances. 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.3 (82. 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.9-92. colognes. 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.9. soaps. and 03-04 are 1.5) 81.Phthalates Diethyl Phthalate CAS No.2-102) 95. 2001-2002. 84-66-2 General Information Diethyl phthalate (DEP) is a solvent used in many consumer products.4 (62.S.. Workplace air guidelines for external exposure to DEP have been established by ACGIH and NIOSH.7 (70. interval) 179 (156-204) Selected percentiles ( 95% confidence interval) 50th 164 (136-201) 169 (141-194) 174 (151-208) 75th 454 (370-538) 465 (415-527) 502 (457-555) 90th 1260 (1010-1480) 1230 (1040-1440) 1380 (1170-1750) Total 178 (159-199) 193 (169-220) Sample size 2840 (2150-3770) 2536 2500 (1860-3220) 2782 2700 (2160-3310) 2605 95th Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 91.3 (74.. Products that may contain DEP include perfumes. see Data Analysis section) for Survey years 99-00.4.8-111) 85. shampoos. Biomonitoring Information MEP levels in the NHANES 1999-2000. Neither IARC nor NTP has evaluated DEP with respect to human carcinogenicity. 2002). In contrast. 2003) and African-American women in Washington.

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.6 (77.0-156) 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 . In an analysis of NHANES 1999-2000.9-110) 96. Median MEP levels found in a small sample of German residents (Koch et al. population from the National Health and Nutrition Examination Survey.Phthalates 2002 (Brock et al.2 (66.6 (65.5-114) 101 (87. 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. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. 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. 2003) were slightly lower than levels found in NHANES 2001-2002. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 2004). 2005)..5-113) 122 (93.0 (66.. 2002).3-105) 87.9 (82. 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.7-110) 81. Other population estimates also differed by sex and race ethnicity (Silva et al. Analysis of NHANES 2001-2002 showed similar findings. This age-related trend is opposite the direction seen for other phthalates..S. 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. 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.

Ryan L. Urinary levels of seven phthalate metabolites in the U. Silva MJ. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. 274 Fourth National Report on Human Exposure to Environmental Chemicals .Phthalates References Adibi JJ. et al. 112(5):A270]. Koch HM. Rossbach B. Third National Report on Human Exposure to Environmental Chemicals. Prenatal exposures to phthalates among women in New York City and Krakow. Barr DB. Angerer J. Silva MJ. Barr D. et al.22(3):688-695. Environ Health Perspect 2004. Hum Reprod 2007. et al. Reidy JA. Needham LL. Phthalate monoesters levels in the urine of young children. Hoppin JA. Jacek R. Duty S. Baird DD.110(5):515-518. Hilborn ED. Atlanta (GA).68:309-314. Caudill SP. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Drexler H. Perera FP. Hauser R. Davis BJ. 2005. Environ Health Perspect 2003. Environ Health Perspect 2002.112(3):331-338. Meeker JD. Jedrychowski W. Brock JW. Environ Res 2003. Malek NA. Caudill SP. Hodge CC. Poland. Brock JW.111(14):1719-1722. Silva MJ. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Bull Environ Contam Toxicol 2002. Singh NP. Camann DE.S.93:177-185. Centers for Disease Control and Prevention (CDC). Reproducibility of urinary phthalate metabolites in first morning urine samples.

0-84.70) 7.70-3.70-6.9 (26.31-4.0 (16.6) 15.80 (4.6) 39.3) 28.1982).80 (8. DEHP present in medical devices and parenteral delivery systems results in the diester rather than the monoester form being directly introduced into the blood. respectively.00 (5.0 (13.80-3.Phthalates Di-2-ethylhexyl Phthalate CAS No.10-5.00 (2.9.40 (4.80-4.0) 23. 117-81-7 General Information Di-2-ethylhexyl phthalate (DEHP) is primarily used to produce flexibility in plastics.9 (29.70-4.82 (3.26-2..20 (3.50-2.9) 13.89-3. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.51) 4.54) 4.67-4.4) 13.0) 31.6 (11.0-29.2-35.5) 32.10) 3.9 (15.80-5.40-11.1 (10. as glucuronide conjugates (Albro et al. packaging film.70 (5. Albro and Lavenhar.8-50.6-60.9-57.10-11.9 (13.90 (1.20 (4.40) 4.80 (2.10 (4.5-27.7-58.92-2.0-18.40 (2.9) 27.5-28. Four metabolites were measured in this Report: mono-(2-ethyl-5-hexyl) phthalate (MEHP).4) 33.5 (12.10) 3.5) 31.90 (4.0) 11.19-3.6-28.00) 1.7) 37.80-8.2.57 (3. DEHP is metabolized to more than 30 metabolites which are rapidly eliminated in urine.85 (3.9) 15.1) 25.32 (3.5) 40. MEHP is primarily formed by the hydrolysis of DEHP in the gastrointestinal tract and then absorbed. 1982.5-41.90) 4.S.60) 7.7-18.60) 10.9 (17.50-11.75-4.42-5.50-20.80-27.0 (9.6 (16.00-3.23 (2.3) 13.10 (3.40) 1.10-2.10 (4.10) 2.8-36.00) 9. and 0.5 (12.6) 14.40) 4.1) 29.90-8. 2002.5 (20. 1989.85) 4.40-12.10-3.84 (2.50 (3.23) 3.10-5.2) 6.9) 5.3-49.8 (19.6) 5.16-3.91-3.27 (3.5 (25.7) 6.2) 23.70 (1.60) 3.00) 5.40-9.50-5.5-17.1-17.43 (3.4 (13. mono-(2-ethyl5-hydroxyhexyl) phthalate (MEHHP) and mono-(2-ethyl5-carboxypentyl) phthalate (MECPP).90) 7.1-17. mainly polyvinyl chloride.00) 19.50 (8.1-27.6 (10. 1.3) 52.9 (7. and 03-04 are 1.50-16.3 (24.40 (6.20 (1.5 (31.92) 4.03-2.0 (18.8 (17.9 (16.10 (6.2 (31.5 (24.50 (3.50-6.70 (3.50-3. DEHP has been removed from or replaced in most toys and food packaging in the United States.6-130) 31.84) 3.4-27.94-3.49 (3.00 (7.40) 2.2 (11.2) 42.3 (11.27) 2.96-5.62) Sample size 2541 2782 2605 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 5.40) 75th 7.70-2.50-14.70 (7.40 (4.40) 9.1-48.9) 18.6-25.6-38.30-8.40) 8.92-2.9 (29.2-39.86) 2.1) 19.9-49.90-3. Urinary Mono-2-ethylhexyl phthalate (MEHP) Metabolite of Di-2-ethylhexyl phthalate (DEHP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.6 (9.50) 4.46) 3.5 (11.0) Total 4.8-47.56 (2.3 (15.0) 35.90 (3.5 (18.4-20.7) 35.41 (3.6 (12.31 (3.0.60) 9.2) 29.39) 3.80) 6.35) 4.37-4.0) 23.80-4.00-5.80 (1.5) 19.00 (4.10-4.24-4.70) 16.60-11.10) 4.00) 1.90-5.4) 22.70 (1.61 (3.30